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Contents

.......

Contributors
Preface
Acknowledgments .

1

1.3.5

xxlll

xli

.

1.4

1.4.2

1

Wesley

1.1.1 MotorAbnormalities.... 4
1.1.2
1.1.3

StructuralDisorders

....

Disorders

1.5.3

7

1.5.4 Tirmors
Wesley

1.1.4 InfectiousDisorders.... 8
1.2 Liver..

9

1.6.2

Wayne J. Farnsworth

9

1.6.3

David G. Heisig

1.2.1 Hepatitis

l0

1.6.4

David G. Heisig

1.2.2 Cirrhosis.
1.2.3

Prince
1.3.1 Cholecystitis
Louise A. Prince
1.3.2 Cholangitis
LouiseA. Prince
1.3.3 Cholelithiasis and

Choledocholithiasis. . . .
Louise A.

Prince

....

Inflammatory Disorders
Paul E McGuire

InfectiousDisorders

.

....

33
34
35
37
39

Paul E McGuire

Failure.

Gallbladder and Biliary Tract . . . .
Louise A.

StructuralDisorders
Paul F McGuire

1.6.5 Tumors

Hepatic/Hepatorenal
14

1.7

David G. Heisig

1.3

Paul E McGuire

33

Paul E McGuire

12

David G. Heisig

1.2.4 Tumors
David G. Heisig
1.2.5 Abscess.
David G. Heisig

32

P Eilbert

1.6 SmallBowel..
1.6.1 MotorAbnormalities....

Wayne J. Farnsworth

26

P Eilbert
Inflammatory Disorders 28
Wesley P Eilbert
Peptic Ulcer Disease. . . .
30
Wesley P Eilbert
Wesley

4

Wayne J. Farnsworth

1.1.5 Tumors

24

P Eilbert

1.5.2

Wayne J. Farnsworth

Inflammatory

23

1.5.1 StructuralLesions......

4

Wayne J. Farnsworth

Ilayne J. Farnsworth

Carcinoma

1.5 Stomach

Gary A. Johnson

1.1 Esophagus

20

Louise A. Prince
Tumors and
Louise A. Prince

I

Disorders

19

1.4.1 Inflammatory

ABDOMINALANDGASTROINTESTINAL
Chapter Editor: John B. McCabe
1.0 AbdominalandGastrointestinal

pancreas.

Louise A. Prince

xliii

DISORDERS

l9

Tumors

LouiseA. Prince

David G. Heisig
1.7.1 MotorAbnormalities. . .
David G. Heisig

14

15
.

17
.

17

1.3.4 Gallstonelleus........ 18
Louise A. Prince
vll

39
40

.

1.7.3 Colitis.

15
15

1.6.6 VascularDisorders .....
Bowel.

Large

42
43

David G. Heisig

1.7.5 Tumors
1.8

44

David G. Heisig

.

Rectum and Anus
llayne J. Farnsworth
Structural Disorders . . .
Wayne J. Farnsworth

1.8.1
1.8.2

Inflammatory

44

.

Disorders

45
48

Wayne J. Farnsworth

1.8.3 Tirmors

Wayne J. Farnsworth

50

viii /

CoNrrNrs

2

CARDIOVASCULARDISORDERS ....
Chapter Editor: E. Jackson Allison, Jr.

2.5.3 Ll,rnphatics

52

2.0

Cardiovascular Disorders
Marc C. Restuccia

2.1

Pathophysiology....
2.1.1 CongenitalDisorders....

52

2.6

Congenital Abnormalities of the
Cardiovascular System

2.6.1

FamiliaVGenetically

TransmittedDisorders.
RichardA. Craven

54

2.6.2

Marc C. Restuccia

2.1.3
2.2

Effects ofAging on
the Heart.

2.7

Acquired
2.2.1

57

Cardiac Failure .
John T Meredith and
Charles K. Brown

2.2.3

John T. Meredith and
Charles K. Brown
Ischemic Heart
65

2.9

2.2.4 Endocarditis

79

2.10

Michael K. Kerr and
Charles K. Brown
Valvular Heart Disease .
Michael K. Kerr and
Charles K. Brown

.

81

150

152

154

154

156

Robert L. Brown and

Wlliam J. Meggs

2.10.3 Rheumatologic

95

157

Robert L. Brown and
IVilliam J. Meggs

PericardialEffirsion/

Tamponade

2.10.4

96

John T Meredith
Diseases of the Conduction System
(Disturbances of Cardiac

Renal

.

158

Robert L. Brown and

llilliam

2.10.5

Rhythm).

98

John E. Gough and
E. Jacl<son Allison, Jr

J. Meggs

Toxic Exposures. . . . . .
Robert L. Brown and

.

159

Ililliam J. Meggs

2.11

2.4.1 Dysrhyhmias

100

John E. Gough and
E. Jackson Allison, Jr
ConductionBlocks. . . .
John E. Gough and

Treatment

2.11.1

Therapy.
.

160
160

Richard C. Hunt, and

111

Francis L. Counselman

2.11.2 PharmacologicAgents...

Jr

Acquired
2.5.1 Arterial

Modalities

Thrombolytic
Robert L. Brown,

Diseases of the Circulation,

ll4
ll4
2.11.3

Peggy E. Goodman and
Amy A. DeStefano
Pegglt E. Goodman

144

Diseases
94

John T. Meredith

2.5.2 Venous

142

Robert L. Brown and
lVilliam J. Meggs
Endocrine and Metabolic

John T Meredith

2.5

139

MyocardialManifestations
of Systemic Diseases
Robert L. Brown and

2.10.2

Pericardium

E. Jacl<son Allison,

.

Gary S. Setnik and
Arshad Khan
2.8.2 Chronic Hypertension . .
Gary S. Sernik and
Arshad Khan
PrimaryTumorsoftheHeart . . ., .
G. Richard Braen

Diseases of the

2.4.2

..

AcuteHypertensive
Crisis .

92

2.3.1 Pericarditis

2.4

.. . ..

Lltilliam J. Meggs

John T. Meredith and
Charles K. Brown

2.3.2

134

2.10.1 Infections

2.2.6 Myocarditis.
2.3

.

Gary S. Setnik and
Arshad Khan

2.8.1

David P Hightower and
Charles K. Brown

2.2.5

CardiacTransplantation .
Francis L. Counselman

62

Disease

131

RichardA. Craven

2.8 Hypertension

57

2.2.2 Cardiomyopathy

..

Disorders Due to
Anatomic Anomalies. . .

57

Marc C. Restuccia
Diseases of the Myocardium,

130

RichardA. Craven

52
52

Marc C. Restuccia

2.1.2 AcquiredDisorders.....

129

Pegg E. Goodman

125

Robert L. Brown,
Richard C. Hunt, and
Francis L. Counselman
CardiacPacemakers ....
Robert L. Brown,
Richard C. Hunt, and
Francis L. Counselman

161

163

CoNrnvrs
2.11.4 Surgicallnventions..... 165
Robert L. Brown,
Richard C. Hunt, and
Francis L. Counselman

3

3.2.4 Vir.f..
3.3

l7l
CUTANEOUS DISORDERS . . .
Chapter Editor: RichardVAghababian
3.0
3.1

Disorders
and
Ciottone
Dermatitis
Eric W. Schmidt and
Constance G. Nichols
3.1.1 Acne. .

Cutaneous
Eric W Schmidt
Gregory R.

Constance G.
.l

.2

3.3.2

172

3.3.3

172

Nichols

3.4

173

Dyshydrotic Eczema. . .

.

Nichols
3.1.6 Lichen Simplex
Chronicus
Eric W Schmidt and
Constance G. Nichols
3.1.7 Psoriasis
Eric W Schmidt and
Constance G. Nichols
3.1.8 Seborrhea
Eric W Schmidt and
Constance G. Nichols

3.4.5

174

l8l
181

Nichols

l8l
181

181

Douglas Scudder

3.5.2

174

ErythemaNodosum . . .

.

182

Eric W Schmidt and

174

3.6

Douglas Scudder
Vesicular/Bullous Lesions
3.6.1 Pemphigus/Pemphigoid.
Eric W Schmidt and

174

Scalded Skin

Syndrome

3.7

Cancers
3.7.1

182

E Siraco and

Constance G. Nichols
Basal Cell Carcinoma . .
Steven E Siraco and
Constance G. Nichols

.

3.7.3 Melanoma.
3.7.4

176
177

182

Schmidt and
Douglas Scudder

175
175
175

182

l(

Steven

175

182

.

DouglasScudder

3.6'2

Eric

Eric W Schmidt and

Nichols
3.1.10 Actinic Keratosis/
Photosensitivity
EricW Schmidt and
Constance G. Nichols
3.1.11 Nummular
Eczema.
Eric I4! Schmidt and
Constance G. Nichols
Infections
3.2.1 Bacterial
Eric W Schmidt and
Douglas Scudder
3.2.2 Fungal.
EricW Schmidt and
Douglas Scudder
3.2.3 Parasitic
Ericll! Schmidt and
Douglas Scudder

Nevi . .
Eric W Schmidt and

Erythemas
3.5.1 Erythema
Multiforme

Constance G.

3.2

181

Eric W Schmidt and

Keratoacanthoma...... 174

.

180

Douglas Scudder

3.5

Eric W Schmidt and
Stasis

Urticaria/Angioedema. . .

Eric W Schmidt and

173

Constance G.

3.1.9

180

Douglas Scudder

EricW Schmidt and

Constance G.

.

Douglas Scudder
PapularA'{odular Lesions
3.4.1 Epidermoid Inclusion
CYst . .
Eric W Schmidt and
Douglas Scudder

173

Eric W Schmidt and

3.1.4

Douglas Scudder
Purpura and Petechiae. .
Eric W Schmidt and
Douglas Scudder

Millium.

Nichols

3.1.3 Contact

Nichols

180

171

Eric W Schmidt and

Constance G.

180

3.3.1 PityriasisRosea........

Eric W Schmidt and

Atopic.

Constance G.

Douglas Scudder
Maculopapular Lesions

Eric W Schmidt and

Eric W Schmidt and

3

178

EricW Schmidt and

183

183

Steven F Siraco and
Constance G. Nichols
Squamous Cell

Carcinoma

184

Steven E Siraco and
Constance G. Nichols

Pigmented Lesions of
the Skin
Steven E Siraco and
Constance G. Nichols

BenignNeoplasms.'...
Steven

F Siraco and

Constance G. Nichols

184

185

/ ix

x /

CoNrBNrs

4.0 ENDOCRTNE, METABOLIC,AND
NUTRTTTONAL DISORDERS .........
Chapter Editor: John B. McCabe

4.1

4.2
4.3

4.4

4.5

4.6

4.7
4.8

tB7

Disturbances
187
Singer
4.1.1 Metabolic
189
Andrew Singer
4.1.2 Mixed Acid-Base
Disorders
192
Andrew Singer
4.1.3 Respiratory
193
Andrew Singer
Adrenal Disease
195
Mark D. Crockett
Fluid and Electrolyte
Disturbances
197
Daniel M. Joyce
4.3.1 Calcium
197
Daniel M. Joyce
4.3.3 Magnesium
200
Daniel M. Joyce
4.3.4 Phosphorus
201
Daniel M. Joyce
4.3.5 Potassium
202
Daniel M. Joyce
4.3.6 Sodium
204
Daniel M. Joyce
4.3.7 Water .
207
Daniel M. Joyce
4.3.8 Syndrome of Inappropriate
Secretion of Antidiuretic
Hormone.
207
Daniel M. Joyce
Hypernatremia 208
Daniel M. Joyce
Glucose Metabolism.
210
4.4.1 DiabetesMellitus...... 210
Sandra M. Schneider
4.4.2 Hypoglycemic
Syndromes
210
Sandra M. Schneider
Hyperglycemia....,... 212
SandraM. Schneider
Nutritional Disorders
217
Rob J. Edwards
4.5.1 Wernicke/Korsakoff
Syndrome
218
Rob J. Edwards
4.5.2, Vitamin Deficiency and
4.5.3 Vitamin Excess .
219
Rob J. Edwards
Parathyroid Disease
221
Tomer Feldman
Hyperparathyroidism .
222
Tbmer Feldman
Hypoparathyroidism. .
223
Tomer Feldman
Pheochromocytoma . . .
223
Michael A. Pellegrino
Pituitary Disorders
225
Jerry R. Balentine

4.8.1

panhypopituitarism. . . .

4.8.2

Jerry R. Balentine
Growth Hormone

Acid-Base
Andrew

.

Abnormalities

226

226

Jerry R. Balentine

Acromegaly

227

Jerry R. Balentine

4.8.3 Tumors
4.9

22].

Jerry R. Balentine

Thyroid

Disorders

228

Gary A. Johnson

4.9.1
4.9.2
4.10

Hyperthyroidism/
Thyroid Storm. .

22g

Gary A. Johnson

Hypothyroidism/

Myxedema

229

Gary A. Johnson

Endocrine Manifestations

Neoplasia.

of
229

Jerry R. Balentine
Syndrome of Inappropriate

DietaryHormone......

230

Jerry R. Balentine

Hypercalcemia

230

Jerry R. Balentine

Hypoglycemia

231

Jerry R. Balentine

5

ENVIRONMENTAL DISORDERS..... 233
Chapter Editor: E. JacksonAllison, Jn

5.0
5.1

Disorders

Environmental
Eunice M. Singletary
Diving Emergencies/Dysbarism . .
Eunice M. Singletary
Acute Gas Embolism . .
Eunice M. Singletary
Decompression

5.1.1

5.1.2

5.2

234

.

236

.

240

Sickness

241

Eunice M. Singletary
Submersion
E. Jacl<son Allison, Jr and

Incidents

242

MichaelB.Seim

5.2.1 NearDrowning........
5.2.2

5.3

.

Injuries.

Electrical
Gordian W O. Fulde and
Eunice M. Singletary

5.3.1

5.4

E. Jackson Allison, Jr
and Michael B. Seim
Cold Water Immersion .
E. Jackson Allison, Jr. and
Michael B. Seim

Lightning Injuries . . . . .

243

243

244

.

247

Gordian W O. Fulde and
Eunice M. Singletary

High-Altitude Illness .
249
Eric M. Kardon
5.4.1 Acute Mountain Sickness 251
Eric M. Kardon
5.4.2 High-Altitude Cerebral

Edema.

Eric M. Kardon

253

1. ..4 Reptiles. Levin and Vijai V Chauhan 326 6.1.1. 330 James M.3 MarineOrganisms..singletary 5.9. W John Zehner 6.3.2. Leonard 268 Poisonous Plants.1. William J.5 5. Singletary 6 HEAD.EYE. 6'4 .10 RetropharyngealAbscess 343 . W John Zehner Foreign Bodies W John Zehner 6..2 Gingivitis 339 W John Zehner 6.3.3.. .8. Robey III and Michael B. ' 6. .3. .4 Ludwig'sAngina...0 Hea4 Ear.EAR. Walter C.3.1. . 329 Mlliam J.2.. Jr 291 5. ... Levin and VijaiV Chauhan 6.3.7 5.15 Uvulitis. Singletary 306 5. I 343 W John Zehner I Sialadenitis 344 W John Zehner 6.3. .12 Sialolithiasis 344 W John Zehner 6'3'13 Stomatitis 344 W John Zehner 6. 285 285 5.1 Heat .1 Epistaxis Anterior.8 5. Kornegay. .1 338 . .. . .3 Labyrnthitis.... Levin and Vijai V Chauhan 6. 6. .3. 342 lT John Zehner 6. Thomas and Robert P Ferm 280 Smoke Inhalation. Kardon 259 Radiation Injury. Levin and VijaiV Chauhan 327 6.3.6 5. Singletary 303 5. EYe.8 328 328 William J.3..1 Ear. George Podgorny and Eunice M.3 Larynx/Trachea.9 Pharyngitis WJohnZehner 342 .2.. IVilliam J.3 5. 330 James M. 328 Itilliam J. .1 Arthropods George Podgorny and Eunice M.2 Cold. Levin and Vijai V Chauhan 327 6.3 335 James M.5 Mastoiditis William J.1... Levin and VijaiV Chauhan 326 6.. .. Levin and VijaiV Chauhan 6. . 308 JohnE.4 Rhinitis. James M. Robey III and Hervy B.1..2 Mammals George Podgorny and EuniceM. Levin and Vijai 11 Chauhan Otitis Media 6. Seim 298 5. .. Ralph B.9. 338 6..1 I Cellulitis IfilliamJ. . Jerry D. Leaming .9 Tympanic Membrane Perforations.3.3. 334 James M. . Levin and Vijai V Chauhan Otitis Externa lililliam J.. Leonard and Roy L. Levin 326 6.8 Peritonsillar Abscess . Levin and VijaiV Chauhan 6.5 Sinusitis 6.4'l 345 W John Zehner 345 .2. .. McCabe 6.6 M6nidre's Disease..1.NOSE. 6. . Oropharynx/Throat.2 Frostbite Walter C.9 Pulmonary Edema. GeorgePodgornyand Eunice M.3. James M. External Eye. Leaming 345 / xi . Leaming 6.. 332 333 James M...2 EpistaxisPosterior.8. Leaming 6.4 Malignant Otitis Externa 327 IVitliamJ. WJohnZehner '. Tonsillitis/ 6. 323 Throat Disorders . Ralph B..7 342 WJohnZehner Periodontal Abscess..9. James M' Leaming 6.3 Nasal Foreign Body . Eye.8.2 Nose. William J.3.7 High-Altitude 6.THROAT 323 DISORDERS Chapter Editor: John B. Ll'alter C. Nose. Leaming 6.. 339 341 W John Zehner 6. Alson Temperature-Relatedlllness.9. Robey III and Rffi V Terzian 302 Bites and Stings . ' 342 W John Zehner 6. . Leaming 6. 255 Eric M.14 Temporomandibular Joint Disorders 345 W John Zehner 6.6 Pericoronitis 6. Leaming 6.'.3.2.8.5 OralCandidiasis..Cox-rrNrs 5.4. .2.Gough 315 5..2 Foreign Bodies . Wtilliam J..

Billittier Robert F Reardon. Krause 8.5.... 357 James M..5 SerumSickness. . 395 Michael S. Jehle Transplant-RelatedProblems. Migden 7.2 Lymphomas Michael W Ardagh HEMATOLOGIC Hodgkin'sDisease.1 Anemia. Billitner Ill Robert E Reardon.. and Douglas R... Suchard 7.8.2 8... Jeffrey R.. Migden 7.. Leaming 6.1. 370 8. . Anthony J. 414 Susan P.. 401 HIV Disease/AIDS . 423 .6... Michael Jehovah's Witnesses and 388 Thomas Nowicki and 6.3 Platelet Disorders .5.3 ComponentTherapy.1 Clotting Factor Disorders Jeffrey R. Graham 8.1 350 DISORDERS Chapter Editor: G. ... . Krause Drug and Food Allergies 421 Richard S..2 Anterior Pole. . 387 IV and Migden . Jeffrey R.8 Hypersensitivity.4 Red Blood Cell Disorders 7. 414 8. Suchard 7.. Beeson 8. and Douglas R.5.1.3 8. 8.Suchard 7.. . W Ardagh Non-Hodgkin's Lymphoma Michael W Ardagh 7.5 Vasculitis 374 8.. .6. .1 Hemostatic Disorders JelfreyR. . Krause Allergic Rhinitis 421 Richard S.2 7. 401 Immune Deficiency Syndromes.1 372 397 ...4. and Douglas R.8. Basior 7. .. . Migden Alternatives to Transfusion of Blood Products Anthony J.3 PosteriorPole. 8.. Beeson Humoral Immunity. 422 Richard S... .2 369 8. . Preisz Acute Rheumatic Fever . 393 Thomas Nowicki and Marc Borenstein 361 8 362 IMMUNESYSTEMDISORDERS Chapter Editor: G.4.7 381 381 401 . Gregory A.. ..0 8. Richard Braen 7.8.4 von Willebrand's Disease Jefftey R. . . Douglas R.Preisz Collagen Vascular Diseases 399 Paul T.. . Beeson 396 Chemical 396 Mediators Michael S. Beeson 8.5 Transfusions. .. Leaming 7. Basior 7...2 Polycythemia Jeanne M. 392 392 Thomas Nowicki and 7.5. .1 Anaphylactic/Anaphylactoid Reactions 384 8.xii / CoNrrNrs 6.2 Disseminated Intravascular Coagulation. 354 James M.4.. Billittier Ill RobertE Reardon. Leaming 6. Jehle 8.6. Thomas Nowicki and Marc Borenstein 7.. Richard Braen 8. .4 361 Marc Borenstein MultipleMyeloma . White Blood Cell Disorders .4 Complement.1 381 Dietrich V K. MarcBorenstein Leukemoid Reaction. Jeanne M.7. 7. Disorders 395 395 Michael S.5. .. . 388 BloodTranstusion. 398 PaulT.3 Pancytopenia Jeanne M.4. Krause 9 SYSTEMIC INFECTIOUS DISORDERS 423 Chapter Editors: RichardVAghababian and GregoryA.4 Orbit. Anthony J.3 Immune System .1 Transplant Rejection.6. Preisz 8.3 Leukopenia.0 Systemic Infectious Disorders . Volnro .1 367 8.. Michael S. .2 Complications Anthony J.5 Cavernous Sinus Thrombosis 357 Peter W MaxweU 7 Leukemia 417 417 Richard S.2 373 39't.6 .. Krause Angioedema and Urticaria 420 Richard S. Basior 7. Billittier IV Robert E Reardon.8.Volturo 9.6.1...8. Suchard 7...5 371 Diseases Autoimmune Paul T. James M. ..4 387 . Suchard 7.. Dietrich V K.1.6 374 374 PaulT Preisz 8. Beeson Cellular Immunity Michael S.4.

4. Kocjancic 10. Singh 9. .5. 5ll Syndrome 5l I Lauren Pipas / x\ii . 495 Osteogenesis 10. 505 DiskDisorders ... Laura Peterson American Trypanosomiasis (Chagas' Disease)..2 10.3 . 430 9.4 9.. Kocjancic Low Back Syndromes. James D.1.. 426 Thomas Germano 9. Valerie Schevon Nicoletti 465 9. 10.7 Tetanus Ajeet J. . .5 Rania Habal Bone Rania Habal Cysts 499 Osteoporosis 500 10.5.3 Protozoan-Parasites .4 Mumps 492 (NONTRAUMATIC). Kocjancic .1. 424 9..5. .1 Lyme Disease 450 Thomas Germano Leptospirosis..8 Toxic Shock Syndrome.. Volturo 9. 9.4 9.1.6 Plague. Gregory 488 Laura Peterson Laura Peterson 9. Singh 483 Overuse 10.5. .9 Spirochetes 450 9. 444 Gregory A.1. . 424 ThomasGermano 9. Humanlmmunodeficiency 9..8 Rania Habal Bone Rania Habal 501 Spurs Paget'sDisease...10 Chlamydia. .3 501 Artlritis 467 501 Spine 10.. ..5 LauraPeterson Herpes Simplex Virus . .5.5 Thomas Germano Mycobacterial Diseases. .5. Volturo Gregory A. 9.2 Toxoplasmosis CoNrENrs Fibrositis. 501 10.1.1 Ajeet J..7 Osteomalacia 500 10. Lauren Pipas Muscle Strains Lauren Pipas Carpal Tunnel 5l I . ..2 JointAbnormalities.4. 489 MUSCULOSKELETAL DISORDERS 10. 9.. .5 487 Tendonitis 510 Bursitis 510 Lauren Pipas 485 Ajeet J. .3. .4 Infectious Mononucleosis. Valerie Schevon Nicoletti 9. 448 Ajeet J. James D.3.. ..5 474 Spinal Stenosis. 505 Ankylosing Spondylitis..2 GonococcalDisease. .4. McCabe l0. Ferraro Disorders of the James D.4.. ..1. . Kocjancic 10..2 470 10. . Volnro 10 9.3 472 James D. . 509 James D. Kocjancic 10.9.1 .1 Bacterial.. 453 Thomas Germano 454 9. 442 Gregory A.1..1.5.2 Syphilis.l Bony Abnormalities .1.1.4 486 10.5 Poliomyelitis of Imperfecta.1. Laura Peterson African Trypanosomiasis (Sleeping Sickness). Volturo 447 9. Thomas Germano 459 9.1.6 Rabies. .. Kocjancic 470 10.5.4. .4 Tumors 498 10.6 Rania Habal 10.3. 482 Ajeet J. Singh Influenza.4.2 9. Viral 9.1 469 Carl M.1.3. 507 James D. . Singh 509 Lauren Pipas 484 Ajeet J.. 10.. Laura Peterson 9. Singh Syndromes Lauren Pipas 10. Singh Laura Peterson 497 Rania Habal Valerie Schevon Nicoletti 9.1.3. .8 Roseola.2 Osteomyelitis 10.9 Varicella-2oster.3 495 Chapter Editor: John B.1 Malaria 9. 9.. .3 10.1..1 503 .4 Rickettsial 9.2.5.3..1.1 Botulism..10 A.. Singh 9.1. ...1. Ajeet J.9 9..9. 461 461 9.5.3.3 Sepsis .4.2 Ehrlichiosis.1 Aseptic Necrosis the Rania Habal Hip 10. . 434 .1.1 Rocky Mountain Spotted Fever.1. Rania Habal 495 10. .1..7 Rubella 496 Rania Habal Rania Habal Virus. 504 Spondylosis/Spondylolysis/ Spondylolisthesis .. Thomas Germano Meningococcemia.

..5 FlexorTenosyovitis. 516 Christopher J. .l.5. Robert C.3...3.2 Gangrene 515 Christopher J.2 Malformation Brunett Patrick Hemorrhagic Stroke . Michalakes 12...4.. 558 Robert C. . Eustacia Su Lauren SoftTissue NERVOUS SYSTEM DISORDERS. and Francis P Renzi Tumors of the Central Nervous System.. . Reiser FebrileSeizures. Michalal<es 12.3 CNS Shunt 549 550 Malfunction 514 10. 519 Patrick Brunett Cerebrovascular . Markus 10. Michalakes Pregnancy. 565 Philip D. 581 .2 .l Cerebral Aneurysm.3... ..1 Complicated Ectopic 12. Anthony Cirillo ll. Uncomplicated 581 582 Chris J. Gretchen K. Pipas 10. Chris J.5.3..6 11 Myositis Ossificans.2 Chris J.l.. Michalakes 12....2. Chris J. Markus 10. Reiser ll. Anthony Cirillo I1. l1.2 Trigeminal Neuralgia (Tic Douloureaux) 534 L.l2 Disorders 519 l1..1.. .5. .6. 585 585 582 Chris J.. .3 Abortion 587 Chris J.1.1 Seventh Nerve Palsy/ Bell's Palsy 532 L. . ..4 Transient Ischemic Attack . Hypertension.5.. . 551.l0 Headache 519 ll.4 10.1. 514 Christopher J. 521 Brunett ll. Marlan 10. Markus 552 Eustacia Su 11...6.. ...4. Chapter Editor: John C..2 CranialNerveDisorders. .. . .1.1 Necrotizing Fasciitis . 513 Eustacia Su 11. 513 11..I Muscular Dystrophies . Michalakes Subdermal and Injectable Contraceptives 12.6. DeFlitch. Gravidarum...2 Rhabdomyolysis.. 540 Eustacia Su I1.4 AbruptioPlacentae. . . 12. 516 ChristopherJ.l. Lipke.. Michalakes 589 589 590 . .2 Arteriovenous ll.. Anderson and Ron Medzon 11.2.. Reiser ll. Marhts 10. Reiser Alcohol-related Seizures 559 RobertC. .5 12.7 Lauren 10. ScottW Jolin 560 Christopher J.1 Contraception 578 Chris J.3 Paronychia 516 Christopher J. 542 Scott W Jolin 11. 512 10... .8.5 Muscle Lauren Abnormalities Pipas 10. .6 Chris J.l.3 Myositis Lauren Pipas I 512 L6 ll.6.3 12. Michalakes Hyperemesis Pregnancy.2 EpiduralAbscess..3 IschemicStroke. 525 Patrick Brunett I 1.0 Obstetrics and Disorders Pregnancy of 571- Chris J... Michalakes 12.xiv / CoNrnNrs 10..3 Demyelinating Diseases 536 L.. 531 PatrickBrunett ll. .. Anthony Cirillo 11. Pipas Infections.. Michalakes Intrauterine Devices ..4 Felon..9 Seizures 556 Robert C. Anthony Cirillo 11.2 Chris J. .l Peripheral L.l Status Epilepticus. Michalakes OralContraceptives.. . Lauren Pipas 512 11.. .1 Landry-Guillain-Barr6 Syndrome 542 Scott W Jolin 12 OBSTETRICSAND DISORDERS OF PREGNANCY 577 Chapter Editor: G. Michalakes pregnancy-Induced . ..l Brain Abscess 538 Eustacia Su 11. Richard Braen 12. Anthony Cirillo Visual Disturbances Due to Cranial Nerve Disorders 534 L. Moorhead Myasthenia Gravis .3. 532 L.9. Anthony Neuropathies 544 546 Cirillo AcuteSpinalCordCompression. Michalakes Placenta Previa Chris J.8 Hydrocephalus...3.6.. .5 Neuromuscular Disorders.5.5. 578 ChrisJ. Patrick 520 . . .

. Pundt Preterm Labor.4 Delivery 592 595 Membranes 12. J. . .7 Mark R.l0 13. Kerryann B.4 Pyloric Stenosis David T. . .6 . .1. .4. Nelson Neurosurgical Emergencies 13. Paula J. Appendicitis Jffiey 640 643 Jay Fisher Gastrointestinal 1 . Schweich and L. 681 Disease II E lliley 598 598 Kerryann B. 1 .3.7.1.1 Dysrhythmias 598 Kerryann B. 13.. Bachman and Craig W Lillehei 596 . 596 Mark R Pundt 12. Pundt Distress Fetal 1. Pundt RupturedUterus. Mark G.7. Pundt 12. Broderick 13 681 Brian A. . . Weiner and Mark S. .7 12. 730 733 / xv .1.3 Mastitis. Roback 605 607 686 694 Ketoacidosis . Hanly Neoplasms June G.3 Judith K.. Pundt FailuretoProgress .2 .8 Tucker Gastroenteritis 13. . Pundt Multiple Births ..1. . 12.4.1 RetainedPlacenta. Lucas Vaginal Bleeding in Prepubertal Females . Fleisher.5 Uncomplicated Labor. Broderick 12. Mason Cobb 598 598 667 Jacalyn S. .2 . .3 Inborn Errors Metabolism. 597 Section 654 654 Carmen Teresa Garcia 597 Stillbirth 650 . Complicated Dystocia Mark R. . Teach 13.. Pundt Postpartum 657 663 596 Mark R. . Chris J.3 ProlapsedCord.. . Gastrointestinal Bleeding Mark R.. . Mark R. Bates Acquired Heart James Kerryann B. Mark R.. . Manno Intractable Crying in Infancy 622 and Childhood Robert G. Bolte 630 Limp. 12.2. Pundt 3.4 12. Pundt Labor.2 Abdominal Pain in Donna M. .4 Hematology/Oncology 13.5. Manno 13. .. Broderick 12.4 June G. Bhisitlai Apnea Susan B.. .l 595 13. Manno Hyperplasia. . ...5. 12.0 Pediatric Disorders Endocrine/Metabolic . . Hanly Ventricular Shunts. Mary Christine Bailey.2 634 592 607 710 715 Meningitis and Encephalitis 715 Peter L. . Pundt Uterine Inversion . Chris J. .5.5 Mark R.5.2.1. 12.1 698 of 602 SickleCellDisease. Complicated . Corneli l3.8 593 Howard M. Mariann M. Mark R. June G.5. Vomiting.'7...2.5.11 Midgut Hemorrhage Endometritis 13.5. . 12. . Maller 597 Emergency Cesarean Complications 12. 13.3 Seizures 721 Douglas S.7. Etzwiler of 12. Pundt 12.8 HydatidiformMole (MolarPregnancy) .8.1 Congenital Adrenal 599 Mariann M. .CoNrrNrs Stridor.3. Mark R. . . Michalakes Guidelines for Describing Drugs in Pregnancy.3 Volvus 13. Kharasch Intussusception.2 Cardiac. Michalakes .6 12.2 Emergency Management of Diabetic Children 694 Mariann M.5 12.5.5 Neurologic 13. . . Manno 13. .2.. Mark R. Kristen J.4 672 677 13.1 Premature Rupture I2. Paddon Inherited and Acquired Bleeding Disorders ..'l Lisa S. 13. Broderick 12. Dehydration ..8.8. 13. l3. 701 707 707 . . 603 Debra L.. Mark R. . Korson 13.2 596 13.3 PEDIATRIC DISORDERS Chapter Editors: Gary R.3. Hanly 729 . . Stephen J.8 597 Sigmund J.8. Barnett 615 Tbrrey 618 Fever.3. . and Mariann M.l..'l .

8 David H.9 Sinusitis. . 777 MralExanthema..3 . Tbrrey Carol Ledwith 13.8. .6.. Infections 736 13. Perron 13. . Hanly Spinal Cord 13. David H. . Torrey June G. ... Richard Malley 13.7.7.9 Respiratory..12. Keneck 13. 13.6. .3 Osteomyelitis 13.7. . 782 Genitourinary. . . .6 736 739 Louis M. Dorfman PeritonsillarAbscess.2 Penile Problems . Fitzmaurice 814 . Tbrrey 742 Disease Cystic Richard M. Keneck l3. . . June G. Jr Legg-Calv6-Perthes Disease/Avascular Necrosis ofthe Femoral Head .2 Infectious Rashes . Hanson 47 777 . . Pewon 13. Carol Ledwith 13. .7. Fairley and Ralph M.8. ..6 David H. Dorfman 13. .. Dorfman 746 7 Tonsillitis .. .7 Pharyngitis and 13.12 Skin and Soft Tissue Infections .12 Tracheitis/Bacterial.7. Hanson 13. Fairley and Ralph M.. . David H. Fairley and Ralph M. Laura S.. Hanson Mananda S.l Juvenile Rheumatoid 742 Carol Ledwith Traumatic Pediatric 13. Germaine Brent Nephritis and Nephrosis . 775 Ochsenschlager 744 David H. . Pneumonia Susan B. Alison St.10 l3. Dorfman 13. .3 TesticularProblems. .8. Perron 13.. 735 735 13.3 Depression/Suicide. Bell. . Dorfman 13. 786 Catherine E. Fairley and Ralph M. Baruch S. 741 Carol Ledwith Septic Joint... Hanly 13. 797 749 749 ..l l. Pinkert .:. . Richard Malley 13.5 BehavioralDisorders.. Hanson June G. . Hanly PseudotumorCerebri.6 Tumors 759 Tamara Ingrid Pottker and 742 Toxic Synovitis. 13. Krauss Pediahic Human Immunodeficiency Virus 750 (HIV) and Acquired 751 Immunodeficiency Syndrome (AIDS).4 774 Daniel Warne 13.. . Germaine Brent Sexually Transmitted 787 788 791 747 Diseases 793 748 Alison St. . . . . .4 759 Lower Respiratory Tract Compression.9. Dorfman 13 . Ruddy 13.4 (Croup). Dorfman 13...7.2 Eating Disorders. Dorfman Otitis Externa David H. 765 Eileen A. .l I 743 743 Purpura.7.13.8 Psychiatric Michael J. Bell. . Jr Slipped Capital Femoral Epiphysis 13. ..7 761 Pertussis Bacteremia and Richard Bachur l3. Keneck Henoch-Schiinlein Eileen A.xvi / CoNrnNrs 13. 744 746 David H.. 13.6 Orthopedic 13..7 .9.7. Catherine E. .3 Orthopedics Fibrosis Susan B.4 Urinary Tract Infections .6. .6. .6.. . . Bhende Pediatric Sedation. Michael J.6. 741 Louis M. ..7 Carol Ledwith 13. 752 Newborn Resuscitation in the Emergency Department . . .9. .5 Nasopharyngitis (Upper 13. Pressure 13. Cerebrovascular Disorders 734 June G.2 755 Michael J. Dorfman Otitis Medea David H.5 758 Susan B.6.1 753 Michael J. . 772 Eileen A. ..ll. Hanly Increased Intracranial .3 767 Meumatologic.12. 802 807 Heidi M. Dorfman 13.13. . . Catherine E.13. David H.7 13. Keneck Lyme Disease Eileen A.1 Epiglottitis Sepsis Arthritis Carol Ledwith Osgood-Schlatter HeadandNecklnfections ... .. . David H. .13 Laryngotracheobronchitis RespiratoryInfection)... .

1 Glomerulonephritis. 837 866 866 Tanvir M.6 Addictive ..1 818 Disorder 821 Pamela Edwards and Katherine Thomas Chapter Editor: John C. Nephrotic Syndrome. .2. Edwards and Katherine Thomas 14. .3 14.5 847 847 849 15.. 15.3.2 MoodDisorders. 82'7 Disorders 15 RENAL 15.3 AntisocialPersonality 8T7 867 Tanvir M. .3 Renal Obstruction.3.2 BulimiaNervosa. Dara 839 15. 14. . Pamela J. . Dara Adenocarcinoma of Prostate. 854 15.7 847 Angeline D. .2 . Hong and Leonard Gomella 15.3 Katherine Thomas 14..3. Katherine Thomas Opioid Katherine Thomas Eating Disorders. .CoNrrNrs 14 14.2 DISORDERS Gerald Patrick Igoe Behaviors Drug Abuse. Dara .0 15. Edwards and Katherine Thomas 845 Chapter Editor: G.6. Krause 831 Nephritis Acute Interstitial Ronald M. Hong and Leonard G. 15.1. 866 . Gerald Patrick Igoe 831 Abuse 14. 856 . Obstructive Uropathy and 15. 15.. 857 857 ..7..4 14. Hong and Leonard Gomella 15.2. Dara Tumors of the Urinary 838 Collecting System.6 . . . Nephroblastoma... . ..1 840 14.4 Katherine Thomas 14. Gomella Structural Disorders 15.. Pamela Edwards and Katherine Thomas 847 853 830 831 Disorders Katherine Thomas PersonalityDisorders Pamela Edwards and Katherine Thomas Renal Disorders Robert D.. 862 Gerald Patrick Igoe Acute and Chronic Renal Failure and Interstitial Tirbular Necrosis Acute Renal Failure . Nichols 868 / xvii . . . ..3.2 HistrionicPersonality Schizophrenia Katherine Thomas 14.. Moorhead l4.4.'7.. BorderlinePersonality Disorder (BPD).2. . Edwards and Katherine Thomas Posttraumatic Stress 830 Disorder 830 Pamela J.1 .. . Richard S.7 Tumors... 834 . Katherine Thomas 824 Katherine Thomas Criteria for Manic Anxiety IntoxicationandWithdrawal.3..8 Complications of Dialysis Constance G. 15. . . . Tanvir M.1 Pyelonephritis GeneralizedAnxiety Disorder and Phobias . 867 Renal Cell Carcinoma. . 14.5 Substance Abuse 833 .6. Edvards and Katherine Thomas 14..3.2 Infection. Dependence Disorder Depressive Episode.. . Katherine Thomas 841 Katherine Thomqs Criteria for Substance Katherine Thomas 14.. Robert D. . .1 Obsessive-Compulsive Disorder Pamela J.1.1 PSYCHOBEHAVIORAL DISORDERS Disorder(ASPD) . Richard Braen 827 Pamela J. . Thought Disorders Katherine Thomas 817 Pamela Edwards and Katherine Thomas 14..1 Renal Calculi Robert D.2.7. . Katherine Thomas Criteria for SubstanceAbuse . Krause Chronic Renal Failure. Katherine Thomas Diagnostic Criteria forAnorexia Nervosa . Edwards and Katherine Thomas Panic 841 826 Katherine Thomas Criteria for Major 14... . Richard S.. .8.1 Disorder 828 Pamela J. . Moscati 864 15. ..1. Brunetto Glomerular Disorders. . 838 Tanvir M.1. 14.l 14. Katherine Thomas Diagnostic Criteria for 845 849 849 15.2 MajorDepressive Disorder Bipolar 822 Episode. ..

Jackson Allison.. Jr.. Garry J. Garry J. Beveridge 16.7.1 Asthma 912 912 Eric S. 16.9.2 891 16...8 892 16.6.2 Tumor.1 931 16. Kathleen A. 905 16.. ... PulmonaryEmbolism/ Infarction Mediastinitis 16. Mediastinum. Thomas Contents Stephen H. . Jacques S. 903 . 16. Crespo 16. llilkes 901 16. Andrew T McAfee and Rita A. . BrinsJield Disorders of Pleura. Aspiration of Gastric PulmonaryHypertension David Langleben and Kathryn H. Steven G. James and 933 Stephen H. lVilkes 16.. Beveridge 899 16.12 16.9 Viral.. Robert E McCormack NoncardiogenicPulmonary Edema/Adult Respiratory Distress Syndrome.1 Environmental/Industrial Exposure. L.1 Costochondritis. . Manfredi 949 Garry J.2 Fat.6 16.10. 933 Stephen H.4 948 .2.3 Foreign Bodies Stephen H.2.. 16..6.8 Tuberculosis Garry J.4 945 Thromboembolism.3 ChronicObstructive 16. Brinsfield 16. Thomas Kathryn H.7. . Thomas N. Nadel and Rita A. 894 James Ducharme and Robert C. Wilkes 16.. Thomas Thea L... 928 16.13 .10 PulmonaryInfections Pleurisy.5 Pulmonary Disease.3..4 Lung Abscess Garry J..5 Septic James Ducharme and Robert C.3. 93s James Ducharme and Robert C.3 896 898 Empyema James Ducharme and Robert C.. . 16.6.3 939 Jimmy B..l0. Lee 974 . Sivilotti Pulmonary Tumors Marco L.A. . Tracheostomy/ Complications 890 16. Thea L. James and 16. Jn 16.5 Pneumomediastinum. Manfredi 16.11 ThoracicOutletSyndrome.3 .. and Chest 934 .. Heramba Prasad and E.. .7 .6.6 908 Todd C. PleuralEffirsions/ Stacey Sperling 16. l6. Brinsfield . Manfredi 16. James and Kathryn H... Rothenhaus Obstructive/RestrictiveLung Disease.7 Pneumothoraces .1 Venous Thea L. Gutman 893 . . . Wilkes 16. 950 962 963 963 . Marco L... . 923 .. . .9. 901 .xviii / CoNrsNrs 16 THORACIC-RESPIRATORY 16. 16.. Wlkes Bacterial Garry J.10.6 Opportunistic Garry J. Raftery InterstitialFibrosis .3. Kristian Arnold 16..3. James Ducharme and Robert C.5 Bronchiectasis Garry J.2. . Beveridge 16. ..1 ChemicalAgents. Wilkes 16.9. 10..3.A. Jr.1 Acute Upper Airway 873 Obstruction 874 16.2 Bronchitis 920 Kathleen A. llilkes 16.2 BreastDisorders.6.. . Brinsfield 16. James and Fibrocystic Diseases Thea L. Beveridge Steven G. Beveridge L. Kristian Arnold 16. 16.. Sivilotti Sarcoidosis.4 AmnioticFluid. . .10. Heramba Prasad and E. . Wlkes 16. 892 16.7 N..7 Septic Emboli Garry J. Crespo 16.6 DISORDERS Chapter Editor: E. .3 Mycoplasma (and Other Atypical Agents) Garry J.10.. 16. Stacy Sperling Hyperventilation Syndrome .9 Kathryn H. Crespo 16. Jackson Allison.2 Fungal. Nicole Bruner and Rita A.9.. Manfredi Physical and Chemical Irritants/Insults.2 Mediastinal Masses.l Stacy Sperling ....3.3 Infections 893 Wall L. Mlkes 16. Wilkes 16.. Raftery and Rita A.10.3.. . JacksonAllison..10. Steven G.10..1.

... Chapter Editor: Chrislopher Keyes 17.1 4.12 1097 David B. lI57 Robert W Wolford and Lance K.22 Household Industrial .. . 976 17. Lewis S.2.2.. Geller 17. Dreschet Marc Bayer and Charles A.. and Robert Skoglund Heavy Metals Kimberlie A. 1010 Caustics Alcohols Cocaine.6 Anticonwlsants. ll43 . . Bates 1063 17.34 MushroomToxicity. .4. 1072 for Toxicologiclnformation 17.2.23 Steroid and Thyroid Richard J. Graeme.2.5 1081 Robert W Derlet 17.14 Curdiouur. . Chandler Robert 0t4 Christopher Keyes Anticoagulant 1'7.Drugs . Ferndndez Intoxication and Overdose . Cyanide Salts. . 1045 Intoxicationby AntiparkinsonDrugs.2 Agents .1 Poison Centers: A Resource Guide Sandra 981 Vivek Chander 17. . 17. .2. 1048 17. .24 17.2 Centrally Acting Jacques S.ulu. Jimmy Quir6z Rodriguez Antihistamines . 998 Mahesh Shrestha 17.2 Monoamine Oxidase Inhibitors-Toxicity .1.31 Toxic and Irritant Gases Robert J.2.2.3DigitalisToxicity.2. . Steven C.14.7.. Judith Kassner Lucas 17...2. 1051 1054 Saundra Gilfillan l7.3 CyclicAntidepressants ... Lee Antihypertensive l7 TOXICOLOGIC DISORDERS . . Freeman Hill 17. . Smeel<s ll34 and Leslie R.' . . McKaY and 17.2. . 17 .2..20 and Robert Skoglund Toxicologic Information Resources Equipment 1028 Rodenticides 1107 l'l . . Lugo 17. .. . .ll Bronchodilators. . 1061 17.2.25 Hypoglycemics/Insulin. . and Christopher Keyes 1041 Robert L.17 Hydrogen Cyanide.30 Locally Acting Drugs . Douglas M..... Rosen Jackson Smood t 1075 Christopher J.10 Miguel C.4 HydrogenSulfide.2.2.3 Gastric Decontamination.13 Carbon Monoxide Poisoning Hydrocarbons Frank C. ll45 ..2.2. Lithium. Hill 17. Wolf .33 Methemoglobinemia. 992 Maria I. 1079 Patricia B.2..2. McKaY 17. .32 MarineToxins. Curry.. 984 Charles A. Poisons 1032 1035 1122 Andrds M.2.7.7. .2.8 Hazardous Material Spills 1090 David B.' . . with AntiPsYchotic Agents . Neil S.16 Wu 17.14 Sleep Apnea Syndromes..2. Douglas M. . Norton Douglas M.9 17.. RoY. Smill<stein Michael lil'ainscott 17.2... 1130 17. .2.2.1. . and Robert Skoglund Personal Protective 1026 Robert Rodriguez 17. Nelson 17. 17. Warden 17. 1005 John E HaYnes 17.2. 1139 Kim Sing 17.5 Withdrawal Syndromes. . 1148 I 153 Collin S. . .3 Analgesics/Anesthetics.. Chandler Robert RoY. DeFlitch Diagnostic Modalities for the Toxicologic Patient .2.2.14.4 Calcium Channel Blockers L. Cannabis. . ll2'7 Lena Williams.1 Acetaminophen.CouuNrs 16. Jones Hill Toxicity of the Anticholinergic Agents .2. . l't. . B..2. Meehan 979 1064 Michael J. 17. .2 1069 lT. David B.2.1 1085 Ross E....2. ..1.1. ll59 Christopher Keyes and Harold W Keller . ...1..29 LocalAnesthetics .2.15 Alan H.2. / xix 1069 l7 . and Craig R.27 Iron. Chandler Robert Shu Shum 17.2..2. ... Kozak and Hormones Martin J. Goto Brian A. . and 1113 Michael Shannon 1030 17. . Rudis and Christopher KeYes 17.21 RoY.3 Toxidromes: An APProach to the Poisoned Patient . Gffin 17.. ...

Smood Computed Tomography Scan. 1164 Organophophate Poisoning Oliver L. Rama B.1.2..2. Moorhead Ultrasonography . Lipke Ophthalmologic Trauma Gretchen K.1 Plain Radiography l20l StevenA. .Volturo 18. .l ..39 18. Volturo and . ..3 Resuscitation and Stabilization 1194 RichardVAghababian and Gregory A.vis S. Richard V Aghababian Gregory A. Rao and Lewis S.Y.12.4. the Emergency 18. DiCastro Richard S. ... . La. ll92 RichardVAghababian and Gregory A.4. Physiologic..5. Nelson 18.4.2. . George Kondylis and Kevin M. . Cutaneous Wounds and Injuries 18. .40 Sedative-Hypnotic Drugs 1203 StevenA.. Gregory A.17 DiCastro Genitourinary Trauma . Burnhamand RichardJ.Volturo 18.1 Spinal Fractures . Panacek AbdominalTrauma. Diagnosis and Treatment in 18. Mullins 18.2. Warden 1204 StevenA. ..2 Triage .13 ExtremityTrauma.1.1. Volturo 18. Volturo. Jackson Bryan 17.4. James lZjT F Holmes and Edward A.37 Nonsteroidal Antiinflammatory Drugs. 1238 Maryanne lI1 Lindsay Specific Abdominal Injuries 1244 MaryanneW Lindsay 18. 1250 18.2 Contrast Radiography . Lipke Otologic Trauma 18. 18.7.0 Traumatic Disorders .2.. 1192 18.. .8. Nelson 17. I2l7 Gretchen K. ll72 17..4.2. Nelson 17. .. Penetrating Neck 18. 1198 Richard V Aghababian and Gregory A.11 AbdominalTrauma. .4.1.1 ll77 James H. Volturo l8..6 Il74 18 1183 18.9 Indications for Consultation ll97 Richard V Aghababian and Gregory A. Volturo 18.. Hartoch Facial Fractures. DiCastro 18.. l2l0 1210 Armida Nufiez-Finley and 18.10 ChestTrauma Lilly 1229 C. Craig R. 1204 A. l22l 1223 Trauma 1224 ErinM. Lee and RichardV Aghababian 18. 1166 Steven 18. Panacek 1278 . Panacek 18.36 17. 1204 DiCastro Trauma. Head 18.4..11 Injury Prevention and Control 1198 RichardV Aghababian and Gregory A. DiCastro Steven A. 1200 Steven A.4.4.1 . .7 Gretchen K.4. 1196 Richard V Aghababian and GregoryA. Upper and Lower . James E Holmes and Edward A.2.2. Ciottone Steyen A... Klauer .1.4.2..5 1265 1267 Neil S.. Lipke 18. 18.. Meehan Trauma in Pregnancy 1277 James E Holmes and EdwardA...4 Angiography. 1202 Steven A.. DiCastro Magnetic Resonance Imaging .5 Salicylates.4.4.2.. Volturo 18.. Lipke 18..3 RobertW Derlet and James E Holmes Injuries of the Spine . 18.5 SoftTissueFacialInjuries 1220 18. DiCastro 18. .38 Opioids and Opiates .3 .. .2 . and John C.10 Disposition from the Emergency Department.41 Stimulants.4.5 TeamResponse. .1 Anatomic.9 Laryngotracheal Injuries 1228 Gretchen K.2 Radiologic Evaluation of the Trauma Patient. .1. 1261 18.x / CoNrnNrs 17. and Laboratory changes with Pregnancy.6 1192 18. 18. 1205 . . I 193 Richard V Aghababian and GregoryA..4.8 Departrnent..8.DiCastro 18.1 PrinciplesofTraumaCare. .2. Gregory R. Hung and Lewis S.4 TRAUMATIC DISORDERS 1191 ChapterEditors: RichardVAghababian.4.15 PelvicFractures. .4.1.. 16 18.. Volturo 18. .3.2.4.2. ..

.l and Richard C.1. B.3 1336 MichaelRapp Disciplinary Policy .1 Committees. 20 ADMINISTRATMASPECTS OF EMERGENCY MEDICINE Chapter Editor: John C. 20. Ililliams. Michael Rapp . Brinsfield 19. Panacek 1313 Improvement. . E. .4. James E Holmes 1324 Christopher M. .4 Cervix.4. 1329 Robert W Derlet.1.1 Faculty Development.1 OvarianDisorders. Panacek l3l7 Continuous Quality MaternalAbuse..1. Gary P Young.6. Fernandes andA. Bennett and G. E.l . 1336 MichaelRapp 20. Jehle 19. JuanA. 1280 Informatics James E Holmes Todd B. .9. . Jacl<son Allison. Kathryn H. l31l 2l EMERGENCY MEDICAL SERVICES/DISASTER MEDICINE.6 1282 Hospital Administration 1327 Michael Rapp 20. Jr. .9 Kristi Vaughn Medical Staff. Nicholas J. Restuccia. March. Jr..9.. and Richard C. . Hunt / xxi .0 Emergency Medical Services /Disaster .l. 2l. Panacek 1328 Michael Rapp EdwardA. 19 UROGEI\-ITAL/GYNECOLOGIC 1285 DISORDERS Chapter Editor: G..1 Chancroid DietrichV K. .6.. James E Holmes and Edward A..1 Academic Emergency Medicine. 1335 20...2. Jr. Juan A. 20. 1280 and EdwardA. .2 Genital TracVMale 1295 19. . 1290 Brinslield 1295 19. Jehle 19.2 Governance.3 Structure 1329 Michael Rapp Managed Care .1. Moorhead. Jackson Allison.1. Jr.9..3 Sexual Assault Mary K. llilliams. Kenneth A.4 Structure.9. 1287 Kathryn H. .. Restuccia.5 Infectious Disorders . 1338 Michael Rapp Kathryn H.1.. JacksonAllison. Marc C. Richard Braen 1306 19. 20. Panacek James E Holmes N.2 Granuloma Inguinale. E. .. .4. Juan A. Richard Braen 1285 l9.2 Categorization and Organization 2l. and Edward A. Panacek Emergency Department Perimortem Cesarean 1283 Section James E Holmes and EdwardA. Jackson Allison. Jehle 1309 19.2. Brinsfield 19. 1299 Michael DiBella 1301 19. and Richard C. and John R.3 Uterus.. Marc C. . March.2 Genital Lesions Dietrich T K. . l3l I . Brins/ield 1290 19.1 Congenital Michael DiBella 1297 19. Medicine Kenneth A. Marc C.. Taylor and Edward A.2 Credentialing 20.2..2 Research. Roy Magnusson Evaluation and History . Chapter Editors: E. Marc C.3 Inflammation/Infection. 20.1 Departmental Interaction 1328 Michael Rapp 20. Hunt 21. Panacek Fetomaternal Hemorrhage James E Holmes and 1280 20. Kathryn H. JacksonAllison and Richard V Aghababian 21. Jouriles 1311 .1..2 Stn:ctural Michael DiBella 19.. . Brinsfield . Jehle 19. L34l 1342 llilliams. Wlliams. 1337 Michael Rapp 20. March. and Richard C. .CoNrENrs Burns . Clay Mann Automation and Electricallnjuries.6. Restuccia.4. . Juan A.l Genital Tract/Female Kathryn H. . Brins/ield 1287 19. 1285 Kathryn H. 1309 Dietrich V K. . E. Hunt 1342 EMS System 1342 System Components .1.1.. Designation of Levels of Service 1344 KennethA. Restuccia.3 CondylomaAcuminalata 1309 Dietrich V K..2 VaginaandVulva. Hunt 21.. 1279 20.. Richards Discharge Planning/ 1334 Case Management .3 Specialized Care Centers 1344 Kenneth A. March. .

21.2.5.. Kennedy 1355 Appendix:TheCoreCurriculum Subjectlndex. Kennedy 1345 A. Kennedy Radiation Exposure 1349 N. E. .3.. Taryn E.8 Critical Incident Stress Debriefing(CISD) . and Richard C.. Jr. Restuccia. Kenneth A. Patient Care Protocols..4 Medical Supply/Equipment 21.1.3. 1360 Casualties 1350 N. Heramba Prasad and John E. ll/illiams. Biologic. 1362 1347 Marc C.2.3.. Kennedy N.. Hunt for 1366 Taryn E.4 .. Jr. and Toxicologic Medicine l3j0 Kevin S. Heramba Prasad and John E. .5 1358 Phuli L. 1364 A. Juan A.2 1357 Lucille Gans Pediakic Casualties. PulmonaryCasualties. Heramba Prasad and John E. Jackson Allison..2. .4.3.xxii / CoNrrNrs 21. 1353 Children). Roth DisasterEducation ..4.2 . .4 Blast 1353 Safety. Juan A. Hunt 21. Gaffiey and Paul B.. . March.. March. JuanA. JuanA. Training EMS Continuing 21..1 Communications Crush Syndrome/Injury......3 . Jackson Allison. 1349 21.5 Research 1393 Assessment of New Methods andProcedures.. Gough 1396 Lucille Gans and Richard C. l38l 1385 John K.. E. and Richard C. Kenneth 21. Heramba Prasad and John E.. Restuccia. . Cohan 21. Burkle.1 CardiopulmonaryResuscitation.. Hunt 1354 21. Hunt Medical Control 1348 Kenneth .5..4 AssessmentofEnvironmental.3 EMSEducation.4..5 John K. .3 and Richard C. Lucille Gans System Kenneth Disaster Medical Care..4. Jackson Allison. David E. . .. Marc C. Taryn E. EMS System 1345 Kenneth A.. Restuccia. 1399 l43l ... Hunt Lucille Gans 21.. and Richard C.. Gough 21. llilliams. E. Shock and Its Treatment inFieldSituations. A.2.. 21.1 HealthCareNeeds l3i4 Lillibridge 21.4... . and Richard C. yeskey 21. Marc C. Gaflney and Paul B.1 Rapid Assessment of Emergency . First Ai( and EMS EMT . Jr. . Hunt 21. Hunt Gsting of New Equipment and Technologic Advances t354 N.. Jr. Kennedy MassBurnCare Lucille Gans Marc C..2. Hunt 21.5... Lucille Gans and Richard C. 1347 . .3 135'7 CompartmentSyndrome 1359 Marc C.4 N. . 13 87 Frederick M. Hogan and Lester Kallus Services .4.3. Williams. E. .3. Restuccia. Taryn E.. March. . Disasterlnformation 21. 21. Gough Injury Prevention and Education Management After Disaster Scott R..3. Mlliams. TransportVehicles.3 DataCollectior/Analysis 1396 Lucille Gans and 1354 Richard C...2 Operations.. Jr.6 N. Hunt 21. JuanA..2 Richard C. Heramba Prasad and John E... Gough 21. Taryn E. Jaclcson Allison. 21. Restuccia. Heramba Prasad and John E.. Gough Hazards.4. AwarenessTraining.. E.5 Public Health Issues Teams(DMAIs). l37B DisasterMedicalAssistance 21.. Ililliams. Roth 21. Gough EMS-C (EMS Disaster Injuries..7 InternationalRelief Assistance. Jr.. March.. March.4. 1395 Lucille Gans and 1353 21.. Jaclcson Allison.4. 1368 21.

M. M. Massachusetts Associate Professor of Pediatrics University of Vermont College of Medicine. Victoria 3 0 5 2.D. JacksonAllison. NewYork 14203 xxiii . tructor of Pediatrics Harvard Medical School..O. Barnett. J.B.D. Division of Emergency Medicine Childrenb Hospital Ins 300 LongwoodAvenue Boston. Professor and Chairman Department of Emergency Medicine (Jniversity of Massachusetts Medical Center 55 Lake Avenue North Worcester.D..D.D. Massachusetts 021 I5 Mary Christine Bailey.Ch.H. M.D.D. Barnabas Hospital 4422 Third Avenue Bronx.. NewYork 10457 Peter L. M.Alson. Department of Emergency Medicine Maine Medical Center 36 Oalonont Drive Falmouth.D. University of Pittsburgh Medical Center 230 McKee Place.P. M. M. As si s t ant C linic al P rofe s s or Department of Emergency Medicine Boston University School of Medicine Boston Medical Center 818 Harrison Avenue Boston. M. Associate Director and Assistant Professor Department of Emergency Medicine Philip D. Deputy Director Department of Emergency Medicine Royal Children b Hospital Flemington Road Parkville. Bachman. Massachusetts I 0 65 5 E. Anderson.B. Aghababian. New Zealand L. Massachusetts 02 1 l 8 St.Contributors Richard V.B.D. Balentine. Jr. M.Sc. North Carolina 27 I 5 7. Suite 400 Pittsburgh. Basior. Clinical As sistant Profes s or Department of Emergency Medicine School of Medicine and Biomedical Sciences State University of New York at Buffalo Buffal o G eneral Hospital 100 High Street Buffalo. Maine 04105 I 65 5 Michael W. Ardagh. Australia Jeanne M. M.B. Senior Lecturer in Emergency Medicine Department of Emergency Medicine Christchurch School of Medicine Private Bag 4710 Christchurch.I 089 Clinicql Instructor Department of Emergency Medicine University of Massachusetts Medical Center 0 Richard Bachur.Ch. Clinicql Professor Department of Emergency Medicine Executive Vice President and Chief Medical Officer Emergency Res ource Management.' D. D. M. Inc.S. Kristian Arnold. 55 LskeAvenueNorth Worcester. M. David T. Massachusetts 02 I I 8 Jerry R. Ph. M. M. Assistant Professor Department of Emergency Medicine Bowman Gray School of Medicine Medical Center Boulevard Winston-Salem.D. Pennsylvania I 5 2 I 3-490 I Roy L.. Division of Emergency Medicine Childrenb Hospital 300 Longwood Avenue Boston.

Methodist Womenb and Childrenb Hospital 8 I 09 Fredericksburg Road San Antonio.v. Massachusetts 02 I I 8 . M. Program Director of Residency in Emergency Medicine Vice Chair of Department of Emergency Medicine St. M. M. Richard Braen. Beeson.Sc. Virginia 2 3 5 07 Anthony J.D. M.D. Canada Mananda S.B.. All Childrenb Hospital 801 Sixth Street South St. MC-5380 263 Farmington Avenue Farmington.D. Bhisitkul. Director Children's Emergency Center Donna M. Florida 3 37 3 I -892 0 Kathryn H.v York I 00 I 9 G. Connecticut Assistant Professor D epartment of Ped ia tr i c s of 4209 State Route 44 Rootstown. Professor and Chairman Department of Emergency Medicine School of Medicine and Biomedical Sciences State University of New York at Buffalo uffal o G enera I H o spi t a I 100 High Street Buffalo. Luke's-Roos evelt Medical Center 1000 Tenth Avenue New York. John Dempsey Hospital. NewYork 14203 B Robert C. M. Bhende. M. Associate Professor of Emergency Medicine Assistant Professor of Medicine Dalhousie University Tucker Park Road Saint John. Jr. Brinsfield.D. M. Bates. Bennett. NewYork 14215 As s is ta 60 3 0 Michael S. Na.. Clinical Instructor Department of Emergency Medicine School of Medicine and Biomedical Sciences State University of New York at Buffilo 100 High Street Buffalo. Texas 7 82 29 Marc Bayer.D. Germaine Brent. C linic al As sistant P rofes s or Department of Pediatric s University of South Florida College of Medicine.D. M.D. University of Connec ticut 0 nt C linic al P rofe s s o r Department of Emergency Medicine State University of New York at Buffalo School Medicine Erie County Medical Center 462 Grider Street Bufalo.D. M. New York 14203 of Robert G. Pennsylvania I 9 I 04 Mary K. M. Beveridge. Bell. Bolte. Professor Departments of Pediatrics and Pediatric Emergency Medicine University of Utah 100 North Medical Drive Sak Lake City.D. The Childrenb Hospital of Philadelphia 34th Street and Civic Center Boulevard Philadelphia. Associate Professor Departments of Pediatrics and Pediatric Emergency Medicine University of Pittsburgh / Childrenb Hospital of Pittsburgh 3705 Fifth Avenue Pittsburgh. M.xiv / CoNrnrsuroRs Brian A.D. New Brunswick E2L 4L2. M. Petersburg.D. Assistant Professor Department of Emergency Medicine Boston University School of Medicine Boston Medical Center 818 Harrison Avenue Boston. M.D. Ohio 44272 Louis M. Utah 84113 Marc Borenstein. M..D. Associate Professor Department of Pediatrics Univ er s ity of Pennsy lv ani a . M. Assistqnt Professor Department of Emergency Medicine Northeastern Ohio Universities College Medicine Eastern Virginia Medical School / Children's Hospital of the King's Daughters 601 Childrenb Lane Norfolk.D.A. Billittier IV M. Pennsylvania I 52 I 3 Alison St.

M. M. M.3 09 8 2708 Royster Court Virginia Beach. Oregon 97 201 . M. New York I42l5 Charles K. Department of Emergency Medicine East Carolina University School of Medicine Brody 4W-54 Greenville. Department of Emergency Medicine Oregon Health Sciences University 3 I 8 l Southwest Sam Jackson Park Road Portland.H.D. Anthony Cirillo. M. Virginia 23454 Vivek Chander. Director of the Hazardous Materials Program Nicole Bruner. Resident Department of Emergency Medicine Oregon Health Sciences University 3I8I Southwest Sam Jacluon Pqrk Road Portland. Gregory R. St aff Em ergency P hy s ic i an Portland Veterans Affairs Medical Center 55 LakeAvenueNorth Worcester.D. Chandler. Rhode Island 02860 / xxv .D. Associate Professor of Emergency Medicine Oregon Health Sciences University 3 l 8 I Southwest Sam Jackson Park Road Portland. Ciottone. North Cqrolina 27858 David B.O.. Brunetto.D. Broderick.D. M. Chief Resident Department of Emergency Medicine New York Medical College Metropolitan Hospital Center NewYork. Associate Professor Department of Emergency Medicine East Carolina University School of Medicine Pitt County Memorial Hospital 2100 Stantonsburg Road P.P. UHN-52 Portland. NewYork 10021 Angeline D.D.D. Oregon 9 7 2 0 I .3 098 L. Brown.D.D.D. Tbnnessee 37122 James H. Chauhan. John A. Department of Emergency Medicine University of Massachusetts Medical Center Patrick Brunett. Oregon 97 20 I . Assistant Professor Department of Emergency Medicine Oregon Health Sciences University 3181 Southwest Sam Jacl<son Park Road. North Carolina 2 78 3 5-6028 CoNTRTBUToRS Frederick M. Burns School of Medicine I319 Punahou Street Honolulu. M. Mas sachusetts 0 I 65 5 VijaiV..vsterStreet Pawtucket. Massachusetts 0 I 6 5 5 Consortium 1599 Country Haven Trail Mount Juliet. M. Box 6028 Greenville. Ph. Emergency Physician (Resident) Department of Emergency Medicine State (Iniversity of New York at Buffalo Hospital Assistant Professor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worces ter. M. Clinical Assistant Professor of Surgery Department of Emergency Medicine Memorial Hospital of Rhode Island Brown University Medical School Ill Bra. Kerryann B. M. Oregon 97 20 I -3098 Robert L.D. M.D. Hawaii 96826 Erin M. Jr.. Assistant Professor Department of Emergency Medicine State University of NewYork at Buffalo 462 Grider Street Bufalo.D. Burkle. M. Burnham.D. M. Brown. Bryan. Professor ofPediatric Surgery and Public Health Chair of Division of Emergency Medicine Director of Center of Excellence in Disaster Management and Humanitarian Assistance University of Hawaii. M. Oregon Poison Center.

DeFlitch. DiCastro. Dorfman.D. Massachus etts 0 I 6 5 5 David H. Derlet. Massachusetts 0 I 84 2 Howard M.I 99 9 Department of Emergency Medicine State Uniyersity of NewYork at Buffalo Buffalo General Hospital 100 High Street Buffalo. Massachusetts 02 I I 8 Mark D. Room 304 600 Gresham Drive Norfolk. Illinois 606 I 2-7 3 5 4 Steven A. Curry. Clinical As sis tant Profes s or Department of Emergency Medicine State University of NewYork 100 High Street Buffalo. NewYork 14203 Steven G. Cohan. PSSB Suite 2100 Sacramento. College of Medicine West l8l9 West Polk Street Chicago. M. Counselman. Attending Surgeon Department of Surgery Mary Bridge Children's Hospital 314 South Martin Luther King Jr Way.D. Clinical Instructor of Emergency Medicine Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenueNorth Worcester. M.D. #306 Thcoma. M. Craven. M. Room 304 600 Gresham Drive Norfolk. Califurnia 958 I 7 AmyA. Department of Medical Tbxicologlt Good Samaritan Regional Medical Center 925 East McDowell Road. M.D.D. I4/as hington 9 8 4 0 3 Steven C. Department of Emergency Medicine Wake Medical Center 3000 New Bern Avenue Richard A. NewYork 14203 Christopher J. Associate Professor and Chairman Department of Emergency Medicine Eastern Virginia Medical School Raleigh Building. Associate Profes sor of Pediatrics Departments of Pediatrics and Emergency Medicine Primary Children's Medical Center 100 North Medical Drive Salt Lake City. M.D. Arizona 85006 Tanvir M.2 28 2 Robert W. M. M.D.D. Associate Professor of Emergency Medicine Department of Emergency Medicine Eastern Virginia School of Medicine Raleigh Building. Department of Emergency Medicine M/C724 University of lllinois at Chicago Room 618.D.D.xxvi / CoNrnrsuroRs L. Clinical Instructor Phuli L. M.D. Department of Emergency Medicine Westmoreland Regional Hospital 532 West Pittsburgh Street Greensburg. Assistant Professor D ep artment of Pe diatr i c s Boston Medical Center 818 Hanison Avenue. Assistant Professor Department of Emergency Medicine Boston Medical Center One Boston Medical Center Place Boston. Virginia 2 3 5 07 . M. Davis 2315 Stockton Boulevard. Corneli.D. Utah 841I3 Francis L.I 9 99 Raleigh. Virginia 2 3 5 07 . Department of Emergency Medicine Laurence General Hospital I General Street Lawrence.D. M. Massachusetts 02 1 1 8 . Pennsylvania I 5 60 I . DeStefano. Crockett. M. North Carolina 27610 Michael DiBella.D. Professor Department of Emergency Medicine University of Califtrnia. 2nd Floor Phoenix.D. Mason Cobb. Dara. M. M. Crespo. M. Dowling 3 South Boston.

Etzwiler. B. Edwards. Louis. M. Pqulb Hospital 1081 Burrard Street Vancouveri British Columbia l/62Jy6. M.Syracus e 750 East Adams Street Syracuse. Fernandes. Nevada 89102 / xxvii . Suite 6006-8 St. New York I 32 I 0 80 Seymour Street PO. Louis University School of Medicine. M. M.D. Michael J.B. B.D. Eilbert. Canada Westmead. New Brunswick E2L 4L4. Ferm. Cqnada Pamela J.O. Assistant Professor of Psychiatry Director of Adult Psychiatry Clinic Oregon Health Sciences University Southwest Sam Jacl<son Drive Portland. Illinois 606 I 2 Lisa S. M. Atlantic Health Sciences Corporation Department of Emergency Medicine P. Box 5037 Hartfurd.D. M. Drescher. Australia Wesley P.D.5 0 3 7 James Ducharme. M.D.D. Assistant Professor Deparhnent of Emergency Medicine University of Massachusetts Medical School 55 LakeAvenue North Worcester. Farnsworth.Syracus e 750 EastAdams Street 06 I 0 2 . Consultant in Emergency Medicine Emergency Department Westmead Hospital Hannesbury Road Tomer Feldman. Assistqnt Clinical Professor of Pediatrics St. New South Wales 2145.CoNrRrBUroRs . John's Mercy Medical Center 615 South New Ballas Road.B. Clinical Assistant Professor of Pediatrics University of Nevada School of Medicine.D. Fairley. Texas 7 8 2 84-7 8 3 4 Chicago. Attending Plrysician Cardinal Glennon Childrenb Hospital. M. Director of Pediatric Emergency Services St. Oregon 97201 3l8l Rob J. Box 5200 Saint John. Cl inic al As s i s tant Profe s s or Department of Emergency Medicine University of lllinois. M.. M.D. Connecticut Wayne J. C. Department of Emergency Medicine State University of New York at Syracuse H e alth S cienc e C enter. Fernfndez. Chicago 1740 West Thylor Miguel C. Clinical Associate Professor of Surgery University of British Columbia.D. M. Australia Carl M. Edwards.B. Associate Professor Division of Emergency Medicine Dalhousie University.S. Department of Emergency Medicine St. New York I 3 2 I 0 Robert P. Mass achusetts 0 I 6 5 5 -02 2 8 Christopher M. Pediatric Emergency Servic es Department of Emergency Medicine University Medical Center Las Vegas. Box 3515 Parramatta.M.D. Illinois 606 I 6 Jay Fisher.. Missouri 63141 Michael J. New South Wales 2124.D. Departmenl of P sychologicql Medicine The New Childrenb Hospital PO. Assistant Professor Departments of Traumatology and Emergency Medicine University of Connecticut School of Medicine Hartford Hospital Syracuse. Ferraro. M.D. Assistant Professor of Emergency Medicine Department of Emergency Medicine State University of NewYork at Syracuse Health Scienc e Center. M. M. South Tbxqs Poison Center University Hospital 7703 Floyd Curl Drive Sqn Antonio.S. C linic al As s o ciate Profes s or Department of Emergency Medicine Mercy Hospital qnd Medical Center University of lllinois 2 5 2 5 South Michigan Avenue Chicago.

M. Massachusetts 0 I 65 5 Sandra L. Giffin. Director Rural Emergency Medical Service and Disaster Medicine Department of Emergency Medicine University of New Mexico Health Sciences Center Ambulatory Care Centeri 4 West Albuquerque.3 8 0 75 2 3 5-9070 Leonard G. Geller. Associate Professor D epartment of Pediatrics Section of Emergency Medicine University of Missouri. R.B. Medical Director Georgia Poison Center 80 Butler Street Southeast Box 26066 Atlanta. M. Fleisher.T. Clinical Instructor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcester.E. Assistant Professor Department of Emergency Medicine St. Associate Professor of Pediatrics Emory University School of Medicine.D.D. Australia Richard J. Georgia Clinical Instructor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcester. Fulde. Assistant Clinical Professor of Emergency Medicine Tufts University. Gabor. Missouri 64108 Lucille Gans. M.D. Gaffney. D. M. Michigan 48 60 2 Gordian W. The Bernard W Godwin.R. B. s s or of Pe di atri c s Harvard Medical School.B. Children b Mercy Hospital 2401 Gillham Road Kansas City. Associate Professor of Prostqte Cancer Director of Urologic Oncology Kimmel Cancer Center Thom as Jeffer s o n Un iv ers i ty l0I5 Walnut Street #I102 Philadelphia.D. Arizona 8 5 008-4 9 7 3 Robert J. 2010.D.S. Oregon 9 7 2 0 I . Fitzmaurice. Pennsylvania I 9 I 07 .B. Lukeb Hospital / Michigan Stqte University 700 Cooper Saginaw. M. M.xxviii / CoNrnreuroRs Laura S.D. M. M. Gomella.. Director of Emergency Medicine St. Senior Lecturer University of New South Wales Victoria Street Darlinghurst. M.3 09 8 Saundra Gilfillan. Texas I 3 03 3 5 .O. Massachusetts 2601 East Roosevelt Street Phoenix.A. Massachusetts 0 I 65 5-02 28 Carmen Teresa Garcia. New South Wales.M. Kansas City. Massachusetts 02 I I 5 Lance K.D. O. Vincentb Hospital Sydney. Jr. M. University of Texas Southwest Medical Center 5323 Harry Hines Boulevard Dallas. Freeman. Attending Physician D ep artment of Pe di atric s Maricopa Medical Center Gary R.D. M. 0 I I 99 John K. Department of Emergency Medicine Oregon Health Sciences University 3l8l Southwest Sam Jacl<son Park Road Portland. Profe Chief of Emergency Medicine Children's Hospital 300 LongwoodAvenue Boston.D. Director of Pediatric Emergency Department Baystate Medical Center 759 Chestnut Street Springfield. New Mexico 87 I 3 I -5 24 6 I I Thomas Germano.. N.-P.N.S.

Graham. Assistant Professor Department of Emergency Medicine East Carolina University School of Medicine Brody Medical Sciences Building Greenville.M.D. Kansas 66204 Douglas M. Colorado 802 29-4 3 6 I . Physimed Clinic 6363 Transcanada I2I Saint Laurent. Hanly.. M. Massachusetts 0 I 6 5 5 Ralph M. M. M. Co-Director of the North Suburban Medical Center 919l Grant Street Thornton. Arizona 85006 Portland Veterans Administration Medical Center.D. Jr. Oregon 97 20 I . M. Oregon Health Sciences University 3 1 8 1 Southwest Sam Jackson Park Road Portland. Gutman.D. New South Wales 2124. Suite 412 El Paso.D. Assistant Professor D ep artm ent of Pe diatric s University of Massachusetts Medical Center 55 LakeAvenue North Worcester. M. M. Heisig.D. Susan P. L. M. D. M. NewYork 10029 P.P. Haynes..M.A. Graeme. 2nd Floor Phoenix. Assistant Professor Department of Pediatrics Division of Pediatric Emergency Medicine University of Tbxas Southwestern Medical Center at Dallas / Children s Medical Center of Dallas 5323 Harry Hines Boulevard Dallas.D. M.S. Goto.D. North Carolina 2 78 5 8-4 3 5 4 CoNTRIBUToRS / xxix June G.D. Hanson.D.C.. Assistant Professor Department of Emergency Medicine John E. Hightower.H.. Clinical Associate Professor of Medicine Department of Medicine.D. Goodman.R. M. Assistant Professor and Assistant Medical Director Department of Emergency Medicine E ast C aro lina Univ ers i ty Building A. Assistant Professor Department of Emergency Medicine New York Medical College / Metropolitan Hospital l90I FirstAvenue NewYork. Department of Emergency Medicine Shawnee Mission Medical Center 9100 West 74th Street Shawnee Mission. Hartoch.. Department of Medical Tbxicology Good Samaritan Regional Medical Center 925 East McDowell Road. Australia Richard S.H. Kansas City. Texas 7 5 23 5-9063 M.. Physicians' Quadrangle Greenville. M. M.O. NewYork 14203 Associate Professor Departments of Medicine and Emergency Medicine State University of New York at Syracuse Health Science Center-Syracuse 750 East Adams Street Syracuse. North Carolina 27858 Kimberlie A. Texas 79905 David G.B. Peggy E.B.C. M. M. Professor of Emergency Medicine University of Health Sciences. Hill. M. Division of Cardiology State (Jniversity of New York at Buffalo / Buffalo General Hospital 100 High Steet Buffalo.D. Gough.T.3098 John F. New York I 3 2 I 0 David Jimmy B. Department of Emergency Medicine Sydney University The Royal Alexandra Hospital for Children Hawkesbury Road Westmead.A. Clinical Assistant Professor Departments of Emergency Medicine and Medical Toxicology Texas Tbch University 6090 Sanity Drive.D. Collin S.A.B. Quebec H4T 109 Canada Rania Habal.

Assistant Professor Wce Chairman and Associate Professor Department of Emergency Medicine State University of NewYork at Bulfalo / Erie County Medical Center 462 Grider S*eet Buffalo. M.D. Associate Professor and Vice Chair Department of Emergency Medicine East Carolina University School of Medicine Moye Boulevard Greenville. M.S..D. M. Jehle. M. Hogan.D. Associate Professor Department of Emergency Medicine University Hospital 750 East Adams Street Syracuse. Medical Tbxicology Department of Emergency Medicine New York City Poison Control Center Director of Corporate Tbxicology Bellevue Hospital Center. Resident in Urology Assistant Professor Department of Urology Thomas Jefferson University Hospital Jeferson Medical College I I I South I lth Street. NewYork 14215 Thea L. Jones. James. Assistant Professor Case Western Reserve University. Jolin. Hong. New York I I 7 94 -7 400 . M. Oklahoma 73104 James R Holmes.D. New York 10016 Occupational and Preventive Health Services Texas Instruments 7839 Churchill Way. Jouriles.D. M. C linical As s is tant Profes s or Department of Emergency Medicine State University of NewYork at Buffalo 462 Grinder Street Buffalo. Texas 75251 Nicholas J. Ohio 44109 Daniel M. Hung. NewYork 14215 Oklahoma University Health Sciences Center University Hospital 800 Northeast Thirteenth Street Oklahoma City.. Ross E. Hunt. ScottW.D. Johnson.O.D. Massachusetts 02 I I 8 Lester Kallus. Califtrnia 958 I 7 GaryA. Fellow. Nan York I3210 Clinical Instructor Department of Emergency Medicine Boston University School of Medicine Boston Medical Center 81 8 Harrison Avenue Boston. M. K. M. M. Joyce. M. Suite G6220 Philadelphia. M. D. Davis I 5 Stockton Boulevard 23 Sacramento.D. Dietrich V. Associate Residency Director MetroHealth Medical Center 2500 MetroHealth Drive Cleveland. M.D. Mailstop 3938 Dallas. Connecticut 06519 Oliver L. State University of New York at Stonybrook Department of Emergency Medicine Hospital L4 515 Stonybrook. Ph. Richard C./ CoNrmsuroRs David E.D.D. Assistant Professor Department of Emergency Medicine State University of NewYork at Syracuse Health Science Center 750 East Adams Street Syracuse. M. Pennsylvania I 9 I 07 Department of Surgery Section of Emergency Medicine Yale University School of Medicine 464 Congress Avenue New Haven. New York University Medical Center 462 FirstAvenue Nau York. M.D.D. New York I 3 2 I 0 Robert D.P. Assistant Professor Division of Emergency Medicine Department of Internal Medicine University of California.H. North Carolina 2 7 8 5 8-4 3 5 4 Gerald Patrick Igoe.

3 098 Richard Arshad Khan. Kerr. Klauer.D. Kharasch. Ohio 44307 1199 PrinceAvenue Athens.D. M. Associate Professor of Clinical Emergency Medicine Division of Emergency Medicine Athens Regional Medical Center Kevin M. Kennedy.D. M. Massachusetts 02 1 I 8 Hervy B.' M.D. Instructor in Medicine S. M. M. Ed. M. Massachusetts 100 High S*eet 02 I38 S.O. Krauss.D. Department of Emergency Medicine Taryn E. Jr. Krause. M. Pennsylvania I 6 5 0 l HaroldW. Wabash Avenue Alcron.C.D.O. Massachusetts 021 15 Michael K.' B. B. M. Director of Pediatric Emergency Medicine Boston Medical Center Instructor 818 HawisonAvenue 300 Longwood Avenue Boston. al Profes s or As s i s t ant Clinic Department of Emergency Medicine Department of Emergency Medicine State University of NewYork at Bufalo Harvard Medical School 330 MountAuburn Street Buffalo. S e c ti on of Tbxi c o I ogy Division of Emergency Medicine University of Tbxas Southwest Medical School 5323 Harry Hines Boulevard Dallas. University of Massachusetts Medical Center 55 LakeAvenue North Worcester Mas s achus etts 0 I 6 5 5 -02 2 8 Wayne Memorial Hospital Mark S. Office of Research and Biotechnology University of North Texas Health Science Center 3500 Camp Bowie Boulevard Fort Worth. Maryland 2 I I 57 Christopher Keyes. M..B. Massachusetts 0 I 65 5 Boston Medical Center I Boston Medical Center Place Boston.D. Department of Emergency Medicine Oregon Health Sciences University 3181 Southwest Sam Jacl<son Park Road Portland. D. Sigmund J.D.D.CoNrrusuroRs Eric M. M.D. M. Kardon. Westminster.A. Kornegay. Kozack. NewYork 14203 Cambridge. Georgia 30606 James D. C hief. North Carolina 27534 Department of Emergency Medicine . Baruch Assistant Professor Boston University School of Medicine.M. tructor in Pediatrics Harvard Medical School. Texas 7 6 I 07-2699 George Kondylis.H. Texas 7 5 23 5-8579 Richard J. M. Massachusetts 02 I I 8 D ep artm e nt of Pe diatric s Hqrvard Medical School. Clinical Instructor 2700 Wayne Memorial Drive Goldsboro. M.D. Keneck.. As s i s t qnt Res i dency Director Alcron General Medical Center 400 N.P. Assistant Professor Department of Pediatrics Boston University School of Medicine / Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcester. Clinical Instructor Eileen A.O. Professor Department of Emergency Medicine Hamot Medical Center 201 State Street Erie.D.. M. Kellet Ph. Kocjancic. Massachusetts 02 I I 5 Boston.D.H. D. Ins Department of Emergency Medicine Carroll County General Hospital Assistant in Medicine (Genetics) Childrenb Hospital 300 LongvoodAvenue 200 Memorial Drive Boston. Oregon 97 20 I . Childrenb Hospital / xxxi . Korson.

D. Ph.D. Davis Jewish General Hospital 3755 Cote Saint Catherine Montreal.P.D. B.D.D.D.D.I. D. Box 251 Denver. CraigW. Lindsay.D. Massachusetts 02 I I 5 Scott R. M. Pennsylvania I 9 I 04 .Sc. NewYork 10021 I 608 Judith K.. Ontario KIY 489. 0 Regional Poison Center 4815 Alameda El Paso.D. Chief Resident Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcester.xxxii / CoNrnrsuroRs David Langleben. Division of Emergency Medicine Ottawa Civic Hospital 1053 CarlingAvenue Ottawa.D. Canada Lilly C. New York I 3204 2 052 3 - 4 43 Maryanne W.D.M. Canada Assistant Professor of Surgery Associate in Surgery Childrenb Hospital James M. Associate Professor of Medicine D ep artment of C ardi o I o gy McGill University / Sir M. Texas 79905 A.Sc. Clinical Instructor of Emergency Medicine Carol Ledwith. Emergency Department Childrenk Hospital 1056 East l9thAvenue.D. Room 2Al8 NewYork. Lipke.49 7 3 Andr6s M. Colorado 80218 Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcestef Massachusetts Jacques S. Leaming. Roy Magnusson. M. M.. North Carolina 2 7 I 5 7 . Oregon 9 7 2 0 I . 300 Longwood Avenue Boston. Assistant Professor of Emergency Medicine Department of Otolaryngology / Head and Neck Surgery Nau York Eye and Ear Infirmary. Massachus etts I 0 I 65 5 Associate Professor Department of Emergency Medicine Bowman Gray School of Medicine I Medical Center Boulevard I4/inston-Salem. M. M. Quebec H3T IE2. C.D. Arizona 8 5 008 . Thomason Hospital West Texas Ralph B...A.S. M. North Carolina 2 7 I 5 7. Maller. B.D. M. Lee. Harvard Medical School . Department of Primary Care Pediatrics Children b Hospital of Philadelphia 34th Street and Civic Center Boulevard Philadelphia. M. Lucas. M.3 09 8 Jacalyn S. Associate Professor Department of Emergency Medicine Oregon Health Sciences University 3I8l Southwest Sam Jaclson Park Road Portland..D. M. S. Lugo. School of Pharmacy Tbxas Tech University El Paso Campus University of Houston. School of Pharmacy University of Nan Mexico. M. M. Leonard. Lillehei.S. Clinical Assistant Professor of Pediatrics University of Pennsylvania School of Medicine. C. Levin. M. AID-OFDA Clinical Instructor and Research Fellow Department of Emergency Medicine State University of NewYork at Syracuse Health Science Center-Syracuse Washington. Lee.. Lillibridge 750 East Adams Street Syracuse. M. Department of Pediatric Emergency Maricopa Medical Center 2601 East Roosevelt Phoenix. Department of Emergency Medicine Bowman Gray School of Medicine Medical Center Boulevard Winston-Salem.I 089 William J.I 089 Gretchen K. M. M. Deparfment of Emergency Medicine Metropolitan Hospital l90l FirstAvenue.

M. Instructor of Pediatrics Harvard Medical School . Ph. Connecticut Christopher J. M.D.D. Clinic al As RitaA. Dowling I South Boston. Attending Physician Department of Emergency Medicine St.O.D.D. Massachusetts 02 I 18 Neil S. Massachusetts Andrew T. March. Professor of Emergency Medicine Vice President and Vice Dean for Clinical Affairs State University of New York at Syracuse Health Science Center-Syracus e 750 East Adams Street Syracuse.D. A s s is t ant C linical Profes s or Department of Emergency Medicine Mercy Hospital and Medical Center 2525 South Michigan Avenue Chicago. Manfredi. Instructor Worcester. North Carolina 27 8 5 8-4 3 5 4 Hartfurd. M. M. Department of Traumatology and Emergency Medicine University of Connecticut School of Medicine Assistant Professor and Director 80 Seymour Street Division of Emergency Medical Services East Carolina University School of Medicine Greenville. M.D. Attending Physician Department of Emergency Medicine Boston Medical Center 818 HarrisonAvenue. New York 12054 06 02 . McCormack.C. Clinical Instructor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North 0 I 65 5 William J. North Carolina 27858 . Department of Emergency Medicine Division of Infectious Diseases Childrenb Hospital 300 Longwood Avenue Boston. M. M. NewYork 14203 N. M.5 03 7 Department of Emergency Medicine Boston University School of Medicine. Nau York I 3 2 I 0 Robert F. Hartford Hospital CharlesA. Ph.D. Manno. Maxwell.D.' B uffa I o G en era I H o sp it a I 100 High Street Buffalo.D. Ctay Mann. Department of Emergency Medicine Harvard Medical School Brigham and Women's Hospital 75 Francis Street Boston. Massachusetts 02 I I Ron Medzon.CoNrrusuroRs Richard Malley.D. D.D. Peterb Hospital Albany. Paul F. New York I 3 2 I 0 Mariann M. Assistant Professor Oregon Health Sciences University 3 I 8 I Southwest Sam Jackson Park Road Portland.. Massachusetts 02 I I 5 John B. M. McCabe. M.O.D. Instructor 6 l / xxxiii Associate Professor Department of Emergency Medicine University Medical Center of Easlern Carolina 600 Moye Boulevard Greenville. Oregon 9 7 2 0 I . Illinois 606 I 6-2 47 7 PeterW. Assistant Professor Department of Emergency Medicine Georgetown University School of Medicine 3700 Resevoir Road Washington.D.3 098 Resident Physician Department of Emergency Medicine State University of New York at Syracuse Health Science Center-Syracus e 750 EastAdams Street Syracuse. Meehan. Markus. McAfee. 20007 sis tant Profes or s Department of Emergency Medicine State University of New York at Buffalo School of Medicine and Biomedical Sciences. McKay. McGuire. M.D. Assistant Professor Departnt en t of Pediatrics University of Massachusetts Medical Center 55 LakeAvenue North Worcesteti Massachus etts 0 I 60 5 Assistant Professor JuanA. D. Meggs. M. D.

Douglas R. Professor John T.D. Nichots. Meredith.xxxiv / CoNrrusuroRs M. Mullins.D. Thomas Nowicki.D. J.D.D. Massachusetts 02115 S.C. Norton. Douglas S. North Carolina 27858-4354 Chris J. Moscati. D.D. Emergency Physician 3181 Southwest Sam Jackson Park Road.O.D. Oregon 97216-2599 8 M. Portland. Massachusetts 01655-0228 Department of Emergency Medicine Oregon Health Sciences University 3l8l southwest sam Jaclcson Park Road Portland' oregon 97201-3098 Ronald M. Connecticut 06519 Daniel Warne Ochsenschlager. Department of Surgery Oregon Health Sciences University Portland. ProJbssor M. D. M.D. Utah 84113 Department of Emergency Medicine Brady Medical Sciences Building 4W54 East Carolina University School of Medicine Greenville. Nadel. Professor Lewis S.D. Section of Emergency Medicine Yale University School of Medicine 464 Congress Avenue New Haven.D. M. Robert L. 20010 of . Instructor of Medicine Associate Residency Director Harvard Medical School. Assistant Professor of Clinical Medicine Emergency Department of Emergency Medicine State University of New York at Buffalo Buffalo General Hospital 100 High Street Buffalo' New York 14203 constance G. M.3 09 Portland Adventist Medical Center 10123 Southeast Market L223A Portland. Migden. NewYork 14215 Erie County Medical Richard J. Assistant Assistant Professor ofPediatrics Department of Pediatric Emergency Medicine University of Utah / Primary Children s Medical Center 100 North Medical Drive Salt Lake City. CrockerAvenue West Hartford.. 9 7 2 0 I .D. M. Michalakes. Nelson. Oregon 97201-3098 UHN52 Department of Emergency Medicine State University of New York at Buffalo / Center 462 Grider Street Buffalo.s. washington 981t I John c. Brigham and Womenb Hospital 75 Francis Street Boston.D. Nelson. Connecticut 06110 Armida Nufrez-Finley.D. clinicalAssistant ProJbsso. Emergency Physician Group Hearth cooperative oJ puget sound seattle. D. New York I 4 2 0 3 . Moorhead. Childrenb National Medical Center I I I Michigan Avenue Northwest Washington. M.O. Eric Schevon Nicoletti' M'D' Assistant Professor Department of Emergencl' Medicine university of Massachusetts Medical Center 55 Lake Avenue North worcester' Massachusetts 01655-0228 :?-I-lt Clinical Resident in Emergency Medicine M. Oregon Assistant Professor Department of Emergency Medicine University of Massachusetts Medical Center 55 Lake Avenue North Worcester. M. M. Clinical Assistant Professor of Emergency Medicine State University of NewYork at Buffalo Buffalo. Department oJ Emergency Medicine Oregon Health Sciences University 3l8I Southwest Sam Jacl<son Park Road. M. M.. Professor of Pediatrics Emergency Medical Trauma Center George Washington University School Medicine.

Assistan Residency Director Department of Emergency Medicine Harvard Medical School .D. M. Preisz.B. M.D. M. Assistant Professor Department of Emergency Medicine State University of New York at Syracuse Health Science Center-Syracuse 750 East Adams Street Syracuse. Na'v South Wales 2092.D. Mail Stop 677 Milwaukee. NewYork 10016 Associate Profes s or of Clinical Surgery Department of Surgery Bowman Gray School of Medicine Michael Rapp. M. Arlington Hospital Forest University GeorgiaAvenue Winston-Salem. M. B.D. Building M Greenville. Tamara Ingrid Pottker. Department of Emergency Medicine New York University Hospital 462 FirstAvenue NewYork. Assistant Professor Department of Emergency Medicine State University of New York at Syracuse Health Science Center 750 East Adqms Street Syracuse. Medical Tbxicology Attending Physician. Paddon. Panacek.O. C linical As s istant Profe ss or Department of Emergency Medicine State University of NewYork at Buffalo 6167 Bridlewood Drive South East Amherst.I 9 I 7 Department of Emergency Medicine I70l North George Mason Drive Arlington. Ohio 45229 9000 West Wisconsin Avenue. Virginia 2 2 2 0 5 . Heramba Prasad. M. Assistant Professor Department of Pediatr i cs Section of Emergency Medicine Medic al Co I I ege of Wis cons in Department of Pediatric Emergency Medicine Childrenb Hospital Medical Center of Cincinnati 3333 BurnetAvenue Cincinnati. NewYork 10025 Lauren Pipas.3 67 I Wake 2II5 / .S. George Podgorny. Lecturer in Emergency Medicine University of New South Wales.CoNrRrsuroRS Kristen J. tant Clinic al Ins truc tor N. Neyv York I 3 2 0 I Hospital LouiseA. M. D. New York I 3 2 I 0 Catherine E. M. Brigham and Women's Hospital 75 Francis Street Boston.D. Australia A s s is Syracuse.D. Assistant Professor Department of Emergency Medicine Universiht of Massachusetts Medical Center 55 LakeAvenue North Worcester. Associate Professor Department of Emergency Medicine East Carolina University School of Medicine Physician's Quadrangle. Luke's-Roosevelt Hospital Center llll AmsterdamAvenue NewYork. Rao.D. Perron.D. University of Califtrnia at Davis Medical Center I 5 Stockton Boulevard 23 Sacramento. Pundt. M. M.D. M. Pinkert. Massachusetts 02 I I 4 Rama B. M.D. North Carolina 27 I 04. Raftery. M. Califtrnia 958 I 7 Michael A. Assistant Profess or of Clinical Pediatrics Department of Pediatric Emergency Medicine St. M.. Pellegrino.D.D. New York I 405 l Kathleen A. M. Clinical Instructor in Pediatrics Departntent of Medicine Harvard Medical School Children s Hospital : 330 Longwood Avenue Boston. New York I 3 2 I 0 Mark R. Massachusetts 02 I I 5 Laura Peterson. LTisconsin 5 3 2 2 6 Edward A. Prince. Fellow. Department of Medicine Health Science Center St. North Carolina 2 78 5 8-43 5 4 Department of Emergency Medicine State University of New York at Syracuse Paul T.D. Vincentb 750 East Adams Street Victoria Road Darlinghurst Sydney. B ellevue Hospital .D. Massachusetts 0 I 6 5 5 Heidi M.

Rosen. Box 35926 Dallas. Califurnia 9 5 8 I 7 Boston Medical Center Boston. North Carolina 2 7 8 5 8-4 3 5 4 Robert Rodriguez. M. Box 251 Denve4 Colorado 80218 Walter C. Professor of Clinical Pediatrics Department of Pediatrics University of Cincinnati College of Medicine Childrenb Hospital Medical Center 3333 BurnetAvenue.D. Pitt County Memorial Hospital Richard M.D. M. Clinical Instructor Jimmy Quirriz Rodriguez. OSB 4 Cincinnati. Assistant Professor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North WorcesteL Mass achus etts 0 I 6 5 5 -0 2 2 8 Jefatura.D. Emergency Medicine Division University of California at Davis Medical Center 2315 Stockton Boulevard. M. Renzi. Box 10014 Charlottesville.D..D.P. Texas 75 2 3 7-8 5 79 Maria I. Department of Emergency Medicine State University of New York at Buffalo 100 High Street Buffalo. NewYork 14203 Robert C. M. Toxicology Services Assistant Professor of Pediatrics Section of Pediatric Emergency Medicine The Childrenb Hospital / University of Colorado Health Sciences Center 1056 East |9thAvenue. M. Massachusetts 0 I 65 5 Marc C. Virginia 2 2906-00 I 4 Francis P. 3M Medical Department. M. M. Ohio 45229 Greenville. Associqte Professor Tbxicology Graduate Program Univ ersity of Minn es o t a Minneapolis.D.D. Assistant Professor Department of Emergency Medicine University of Virginia School of Medicine University of Virginia Health System PO.H. New Mexico 87131 Todd C. M. University ofTexas Southwest Medical Center 5323 Harry Hines Boulevard Dallas.D. Reardon.D. Reiser. Pharm. M. Minnesota 5 5 4 5 5 / Robert Roy. Clinical Insh'uctor Department of Emergency Medicine Boston University School of Medicine John R. Roback. Box 10105 San Jose. M. Building 2100 Sacramento.D.D. Rothenhaus. Scott and White Memorial Hospital 2401 South 3lst Street Temple. Rudis. Assistant Professor and Associate Residency Director Department of Emergency Medicine East Carolina University School of Medicine. Richards. Restuccia. Roth. Texas 75235 / .xxxvi / CoNrnrsuroRs Robert F. Dean University of New Mexico School of Medicine Health Sciences Center BMSB. Texas 76508 Paul B. M. Servicio de Urgencias Hospital Mexico La Uruca PO. Robey III. M. Ruddy. Assistant Professor Department of Emergency Medicine Tbxas A&M University College of Medicine.D. Room 177 Albuquerque. M.D. Costa Rica Patricia B. Director of Residency Training Program Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcester.D. Massachusetts Mark G. Ph. M.D. North Texas Poison Center 5201 Harry Hines Boulevard PO.

. Schneider. M. 5 54 3 l M. Department of Emergency Medicine Connecticut Children b Medical Center 282 Washington Street Hartftrd. M.D. Anthony Hospital . Texas 75235 Steven F. M. Texas 79106 Sandra M. M. Massachusetts 02 I 38 Michael Shannon.D.D. Clinical Instructor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcesteri Massachus etts 0 I 65 5 Michael B. Assistant Professor Toxicology Graduate Program International Univ ers ity of Minn es ot a Minneapolis. M.D. Schmidt. Massachusetts 02I I 5 Mahesh Shrestha.Sc. Minnesota Gary S. Associate Professor of Pediatrics Harvard Medical School .D.D.A. Setnik. Emergency Physician Professional Associqtion Methodist Hospital 7900 Xerxes Avenue South.D. M. Associate Chief of Emergency Services Director of the Lead & Toxicology Clinic Children's Hospital. M. Ph. Ontario KIY 489. Senior Tbxicologist Pois on C enter . M. New York 14627 Kim Sing.3 09 8 Paula J. Professor and Chair Department of Emergency Medicine University of Rochester S*ong Memorial Hospital 601 ElmwoodAvenue. Canada Robert Skoglund.D.D.D. Oregon 9 7 2 0 I . M. Associate Professor Department of Emergency Medicine Eastern Virginia Medical School Raleigh Building. Texqs kch University Health Sciences Center 1400 Wallace Boulevard Amarillo.CoNrnrsuroRs EricW. Virginia 2 3 50 I Instructor in Medicine Department of Emergency Medicine Harvard Medical School 330 Mount Auburn Street Cambridge. Seim.D. Adjunct Professor of Medicine and Surgery E mergency M edi cin e D iv i s ion University of kxas Southwestern Medical Center Dallas.D. M. M.D. Siraco. Connecticut 06 I 0 6 Andrew Singer. M. M. Assistant Professor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenueNorth Worcesteti Mas sqchusetts 0 I 65 5 Shu Shum.. Department of Emergency Medicine Oregon Health Sciences University 3I8I Southwest Sam Jacl$on Park Road Portland. Suite 740 Bloomington. Schweich.H. M. Emergency Department Douglas Scudder. Room 304 600 Gresham Drive Norfolk. B aptist-St. Singh.P. Box 49200 Rochester.D. Assistant Professor Division of Emergency Medicine University of Ottawa Ottawa. M. Clinical Instructor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcesteri Mass achusetts 0 I 65 5 Marco L. New South Wales 2076. Ausfralia Worceste4 Massachusetts 0 I 65 5 Eunice M. Sydney Adventist Hospital 185 FoxValley Road Wahroonga. M.D. Minnesota 5545 5 / xxxvii . Clinical Instructor Ajeet J.D. Northwest Texas Hospital. Singletary. Sivilotti. StaffToxicologist Massachusetts Poison Control System 300 Longwood Avenue Boston.

M. Affi liate As s i s t ant P rofe s s or Division of Clinical Education Arizona College of Osteopathic Medicine. M. M. Terzian. Massachusetts 021 I5 Jeffrey Tucker.S. Associate Professor Department of Emergency Medicine Oregon Health Sciences University 3I8I Southwest Sam Jacl<son Park Road Portland.P.D. M.D. 1323 East El Parque Drive Tbmpe. M. M. Department of Emergency Medicine Wright State University School of Medicine 3 5 2 5 Southern B oulevard Kettering... NewYork 14222 CherylVance. M. Chief Resident Department of Emergency Medicine East Carolina University School of Medicine Pitt County Memorial Hospital 600 Moye Boulevard Greenville. Childrenb National Medical Center I1 I Michigan Avenue Northwest Washington. Oregon 9 7 2 0 I .C.H. Georgia 3 03 0 3 . Oregon 97210 Jackson Smood.D. Department of Emergency Medicine Assistant Professor of Emergency Medicine and Harvard Medical School.D. Mass achusetts General Hospital Pediatrics Department of Emergency Medicine Oregon Health Sciences University Hospital 3l8I Southwest Sam Jacl<son Park Road. UHN 52 Portland. Oregon 97221 Jeffrey R.xxxviii / CoNrrunuroRs Frank C. Oregon 97 2 0 I -3098 Stephen H. D. North Carolina 27858 Jerry D. tor of Pe di atric s Department of Emergency Medicine Harvard Medical School. Thomas. Ohio 45429 Martin J.D.P. M. Califurnia 9 5 8 I 6 Kristi Vaughn. Arizona. Children's Hospital at Buffalo 219 Bryant Street Buffalo. Second Floor Phoenix. M. M.D.H.D. M.3 2 I 9 Katherine Thomas. M. M. M. Smeeks. Assistant Professor Department of Emergency Medicine Boston Medical Center One Boston Medical Center Place Boston.3 098 / . Room I 16 Boston. Arizona 8 5 2 8 2-2 649 Stephen J. Fellow Department of Medical Tbxicology Good Sqmaritan Regional Medical Center 925 East McDowell Road. M. Assistant Professor Department of Emergency Medicine Emory University School of Medicine 68 Armstrong Street Southeast Atlanta. Instructor Eustacia Su.N. Massachusetts 02 I I 4 Susan B.D. Oregon 97 20 I -3 098 Stacey Sperling.S.. Smilkstein.D. Suchard. M.D. Attending Em ergency P hy s i c i an Good Samaritan Regional Medical Center and Phoenix Children b Hospital Phoenix. Teach.D. M. Ins truc Children's Hospital 300 Longwood Avenue Boston. Assistant Professor of Pediatrics and Emergency Medicine George Washington University School of Medicine. M.Taylor. Department of Emergency Medicine Oregon Health Sciences University 3I8I Southwest Sam Jaclaon Park Road Portland. Torrey.D.N. 20010 32 Fruit Street Clinics Building.D. Thomas. R. University of Caffirnia at Davis Medical Center 2315 Stochon Boulevard Sacramento. Instructor Oregon Health Sciences University 3181 Southwest Sam Jacl*on Park Road Portland.. Arizona 85006 Todd B. Massachusetts 021 l8 RaffiV.D.D. M. artment of P sy chiatry D ep Oregon Health Sciences University 3181 Sam Jacl<son Park Road Portland.

Connecticut 06 I 02 II. Associate Professor University of Tbxas Southwest Medical Center 5323 Harry Hines Boulevard Dallas. al P rofe s s or University Hospital State University of New York at Syracuse As s i s t ant Clinic Health Science Center. B. M.Wu.D. or/Tbxicology Co ordinator Department of Emergency Medicine Wright State University PO.O. Box 35926 Dallas.. Laboratory Medicine Department of Pathology and Laboratory Medicine Hartford Hospital University of Connecticut Health Center 300 Longwood Avenue Boston.Volturo. Box 927 Dayton. John Zehner. M. Assistant Professor Department of Emergency Medicine University of Massachusetts Medical Center 55 LakeAvenue North Worcester.Young.D.D. Wilkes.Weiner.B.Warden. Director of Trauma and Retrieval Services Kevin S. M.Vf .f. Western Australia 6009. Division of Emergency Medicine Children s Hospital Profes sor.D. Massachusetts 0 I 6 5 5 W.S.3098 Saginaw.D.Witey / xxxix 80 Seymour Street Hartford. M. Director Clinical Chemistry Debra L. Associate Professor Program in Emergency Medicine Michigan State University College of Human Medicine.O. Oregon 97401 Department of Emergency Medicine Sacred Heart Medical Center Kenneth A.D. M.Yeskey. B. M.C.. Australia 1255 Hilyard Steet Eugene.S. R. Associate Professor D ep ar tment of Pe di atric s The School of Medicine of the University Connecticut Health Sciences Center of Connecticut Children s Medical Center 282 Washington Street Harford.N. Ins truc tor of Pe di atri c s Harvard Medical School . Leslie R.D.D. North Tbxas Poison Center 5201 Harry Hines Boulevard P.I. Emergency Department Sir Charles Gairdner Hospital Verdun Street. Ohio 4540 I -0927 RobertW. Associate Professor and Vice Chair Department of Emergency Medicine University of Massachusetts Medical School As sis tant Profes s 55 LakeAvenue North Worcesten Massachusetts 0 I 65 5 Michael Wainscott. Vf . Department of Emergency Medicine Saginaw Cooperative Hospitals 1000 HoughtonAvenue Craig R. M.Wolford. Oregon 97 20 I .B.CoNrnreuroRs GregoryA. Associate Professor Department of Military and Emergency Medicine Unifurmed Services University of the Health Sciences 4301 Jones Bridge Road Bethesda. Maryland 208 I 4 Gary P. kxas 75 2 3 5-8 5 7 9 l.P.D. Department of Emergency Medicine Oregon Health Sciences University 3I8l Southwest Sam Jacl<son Park Road Portland.D. M. Nedlands Medical Director Perth. Josephb Hospital Medical Center 301 ProspectAvenue Syracuse NewYork 13203 . M.C. M. Williams.D. Texas 75235 Attending Physician Department of Emergency Medicine St. Massqchusetts 02 I I 5 James F. M. Lena Williams. Michigan 48 64 2 Alan H.S. Woff. Ph. Connecticut 06 I 06 Garry J.

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Payers would like to see the nonurgent portion ofthe over 90 million annual visits to the U. In addition. and (4) provide a list of key references for those who wish to investigate a clinical entity in greater depth than in the textbook.Preface Emergency medicine is a young and vibrant speciality with a rapidly expanding body of knowledge.The table of contents of this textbook parallels the clinical and administrative sections of the current version (June 1997) of the Core Contentfor Emergency Medicine. Once a diagnosis has been determined. To achieve this goal it was decided to follow as closely as possible the outline of the Core Contentfor Emergency Medicine. emergency medicine has been subjected to particularly intense scrutiny. As a new specialty with a reputation of providing efficient but sometimes costly medical care. performance of stabilizing procedures based on a provisional diagnosis. The textbook has been designed to present the body of knowledge that forms the basis of emergency medicine. In light ofthese practice characteristics. xli .The chapters within the 21 sections of the text cover the vast majority of topics identified inthe Core Content. emergency departments referred to alternate practice settings in an effort to reduce costs. This is an attempt to avoid the inclusion of redundant materials and subjects that were thought to require little discussion or elaboration. The Core Contenl is also found in the Appendix at the back of the book. emergency departments have begun observing patients up to 24 hours to complete diagnostic evaluation treatment protocols that would otherwise have to be performed as part of a hospital admission. this textbook has been designed to allow emergency physicians to (l) study for the boards using a focused and pertinent guide. (3) provide background information about disease processes and mechanisms or injury that will assist in the bedside instruction of patients as well as the classroom instruction of medical personnel. there continues to be a public demand for care through emergency departments for those who have no other alternative. (2) rapidly access specific information about illnesses and injuries in a manner that will facilitate the cases of emergency department patients. Emergency department observation medicine is one innovation in the management of emergency departments that is addressed in Chapters 2 and20 of this textbook. and then further diagnostic assessment to identify a more definite diagnosis. In a busy emergency department. Not all items that appear in the Core Contenl are included in the textbook.S. it is often up to the emergency physician to arrange access for the patient to appropriate resources available within the local health care system. it is sometimes difficult to gather all available clinical data and use that data to construct a working diagnosis. To facilitate the reader.MosI of the headings match those in the Core Content. We are now witnessing rnajor changes in health care delivery across the globe. we have put the number of the Core Content section in parentheses next to the corresponding section in this text. Despite this pressure. The specialty is somewhat unique in that the approach to the patient in acute distress focuses on the rapid identification of lifethreatening conditions.

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and Frank Livesay in the Department of Emergency Medicine at the University of Massachusetts. Moorhea4 as well as the contribution of the associate editors Mary Christine Bailey. Fleisher. and Andrew. Jr. G. Jennifer Cederberg. Volturo. McCabe. and Gregory A. Christopher Keyes. John B. Special thanks to Carol Bloom.. Richard Braen. xliii . The chapter authors are to be commended for their work. Gary R. Emily. Pat Keith. Thanks to my family. Ann.Acknowledgments I acknowledge the dedication of the editors E. Mariann M. who have put up with me despite the fact that I have been devoted to this scholarly pursuit. Manno. Alicia Galvan. and John C. JacksonAllison.

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Rectum and Anus (1. Farnsworth Esophagus (1. is often not definitively diagnosed but can represent a life-threatengency department (ED) presentation that ing disease that requires immediate intervention.4) Wesley P. acute pancreatitis. necrotizing endocarditis. and constipation. Prince Gallbladder and Biliary Tract (1. These illnesses include diabetes mellitus. intestinal obstruction. acute cholecystitis. only 7o/o required hospitalization after hospital admission for nonspecific abdominal pain. They also may have intussusception. Both school-age and adolescent children may have a psychosocial cause of abdominal pain. gastroenteritis. various authors have found that nonspecific abdominal pain is the preliminary diagnosis in4lohto 50o/o ofall patients. Approximately 15% of patients seen for abdominal pain will require operation and 27o/o wlll Abdominal pain is one of the emergency physician's most challenging chief complaints. Pancreas (1. Epidemiology After ED evaluation. Toddlers frequently have belly pain with pneumonia or pharyngitis. urinary tract disease. Age of patient greatly impacts on the differential diagnosis and incidence ofsevere disease and illness. and urolithiasis. . It is a common emer- require hospitalization. Approximately 5% of these require hospitalization.2). Infants commonly present with colic. Adolescents may have other abdominal disorders such as pelvic inflammatory disease. Eilbert Stomach (1. These patients often have a benign prognosis.7) Louise A.0) Wayne J. perforated ulcer.6) ABDOMINAL AND GASTROINTESTINAL DISORDERS (1. or other serious diagnoses including Meckel's diverticulum or appendicitis. malrotation.5) Paul F. intestinal ischemia. volvulus.1).0) (See 13. Presentations often vary by age. McGuire Small Bowel (1. These diagnoses include appendicitis.3). pelvic inflam- Porphyria. Chronic illnesses may present acutely with belly pain. Johnson Abdominal and Gastrointestinal Disorders (1.0) matory disease. renal neoplasm. Mediterranean fever. and inflammatory bowel disease.8) David G. Large Bowel (1. or incarcerated hemia. Heisig Liver (1. One out of five children seeks medical help for abdominal pain by age 15. sickle cell anemia.CFIAPTER 1 Abdominal and Gastrointestinal Disorders Gury A. Many conditions that present as abdominal pain represent severe disease that requires immediate intervention. In a prospective study of 230 patients followed-up for 5 years. and cystic fibrosis.

Appendicitis pain classically occurs before vomiting. (ll Pathophysiology Most abdominal pain is transmitted through visceral components. as well as the capsules ofsolid organs. Episodic sharp pain that comes in increasing waves is often considered "colicky. This withdrawal will move abdominal contents including the peritoneum and may indicate peri- tonitis. A positive iliopsoas sign is pain that occurs when the patient has right lower quadrant pain when he . Nonspecific abdominal pain as a discharge diagnosis is relatively unusual (9% to lgo total). aggravating or palliative factors should be queried. however. the history should include location of pain.2 / EunnctNcn MtuctNn: THn Conn Cunnrculurr. tapping the patient's heel in order to move the abdomen. Many additional physical tests have been described. and -5 distribution).g.. appendicitis). is characteristically vague. movement of pain. this rule is violated in many appendicitis patients. malignant disease (l3o/o). Rebound tendemess may indicate peritonitis. and presence or absence of bright red blood or melena must be queried. Somatic pain often originates in the peritoneum and is much better localized than visceral pain. Physical Examination Abnormal vital signs including tachycardia and elevation of temperature can be important clues to patients who have truly emergent or surgical presentation of disease. It is wise to begin palpation away from the most tender area since the patient may provide more voluntary guarding after a tender area is elicited. simple inspection will reveal a localized mass or general distention of the abdomen. This may be indicative of appendicitis.. it is considered a positive Murphy sign. time of onset. Murphy's sign tests for possible cholecystitis. and pancreatitis (4 to 5%o) are common diagnoses.g. The iliopsoas sign also looks for possible appendicitis. Referred pain is frequently involved with evaluation of abdominal pain. pain is well localized and more easily described. Common referral patterns include pain in the chest (e." Such pain may increase the suspicion of a hollow viscus as the origin (e. The abdomen should be palpated for the point of maximal tenderness and total area oftenderness. Often the general appearance ofthe patient can be helpful. however. urinary frequency. Pain often moves and in many cases its final destination is more predictive of the final diagnosis than its original location (e.g. Patients with peritonitis will lie very still to avoid any movement that may irritate their inflamed peritoneum. Associated symptoms provide important clues to the diagnosis. incarcerated hernia (5 to l0%). Masses and organomegaly must specifically be searched for. Pain that has been present for a long period of time is less likely to be emergent. Bowel symptoms including frequency and nature of stools. Simply moving the stretcher. or discoloration of urine should be noted as should menstrual history in female patients. or diabetes) will impact and complicate the presentations of abdominal pain. Once the peritoneum is irritated. Infrequently. While palpating the right upper quadrant the patient is asked to take a deep breath. Possible neural mechanisms include stretch fibers. Hepatic or sphenic enlargement should be noted.r Acute abdominal pain in the elderly is frequently a lifethreatening illness. Emergency Department Evaluation Historical Factors For patients who present with abdominal pain. giving a sensation in the neck or the back of the shoulder blade (C-3. atherosclerotic risk factors. Rovsing's sign is positive when pain in the right lower quadrant occurs with palpation in the left lower quadrant. and duration of pain. The test must be interpreted with care since abrupt movements startle patients and their response to the test may be difficult to interpret. Visceral pain is often poorly localized. If the patient suddenly halts inspiration in response to pain in the right upper quadrant. and pain near the diaphragm. Also. Mortality in this patient population is significant to l4oh) and one-third of patients required operations. which are in the wall of all organs. Patients with colic will frequently be very mobile and be difficult to examine because of their unwillingness to lie still. Dysuria. Very active bowel sounds may be a clue that the patient has increased gastrointestinal motility. The presence of nausea or vomiting may help indicate the presence of hollow viscus disease. A past history that reveals prior abdominal pathology or prior surgical procedures may provide important clues as to the final diagnosis. bowel or ureter). The abdomen should be auscultated for presence or absence of bowel sounds. Symptoms referable to organs in the chest or retroperitoneum must also be queried. giving an upper quadrant tenderness. It is important to note location of prior surgical scars. Acute cholecystitis (26 to 4loh). -4. or lightly percussing the abdomen may provide alternative tests for detecting peritonitis. many patients with acute appendicitis or cholecystitis present more than 12 to 24 hours after the onset of pain. and. pneumonia). Multiple medical diseases (cardiac orpulmonary disease. Input from these organs is conducted along afferent nerve fibers that return to the spinal cord at various levels.. A traditional method of testing for rebound tenderness is to palpate the abdomen somewhat deeply and then rapidly remove the hand.

Lipase has been reported to have higher predictive value than serum amylase. Br Med J 1979. A hemodynamically unstable patient should have large-bore IV catheters placed and isotonic fluid administered. Complete blood count is often ordered to examine the patient's hematocrit and white blood cell count. and pancreatic disease. it is clear that judicious use of anal- gesics in closely observed patients may be safely performed. Testing for hepatic enzymes may be very helpful in the setting of acute hepatitis. Pyuria may occur with disease that is not intrinsically renal such as appendicitis. Bilirubin. Buchert GS. bowel perforation is suspected anaerobic and enterococcal coverage should also be provided. angiography. Acute bleeding will have a normal hematocrit. If SELECTED READING Analgesia and the acute abdomen. Abdominal pain in children: an emergency practitioner's gide. Amylase is present in nearly all hollow organs and therefore may be elevated with salivary gland or gastrointestinal disease. should be measured to screen for hepatobiliary disease. Testing for occult blood may be helpful as well. Patients with suspected urinary tract infections or bowel perforations require antibiotic administration. and quality of stool. Alkaline phosphatase will also be elevated in hepatic disease but more severely elevated in most cases of biliary tract disease. Brewer RI. The obturator sign also looks for appendicitis. the hip is rotated internally. Gunn AA. Bower RI. With the right leg flexed at the hip. Golden GT. antibiotic therapy.. or pancreatitis. or free intraperitoneal air. Abdominal pain an analysis of 1. alanine transaminase) will be elevated with hepatic inflammation or masses.. Other patients may have a life-threatening presentation or a confusing presentation that requires multiple lab tests to be performed. Abdominal radiography may be performed to look for evidence of bowel obstruction. calcifications. gastroenteritis). biliary tract disease. Total white count and white count differential may imply presence of bacterial or surgical disease. Am J Surg 1976. computed tomography.g. However. Palpation ofthe back and percussion over costovertebral angles should always be performed. Hepatocellular enzymes (aspartate transaminase. Pelvic examination should be performed on all women with lower quadrant pain. Emerg Med Clin North Am 1989. . Special radiographic Laboratory Evaluation phv. Bell MJ. Despite traditional concerns. but chronic blood loss with an insufficient compensatory mechanism may reveal a low hematocrit. foreign bodies. Diagnostic value of the white blood count and neutrophil percentage in the evaluation of abdominal pain in children. Adequate gram-negative coverage is required in either case. Laboratory evaluations of patients with abdomen pain may be very specifically or very broadly undertaken. appendicitis.2:1093. examination of male genitalia is mandatory in all patients with lower quadrant pain. Similarly.7(3):497-517. Amylase and/or lipase may be measured to look for pancreatic inflammation.131:219-223. All patients should have pulmonary and cardiac examinations as well.g. urolithiasis) or a more systemic insult (e. and ultrasonogra- Since many patients have a potentially serious disease that is difficult to diagnose.AloourNer eNo GIsTRoTNTESTTNAL DrsonoBns / 3 tries to flex at the hip against resistance. it may be elevated in a large number of non-pancreatic disease states also. Disposition Certainly some patients may have a clear diagnosis based on history and examination alone and laboratory analysis is not required. The literature has addressed the place of leukocye and neutrophil counts in the evaluation of appendicitis. Temberg JL. and analgesia. These tests would include intravenous pyelogram. Control of emesis with antiemetics or nasogastric suction may aid in maintaining appropriate fluid hydration. Br J Surg 1 988. Treatment Emergent treatment of these patients include hemodynamic management. A pregnancy test should be performed in all female patients of child-bearing age who have not had a hysterectomy.000 consecutive cases in a university hospital emergency room. Rectal examination should be performed for presence or absence of mass. a low threshold should be present for obtaining consultation and admitting patients with acute abdominal pain. The test is positive if pain is elicited with this motion. there is extensive crossover with other diagnoses including benign diagnoses (e.g. Diseases that are notoriously difficult to diagnose include ischemic bowel disease. Plain abdominal radiographs and acute abdominal pain. Patients with appendicitis do tend to have higher white counts and higher percentage of neutrophilia. However. both total and direct. pain.. It is clear that patients who have tubal ligation are still at risk for pregnancy-related diseases.75:554-556. Surg Gynecol Obstet 198l. Campbell JPM. Urinalysis should be performed on all patients with suspicion of urinary tract infection (UTI) or a suspected tests may be considered in patients after initial evaluation. These will also be elevated in other disease states. emergent cause of pain. This will also be more modestly elevated with biliary tract disease. endocarditis).152:424426. Hematuria may indicate renal disease (e. Administration of analgesics has always been controversial in the setting of acute abdominal pain. Hitch DC.

2) Varices (1. et al. of acute will present with a history that may difficult and. DeDombal FT. The occurrence of a variceal bleed portends severe disease with high mortality.ll(1)47-52. isoamylase. A patient with a variceal bleed will typically present with massive hemorrhage and shock./or painful swallowing. It is a common cause of esophageal chest pain.1.143:751-754. but is less common than reflux and spasm. J Clin Gastroenterol 1989. Staniland JR. It is the most posterior component of the mediastinum. The diagnosis is made by lack of motility on barium swallow and confirmed by esophageal motility stud- telangiectasia. Symptomatic relief from esophageal spasm may be accom- plished with nitrates.144:338-340. The diagnosis is typically not made in the ED. The contraction and consequently the pain may last just a few seconds or many hours. In the evaluation of the patient presenting to the ED for dysphagia. sclerotherapy. jaw. patients with dis- covered ESOPHAGUS (1. The esophagus is the proximal poftion of the upper gastrointestinal (GD tract originating just distal to the epiglottis and ending at the entry to the stomach. Ditchbum J. The true incidence and etiology are unclear.1. Emergency therapy consists of vasopressin infusion at 0. calcium channel blockers. Air. Structural Disorders (1. 1. Trapped fluid may slosh or splash. 1) Esophageal spasm results from synchronous contrac- tion of esophageal smooth muscle along the length of the esophagus and is typically associated with pain. and lipase in the acute abdomen. leading is increased collagen to fibrosis and a thinning of the mucosal elements. Portal hypertension is most commonly seen with hepatocellular disorders such as cirrhosis or cancer and should be suspected in patients with these disorders. large food boluses.4/ ErunncrNcv MnucrNr: Tnn Conn CunrucuLUM Fenyo G. Nearly one-third of deaths from upper GI bleeds occur in these patients. or Sengstaken-Blakemore .1.5 units per minute with emergency embolization. but on occasion this cannot be accomplished in the ED. Clinical presentation abdomen: study of 600 patients. along with other etiologies that impair contraction of esophageal smooth muscle.1. or gas. is associated with decreased and absent esophageal peristalsis. The patient will typically complain of substernal chest pain. and cyclic antidepressants.Wang SS. however.2 to 0. (1. LinXZ. which may radiate to the arm. Histologically there deposition. et al. Prognosis ofacute nonspecific abdominal pain: a prospective sfidy. visualized in the esophagus on posteroanterior (PA) and lateral chest films may suggest the diagnosis of scleroderma as an etiology for dysphasia. Persistent bleeding requires urgent gastroenterology consultation. Acute abdominal disease in the elderly experience from two series in Stockholm.3:393-398. Portal vein thrombosis may occur in patients with normal hepatic function. or neck. Spasm may be precipitated by reflux. Scleroderma. or exercise. Motor Abnormalities (1. Progressive esophageal dilation may result in prolonged retention or regurgitation of undigested food. Am J Surg 1982. Bjerregaard. Achulasia (1.1) Esophageal Spasm Scleroderma or Raynaud's phenomenon should prompt a rheumatologic referral for further evaluation. It serves as the portal of entry to the GI tract.2. ies.2) Achalasia is a syndrome manifested by absent or abnormal esophageal motility often coupled with a rigid lower esophageal sphincter. the presence of sclerodactyly. 1. swallowed materials at extremes of temperature. Underlying hepatocellular disease may also induce coagulopathy and other metabolic disorders. It is supplied from short branches off of the thoracic aorta and from the inferior thyroid and left gastric arteries. many patients with noncardiac chest pain suffer from unrecog- nized achalasia. It is innervated by the spinal accessory and vagus nerves and the autonomic nervous system. Jess P. Serum amylase. Br Med J 7972. TsaiYT. Nasogastric tube placement evaluation of continued bleeding should be performed. anticholinergics. Fluid and blood resuscitation is mandatory.1. Brynitz S. The lower esophageal sphincter also may become incompetent in scleroderma. but several authors report an association with a decrease in the numbers of ganglion cells in the esophageal mesenteric plexus. During the course of the spasmodic episode the patient will also have difficulty in further attempts at swallowing. There is presently no evidence to suggest that careful for instrumentation causes variceal trauma or induces bleeds. also known as progressive systemic sclerosis. calcinosis. The emergency physician must attempt to differentiate this pain from that of cardiac etiologies.1) or suspected achalasia should be referred to ensure appropriate follow-up. Am J Surg 1982.1) Esophageal varices are dilated veins that occur as the result of portal hypertension. The patient is consequently The typical patient span several years of more prone to aspiration and pneumonia. The motility disorder is most commonly recognized in the lower two-thirds of the esophagus. and has venous drainage through both portal and systemic distributions.

or as a complication of carcinomatous spread. Tears (Mallory-Weiss Syndrome) (1. increased risk for esophageal foreign body occurs in alcoholics and those with dentures. Perforation of the cervical esophagus in the setting of flexion-hyperextension trauma has been reported. cases of mediastinitis from Boerhaave's syndrome are usually fatal in 2 to 3 days.2. esophageal rupture. regurgitation. Regardless of type. Small objects (i. carbon tetrachloride inhalation. esophageal hematomas may be associated with bleeding or mass effect resulting in dysphasia or chest pain. Etiologies include hemophilia. is best demonstrated radiis less likely to Gastrografin Although ographically. which is a characteristic crunching sound accompanying systole. Vomiting. A case report of perforation following the Heimlich maneuver has been documented. aortic arch. Perforation also may also occur following erosion or ulceration.. The most common offending instrument is the rigid endoscope. or left-sided empyema are all suggestive of Boerhaave's syndrome. In pediatric patients. objects may lodge at the thoracic inlet' Patients with esophageal canceq esophageal webs and rings.5) Esophageal hematomas are a relatively rare finding and can be either traumatic or nontraumatic. Mediastinal gas may be by auscultating Hamman's crunch. A small percentage of small perforations have been shown to heal spontaneously without infectious sequelae. In the absence of treatment. The evacuation of a pneumothorax may be indicated in the ED as well.AgooN. or performing the Valsalva maneuver against a closed glottis can also result in esophageal detected rupture. coagulopathy. surgical vagotomy. The treatment of Boerhaave's syndrome is surgical. uremic hypocoagulation. vomiting. Inmates in correctional institutions are a special risk. in addition to the above.) Foreign-body ingestion occurs most commonly in toddlers. the patient should be admitted for observation and therapy. then a barium esophagram should follow.2. Those with a communication radiographically appear with the "double-barrel" lumen sign and are thought to represent a paftial rupture of the esophagus. sclerotherapy of esophageal varices. and motility problems may present with obstructing objects at other levels. typically results from a force applied against a weakened esophageal wall as occurs with repeated emesis or prolonged gastric intubation. 2.1. as it is better tolerated in the mediastinal demonstrate employed space and does not obscure visualization for endoscopy.3) Perforation may occur from penetrating trauma.1. Perforation when unrecognized and untreated can lead to indolent and eventually overwhelming infection simi- lar to that with rupture. foreign-body ingestion. <2 to 5 cm) are more likely to pass through the esophagus. If a Gastrografin swallow does not demonstrate a perforation when one is suspected" especially with penetrating trauma. a mediastinalbased left pleural effirsion.IINAL AND GASTRoINTESTINAL DIsonoEns / 5 intubation reserved for massive persistent bleeding in most commonly are the result of recurrent or violent patients who are vasopressin failures. These esophageal rents are usually superficial and mild with minimal self-limited bleeding.6) Aside from children and those with cognitive impairment. Objects that lodge do so at the predictable narrowings located at the cricopharyngeus. Hemodynamically stable patients without evidence of active upper GI bleeding on nasogastric evaluation may be managed conservatively as outpatients. The presence of mediastinal emphysema. foreign body ingestion. Foreign Body (1. erosion from aortic aneurysm. in that they will attempt concealment of restricted material or will ingest material to seek a temporary medical release from the facility. More that 95% of . Esophageal perforation an esophageal perforation. The combination of chemical and bacterial insult produces a rapidly progressive and profound mediastinitis.1. esophageal strictures. and the lower esophageal sphincter. There are scattered case reports of spontaneous intramural esophageal hematoma. In cases with ongoing or massive blood loss. Iatrogenic precipitants are as follows: upper endoscopy. and blunt trauma (including minor head injury). The patient will typically present with a complaint of bright red blood in the vomitus after series of regurgitations. it should be first.2. either direct or pneumatic.4) Mallory-Weiss tears are longitudinal disruptions in the esophageal mucosa at the gastroesophageal junction that Hemstoma (1.e. Intramural esophageal hematomas are of two main types: those with and those without a communication with the intraluminal space. (Body packing for the smuggling of illicit drugs may also cause obstruction. 1. or iatrogenic causes. hiccuping. Rupture (B oerhaave's Syndrome) (1. and esophageal dilation. In some cases the amount of bleeding may be massive and require fluid and blood therapy. 2. left mainstem bronchus. 1. Historically the treatment has been that of surgical repair. 2) Boerhaave's syndrome. and emetic administration. Perforation (1. Fluid resuscitation and rapid broad-spectrum antibiotics are important ED interventions.

7) Diaphragmatic hernias can be either congenital or traumatic. is operative. stridor.6 / EN. Localization can be aided by the use of contrast radiographs. gagging. and a sunken abdomen. and second. Nondigestible objects that pass through the esophagus into the stomach require surveillance to ensure successful passage. 2. Attempts at esophageal foreign body removal with Foley or other balloon catheters should be discouraged" even under fluoroscopic guidance.2. The aspiration offood contents from this cavity may occur when the patient lies down. The neonate born with congenital diaphragmatic hernia typically has early severe respiratory distress. Both nifedipine and nitroglycerin also relax the smooth muscle of the esophagus and may be utilized. particularly in children. the presence of barium makes endoscopic removal difficult. if a perforation has occurred. In the ED small esophageal foreign bodies. because of the risk of pulmonary aspiration and respiratory compromise. thereby eliminating the risk of aspiration. The treatment of diaphragmatic hernias. retching. plain radiographs can make this determination. The battery may cause esophageal electrical burns in as soon as 4 hours after ingestion and esophageal perforation in as soon as 6 hours. is made when abdominal viscera are seen above the diaphragm on the chest roentgenogram. A barium-soaked cotton ball may be employed. The failure to identify a foreign body by plain radiographs does not exclude its presence. In the evaluation and management of the patient with an ingested foreign body. In the case of ingested coins. and should not be employed. Treatment is sup- portive initially with endotracheal and gastric intubation for respiratory distress with eventual surgical repair. Esophageal coins will be viewed in the anteroposterior (AP) or head-on projection on standard AP or PA radiographs.rsncsNcy MrorcrNr: THn Conn CunrucuLUM patients with a piece of meat impacted in the esophagus will have predisposing pathology. coughing. Hiatal Hernia (1. if not impossible. Objects have been known to lodge in diverticula or in the appendix with infectious and obstructive consequences. Tracheal coins will be viewed in the lateral or edge-on projection on standard AP or PA radiographs. 1. Treatment is surgical. patients with severe respiratory distress may require endotracheal and gastric intubation with more urgent repair. 1.1. because of impairment of visualization. Patients who do not have an early radiographic diagnosis made will present with respiration compromise and dysp- nea. small lung volumes.5 to 1. Although the use of enzymatic degradation of impacted food has been advocated in the past. whether penetrating or blunt in etiology. Diaphragmatic Hernia (1. Children are often not observed to have ingested anything and may manifest with drooling.8) Zenker's diverticulum is the most common esophageal diverticulum and is a pharyngoesophageal pouch that may result from incomplete relaxation of the cricopharyngeus. other than sharp objects and batteries. Healthy patients with small objects in the distal third of the esophagus can be considered for glucagon administration (0. Traumatic diaphragmatic herniation can occur as a result of blunt trauma or with penetrating injury . If a perforation is suspected but cannot be demonstrated with water-soluble contrast. can be observed for up to 12 hours to allow for spontaneous passage. The patient may complain of regurgitation of food ingested several days earlier. Ninety percent of congenital diaphragmatic hernias occur on the left and correspondingly displace the apical impulse of the heart to the right. It is thus imperative that an esophageal battery be removed or advanced into the stomach immediately. if not made in utero. An easy way for the clinician to remember this may be to consider that the coin must turn sideways to pass through the vocal cords into the trachea.2. it is important to maintain and protect the airway. With right diaphragmatic hernia the diagnosis may be delayed as the presence of the liver slows this translocation. Diverticula (1. or an inability or unwillingness to eat or drink. such agents can also degrade the esophagus. Button-battery ingestion represents a special circumstance ofesophageal foreign body. the emergency physician may need to determine the nature ofthe foreign body and confirm that it lies in the esophagus and not in the respiratory tree. Indirect laryngoscopy may be of benefit in some cases. On occasion lodged digestible material can be advanced into the stomach under endoscopic guidance rather than retrieved. Any object that does not pass out of the esophagus requires endoscopic removal.0 mg IV) to relax the esophagus and enhance the likelihood of passage. resulting in perforation. water-soluble contrast is much better tolerated in the mediastinum. In some cases.9) A hiatal hernia is defined as the herniation ofpart of the stomach into the thoracic cavity. The majority of cases are on the left and recognized by early migration of abdominal contents into the thorax. The clinical situation may require intubation to protect the airway. The diagnosis. This chamber may be seen on neck radiographs. The typical adult may present with a history of ingestion or may have the sen- sation that something is lodged. If the gastroesophageal junction and part of the fundus of the stomach her- . barium must be employed before perforation can be excluded. Water-soluble contrast is preferred in the evaluation of esophageal foreign body for two reasons: first.

Reflux esophagitis is worsened by agents or activities that decrease the tone of the LES. chocolate. will provide both symptomatic relief and reduce the dam- monly present decade.10) AND GASTRoINTESTINAL DIsorueRS / 7 estrogens. aspira- . and by age 70 as many as 600/o of patients may have a hiatal hernia. Liquid caustics are associated with more rapid and diffuse injury than are solids that stick on a particular site and burn until they are removed or washed off. fatty foods. Webs and Strictures (1. The physical state of the material is important. caffeine. When they occur in the distal esophagus they are also referred to as esophageal rings or Schatzki's ring.Aroouner niate. The stomach contents also play a role. Cuustic Injury (1. Decreased esophageal motility and diabetes can also worsen reflux and potentiate esophagitis.1. More recently promotility agents such as metoclopramide have been associated with success. calcium channel blockers. Pyloric sphincter tone also plays a role in the duration of contact. materials proximal to the lower esophageal sphincter (LES). or rarely alkaline bilious. smoking. webs present with obstruction. but not to the same degree as that with acidic ingestions.1. It is often associated with decreased LES tone and hiatal hernia. nitrates. below). Ifnot ies. progestins. 2) Caustic esophageal injuries result from ingestion either acidic or alkaline substances. Sucralfate. if the gas- troesophageal junction remains in the abdomen and another portion of the stomach herniates alongside the esophagus through the esophageal foramen. Short courses of proton pump inhibitors such as omeprazole have been reported to be of benefit. Aspiration of caustic alkali may produce glottic and subglottic edema. During this and other periods of recumbency.1. The majority of cases of hiatal hernia are asymptomatic. A sour taste or exacerbation by leaning forward or with the Valsalva maneuver is a common historical feature. stress. preg- nancy.3. lifting. particularly when given as a slurry. of Caustic Alkali tis is also reported.3. The obese and marginally overweight should be counseled that weight loss will also reduce reflux. Plum-"t-Vittto. Patients with severe reflux esophagitis require elective endoscopic evaluation to exclude the precancerous lesion of Barrett's esophagus and to evaluate for stricture formation. The head of the bed can be elevated 4 to 6 inches to reduce nocturnal reflux. The degree of injury with alkaline caustics is related to several factors. Hz blockers can increase gastric pH. A hiatal hernia is often present with a ring. this is known as a sliding hiatal hernia. A hiatal hernia may require repair if it is large or symptomatic. 1.t syndrome is the combination of iron-defi- ciency anemia As rings beco The mainstay of treatment for reflux esophagitis is behavior modification to reduce the risk factors. The presence of a hiatal hernia may enhance reflux or may strangulate or incarcerate.3) Reflux Esophagitis (1. Alkaline caustics will continue to burn until they are removed or diluted by the liquefaction that they induce. Also of concern are precipitants ofincreased gastric acidity such as spicy foods. Stricture-complicating reflux may be more age from gastric acid. the duration of contact and time until dilution portend the degree and depth ofinjury' Ifthe caustic induces laryngeal or esophageal spasm. particularly in the dilution rate. and anxiety. Esophageal Strictures Esophageal stricture formation is a complication of esophigeal inflammation or injury such as with chronic insult from reflux esophagitis or with single wounding as in the case of caustic ingestion (see Inflammatory Disorders. there is no gravitational resistance to proximal migration of gastric contents. producing pain or obstruction. alcohol. 1) Reflux esophagitis is the erosive or digestive injury to the esophagus that occurs with the retrograde propulsion or leakage of acidic gastric. Esophageal Webs Esophageal webs are outpouchings in the squamous epitheiium of the esophageal mucosa that may be cir- cumferential. The patient with reflux esophagitis will often complain of severe heartburn. forward bending. Most of the damage due to reflux occurs at night while the patient sleeps. this is known ur i putuetophageal hernia. Thus.2. Recalcitrant cases can be referred for surgical therapy such as by Nissen fundoplication. it can be held and its effect concentrated in a local area. and anticholinergics. sometimes awaking from sleep. or straining may also precipitate reflux. Exercise. Inflammatory Disorders (1. These include smoking (nicotine).

1. monilial esophagitis may occur in the absence of any oropharyngeal findings. water) dilution should be employed. is manifested by scar retraction. In the evaluation and treatment of caustic ingestion. Alkaline esophageal burns evolve through four distinct phases. Phase 0 is the immediate liquefactive necrosis. A liquid-filled stomacl will demonstrate diffrrse injury. During this time translocation of bacteria from the esophagus to the mediastinum may occur without perforation and lead to mediastinitis. Caustic Acids With acidic compounds.4) Herpetic Esophagitis (1.2) Monilial or yeast esophagitis is manifested by mild odynophagia. Rapid pro- esophagus are somewhat spared. Authors differ on whether or not milk (or. As with other viral lesions. increasing vascular thrombosis and the sloughing of necrotic layers. and the majority of immuno_ onset. In the case of an empty stomach. who should receive acy- clovir therapy. The treatment is ticular attention to t acid-base disorders. Lifelong surveillance is mandated. Consequently. less preferably. and these patients may do better with early surgery. these patients. given the increased risk of squamous esophageal carcinoma following alkaline caustic injury. Phase 1 occurs in the first 5 days and is marked by an acute inflammatory process with mucosal hemorrhage. Monilial Esophagitis (1. the injury is located in the antral and midgastric regions.4. greater contact time is required for injury.5% sodium hydroxide. beginning anytime after 2 weeks postinjury. given the likelihood that all the damage may have already been done. collagen deposition begins. 1. but may last up to 6 weeks. and respiratory-enteric fistulae.B/ EnarncoNcy MeucrNr: Tun Conr CunrucuLUM tion pneumonitis. Any patient with a phase 3 burn should have bronchoscopy to evaluate the degree of pulmonary injury. The predominant site of injury for caustic alkali is the esophagus where rapid liquefaction necrosis has already taken place by the time the patient presents to the ED. The prudent endoscopist will advance the endoscope only to the point of the first circumferential (phase 3) burn and withdraw This will minimize the risk of iatrogenic perforation and confirm that the burn is basically as bad as it can be. Dilution and neutralization of acid is contraindicated secondary to the strong exothermic reac_ tion that ensues. Immediate gastroenterologic consultation for careful early endoscopy should be employed. In the immunocompromised patient. The stomach is most commonly involved and the preingestion stomach con_ tents determine the location of maximal injury. adult respiratory distress syndrome.4. Opponents cite the increased risk of vomiting. and The evaluation of acid ingestion by clinical means is corre- injury rophaof correlate well with gastric injury. It is this progressive contraction of collagen fibers that reduces both circumference and length of the esophagus and that strictures in 7oh will eventually give rise to esophageal to 15% of patients. phase 2 is a repair phase during which granulation tissue develops. Phase 3. It can occur in nonimmunocompromised individuals. unlike the distal injury found with solid-filled stomachs. Should severe pain with swallowing be manifest. and complications are more common in the immunocompromised. Full+hickness esophageal burns are complete in I second of contact with 30% sodium hydroxide. but require a full 10 seconds with22. . Esophageal rest for the first 6 to 8 weeks is universal therapy. the oropharynx and Infectious Disorders (1. It typically follows an upper respiratory infection. it is self-limited in the immunocompetent. another or coexistent process is suspect. These patients require close follow-up and should receive dilation or replacement for stricture depending on the severity. Caustic acids produce a coagulation necrosis with also gas. particular attention must be paid to the airway. l) Herpetic esophagitis is the upper GI manifestation of herpes simplex virus infection. and mucosal reepithelialization begins.1. Phase 2 is often complete by l5 days postinjury. The treatment of acid ingestion also requires careful rapid assessment for tion.

and utilizing avariety of radiologic and nuclear medicine procedures when appropriate. phrenic nerve dysfunction. Motility disorders of the esophagus. The liver stores glucose in the form of glycogen and through gluconeogenesis it is able to supply this source of energy during fasting. and management. A controlled trial of corticosteroid in children with corrosive injury ofthe esophagus. Although the precise diagnosis of liver disorders is rarely confirmed during a single ED visit. Management of foreign bodies of the upper gastrointestinal tract: update. and those with esophageal stricture following caustic ingestion. reviewing the liver function tests (LFTs). The liver and the kidney provide the two most common pathways by which foreign substances are excreted from the body. It is supplied with blood by the portal vein. Rouse TM. Ott DJ. Randolph JG.69:867-876. the esophagus must be narrowed by 50% to 670/o before the patient experiences difficulty swallowing solids. and transport moieties. which serves as a complex biochemical "factory. Gas tro intes t E ndosc 1 995 . Davies HA. Kerr WF. which form the bile ducts and carry bile formed within the liver to the gallbladder and the intestine. Liver biopsy to obtain tissue for histologic review is often mandatory for precise diagnosis and the determination of the extent of liver disease. drinkers. performing an appropriate physical examination. neck mass from tumor. usually (70%) after metastasis has occurred. The occurrence of odynophagia is a poor prognostic indicator. Other modalities used to detect liver disease. Radiol Clin North Am 1994. protected by the rib cage. It is also supplied by the hepatic artery.1. Ingestion ofcorrosive substances by adtrJts. which is heavily innervated. Gastroesophageal reflux. The parenchyma of the liver is devoid of pain fibers but the organ is encapsulated by Glisson's capsule. prevalence.4 I ( I ) :39-5 1. Within the portal triad are the canaliculi of the biliary tree. The typical patient will present after a period of progressive dysphagia and tumor growth. DeMeester TR. SELECTED READING Anderson KD. N Engl J Med 1990.92:412421. It is located in the right upper quadrant of the abdomen lust beneath the diaphragm. The history. a low pressure capillary system relatively permeable to serum filtrate. Treatrnent of acute variceal bleeding. is made in the liver at the canalicular membranes. and prognosis. the patient may also present with voice changes. Puncturing or distorting Glisson's capsule results in the clinical sensation of pain. Unfortunately.92(suppl 5A):5s-10s. the tumor is advanced and has had the opportunity to metastasize before the symptoms have become severe enough to cause the patient to seek medical attention.5) Esophageal carcinoma is a devastating disease. gastroparesis.21 (l): 103-1 18. diagnosis. Gastroenterol Clin North Am 1992. Any patient with suspected or possible esophageal malignancy should have an urgent outpatient evaluation and staging. a careful and focused approach will allow the clinician to determine if management requires an inpatient versus an outpatient . Ketoconazole remains the drug Tumors (1.35:890-897. Peters JH. The liver is the sole site of albumin production and is the source of many other proteins in the body including coag- ulation factors. to the central venules that eventually coalesce to form the hepatic vein. infection. Current diagnosis and treatment of gastroesophageal reflux disease. Depending on the location of tumor and its pattern of spread. thus. Approximately 20% of the cardiac output passes through this vital organ. which solubilizes fat during digestion and contains substances excreted from the body via the liver. through the sinusoidal capillaries. intestinal. The patient may not have difficulty with liquids until the lumen has been narrowed to a diameter of 4 mm by the growth of the cancer. are rarely employed in this setting. Castell DO. Wilcox MC. Patients who progress to systemic infection should receive a course of amphotericin B." Evaluating liver function clinically involves obtaining a thorough history. Am J Med 1992. and certain less invasive radiologic studies such as ultrasound are readily available tools. MatloffDS.AsloN{rNAL AND GASTRoTNTESTTNAL of choice for Candida esophagitis. Esophageal disease in acquired immunodeficiency syndrome: etiology.2) The liver is the largest solid organ in the body.7 3 (6): I t t9-t | 44. particularly the immunocompromise4 may require higher doses or fluconazole. but some patients. Anginal pain ofesophageai origin: clinical presentation. and colonic fields. Thorax 1980. Spontaneous intramural rupture and intramural haematoma of the oesophagus. Bile. Surg Clin North Am 1 993 . those with Barrett's esophagitis. bleeding. LrvER Dnononns / I (1. which drains the splenic. DeVault KR. LFTs. physical examination. Webb WA. a branch ofthe celiac artery. such as the liver/spleen scan or biopsy. 32(6):1117-1134. This results in a lower 5-year survival than that seen with many other malignancies. Am J Med 1992. Gumaste V! Dave PB. If such cannot be arranged" admission may be necessary. which drains the liver. or subcutaneous emphysema. Blood flow within the hepatic microvasculature passes from the portal tria4 which contains the terminal venules of the portal vein and the arterioles of the hepatic arter1y. Patients at greater risk for esophageal can- cer include smokers. tobacco chewers. It typically presents in advanced and/or inoperable stages. Am J Gastroenterol 1992.87( I ): l-5. It detoxifies drugs and metabolites that pass through it via the portal vasculature. 323(10):637440. Some of these methods of assessment are commonly employed in the ED. and is a rich source of nutrients and substances absorbed from the gut. Mayo Clin Proc 1994. complement factors. or pulmonary infection secondary to either aspiration or perforation. which provides the majority of the liver's oxygenated blood.

Although liver transplantation has significantly improved the overall outcome in many of these patients. and malnutrition or excess albumin wastage. This family of enzymes is not exclusive to the liver. as well as failure in the conjugation process. Historical information regarding liver diseases should include the standard detailed "history ofpresent illness" as is usually obtained. are commonly part of a "liver function" panel.1) ^ Hepatitis literally means inflammation of the liver. can lead to hypoalbuminemia despite a functioning liver. alanine aminotransferase (ALT) and aspartate aminotransferase (AST)." Failure of liver synthetic function will lead to an elevated PT and bleeding as well as hypoalbuminemia and its consequences. Acute self-limited hepatitis usually heals without sequelae. family history of liver disease orjaundice. caput medusae. Dupuytren's contractures. fat malabsorption. A cost-effective approach to liver disease requires a working knowledge of the tools available to the practitioner for evaluating liver disease. cytomegalovirus (CMV). Chronic hepatitis may remain indolent and subclinical for decades until the patient succumbs to an unrelated problem. the metabolite of hemoglobin. for example. The multiplicities of etiology and natural course make hepatitis a challenging medical condition. the etiologic agent (a virus or drug for example) will cause fulminant destruction of the liver parenchyma with lifethreatening results. will cause hyperbilirubinemia. Practitioners in this setting should be familiar with the basic evaluation and management of these entities. the syndrome of fulminant hepatic failure still has mortality rates of between 30To and7}o/o. alcohol usage.10 / ErrasncnNcy MnorcrNn: Tnr Conn CunrucuLUM setting and facilitates all aspects of subsequent clinical Excess unconjugated hyperbilirubinemia may result from care. and ascites must be carefully recorded whenever liver disease is suspected. Somewhat arbitrarily hepatitis has been divided into "acute" (less than 6 months in duration) and "chronic" (greater than 6 months) categories. and herpes simplex virus (HSV) are the major viruses responsible for hepatitis. Various types of autoimmune hepatitis exist and these diseases almost invariably become chronic in nature. such as occurs in the nephrotic syndrome. is conjugated to make it lipid soluble within the hepatocyte. Hepatitis. The prothrombin time (PT) and the serum albumin come closest to being actual tests of liver "function. portal hypertension and its complications. as well as a basic understanding of the pathophysiologic processes involving the liver.2. cirrhosis with or without synthetic failure. Alkaline phosphatase levels may be significantly elevated as a result of a biochemical defect in bile production at the canalicular level or secondary to a gross mechanical obstruction to bile flow such as an impacted gallstone. vitamin K deficiency (broad-spectrum antibiotic use. Obstruction to the creation of bile or its flow through the biliary ductal system. Rarely. pahner erythema. Liver function tests (LFTs) are chemical and hematologic studies grouped together due to their potential relevance to hepatic abnormalities. and prior liver dysfunction must receive extra attention during questioning. Hepatitis (1. hepatic neoplasia. However. Elevations in conjugated bilirubin denote pathology in the liver or biliary system. Wilson's disease and crr-antitrypsin deficiency are two rare inherited metabolic diseases that cause chronic hepatitis. Epstein-Barr virus (EBV). The aminotranferases. Viral (1. Specific points such as drug/toxin exposures. Bone tissue has active alkaline phosphatases. malnutrition) can lead to an abnormal PT despite an intact liver. but they take several days to process and are rarely useful for decision making in the ED setting. It may also lead to liver destruction with synthetic failure and portal hypertension within months. blood transfusions. There are many causes for hepatitis. splenomegaly.1. risk factors for viral hepatitis (sexual practices. Many other viral agents can cause liver inflammation as part of their clinical presentations as well.1) Viral hepatitis is common. Hepatotrophic viruses A through E and G (HAV HBV and so on).2. the blockage of the production and flow of bile. may be present for decades without being noticed unless more invasive rneans of evaluation are employed. Viruses. A carefully obtained history and physical examination may not disclose serious liver disease. drugs and toxins (especially alcohol). HAV and HEV are selflimited diseases. The other hepa- . which can cause excess bilirubin formation and overwhelm the normal liver. Although ALT is far more specific for liver tissue than AST. hemolysis. Indolent chronic hepatitis. Alkaline phosphatase actually represents a family of enzymes that are associated with cholestasis. Bilirubin.). They are routinely elevated with hepatocellular damage or death such as would occur in hepatitis. hepatomegaly. The presence or absence ofjaundice. and bone growth or repair leads to elevated serum levels of alkaline phosphatase. intravenous drug abuse. etc. Other LFTs such as the 5'-nucleotidase or 1-glutamyl transpeptidase are useful in determining if alkaline phosphatase abnormalities are liver related. and hepatic abscesses are diseases ofthe liver encountered in emergency medicine. these assays do not measure actual hepatic function and they may be "abnormal" as a result of the dysfunction of organ systerns other than the liver and biliary tree. neither is exclusive to liver tissue and must be interpreted in this light. and hypoxemia are the most cornmon etiologies. It is subsequently excreted via bile. Strictly speaking. "spider" telangiectasias. gynecomastia and tes- ticular atrophy in males.

but follow-up should be timely and include repeat LFTs to ascertain stability. DrsoRorns / 11 and an antibody to hepatitis C (HCV Ab). all potentially exposed contacts should be sought and prophylaxis. Patients require admission for intravenous hydration if severe nausea and vomiting have led to dehydration. Treatment generally centers around the removal of the offending agent and supportive care. Hepatitis A and E are RNA viruses spread via the fecal-oral route through contaminated water or foods. In addition. Substitutions should be considered for any necessary drugs suspected of being the cause of the hepatitis. In HCV over 5070 of those infected become chronically infected. Hepatitis B immune globulin (HBIG) is used to prevent clinical disease after exposure to HBV A successful vaccine against HBV has been in use for over l0 years. HAV is very common in the United States but there has not been an outbreak of HEV in the United States yet. or improvement. HBV (a DNA virus) leads to chronic hepatitis in approximately l0% of cases. such as food handling. should be offered. surface antibody (HBVsAb). When a patient presents with symptoms and signs of liver disease. and core antibody (HBV cAb). The latter is appropriate in the vast majority of cases. HCV is an RNA virus spread by parenteral means. Serologies are needed to confirm the diagnosis (although routine serologic testing is not yet available for HEV and HGV). Virtually all drugs and many environmental chemicals may result in liver disease. Successful prophylaxis against HBV prevents HDV Unexpected births in the ED to mothers infected with HBV should prompt inoculation with HBIG and the first of the three doses of the HBV vaccination series. HB! HCY and HDV may all be self-limited or lead to chronic infection. deterioration. if available. or both. low-grade fever. Patients with viral hepatitis commonly present with flulike symptoms (malaise. a thorough drug and toxin exposure history must be obtained. Alterations in drug dosing might need to be considered when there is the possibility of altered hepatic drug metabolism.AsooNrrNAL eNo GISTRoTNTESTTNAL totrophic viruses may lead to chronic hepatitis. liver failure. Less than 0.4) Drugs and toxins are another very common cause of both acute and chronic hepatitis. Over-the-counter preparations can be just as dangerous and the review should include them as well as prescribed medications and illicit "recreational" drugs. although the subsequent clinical courses are variable from patient to patient. follow-up review of the pending serologic tests should be arranged. Outpatient follow-up with a primary care physician is acceptable for the routine presentations ofviral hepatitis. Further serologic testing may be warranted after these studies have been reviewed. EBV (mononucleosis). Hepatotoxins such as alcohol and excess acetaminophen should be avoided during recovery. Liver disease may manifest as hepatocellular dysfunc- tion. The following serologies should be sent when the diagnosis ofviral hepatitis is suspected: hepatitis A antibody (HAV Ab). Some people are never clinically compromised while others encounter cirrhosis. Pregnant women are advised against travel to endemic areas. Fulminant hepatic failure as a result of drug toxicity often requires transplantation. Chronic autoimmune . HDV is an incomplete RNA virus that requires coinfection with HBV Like HBV HDV is transmitted via the parenteral route and will become a chronic infection if the HBV does so. All unnecessary drugs should be stopped until the precise diagnosis of the liver disorder can be ascertained. Patients with hepatitis should be counseled to avoid behaviors that might spread infection. but obtaining them promptly in the ED facilitates further workup. They also require urgent admission if there are any manifestations of liver failure (as discussed below). Sexual contacts and maternal-fetal infections are recognized" but the rates ofthese routes oftransmission are less than for HBV Intravenous drug abuse with shared needles is a common source of infection for both HBV and HCV Forty percent of HCV infections are considered to be of unknown origin. anorexia) and may not be recognized as having hepatitis without concomitant jaundice. Gamma globulin has not provided prophylaxis and there is no vaccine. hepatitis B surface antigen (HBV sAg). myalgias.2. CMV ("heterophile-negative" mononucleosis). Drugs may cause idiosyncratic liver disease or they may do so in predictable dose-related fashion. Drug and Toxin (1. until the risk of infection can be clarified and more specific recommendations can be made. In the ED it is also necessary to determine whether admission to the hospital is required or outpatient followup is adequate. Viral hepatitis may be reportable to local public health officials. cholestasis. Gamma globulin reduces the clinical manifestations of HAV after exposure. If infectious hepatitis is confirmed. The results of these initial serologic tests will be available hours to days after the initial visit. Other liver and biliary tract disorders can present similarly especially in the elderly and immunosuppressed population. etc. and/or hepatocellular carcinoma. sexual contact.1. Relatively small doses of acetaminophen (greater than 2 g per day) can be dangerous when there is existing liver damage. and HSV infections generally cause systemic infections that may or may not have hepatitis as a major clinical component. A vaccine is available for the prevention of HAV Prophylaxis against HEV is not yet available. Chronicity usually occurs in babies who acquire the virus from their infected moth- ers at birth..01% of the HAV infections lead to fulminant hepatic failure. but l0% or more HEV infections (especially in pregnant women) cause death. blood donation. The natural course of the newly discovered HGV infection is not well characterized as yet.

Table l-l lists several drugs well known to induce liver disease. Good. Liver biopsy can be quite dangerous in the face of severe coagulopathy and is rarely performed in this setting. Most patients can be handled as outpatients unless complications such as portal hypertension or liver failure intervene. If autoimmune hepatitis is suspected. The ED may treat patients with this entity if they have been transported from outlying areas or for some other reason have had time elapsement since the initial hypoxic insult.2) Liver failure refers to the condition in which enough hepatic parenchyma has been damaged or destroyed that synthetic and metabolic function are compromised. However. but very serious. significant leukocytosis. The liver's dual blood supply lessens the likelihood of this occurring at the local level. Alcoholic hepatitis should prompt admission to the hospital and immediate cessation of all alcohol consumption. Hepatitis is a rarer. alcoholic hepatitis often presents with fever. Cirrhosis.12 / ElmncnNcy MnorcrNn: TABLE 1-1.1. Drug doses may need to be altered in patients with liver dysfunction. Autoimmune hepatitis is uncommon. Because of the need for pyridoxine as a coefficient of ALT and ASI and the fact that pyridoxine deficiency is common in alcohol abuse. It may present emergently as fulminant hepatic failure with or without a hemolytic crisis. These definitions are clinical. Often it is recognized as chronic hepatitis due to abnormal LFTs or when family members of known probands are screened. Chronic liver or hepatic failure takes 6 months or longer to transpire. Alcoholic (1. at some point in time. liver failure can lead to the death of the individual. Clearly. can cause hepatitis andlor hepatopathy. In the case of fulminant hepatic failure the hepatocytes are generally destroyed in large numbers leading to metabolic failure. Ischemia. the disorder manifests fully within weeks of the onset of symptoms. Drugs may trigger autoimmune hepatitis. can result from systemic hypotension or an acute restriction of hepatic blood flow. This should not be interpreted as suggesting that alcoholic hepatitis is less serious. the peak levels of these two enzymes are generally much lower than those seen in viral. If this process evolves between 8 weeks and 6 months it is considered subacute or subfulminant hepatic failure. can result from the consumption of alcohol in large quantities for long periods of time. the fibrosis of hepatic parenchyma. '.5) Alcohol causes fatty liver. or ischemic hepatitis. Aceta- minophen should be avoided if at all possible. which is reversible upon disof consumption.2. or dosed sparingly (no more than2 gtotal per day) as patients with alcoholic liver disease are very susceptible to acetaminophen toxicity. and profoundly deranged liver function. Similar to acute tubular necrosis. Unlike the relatively subtler presentations of viral hepatitis and drug-induced hepatitis (excepting fulminant hepatic failure as a presentation).2. In the ED setting the complications of liver failure and portal hypertension are commonly encountered and the practitioner needs to be aware of them. result of ethanolism with a 50% mortality rate. Controversy exists as to continuation whether alcoholic hepatitis is an acute or a chronic hepatitis. ." with significant elevations in transaminases and concomitant synthetic and metabolic dysfunction. or adult respiratory distress syndrome (ARDS).shock liver. this potentially lethal form ofhepatitis requires lengthy and heavy exposure to ethanol. Virtually any drug may be responsible and all should be considered when the diagnosis of liver disease remains obscure. both acute and chronic. Treatment is aimed at removing possible culprit drugs and initiating immunosuppressive therapy with pred- nisone (or an equivalent) and azathioprine under the direction of a gastroenterologist/hepatologist. Maintenance of hemodynamic stability and tissue oxygenation and the avoidance ofpotential hepatotoxins during recovery are the mainstays of therapy. Fulminant hepatic failure has been arbitrarily defined as the clinical syndrome in which a patient with no known prior liver disease suffers deteri- orating liver function and resultant hepatic encephalopathy within 8 weeks. Clinically. balanced nutrition is important to the recovery of these patients and corticosteroids may be helpful in serious cases that are not complicated by gastrointestinal bleeding. Emergent treatment focuses on the management of the portal hlrpertensive complications or emergency orthotopic liver transplantation in the case of fulminant hepatic failure. Tnr Conr CunrucuLUM Common drugs known to induce liver disease Nitrofurantoin Sulfonamides Acetaminophen Aspirin lsoniazid Phenytoin Diltiazam Methotrexate (hepatopathy often without abnormal LFTs) Note: All drugs should be suspected until another etiology for liver dysfunction is found. but many cases are idiopathic. Cirrhosis (1. Wilson's disease is a congenital disease involving inappropriate copper metabolism with subsequent copper overload in the liver and brain. drug-induced. or as a complication of cirrhosis and portal hypertension. prostration. an antinuclear antibody and an anti-smooth muscle antibody should be obtained. hepatitis may result from drug-related hepatitis and require corticosteroids and/or immunosuppressive therapy.

Deficient gluconeogenesis leads to hypoglycemia. disorientation Stage 3: Disorientation. which may worsen the liver disease. hypoxia. Portal hypertension is the condition in which the blood pressure in the portal venous system exceeds ll to 12 mm Hg and blood is shunted back to the systemic venous circulation via ves- tigial venous systems. Second. Radiologic shunts.rrNAr eNo GIsTRoTNTESTTNAL DrsoRnnns Synthetic failure can lead to hypoalbuminemia as well as other protein deficiencies causing defects in immunity. including blood. octreotide. Portal vein thrombosis (or the thrombosis of a major component of the portal venous system. Variceal bleeding should be managed directly with endoscopic sclerotherapy or banding while additional pharmacologic agents such as octreotide or vasopressin with nitroglycerin are used to lessen portal pressure.AenoN. while every effort is may to avoid hepatotoxins and mitigate any ongoing hepatitis. It should be suspected in anyone with a massive bleed who has known liver disease where it is often further exacerbated by concurrent coagulopathy. First. The other method is the reduction of the portal venous system pressure. Urgent intubation and volume expanders. Although cirrhosis with sinusoidal fibrosis is by far the most common cause of portal hypertension in the United States. Management of variceal bleeding via shunting procedures as described below will often exacerbate HE as more blood bypasses the hepatic sinusoids. Clinically patients manifest with increasing CNS inhibition such that they initially become irritable and subsequently become more confused and / 13 TABLE 1-2. The resultant condition mimics the Budd-Chiari syndrome in many ways. Gastroesophageal varices may bleed massively. and propranolol have been used to decrease portal blood flow and pressure. which lessens the uptake of urea. Massive hemorrhage and death can result. drowsy. unarousable. which would normally process them. and sedating medications (especially benzodiazepines and barbiturates) can induce clinical HE or exacerbate it. Varices that are known to be present but have not bled should be managed with nonselective beta-blockade using propranolol. This parasite's eggs are deposited in the small venules of the portal venous system within the liver parenchyma but before the sinusoidal capillaries. compromising the patient's airway and causing hypotension and shock. The Budd-Chiari syndrome refers to the obstruction of the hepatic vein. somnolent but arousable to stimuli Stage 4: Deep coma. and ascites. they tend to do better even if their elevated portal pressure causes massive bleeding. Stages of hepatic encephalopathy Stage 1: Restless. such as the splenic vein) can result in shunting. benzodiazepine-like substances. Since the hepatic parenchyma and synthetic function are preserved in patients with schistosomiasis. potential airway compromise somnolent until frank coma ensues. Variceal bleeding is the most dramatic and imminently life-threatening complication of portal hypertension. variceal bleeding. shunted away from the liver and into the systemic circulation. y-aminobutyric acid. Hepatic encephalopathy can be treated with bowel purging and the acidification of the luminal contents. carries substances that would normally be metabolized in the liver in greater concentration to the central nervous system (CNS). Chemotherapy and bone marrow transplantation can cause clotting at the level of the initial hepatic venules. Refractory bleeding may be controlled by placing one of several specially designed intraluminal balloons into the stomach and esophageal lumina. This results in neuroinhibition of the CNS. Massive bleeds naturally decompress the system but may cause death before the bleeding stops. Hepatic encephalopathy (HE) is a clinical condition in which blood. Additionally the liver is deprived of its metabolic needs. The hepatic sinusoids are bypassed. metabolites and drugs from the gut bypass the liver. This creates two basic problems. portal hypertension presents a mechanical problem. This compromises blood flow into the liver from both the portal vein and the hepatic artery. other lesions can cause this condition. Vasoactive substance such as vasopressin. but conclusive proof of the precise etiologic agent or agents remains elusive. asterixis present. with an overall mortality rate of 30o/o to 50%. agitation Stage 2: Cognitive impairment obvious. are required as a gastroenterologist is summoned to attempt variceal sclerosis or banding. Hypoglycemia. Lactulose is commonly employed to create an osmotic diarrhea and to acidify the gut contents. acid. Ammonia. disruption of sleep/wake cycle. known as transjugular intrahepatic portosystemic shunt stents (TIPSS). intercurrent illnesses and infections. This leads to an increased levels of a variety of substances in the systemic circulation. Thin-walled vestigial veins may not be able to tolerate the increased blood pres- sure and rupture. Schistosomiasis infection is the most common cause of portal hypertension worldwide./base disorders. nitroglycerin. These entities should be sought out and aggressively corrected when a patient presents with HE. The balloons are then inflated to tamponade the variceal bleeding. Direct variceal tamponade is one of two basic ways in which the bleeding can be controlled. The three main complications of portal hypertension are hepatic encephalopathy. can be placed under fluoro- . The stages of "coma" in hepatic encephalopathy are noted inTable 11. Ischemia and metabolic failure can ensue and the liver can become severely compromised. and carrier mechanisms. In this setting pressure is transmitted back through the sinusoidal system and into the portal system. and other substances have been implicated in the pathogenesis of this condition. mercaptans. some of which have untoward biologic effects. electrolyte abnormalities. short chain fatty acids. subtle cognitive impairment. slurred speech. coagulation.

in conjunction with strict dietary sodium restriction (as low as 500 mglday)." Cirrhotic livers have been observed to be "weeping" during laparoscopic visualization. if portal hypertension is presinusoidal. Appropriate antibiotics include cephalosporins and penicillinase- resistant penicillins. it should be assayed for cholesterol.4) The liver is a common site for benign and malignant neoplasia (both primary and metastatic). It can be triggered by therapeutic attempts at managing the ascites and edema resulting from portal hypertension. An albumin gradient is calculated by subtracting the ascites albumin level from the serum albumin level. Chronic pancreatic fistulae. Antibiotics and the drainage of the ascites are the means by which this infection is managed. A low gradient and a history of malignancy. malignancies. Emergent sists referral for liver transplantation should be considered adding loop diuretics as needed subsequently. HRS appears to result from disordered hemodynamics and the decrease in effective arterial volume seen in cirrhosis. Several theories exist to explain various aspects of the HRS. and often deadly complication of end-stage liver disease. tense ascites will lead to umbilical rupture and rapid decompression. which have loose junctions and tend to be "leaky.1 or greater suggests a portal hypertensive etiology. Hepatocellular carcinoma (HCC) is a common malignant tumor worldwide. especially if the patient had been receiving diuretics. There are reports of improvement in patients suffering from HRS with the placement of TIPS stents. The increased pressure ofthe portal system forces filtration of the blood plasma through the sinusoidal capillary walls. A diagnostic paracentesis should be performed to distinguish the cause and rule out infection. Ascites causes restrictive lung disease at greater volumes. The third major complication of portal hypertension is ascites. It may be triggered by the use of nephrotoxins as well. Rarely. Oliguria accompanied by azotemia and a rising BUN and creatinine. Kidneys from patients dying of HRS will function upon transplantation if acute tubular necrosis has not supervened. It results from cirrhosis . It can have profound effects on the hemodynamics of the body and self-perpetuate. It may lead to early satiety and anorexia due to gastric compression. but the only routinely (albeit not always) successful intervention is orthotopic liver transplantation. The history and physical examination are often useful in suggesting the underlying etiology. This technique increases the culture sensitivity by approximately 40o/o to 50%. This fluid is relatively protein-poor and can serve as culture media for bacteria. Tense ascites.2. Asymptomatic neoplasia is noted when radiologic studies such as ultrasounds or CAT scans are performed for abnormal LFTs (detected as part of screening surveys if the patients are asymptomatic) or for unrelated reasons that include a liver window. whereas a gradient less than 1. an amylase level should be checked. Spontaneous bacterial peritonitis (SBP) is likely due to hematogenous contamination of this fluid although transmural contamination from the gut has been postulated. A low urine sodium. Studies have shown improvement in response to paracentesis and the resultant hemodynamics with the use of salt-poor albumin. and SBP can be managed by therapeutic large-volume paracentesis with the goal of removing as much fluid as possible. and albumin should be infused intravenously (25 g) at the time of the paracentesis. and intestinal lymphatic obstruction are readily identifiable causes of free intraperitoneal fl uid collection. The fluid should be sent for a cell count and differential. Prostaglandin inhibition can cause or seriously exacerbate the hepatorenal syndrome and should be avoided. Ascites is an example of "third-spacing" in which fluid collects within the body but outside the vascular and interstitial compartments. but isolate sensitivities should dictate specific therapy. should if prompt the clinician to send the fluid for cytologic review Management of portal hypertensive ascites con- therapy using aldosterone first. A gradient of 1. especially the fluid is cloudy. Tlrmors (1.1 cautions the practitioner to look for another cause. Ascites is not exclusively the result of portal hypertension. is suggestive. Ifthe patient has a history ofpancreatitis and/or pseudocysts. and a "bland" urinalysis in the face of serious liver disease suggest this syndrome. The use ofnon- steroidal antiinflammatory drugs (NSAIDs) should be avoided in all patients with cirrhosis or ascites of uncertain etiology. Transplantation provides definitive care for cirrhotic ascites. All patients with suspected HRS should be admitted and a urine sodium should be checked. which is a final pathway in the development of the qmdrome. This phenomenon can occur in the gut venous system.If the fluid is milky.3) The hepatorenal syndrome (HRS) is another common. and Streptococcus pneumoniqe is the second most often identified. refractory ascites. as well. and for culture using direct inoculation of 10 ml of ascitic fluid into each blood culture bottle directly at bedside. Intrarenal prostaglandin inhibition has been shown to decrease intrarenal blood flow. Aminoglycosides may precipitate renal insufficiency in cirrhotic patients and should be avoided. Escherichia coli is the most common bacterial isolate. Salt-poor when appropriate. The first step in managing ascites is to ascertain the cause. an albumin level. Simultaneously a serum albumin level should be checked.2. TIPS stents may lessen portal pressure and reduce refractory ascites. Hepatic/Hepatorenal Failure (1.14 / EnrnncnNcy MnorcmE: TFrn Conr CunnrculuM of diuretic scopic control to decompress the portal system. a low urine sodium.

and hematogenous spread are cofilmon sources. Pagliaro L. abdominal pain (if there is distortion of Glisson's capsule). 23 26. Schiff ER. most notably the gallbladder and biliary tree.54% of autopsies and at half that rate in hospitalized patients. La Villa G. DsonnnRs / 75 droemetine are effective against E. or bulky disease.47(6): 1435-1441. Massive infiltration by primary or metastatic disease might lead to frank liver failure. HCC is resistant to radiotherapy and chemotherapy. Surgical resection of limited HCC affords the only real hope for cure. If the amebic abscess ruptures and contaminates the pericardium (extension from the left lobe of the liver). Pyogenic abscesses have a 25Yo or greater mortality rate. histolytica. the initiating factor is obstruction ofthe neck ofthe gallbladder or the cys- . cholecystitis. Morgan MY The treatment of chronic hepatic encephalopathy. Current therapeutic approaches to vital hepatitis. fertility. but serious diseases of the biliary tract include ascending cholangitis and gallstone ileus.g. Carcinomas of the biliary tract are much less common.3. and dyhy- Vukmir RB. or biliary colic. Portal hypertension: diagnosis and treatment. Clin Inf Dis 1995. N Engl J Med 1994. 13(4):42343s Runyon B. and obesity. Both of these entities are most commonly caused by cholelithiasis. Evaluation 1994. Care of patients with ascites. and shock. various streptococcal species. Jensen DM. metastases. Smaller or multifocal abscesses may be treated with pharmacotherapy alone. which is inflammation or infection of the gallbladder. Diagnosis and managetnent of fulminant hepatic failure. Abscess (1. GALLBLADDER AND BILIARY TRACT (1. Pyogenic abscesses account for 90% of cases and often are caused by E. Referral for further evaluation and management is the general rule for liver masses detected in the ED unless a related complication provokes a crisis. They are more common in areas where human feces is used as fertilizer or in institutions such as facilities for the mentally handicapped. hypotension from hemorrhage. associated with abnormal LFTs. are far more common causes for these presenting symptoms and signs. although approximately one in five cases remains cryptogenic.1) Acute inflammation of the gallbladder is one of the most frequent causes of abdominal emergencies. Hepatctgctstroe ntero I ogv1'99 1 :38:37 7 -387 . however. Management ofend-stage liver disease. Reddy KR. which is pain due to temporary obstruction of the common bile duct. It is estimated that approximalely 20 million Americans have gallstones. Biliary tract infections. and hepatopathies such as hemochromatosis.. Less common. Cholecystitis (1. intraabdominal infections (e. Broad-spectrum antibiotics should be employed in addition to drainage. Fregia A. Comp Ther 1995. the mortality rate may exceed 25oh. they are seen in up to 0. Risk factors include increasing age.23(suppl l):3644. The majority of patients present with acute cholecystitis.20(r):50-54 of abnormal liver tests Contp Ther Hirschman SZ.20:741-746. Segmental resection or orthotopic transplantation may help unless the patient already has symptoms. Liver tumors present with pain if they grow big enough to distort Glisson's capsule. J Hepatol 1995. Entamoeba histolytica causes abscesses with less symptoms of inflammation than pyogenic types. Drainage of an amebic abscess should be undertaken ifit appears large enough to rupture or when a pyogenic abscess is suspected.AsroN4rNrAL eNn GesrnorNTESTrNAr of all kinds. D'Amico G.21(4):166 17l. female gender.14(1):71-tll Nizam R. 29-33.25 (5):29 48-29 52. Kirsh BM. with poor 5-year survival rates ranging from 2oh to 5o/o. and very large tumors (both benign and malignant) can rupture leading to pain. and tumors. even if small. Approx- imately 900/o of cases of acute cholecystitis are caused by gallstone disease.3) Acute diseases of the biliary tract. and tissue densities might suggest that it is not solid. or concomitant biliary obstruction. suggests the diagnosis. Wiley TE. Am Fam Physician 1993. Drug-induced hepatic disorders Pharmucol Ther 1996. are responsible for a large number of ED visits. Percutaneous or open drainage will confirm the microbiology and is very important in the management. Fever. coli. Layden TJ.330(5): 33'7-342. Buniak B. Pathophysiology In most cases of acute cholecystitis. They can trigger fever and this may prompt the patient to seek medical attention. Laffi G.2. although an elevated alpha-fetoprotein is suggestive. Carson JL. Changchien CS. various staphylococcal species. appendicitis). Pyogenic liver abscesses. Acalculous cholecystitis accounts for only approximately 5Yo of cases. Approach to a liver tnass. Luca A. chloroquine. Cholangitis. Amebic abscesses occur in approximately l0% of patients with liver abscesses. et al. leukocytosis. and anaerobes. but larger abscesses will require drainage. Gentilini P Pathogenesis and management of the hepatorenal syndrome Semin Liver Dis 1994.5) Hepatic abscesses are rare. Ultrasound and CAI scan will suggest a space-occupying lesion. Tiznsp I ant P ro c 1 993 .2 I (I): 16. Sarrtln Liver Dis 1993. SELECTED READING Chiou SS. Malignant tumors often produce anorexia and wasting. chronic hepatitis (especially viral). while uncomplicated amebic abscesses are lethal approximately l%o of the time. The diagnosis requires histologic confirmation. Antiamebic therapy with metronidazole. Strategic placement within the parenchyma may cause biliary obstruction with jaundice. Lam N. the ingestion of aflatoxins and exposure to hepatotoxins.

and pancreas. or multiple system failure. Ensuing infection can serve to worsen the preexisting inflammatory process. Visualization of both the gallbladder and common duct is a negative test with a negative predictive value of 98%. hepatic abscess. myocardial ischemia. This bacterial invasion occurs either from blood-borne organisms or from bacteria ascending from the duodenum via the common bile duct. or perforation. For patients with total bilirubins greater than 5 to 7 when the sensitivity of HIDA scanning declines. Prompt surgical consult is warranted. Abdominal x-ray may show evidence of localized small bowel loop dilatation in the area of the gallbladder (a sentinel loop) indicating an ileus. may be detected as well. Inflammation may also be attributed to the cytotoxic constituents of the bile itself including phospholipase and its conversion to lysolecithin. and pericholecystic fluid has positive predictive value of 90%. most commonly gram-negative rods (E. The isotope is taken up by hepatocytes and is secreted into the bile canaliculi allowing outline of the gallbladder within approximately t hour. ovarian disease. tachycardia. Evidence of other disofthe liver. fevers. Significant physical findings include temperature elevation. and possibly antibiotic therapy. burns. The literature suggests a misdiagnosis rate of approximately 20%o when relying on clinical diagnosis alone. These episodes of pain may be in direct relationship to the consumption of a heavy meal or fatty foods. This obstruction causes increased secretion of fluid from the glands within the gallbladder wall. The dilated gallbladder may be palpable in30% of patients. The presence of gallstones. Even though their use is questionable. narcotic use. Patients may report a prior history of similar pain that had resolved spontaneously. hepatitis. and congenital absence of the gallbladder. antimicrobials are still recommended. tis or other acute renal Management Most treatment in the ED is supportive and symptom oriented. and fevers may be present. but may be present in acute cholecystitis as well. Patients most at risk include those with diabetes. gangrene. Ultrasonography has now become the radiologic test of choice for acute cholecystitis in the emergency setting. peptic ulcer disease. Evidence ofjaundice may indicate a stone in the common bile duct. chronic cholecystitis. This pain may initially be colicky in nature. coli) and anaerobes (Bacteroides fragilis). vomiting. Nausea. False positives may occur in certain conditions such as fasting for extensive periods. Radiation of the pain is usually to the tip of the right scapula. pancreatitis. Contributory factors implicated in acalculous cholecystitis include fasting. kidney. Nuclear scintigraphy with 99m-technetium-labeled hepatobiliary inodiacetic acid (HIDA) is generally now considered the gold standard for the detection of acute cholecystitis. or to the use of a narcotic analgesia. the use of diisopropyl IDA (DISIDA) allows the visualization of the a eases. It is possible that keeping the stomach empty with nasogastric suctioning may diminish gallbladder stimulation. tenderness in the right upper quadrant most notably with deep inspiration (Murphy's sign). and possibly evidence of peritonitis including guarding and rebound tenderness. However. sepsis. thickened gallbladder wall. Ancillary Tests There are no truly diagnostic laboratory studies for cholecystitis. Narcotics are effective in controlling the pain of acute cholecystitis. The resultant increase in hydrostatic pressure causes distention of the gallbladder and subsequent ischemia of the wall. Coverage with a broad-spectrum second- or third-generation cephalosporin is usually adequate . Liver function tests such as serum aminotransferase and alkaline phosphatase may be within normal limits or slightly elevated. Aggressive treatment of dehydration with crystalloids is warranted. pyelonephridiseases. Failure to visualize the gallbladder indicates cystic duct obstruction and is considered a positive test. dehydration. The pathogenesis of acalculous cholecystitis remains a mystery. Meperidine is preferred over morphine since the latter may cause spasm of the sphincter of Oddi. which causes spasm of the sphincter of Oddi.16 / ElrnRcrNcy MrucrNr: Tsr Conr Cunnlculuu tic duct by a gallstone. Presentation The most common presenting complaint in patients with acute cholecystitis is right upper quadrant or epigastric pain. The accuracy of ultrasonography approaches 100% for the detection of gallstones. Nausea and vomiting usually can be relieved with antiemetics and possibly nasogastric suctioning. extremely high white blood cell counts may be due to complications such as cholangitis. and ectopic pregnancy. Dffirential Diagnosis Other considerations in patients suspicious for acute cholecystitis include appendicitis. including those biliary tree. Leukocytosis with evidence of a left shift on differential is common. chronic diseases. Bacteria are only isolated in 50Yo to 75oh of cases. An elevated amylase is indicative of acute pancreatitis as a diagnosis either solely or concurrent with acute cholecystitis. total parenteral nutrition. but eventually becomes constant. Higher elevations of aminotransferases and total bilirubin are suggestive of a common bile duct stone. right lower lobe pneumonia.

3. Blood cultures should be obtained immediately and coverage with broad-spectrum antibiotics should be initiated as soon as possible. Definitive therapy is to drain the biliary tree either by surgical. Ancillary Tests Leukocytosis with a left shift is common. via blood from the portal vein. the patient should have early surgical intervention. mortality rates are as high as 30oh to 40o/o. which is the obstruction of the common bile duct by gallstones. and Enterococcus. Bacteroides. Serum aminotransferases may be mildly elevated. The most common pathogens include E. Often. Immediate cholecystectomy is usually reserved for patients with evidence ofcomplications such as gangrene or perforation. Cholangitis was first described by Charcot in 1877. and gentamicin is warranted. and anaerobes. clindamycin. vasopressors may be necessary. Klebsiella. The differential . This process is almost exclusively a disease ofthe elderly. Hyperbilirubinemia and an elevation of alkaline phosphatase are often seen. has been reported to occur in 8% of patients admitted for biliary tract disease. Other symptoms and signs include nausea.3) Gallstones are present in approximately 20o/o of women and 8oh of men. Bacteria may seed the common duct either by retrograde invasion from the duodenum. Lack ofvisualization during nuclear scintigraphy may be useful to diagnose common duct obstruction early on in the disease process. All patients diagnosed with acute cholecystitis should be admitted and have inpatient evaluations and treatment. percutaneous transhepatic cholangiography (THC). An alternative to triple antibiotic coverage is mezlocillin since it is actively secreted into the biliary tree and covers gram-positive cocci. depression of the white blood cell count may be seen in cases with evidence of sepsis.Asno\arNAr AND GASTRoINTESTINAT DtsoRor. The onset of laparoscopic cholecystectomy has made it advantageous to put off surgery until the gallbladder inflammation has 75o/o have resolution decreased or resolved. coli. Cholelithiasis and Choledocholithiasis (1. If acidosis is a concern.000 operations are performed per year due to the complications of cholelithiasis. Diagnostic alternatives include computed tomography (CT) scanning. or endoscopic means. Disposition Patients who are afebrile with relatively normal liver function tests and white blood cell counts and whose pain subsides with narcotic analgesia are thought to have biliary colic. They should be advised to return immediately for persistent pain or fevers. Approximately 500. and tachypnea. Fluid resuscitation with crystalloid is usually necessary to stabilize blood pressure. Most often it is associated with choledocholithiasis. transcutaneous. These patients can be discharged with pain medication and scheduled for outpatient workup. making laparoscopic surgery pos- sible. Management Stabilization of the patient from a hemodynamic stand- point should take priority. fever. Allowing a "cooling off" period also provides for the medical stabilization of acutely ill patients. The most common presentation of cholelithiasis is biliary colic. Presentation Right upper quadrant abdominal pain. and endoscopic retrograde cholangiopancreatography (ERCP). Approximately of patients with acute calculous cholecystitis will of symptoms with medical management alone. On occasion. vomiting. In patients in whom the diagnosis is missed initially. and clindamycin or metronidazole. arterial blood gases should be obtained. gram negatives. Pathophysiology The obstruction of the common bile duct either by gallstones. Ultrasonography may demonstrate stones within the gallbladder or biliary tree and possibly common bile ductal or intrahepatic ductal dilatation.Rs unless sepsis is suspected. incomplete obstruction is seen in cholangitis. and jaundice (Charcot's triad) characterize cholangitis. or benign stricture leads to increased intraluminal pressure and bacterial infection. completing Reynold's pentad. or through the lymphatic system. The timing of surgery for acute cholecystitis remains somewhat controversial. one must always keep in mind cholecystitis and hepatitis since their presentations are similar. Usual antibiotic recommendations include ampicillin. Cholangitis (1.3.2) Infection within the biliary duct system. cholangitis. When evaluating these patients. More / 17 severe cases may be associated with altered sensorium and hypotension. tachycardia. Sepsis is a common complication of cholangitis. abdominal x-rays may reveal air in the biliary tree. the use of a triple antibiotic regimen such as ampicillin. aminoglycosides. Early surgical consultation is a must. malignancy. however. The presence of common duct stones (choledocholithiasis) in acute and chronic cholecystitis is approximately 7o/o to l5o/o. In the septic patient. In the face ofsepsis. If there is evidence of complications such as gangrene or perforation.

multiparity. These stones are usually single and larger than 2 to 3 cm. Nausea and vomiting may accompany the pain and may become severe enough to cause dehydration. located anywhere in the upper abdomen but most commonly in the right upper quadrant or epigastrium. to limit the effects on the sphincter of Oddi. These crystals form a nidus for stone formation. This pain may radiate to the tip of the right scapula. extracorporeal shock wave lithotripsy and oral administration of bile acids have been proven to have some effectiveness. There may be evidence of dehydration such as tachycardia and orthostasis. especially meperidine. Removal of the gallbladder by surgical means is the most common intervention. Nausea and vomiting can be relieved by antiemetics and nasogastric suctioning if necessary. Right upper quadrant or epigastric tenderness is often present. diseases of the ovary fallopian tubes. Brown stones can form either in the gallbladder or the intra. Pain is best treated with narcotic analgesia. There are two types of pigmented stones-black and brown.3. Cholesterol stones are formed when there is a high concentration ofcholesterol in the bile. retained common duct stones should be suspected. These episodes may be caused by either the migration of small stones through the common bile duct or temporary lodging oflarger stones in the neck ofthe gallbladder during gallbladder contraction. pyelonephritis. pancreatitis. Fistulous formation may be the result of prior surgery. When patients are asymptomatic.18 / Err. pregnant uterus. Management The management of biliary colic is symptomatic relief.rnncnNcv MsnrcrNl: Tns CoRE Cunnrculurr. Rarely. they may be discharged with a prescription of narcotics to be used for similar episodes. Bacterial as well as parasitic infections such as Ascaris lumbricoides and Clonorchis sinensis have been incriminated. Physical findings are often limited. Leukocytosis may aid in the An unusual complication of cholelithiasis is gallstone ileus.r diagnosis of biliary colic includes acute cholecystitis. Approximately 4Yo calcium by weight is needed for a stone to be radiopaque. Surgical evaluation or referral is necessary for further workup and intervention. Black stones are formed in the gallbladder and of calcium bilirubinate. Serum aminotransferases are important to obtain to help differentiate between this disease entity and hepatitis. family history. obesity. Detection of dilated intrahepatic and common bile ducts is also possible with ultrasonography. begin the process. tracheobronchial tree. renal pelvis. rapid weight loss. sonography is negative.4) Episodes of biliary colic are frequent in the ED. There is a past history of known cholelithiasis in 50Yo to 75Yo. The formation of a fistula is not always to the duodenum but may be to any organ of the gastrointestinal tract from the stomach to the colon.or extrahepatic biliary system and are frequently associated with infection. Commonly associated diseases include major cardiovascular disorders and diabetes mellitus. usually the duodenum. renal colic. This entity is most frequently seen in older women (average age 64). female gender. allowing the passage of gallstones from the gallbladder into the intestinal tract. peptic ulcer disease. Gallstone ileus is responsible for lYoto2%o ofmechanical small bowel obstructions. Both black and brown stones contain calcium bilirubinate. pleural or pericardial cavities. The patient may relate a history of previous episodeg of similar pain and an association to the consumption of fatty foods or heavy meals. . Bilirubin levels will help detect the presence of a common bile duct stone. Dehydration is treated using IV crystalloids. Pathophysiology Adhesions between the gallbladder and intestinal tract. Eventually a fistula forms. hepatitis. and myocardial ischemia. differentiation of acute cholecystitis from biliary colic. or ureter. appendicitis. If a patient has had previous cholecystectomy. Ultrasonography is highly accurate for the detection of gallstones (approaching 100%). jaundice may be encountered. Risk factors include increased age. The pain may be colicky or constant. Presentation Gallstone Ileus (1. Cholesterol crystals precipitate when the cholesterol concentration exceeds the ability of the bile acids and lecithin to reduce it. and drugs such as clofibrate and oral contraceptives. Elevations of amylase and lipase Pathophysiology may indicate pancreatitis. however. cystic fibrosis. This stone then can form an intraluminal obstruction. Oral cholecystography is used to detect gallstones in the highly clinically suspicious patient when ultra- There are two types of gallstones-cholesterol and pigmented. Ancillary Tests Most commonly obtained laboratory evaluations are usually within normal limits. ovarian cyst. These are most often seen in the elderly and those contain a large amount stones patients with sickle cell anemia and hereditary spherocytosis. pneumonia. Plain radiographs provide little clinical information since only l0%o of stones are radiopaque.

hernias. Both ultrasound and CT scanning can be used to image the tumor.3. As an endocrine organ. T! et al. 1989. 1992. carcinoid tumors. Luten RC. Serum bilirubin is often elevated to extremely high levels. Barkin R.5th ed. Ultrasonography may show dilated intrahepatic ducts. glucagon. All lesions are histologically adenocarcinomas. Ultrasonography may be helpful. Nasogastric suction- ing to relieve gastric distention and vomiting will be required. Brown. Wilson J. for definitive diagnosis. et al. In'. Acute acalculous cholecystitis. Spencer F. In: Emergency medicine: concepts and clinical practice. Kadakia SC. weight loss. Emergency medicine.3Yo. Shires G. et al. et al. Ruiz E.131-132. Ancillary Tests The most helpful test in this disease is a radiologic examination of the abdomen. Aghababian RY Fleisher GR. and distention. DsoRlans / 19 of jaundice. 1988. 5-year survival rates range from 32o/o to 620/o. Nuclear hepatobiliary imaging. Plain abdominal x-ray may demonstrate evidence of small bowel obstruction or air within the biliary tree. Acute cholecystitis. the pancreas is an organ that serves multiple functions. Kim EE. Approximately 90oh of patients have had a history of cholelithiasis. 1991. In: Principles ofsurgery. crampy abdominal pain. Acute diseases of the gallbladder. trypsin. but THC is associated with the highest yield. Wide surgical excision is required for cure. Linden CH. chymotrypsin. vomiting. Moon Tumors (1. Antibiotic therapy is usually recommended with the choices being similar to those in cholangitis. These products'primary role is to neutralize gastric . PANCREAS (1.4th ed. 1996. weight loss. The administration of IV crystalloid to replace fluid losses and relieve dehydration is necessary. Five-year survival rates are only 2o/owith9}Yo of patients dying before the end of 1 year. However. NewYork: McGraw-Hill.3 I (4):923-933. lipase. Electrolytes and renal function tests are helpful in evaluation of fluid and electrolyte losses from vomiting and accumulation of fluid in and around inflamed tissues. however. A stone within the gastrointestinal tract may also be seen. Harwood-Nuss AL.77(5): 101 5-1 036. et al. pruritis. Surgical removal of the stone and a search for other stones in the gastrointestinal tract will be necessary. Obstruc- tive jaundice is the usual presenting symptom and appears early in the course of the disease. Characteristic symptoms include rapid onset t60l-1626. 3rd ed. the pancreas supplies insulin. Adenocarcinoma accounts for 80% of the tumors while the remainder are undifferentiated or squamous cell. In: Emergency medicine: a comprehensive study guide. Biliary tract emergencies. Krome R. J Clin Gastroenterol 1992. Carcinoma of the extrahepatic ducts has an average autopsy incidence of 0. nausea. Gallbladder and extrahepatic biliary system. It affects predominantly older women. and abdominal pain.AsooN4rNAL AND GASTRoTNTESTTNAL Presentstion Symptoms of acute cholecystitis immediately prior to gallstone ileus occur in one-fourth to one-third of patients. and somatostatin. Boston: Little. and abdominal pain.5) Gallbladder carcinoma is the fifth most common type of carcinoma involving the gastrointestinal tract and accounts for 5Yo of cancers found at autopsy. 1992.1477-1479' Rosen P. May HL. they fail to identifu tumor in 49olo of cases.495497. Beginning the workup of these patients with an ultrasound or CT scan is reasonable. Schwartz S. Carcinoma of the ampulla of Vater may be the result of tumor extension from elsewhere or a primary site of sarcomas. Amylase. Surgical intervention offers only a small hope for cure.24t. Philadelphia: Lippincott. Early surgical consultation should be obtained. These products are required to maintain glucose homeostasis. The emergency physician should be highly suspicious of carcinoma in any patient who presents with rapid onset ofjaundice.2nd ed. The presenting symptoms are usually indistinguishable from those of cholecystitis and cholelithiasis.4) Lying in the retroperitoneum. This tumor type occurs more frequently in men. Surgical intervention may be curative or palliative. bicarbonate. urgent referral to a gastroenterologist for ERCP or THC will be required. About one-half of the patients appear jaundiced and there is a palpable right upper quadrant mass in two-thirds. ERCP may be diagnostic.15(3): 238. 1358-1368. elastase. SELECTED READING Babb R. These symptoms are then followed by symptoms of intestinal obstruction. Management Resuscitation of the patient is the first priority.1381-1412. Tintinalli J. or adenocarcinomas. Radiol Clin North Am 1 993 . The differential diagnosis is that of other causes of small bowel obstruc- tion including adhesions. Palpation of the gallbladder may be possible in one-third of cases. carboxypeptidase. biliary tract. Med Clin North Am 1993. et al. but ERCP is usually necessary for diagnosis. Due to early detection. Five-year survival rates are approximately 2o/o to 5oh. Disorders ofthe liver. In: The clinical practice of emergency medicine. and pancreas. Diseases of the gallbladder and bile ducts' In: Harrison's principles of internal medicine. and cancer. 12th ed. Cholecystitis and biliary colic. New York: McGraw-Hill. et al. and phospholipase are some of the exocrine products provided by the pancreas.

Patients with acute pancreatitis often present in acute distress. cystic fibrosis. The pancreas can be afflicted with multiple disease processes. Abdominal tenderness in the epigastrium is the norm. acute pancreatitis can also become a life-threatening illness when it deteriorates into hemorrhagic or necrotic pancreatitis. guarding is commonly present. Pancreatic carcinoma often makes its initial presentation in the ED with weight loss and pain. bacterial infection. Drugs associated with pancreatitis Proven Azathioprine Cisplatin Estrogens Furemide Tetracycline Thiazides Possible Acetominophen Carbamazepine Clonidine Cimetidine Enalopril lndomethacin lsoniazid Metronidazole Opiates Procainamide Rifampin Salicylates Valproic acid and pancreatic carcinoma. Tachypnea and tachycardia may be present as well as signs of orthostasis. edema. Acute pancreatitis is present in approximately 0. This may be partly due to improved diagnosis or perhaps to the prevalence of alcohol abuse. Tetracycline.1) Acute Pancreutitis (1. Presentation Constant midepigastric pain accompanied by nausea and vomiting is the usual presentation of acute pancreati- tis. Pathophysiology There are many theories as to the mechanism for the development of acute pancreatitis. cisplatin. or pancreatitis- is also helpful in making the diagnosis. and azathioprine arejust a few ofthe drugs definitively shown to cause acute pancreatitis. Usually 5 to 10 years ofchronic alcohol ingestion is necessary to develop acute pancreatitis. 1) Pancreatitis can be of two types. In the United States. Other mechanistic theories include the reflux of bile or duodenal contents.20 / EuencrNcv MnlrcrNr. and ductal hypertension. there have been cases of acute pancreatitis after sudden binge drinking in the nonalcoholic. Complications of those disease entities include pseudocysts and abscesses. thiazides. acute and chronic. related drug therapy . The incidence of pan- creatitis is increasing in certain areas over the last 20 years. TABLE 1-4. Radiation of pain to the midback is common. Etiologies of acute pancreatitis Alcohol Biliary tract disease (choledocholithiasis. The principal concept TABLE 1-3. acute pancreatitis can be attributed to cholelithiasis and alcohol in 80% to90Yo of patients. or may be seen after pancreatic or gastric resection. furosemide. It is important for the emergency physician to recognize the signs and symptoms of pancreatic disease and provide appropriate intervention and referral. and pain. The list of possible or known etiologies of acute pancreatitis is quite extensive (Table 1-3).: Trtn Conr Cunnrculurrr acid and aid in digestion of proteins. Pancreatic insufficiency is one of the most common causes of maldigestion and can be caused by chronic pancreatitis. and carbohydrates. Inflammatory (1. Acute and chronic pancreatitis are responsible for many ED visits. 1. which are occasionally seen in the emergency setting. fats. However.5Yo of the population of the United States. Drugs are also well-known contributors to pancreatitis (Table l-4).4. alcohol use.4. Usually a mild self-limiting disease. Loss of bowel sounds is indicative of an associated ileus. This autodigestion results in coagulation necrosis and vascular injury causing hemorrhage. carcinomas) Hyperlipoproteinemias Hypercalcemia Drugs Posttraumatic Postoperative Post-ERCP Pregnancy Penetrating peptic ulcer Carcinoma of the pancreas Scorpion bites Vasculitis lnfectious Mumps Coxsackie virus Mycoplasma Legionella Campylobacter Hepatitis B virus Ascariasis of these theories is the autodigestion of the pancreas by inappropriate activation of proteolytic enzymes such as trypsin. A history ofgallstones in the past. Mortality rates reach as high as 5%.

It has a sensitivity similar to amylase but a specificity nearing 100%. other conditions such as perforated ulcer.AsnoNarNAL AND GASTRoTNTESTTNAT DrsoRonns Grey Tirrner's sign. Transfusion may become necessary. . the insertion of multiple large-bore IV catheters or a central line may become necessary. Ranson has outlined criteria for predicting the severity and mortality of acute pancreatitis (Table l-5). Lipase is found primarily in the pancreas. and decreasing stimulation of the pancreas by gastric contents. abscesses. and hemorrhage.000/mm3 LDH > 350 IU/L SGOT > 250 SF units Fluid sequestration > 6 L pOz < 60 mm Hg Hematocrit fall > 10% Calcium < 8 mg% Basedeficit>4mEq/L BUNrise>5mg/dl Adapted from Ranson JHC. secondary infection of necrotic material requiring debridement. The advent of the ability to test serum lipase has increased diagnostic accuracy for pancreatitis.40%o. pseudocysts. Broad-spectrum antibiotics should be reserved for those patients with evidence of biliary sepsis. Plain abdominal x-ray may show calcifications in the epigastric area suggestive of chronic pancreatitis or localized evidence of ileus (sentinel loop) suggestive of acute pancreatitis. or hemorrhage into a pseudocyst. and greater than 6. Arterial blood gases should be monitored to detect decreasing PaO2. It may be helpful in limiting emesis. ecchymosis around the umbilicus. up to one-third of patients with clinical pancreatitis may have normal amylase levels. Its most useful application is for the demonstration of inflammation in the surrounding tissues. and hemorrhages may be identified by ultrasound. Meperidine is preferred over morphine to limit induced spasm of the sphincter of Oddi. Ancillary Tests Elevations of serum amylase and lipase are usually indicative of acute pancreatitis. are indicative of retroperitoneal blood consistent with hemorrhagic pancreatitis. The highest elevations are commonly seen in gallstone pancreatitis. abscesses. l%o.34. Upright chest x-ray may show free intraperitoneal air associated with perforated viscous. but most have a lim- ited role in acute pancreatitis. intestinal obstruction. A falling hematocrit andlor Grey Tirrner's and Cullen's signs indicate the possibility of hemorrhage. Am J Gastroenterol 1982:77:663. Peritoneal lavage has not been proven to be effective. Hypotension either due to fluid sequestration or hemorrhage needs to be aggressively managed. and Cullen's sign. / 27 phlegmons. ruptured ectopic pregnancy. CT scanning can identify the pancreas easily but has a limited role in acute pancreatitis. renal insufficiency. including cardiopulmonary diseases. Potentially surgically correctable problems include abscess. or the use ofopiates can also cause hyperamylasemia. Ideally CT scanning should be performed only when complications are suspected. Therefore. Ranson criteria for prognosis in acute pancreatitis On admission ln 48 hours Age > 55 years Serum glucose > 2O0 mg7" WBC > 16. phlegmons. Elevation of serum amylase carries a reported sensitivity of 95%. l5Vo. Nasogastric aspiration is controversial. Pain control with narcotics such as meperidine is usually necessary. Conversely. 5-6. There are a variety of radiologic imaging modalities available for diagnostic purposes. mesenteric veinous thrombosis. Differentiation is possible using good hisancillary tory and examination skills as well as evaluations. Mortality using the Ranson criteria is based on the number of prog- nostic signs present: 0-2. Etiologic and prognostic factors in human acute pancreatitis: a review. providing gastric and proximal duodenal decompression. An antiemetic may be helpful as well for symptomatic relief. TABLE 1-5. Most patients present with dehydration and will require fluid resuscitation. However. Vigilance in the search for complications can help decrease morbidity. 100%. Insertion of a Foley catheter is helpful in monitoring urine output. ecchymosis in the flanks. Management The management of acute pancreatitis is both supportive and expectant. Dffirential Diagnosis The differential diagnosis in acute pancreatitis is that of the acute abdomen. Amylase levels may remain elevated for up to 72 hours after the onset of acute pancreatitis. Surgical intervention is usually reserved for those patients with acute decompensation. Electrolytes including calcium and magnesium should be closely monitored. and renal or gynecologic disease. Pseudocysts. Pancreatitis is a burn to the retroperitoneal space and can go on to large amounts of fluid sequestration. acute cholecystitis. Ultrasonography in the majority of patients will either be normal or show an enlarged hypoechoic gland. The degree of elevation of amylase and lipase has no clinical correlation to the severity of disease. intraabdominal processes. Gallstones are also reliably detected by ultrasonography. This myriad of conditions associated with hyperamylasemia creates poor specificity for this test. Hypoglycemia needs to be detected and rapidly addressed.

The clinically stable.4. Pseudocysts usually appear in the fourth or fifth decade and are more common in men. The patient may also present due to symptoms related to complications such as intestinal obstruction. chronic patient who is able to achieve pain control with oral medications and take oral hydration may be discharged. some even to the intensive care unit. Pain control is generally achieved with narcotics such as meperidine. fevers. The patient has often had frequent attacks ofacute pancreatitis. Management Treatment of chronic pancreatitis is generally symptomatic and supportive. Alcohol should be discontinued in order to facilitate recovery. while a few will persist and grow to large dimensions. Nausea and vomiting may also be present. They do not have an epithelial lining as do true cysts. There may be evi- of pancreatic insufficiency. and orthostasis may be present. however. Approximately three-fourths of all cystic lesions of the pancreas are pseudocysts. Hyperglycemia is a late finding and is usually accompanied by other evidence of pancreatic insufficiency. however. or hemorrhage into the pseudocyst. steatorrhea. The pain is usually in the epigastrium or left upper quadrant and may radiate to the back. 3) Pseudocyst Pathophysiology. The typical presentation is that of an alcoholic patient who has had repeated presentations with acute pancreatitis. endoscopic retrograde cholangiopancreatography (ERCP) is the most reliable diagnostic tool. and polyuria.22 / EunncrNcy MslrcrNn: Tun Conr CunnrculuM Disposition The vast majority of patients with acute pancreatitis require admission to the hospital for management. Hydration with crystalloids is often necessary. infection. Only a select few with very mild disease and the ability to tolerate oral intake may be discharged. Elevations ofamylase and lipase are unusual as the pancreas has virtually stopped their production due to scarring. Other evidence of dehydration such as dry mucous membranes. In the late stages. Many pseudocysts will resorb spontaneously. or intrathoracic . Pain may radiate to the back and may be partially relieved by sitting forward. The primary cause of chronic pancreatitis appears to be alcoholism. This readily detects abnormalities on the pancreatic ductal system. 1. migration of the pseudocyst. Pancreatic ductal dilitation may be seen on CT or ultrasound. Tenderness in the midepigastric arca may be elicited. Ancillary ksts Laboratory evaluation may be unrevealing. The majority of these patients have evidence of chronic pancreatitis. These calcifications are considered usual. ketorolac may be useful in the patient with no evidence of gastrointestinal hemorrhage or history of peptic ulcer disease. admission may be necessary. Testing for pancreatic secretory insufficiency does not have a role in the ED setting. other entities such as pancreas divisum. Gallstones on occasion do lead to recurrent pancreatitis but do not seem to contribute to chronic pancreatitis. and the inability to take liquids orally. The pain may change from intermittent to constant. C hronic Pancreatitis (1. Most are a result of destruction of the pancreatic ductal system and are unilocular. Vomiting should be treated with antiemetics. weight loss. His- tologically. fever. Nausea and vomiting may occur if this attack has been precipitated by a bout of alcoholism. pain out of pro- portion to the exam is pathognomonic. 2) Pathophysiology Chronic pancreatitis is a result ofrepeated episodes acute pancreatitis. Pseudocyst and Abscess (1. 1. with close follow-up arranged.4. however. Presentation dence Plain abdominal x-rays may reveal calcifications in the epigastric area. In general. These patients should be kept on clear liquids initially and advised to return immediately for worsening pain. Pseudocysts are so named because they are composed of a fibrous cavity filled with pancreatic debris and secretory products. Presentation The typical presentation of patients with pseudocysts is pain. They are a common complication of acute pancreatitis but have been encountered in l}Yo of patients with chronic pancreatitis. Physical examination generally reveals a chronically ill-appearing patient who is malnourished and in moderate to severe distress due to pain. calcifications may occur. especially in the patient with evidence of dehydration or orthostasis. of Initially the diagnosis may be on clin- ical grounds rather than through pathologic changes. This patient generally complains of severe epigastric abdominal pain that may be similar to that experienced during acute disease. and hyperparathyroidism have been incriminated. Malabsorption can be treated with pancreatic extracts. Trauma accounts for 25%o. causing complications to surrounding organs. lobules of functional acinar tissue and islet cells are surrounded by fibrous tissue. tachycardia. For patients with severe bouts similar to acute attacks. and ileus 2 to 3 weeks after acute pancreatitis or trauma. protein malnutrition.

The most common form of endocrine carcinoma is ductal adenocarcinoma (90%). if it is suspected. mortality still remains quite high. seeding of pancreatic pseudocysts 4 to 6 weeks later. Managemenf. Drug therapy consists of pancreatic enzyme replacement. The foremost cause is chronic pancreatitis.2) Carcinoma of the pancreas is the fourth leading cause of cancer-related death in the United States and its incidence is on the rise.4. vomiting. or extensive pancreatic resection. and other evidence of nutritional insufficiencies. If the mass enlarges or the patient develops complications such as infection or hemorrhage. Open surgical drainage and debridement with removal of all necrotic material is necessary. it increases the risk of the disease by two. There is also an Abscess attempt to reduce the symptomatic complaints associated with steatorrhea such as diarrhea and abdominal discomfort. and evidence of ileus are the hallmark symptoms. These patients frequently present as diabetics who have a history ofrepeated attacks ofpancreatitis and now have intestinal malabsorption. immediate surgical intervention will be required. Ancillary evaluation will reveal a leukocytosis with a left shift. 4. Heavy cigarette smoking is the most common risk factor.AsooNdrNAL AND GASTRoTNTESTTNAL DrsononRs Physical examination reveals a nontender or slightly tender abdominal mass in 75%o of patients. Catastrophic hemorrhage may be amenable to angiographic embolization. The primary goals in the treatment of pancreatic insufficiency are to maintain an adequate nutritional status and restore and maintain body weight. The mass may fluctuate in size over time as well as completely disappear. appropriate referral for evaluation and treatment should catheters. There may also be evidence of Brz or fat-soluble vitamin insufficiency. Pancreatic abscesses are not amenable to antibiotic therapy alone (mortality reaches 100%).This disease rarely presents prior to the age of 50 and seems to have a prevalence in males over females and blacks over whites. There are a variety ofpreparations available to replace pancreatic enzymes. Pseudocyst should be suspected in the patient who shows persistent elevation of amylase levels. coli. These preparations Two infectious processes may result in pancreatic abscess. Fever. Patients with cystic fibrosis become clinically apparent in childhood and occasionally in young adulthood. Percutaneous drainage has met with only limited success. / 23 1. abdominal tenderness.to threefold. and possibly signs of septic shock. lipids. This is usually a lifelong endeavor and is quite expensive. to l0% of patients with acute panthe abscess usually reveals multiple creatitis. Pseudocysts that persist for longer than 4 to 6 weeks are unlikely to resolve spontaneously. The loss of pancreatic enzymes leads to failure to digest carbohydrates. nausea. organisms including Abscess occurs in be made. Physical examination reveals fever. carcinoma of the pancreas. Laboratory tests may reveal persistent elevation of amylase in 50Vo of patients. Serum amylase will be normal or slightly elevated. high-protein diets. Pathophysiology tion with packing of the abscess cavity seems to have reduced overall mortality. abdominal pain. Hemodynamic instability may be present in the case of hemorrhage into the pseudocyst. and the bacterial have differing efficacies and should be tailored to the patient's level of malabsorption. The 3-year survival rate is approximately 2Yo. A patient who develops an abdominal mass during an attack of acute pancreatitis should be observed for several weeks. Chronic pancreatitis does not appear to carry an increased risk. is either endocrine or nonendocrine. In general. 2%o and aerobic hemolytic streptococci. Profound weight loss due to pancreatic insufficiency is often seen in pancreatic carcinoma.4) Pancreatic insufficiency is a result of chronic pancreatitis. cystic fibrosis. These patients may present with clinical deterioration as their episode ofacute pancreatitis should be resolving. tachycardia. The mass may occasionally be confused with an abdominal aortic aneurysm. Abdominal plain films may reveal mass effect on adjacent organs but are otherwise unhelpful. infection ofnecrotic pancreatic tissue a few days into the course of acute pancreatitis. ERCP is not generally required. Treatment is composed of drug therapy and dietary counseling. gram-negative anaerobes. weight loss. Radiologic diagnosis is achieved using either ultrasound or CT scanning. Other associated risk factors include diabetes mellitus and the consumption of highfat. and proteins. Diagnosis is generally made by quantitating fecal fat excretion. Exocrine Pancreatic carcinoma . Pancreatic insufficiency is rarely an ED diagnosis. Culture of E. The typical presentation of pancreatic insufficiency is with steatorrhea. however. Drainage may also be achieved using CT:guided percutaneous Pancreatic Insufficiency (1. Ancillary Tbsts. The technique of pancreatic resec- Tirmors and Carcinoma (1. If the patient remains relatively stable and the mass persists. Ultrasound and CT (picture) are the preferred diagnostic modalities. he or she may be referred for elective surgical decompression of the pseudocyst.

and weight loss may help in leading to earlier diagnosis of pancreatic carcinoma. 5th ed. l2th ed. et al. et al.507 509. Fortunately. Luten RC. can be aggravated by mood and emotional stress. This tumor usually results in multiple peptic ulcers. hepatomegaly. 5th ed. et a[. medicine: concepts and clinical praclice. Pancreatic cancer. Kadakia SC. et al. the diagnosis and treatment of stomach disorders has been greatly advanced in the past two decades with the development of fiberoptic technology for endoscopy and histamine (Hz) antagonists. and jaundice. I 988. 459-1490. These patients manifest high insulin levels despite low glucose levels. Elevated glucagon levels usually make the diagnosis. Rosen P. 1992. NewYork: McGraw-Hill. ln Harrison s principles of internal medicine. somatostatinoma. these resections are done in patients with tumors in the head of the pancreas who present with jaundice while the tumor is still small. Emergenq. ambiguous CT or ultrasound findings. For ill patients. and carcinoid. abdominal tenderness.1480-1482.24 / Err. glucagonoma. It should also be noted that disorders of the stomach. The pain is usually described as gnawing and may radiate from the epigastric area to the back. Tintinalli J. This weight loss is initially from anorexia but may also be caused by pancreatic insufficiency as the tumor grows. gastrinoma. Physical findings on presentation include a possible abdominal mass. Etiologic and progrrostic factors in human acute pancreatitis: a review AmJ Gastroenterol 1982. In: Principles of surgery-. The diarrhea associated with this tumor is usually profuse (over 20 L a day). It may become necessary in these patients to replace fluids and lost electrolytes. Pain should be controlled using opiate analgesics. and tail of the pancreas. Pain is usually a more severe problem in those patients with tumors in the body or tail of the pancreas since they may grow quite large prior to presentation. Am J Gastroenterol 1995. CT scanning allows good visualization of the hea4 body. Pain is found in 50o/o to 80% of patients.77:633. 1 1 STOMACH (1. In: P rin c ip le s of surgery. Barkin R. The use oftobacco and alcohol is undoubtedly a contributing factor. Any patient complaining of epigastric pain should be considered for a stomach ailment. 1996. Glucose intolerance and a necrotizing migratory ally benign and erythematous rash are typical of glucagonoma. Krome R. Harwood-Nuss AL.90(9): 1 3 83-l 393. ln: The clinical practice of emergency medicine Philadelphia: Lippincoft. et al. For patients with widely metastatic disease. This is not a specific symptom. pancreas. VIPoma (secretes high levels of vasoactive intestinal peptide). 4th ed.In: Emergency medicine. May HL.s) Disorders of the stomach are a frequent cause of ED visits and hospital admissions in the United States. In: Harrison\ principles ofinternal medicine. et al. Acute and chronic pancreatitis. As for the nonendocrine tumors. Disorders ofthe liver. New York: McGraw-Hill. 3rd ed'. Peritonitis and intraabdominal abscesses. and heart may cause pain here. Wilson J. Haverkort EB. et al. Ruiz E. Gastrinoma is the cause of Zollinger-Ellison syndrome. The diagnosis of endocrine tumors is made by CT scanning in over 80% of patients. Linden CH.77(5): 1015-1037. Weight loss is the earliest symptom in 70o/o to 90o/o of patients with endocrine carcinomas. Biliary tract emergencies. In: Emergency medicine: a comprehensive study guide. and pancreas. 1989. van Leeuwen D. decompression of the biliary tree can be achieved by endoscopic or percutaneous means. 1992. This is only possible in l0o/o to 15% of patients. 1988. median survival is 5 months. ERCP may be used to clarif. In patients with jaundice and pancreatic head tumors. Radiation and chemotherapy with 5-fluorouracil appears to prolong survival and increase the cure rate in comparison to complete resection. Five-year survival rates following pancreatic resection are only 10%. Practically.l tumors include insulinoma (the most common). Ranson JHC.1383-1387. hypokalemia. chemotherapy has not been shown to provide any benefit. and achlorhydria. Shires G. Pancreatitis. 1413-t440. Brown. as several other proximally located organs such as the duodenum. Jaundice is found in 80% of patients with tumors in the head of the pancreas. biliary tract. perhaps more than any other intraabdominal organ. ln'. Schwartz S. SELECTED READING Bruno MJ. Trestment and Prognosis A high index of suspicion in the ED when encountering patients with vague abdominal discomfort. Partial relief may be obtained by sitting forward. I 3 72-1 3 82. These tumors generally present with watery diarrhea. Schwartz S. Wilson J. Med Clin North Am 1993l. Boston: Little. In patients with unresectable tumors. For endocrine carcinomas. 12th ed. Pancreas. 949-951. biliary tract. however. surgical diversion of bile may be necessary. The pancreas may be the site of VIPomas. 1991. 1601-1626.2nd ed. back pain. Treatment of these patients is directed by symptomatology. the only cure is with complete surgical resection. Tytgat G. . Acute pancreatitis. Maldigestion associated with exocrine pancreatic insufficiency: implications of gastrointestinal physiology and properties of enzyme preparations for a causerelated and patient-tailored treatment. Presentation and Diagnosis Carcinomas are generally present for longer than 2 months prior to their diagnosis. et a[. insulinomas are usu- present with hypoglycemia. 989. Ultrasonography is less accurate. Spencer F. Aghababian R! Fleisher GR. This tumor metastasizes quickly and has done so in 60oh of patients by the time of presentation.mncrNcv MnorcINe: THB Conn Cunxrculurr. Acute pancreatitis. New York: McGraw-Hill.

However. The stomach is fixed only at the esophagocardiac junction and the pylorus. pancreas. However. The stomach begins at the esophagocardiac junction just inferior to the diaphragm. hematochezia may be caused by a large proximal duodenal bleed with a rapid transit time. Each region is characterizedby different types and frequency of cells in the gastric mucosa. and is frequently described as crampy or gaseous. sweaty appearance or significant tachycardia or hypotension should receive immediate attention. a coal black. all patients with these complaints would be seen immediately. this is not always done. visceral (splanchnic) pain from these organs is frequently referred to the mid-epigastric area. is through branches GASTRoTNTESTTNAL DrsonorRs of the celiac axis off the descending / 25 aorta. fundus. esophagus. and biliary tree all arise from the embryologic foregut. The stomach is divided into four different regions: the cardia. and inferiorly by the transverse colon and small bowel. can be caused by as little as 60 cc of blood. The left kidney. More serious conditions . In the normal individual. Visceral or splanchnic pain is that which results from stretching of the autonomic nerve fibers surrounding a hollow or solid viscus. Applied anatomy and anomalies of the stomach. Included in this list are iron salts. Finally. Pain that begins abruptly and is maximally severe in intensity at the time of onset suggests a serious disorder (e. Ideally. Its presence implies bleeding proximal to the ligament of Treitz. and beets. The stomach varies in size as determined by its contents or obstruction. The mucosa of the antrum is primarily composed of mucus secreting cells. medially by the liver. the respiratory tract. the vomiting of "coffee grounds" does not necessarily imply the emesis of "old blood. bismuth. the mode of onset of the patients' symptoms is of utmost importance. Hematochezia. Anatomy and Pathophysiology The stomach. For this reason. body. as well as the pharynx and its derivatives. Likewise. order Keeping a few key triage points in mind is helpful in determining which patients must be seen immediately and who can wait. any patient who sits very still or walks cautiously to avoid any agitation of the peritoneal contents may have peritonitis. Emergency Department Evaluation Most patients presenting to an ED with a stomach diswill complain of abdominal pain or vomiting or both. Fondacaro PF. While bleeding from a lower colon source may cause a very dark stool. any patient with a pale. of The gastric mucosa starts at the gastroesophageal junction and ends at the pylorus.) As stated above. is usually caused by lower colon bleeds. The duration of the symptoms is equally important. liver. Bleeding from the stomach and proximal portion of the duodenum is manifested as hematemesis or melena or both. these stools usually lack the shiny and sticky character of true melena. and body of the pancreas lie directly posterior to the stomach in the retroperitoneal space. Any patient complaining of vomiting blood should be evaluated immediately. duodenum proximal to the opening of the common bile duct. Regions of the stomach. It is worth noting that some foods and medications may give stool the false appearance of melena or hematochezia. The stomach normally lies in the left upper quadrant of the abdomen with the pylorus at approximately the midline. 8. with an abundance ofparietal cells that excrete hydrochloric acid.AnnourNer AND A basic understanding of the anatomy and physiology of the stomach is a prerequisite to understanding the various pathologic conditions that affect it. Parasympathetic innervation of the stomach is provided by anterior and posterior branches of the vagus nerve. (From Eisenberg MM. The arterial blood supply to the stomach. a perforated viscus). the passage ofrecognizably red blood from the anus. l-1). various food dyes. suprarenal gland. 1-1. sticky or tar-like stool. Sympathetic innervation is through roots 7. the stomach is bordered superiorly and laterally by the diaphragm. The fundus and body are the acid-producing portions of the stomach. and 9 the thoracic spine by way of the celiac ganglia. History FlG. The abdominal wall is anterior to the stomach with the spleen posterolateral to it. Philadelphia: Saunders. It ends at the pyloric sphincter. charcoal." Melena. a thick band of muscle separating it from the duodenum. Dunn DH. 1995. as well as the distal esophagus and proximal duodenum.. and antrum (Fig. Gastroenterology.g. Since blood exposed to gastric acid changes to a brown color almost immediately.

with men and women being equally affected. NSAIDs. body position or emotional stress). palpation should begin with the non- ofthe abdomen and progress to those embolism. The abdominal exam itself is best performed with the patient as relaxed as possible. approximately 1. vomiting. Physical exam may reveal a distended upper abdomen with a normal. Since many gastric volvuli occur above the diaphragm. biliary tree. salicylates. The inability to pass a nasogastric tube into the stomach combined with pain and violent retching completes a clinical triad that is highly suggestive of gastric vohulus. retrocardiac air-fluid levels.5. or epigastric discomfort with meals. peptic ulcer disease. and menstrual history. Approximately 15% of cases of gastric volvulus Foreign Bodies (1. soft lower abdomen. It should be noted that patients'perceptions ofpain intensity are influenced by cultural and socioeconomic factors. including hiatal hernias. However. A supradiaphragmatic vohulus will characteristically appear as one or two large. this may lead to a closed loop obstruction with ischemia and ultimately necrosis. or pancreas. or other nonalimentary events (e. as even upper abdominal complaints may have a gynecologic etiology. Finally. Endoscopic decompression may be considered in some patients who are poor surgical candidates. usually under I year ofage and associated with congenital diaphragmatic defects. nausea. The inclusion of oral contrast may aid in the radiographic diagnosis. The presence of any abdominal pain in the epigastrum would suggest an ailment involving the upper gastrointestinal tract. the greater the intensity of the abdominal pain. Any reproductive-age female should be asked for a sexual. or a relatively unremarkable abdominal exam if the volvulus occurs above the diaphragm. Patients should be asked about any recent change in the color of their stool. Subdiaphragmatic vohuli frequently appear as a markedly distended stomach with an abnormal lie and one or two air-filled levels. any tobacco. nonspecific symptoms such as heartburn.500 people die yearly in the United States as a . Visual inspection for distention and peristaltic waves as well as auscultation for bowel sounds should be done first. The triad of anorexia. Any diaphragmatic it defects contributing to the volvulus should also be repaired. Abnormal laxity of suspensory ligaments and diaphragmatic abnormalities. By and large. acute pancreatitis. and current medications (specifically steroids. a significant number of patients will complain of anterior chest pain. The peak incidence in adults is in the fifth decade.1) bowel gas in the remainder of the gastrointestinal tract.2) Foreign-body ingestion is not an uncommon complaint in the ED. or pulmonary areas Structural Lesions (1. a rectal exam with stool guaiac testing should be performed.5. and antibiotics). Acute gastric volvulus frequently presents with sudden onset ofsevere left upper quadrant pain with retching and an inability to vomit. the presence of any or all of these symptoms is nonspecific for these conditions. Chronic volvulus is probably underdiagnosed since it is frequently associated with transient. There may be a pauciry of Physical Examination tender areas most tender. a variety of surgical techniques may be used to anchor there. Percussion for intraabdominal organ size and tympany should be per- formed.1) Volvulas (1.26 / ElrpncnNcv MnorcrNr: THn Conn CunnrculuM will usually cause a patient to seek emergent medical attention in a shorter period of time. the stomach can be decompressed with a nasogastric tube. and specifically about any relationship of the pain to eating. Patients with symptoms suggestive of gastric vohulus should have upright chest and abdominal x-rays performed. Any patient with an abdominal complaint should receive a thorough examination including a lung and cardiac exam. While most ingestions are uneventful. aortic dissection. Immediate surgical consultation is warranted as surgical intervention is almost always necessary. or recreational drug used should be noted. If not reversed.1. 5. Finally. Furthermore. pyloric obstruction. surgeries.ulus include IV hydration and nasogastric tube insertion (as discussed above). The patient should be asked about any exacerbating or relieving factors.. The majority of cases of gastric volvulus are chronic in nature. and vomiting is extremely coflrmon in patients with stomach disorders. 1. the more likely the patient to have a serious condition. occur in children. Occasionally. level of education. and cholecystitis. alcohol. Gastric volvulus is defined as an abnormal degree of rotation of one part of the stomach around another. Emergent surgical decompression is indicated if decompression with a nasogastric tube is unsuccessful. reproductive.g. Any reproductive age female should have a pelvic exam. ED interventions for patients suspected of gastric volr. Patients with gastric vohulus above the diaphragm may have symptoms mimicking myocardial infarction. Differential diagnosis includes perforated peptic ulcer. medications taken. After replacement of the stomach into its normal position in the abdomen. and age. are believed to be the two major causes. All patients with abdominal complaints should be asked about any prior medical conditions.

such as sewing needles or razor blades. Furthermore. ileocecal valve. Clear guidelines for the removal of gastric foreign bodies do not exist. duodenum. Between 80% and 93o/o of foreign bodies that reach the stomach will pass spontaneously. Two situations warrant special mention: button battery ingestion and the ingestion ofpackaged illegal drugs for the purposes of concealment (i. Rupture (1. the stomach can decompress into the esophagus and duodenum in the nor- mal individual. Nontraumatic or "spontaneous" gastric rupture appears to have a preponderance among women and a mean age of occurrence of 43 years. the majority of whom complain of some discomfort. alcoholics.e. Most gastric foreign bodies can be safely removed with the use of an endoscope. The stomach is relatively resistant to rupture. Outpatient management of benign gastric foreign bodies should include close follow-up and a high-residue diet to promote passage through the gastrointestinal tract. or fever. and from rapid ascension in diving accidents. Since most patients with gastric rup- . For this reason.. and bleeding.3) Gastric rupture refers to a tear in the stomach wall with release of the gastric contents into the peritoneum.5. Gastric rupture secondary to blunt trauma is accordingly rare. with its muscu- lar wall having the ability to greatly expand with increases in intragastric contents. and prisoners. and anus. Many patients present in shock or quickly progress to it. CT using oral and IV contrast may be helpful. Approximately 80% cases are in the pediatric population. grand mal seizures. the use of emetics is discouraged. Sodium bicarbonate. A small percentage of patients may have subcutaneous emphysema caused by the passage of abdominal air through the mediastinum into the neck. Surgical removal is indicated if the patient becomes symptomatic. Distention can occur because of zealous overeating. This differs significantly from patients with esophageal foreign bodies. Button batteries can leak highly alkaline substances and cause severe burns or perforation in the esophagus. Repeated radiographs to follow the progression of the object through the gut may be performed. individuals with poor eyesight. especially if the object has irregular as opposed to rounded edges. Sharp or pointed objects. Endoscopic retrieval of intentionally ingested packets of ille- gal drugs should not be attempted due to the risk of packet rupture.AsooN. esophageal intubation. used as a remedy for indigestion. with some reporting a bursting sensation. causing gastritis or ulceration. The majority of obstructions caused by foreign bodies occur in the esophagus. Most patients with a gastric foreign body will be asymptomatic. Distention and vomiting together or by themselves can cause gastric rupture. Gastric rupture is a rare condition with both traumatic and nontraumatic causes. pylorus. The stomach's position in the abdomen is well protected by the rib cage and the liver. Obstructing tumors of the esophagus. with exceptions as discussed below Controversy exists as to the timing of endoscopy to remove otherwise innocuous foreign bodies that do not pass through the stomach. One study found only 0. Patients who are to have endoscopy for gastric foreign bodies should be placed in the left lateral decubitus position in an attempt to prevent the passage of the object DrsonorRs / 27 through the pylorus. Patients with gastric rupture complain of abrupt onset of abdominal pain. Gastric rupture has been described secondary to motor vehicle accidents. especially in cases involving sharp or pointed objects and button batteries. may cause gastric distention from the carbon dioxide released during the compound's reaction with stomach acid. psy- of all chotic and demented patients. Any patient with a history of foreignbody ingestion should be evaluated for symptoms of obstruction. Button batteries that have passed into the stomach do not require emergent removal in the asymptomatic patient unless the cell has remained in the stomach for more than 48 hours. should be considered for emergent endoscopic removal since 15% to 35Vo will cause perforation. emergent endoscopy is indicated if the battery is lodged in the esophagus. Abdominal distention may be present. Potentially toxic objects should be retrieved. There is usually severe pain with signs of peritoneal irritation. profuse upper gastrointestinal bleeding. forceful coughing. Adults at increased risk for foreign-body ingestion include denture wearers. and use of the Heimlich maneuver. mouth-to-mouth or bagto-mouth ventilation during CPR. or duodenum may be contributing factors. Most gastric foreign bodies will be visible using plain or contrast radiography. Endoscopy should be considered for objects more than 2 cm in diameter or 5 cm in length. exertion with heavy lifting. perforation. Asymptomatic patients can receive "whole bowel irrigation" with GoLYTELY to expedite the movement of the packet through the gastrointestinal tract. usually at the iliocecal valve. a phenomenon known as receptive relaxation. Diagnostic studies to consider include upright chest xray and lateral decubitus abdominal x-rays looking for air under the diaphragms and flanks.4o/o of patients with severe blunt trauma to have gastric perforation. The main points of obstruction for gastric foreign bodies include the pylorus. Patients should be advised to seek immediate medical attention for any abdominal pain. These retained objects pose the risk of pressure necrosis. vomiting.uNAr eNo GesrnorNTESTrNAr result of swallowed foreign bodies. Peritoneal lavage is felt to be the most sensitive indicator of gastric rupture after blunt trauma. respectively. By and large. "body packers").1.

Inflammatory Disorders (1. Approximately 2oh of all ulcer patients will develop gastric outlet obstruction. steroids. Patients with acute gastritis by definition should not have signs of peritoneal inflammation. Other less common causes are listed in Table l-6. various infections. The differential diagnosis includes all forms of abdominal catastrophe including aortic dissection and rupture. To many emergency physicians. Approximately 90% of patients with gastric outlet obstruction will complain of upper abdominal pain and vomiting. or being diagnosed on clinical grounds only. 1) Gastritis is an inflammation of the mucosa of the stomIt is. there is often little need for diagnostic workup prior to surgical exploration. NSAIDs. uremia.28 / ElanncrNcv MnorcrNr: Tnn Conr CunnrculuM ture present with impressive abdominal findings. may present with symptoms similar to stomach rupture. 5. such as long-standing diabetes or scleroderma. cussed here. Physical examination may reveal a succussion splash (a splashing sound elicited by gently rocking the abdomen) and evidence of chronic malnutrition or dehydration. Definitive management may include endoscopic balloon dilatation or surgical pyloroplasty or partial gastric resection. most commonly secondary to peptic ulcer disease or appendicitis. Routine TABLE 1-6. To this end. and stress. A complete blood count. The true incidence of acute gastritis is unknown. corrosive agents. The term is used. Many will give a history of emesis after the evening meal with food from earlier in the day being present in the vomitus. diagnostic workup in the ED should include a diligent search for other causes of upper abdominal pain and dyspepsia. and has the characteristic small bowel air fluid levels on x-ray. aspirin. many of which would be more appropriately called "nonulcer dyspepsia. by definition. hypochloremic metabolic alkalosis secondary to chronic vomiting. and vohulus. Philadelphia: Saunders. alcohol.4) The complete or near-complete blockage of the flow of gastric contents out of the stomach results in gastric out- let obstruction. and classically causes vomiting with little associated abdominal pain. Gastrointestinal disease. IV hydration is also frequently necessary. It is a transient process that often resolves without sequelae. chronic gastritis. Any perforated viscus. Ulcer complications and their nonoperative treatment.2) Acute Gastritis (1. ED interventions should include nasogastric tube insertion. ED management of gastric rupture should include aggressive fluid resuscitation and early administration of parenteral broad-spectrum antibiotics. Diagnostic workup in the ED should include an upright abdominal film. Acute gastritis can cause a significant amount of bleeding and patients may complain of hematemesis or have hemepositive stools. All patients with suspected gastric outlet obstruction should be admitted to the hospital. There may be a paucity of gas in the small and large colon. Vomiting may be present. These patients typically have a longer than l0-year history of ulcer disease. 1. with attention to the hemoglo- . gastritis probably represents a benign diagnosis ofexclusion. Conditions that may mimic gastric outlet obstruction include gastroparesis and small bowel obstruction. which often results in evacuation of a large amount offoul fluid. however." The World Congress of Gastroenterology in 1990 grouped the many causes of gastritis into three main classifications: acute gastritis. Endoscopy may be performed for definitive diagnosis and biopsy if malignancy is suspected as the cause of obstruction. Emergent surgical intervention is needed for peritoneal lavage and gastric repair. Gastric Outlet Obstruction (1. While never substantiated" most believe gastritis presents with vague upper abdominal complaints including dyspepsia or indigestion. Only acute gastritis will be disach. Causes of acute gastritis include radiation. which often reveals a markedly dilated stomach shadow with a large air fluid level. Chronic duodenal or pyloric channel ulcers are responsible for approximately 80Yo of all cases in adults. Early satiety and recent weight loss will be present in up to two-thirds of patients. 5. by clinicians to describe a variety of disorders. Small bowel obstruction is often of more acute onset than gastric outlet obstruction. bowel infarction. due in large part to the vast majority of cases going undiagnosed. and "special forms" of gastritis. '1 993. blood chemistries may reveal a hypokalemic. Acute gastritis is characterizedby inflammation of the gastric mucosa with polymorphonuclear cells with some loss of epithelium. 2. usually with a severe clinical course. Nasogastric suction may help reduce the amount of peritoneal soilage. Gastroparesis often occurs in the setting ofa predisposing illness. Causes of gastric outlet obstruction other than peptic ulcer disease Tumors Benign Adenomatous polyp Malignant Gastric carcinoma Carcinoma of pancreatic head Lymphoma lnflammation Cholecystitis Acute pancreatitis Crohn's disease Eosinophilic gastroenteritis Miscellaneous causes Adult hypertrophic pyloric stenosis Postsurgical stenosis Pyloric diaphragm Duodenal diaphragm Caustic structure Annular pancreas Ectopic pancreas From Graham DY. rupture of the gallbladder or spleen.5. a diagnosis that can be made only by histologic examination.

AsooNaNAL AND GASTRoTNTESTTNAL Drsonoens

bin level if there is a history of bleeding, liver function
tests, and, in elderly patients, an EKG should be performed. Nasogastric suction should be performed in any
patient with a history of hematemesis.
Treatment of acute gastritis should begin only after
other causes of the patient's symptoms have been
excluded. Antiemetics, such as prochlorperazine, may be
used to help control vomiting. A bland diet as well as
cessation of smoking should be recommended. Antacids,
such as Maalox, should be tried and initiation of Hzblocker therapy is an option. Above all else, the presumed cause of the gastritis, if known, should be discontinued.

Most patients with presumed gastritis can be discharged from the ED with close follow-up. Indications
for admission include intractable vomiting, hematemesis
with evidence of continued bleeding or significant blood
loss, severe dehydration, or the inability to rule out more
serious causes of the patient's symptoms.
Three subclassifications ofacute gastritis warrant special mention in an emergency medicine text: stressrelated gastritis, corrosive gastritis, and drug-induced
gastritis.

Stres

s-

Re I ate

d Gastritis

In experimental models, stress predisposes to both gastric and duodenal injury. While it is well accepted that
physical stressors lead to gastric mucosal injury, some
debate exists as to whether psychological stress causes
damage. Gastric damage is a significant problem in

TABLE

1-7,

of

Treatment involves primary prophylaxis

Drain cleaners

Sulfuric acid (95-99%)
Metal cleaners and antirust compounds
Phosphoric acid (5-80%)
Oxalic acid (1%)

Hydrochloric acid (5-25%)
Sulfuric acid (10-20%)
Chromic acid (5-20%)
Soldering fluxes

Zinc chloride (10-35%)
Hydrochloric acid (up to 40%)

in at risk

patients. Antacids, Hz blockers, and sucralfate have all

been proven efficacious for this purpose, and debate
continues over which agent is best. Treatment in the ED
is the same as for other causes of acute gastritis. Cold
saline lavage has been advocated by some for this condition; however, the efficacy of this action remains questionable.
Corrosive Gastritis

The ingestion of corrosive substances can cause a
severe form of gastritis with both short- and long-term
gastric sequelae. The stomach is susceptible to damage
from both highly acidic and highly alkaline compounds
(Table l-7). Acidic compounds cause a coagulative
necrosis, theoretically leading to eschar formation and
protection from further mucosal damage. Alkaline compounds, in contrast, cause a liquefaction necrosis leading

Acids

Hydrochloric acid (1 0-25%)
Oxalic acid (2%)
sodium bisulfate (70-1 00%)

29

patients with large (>35% body surface area) burns, sepsis, respiratory failure requiring prolonged mechanical
ventilation, trauma, shock or prolonged hypotension,
renal failure, and multiple system failure. Prolonged ICU
stays are a separate risk factor. Of particular importance
to emergency physicians is the increased risk of patients
in extended care facilities.
The most common presentation
stress-related
mucosal damage is bleeding, manifested as hematemesis,
guaiac-positive stools, or frank melena. Clinically significant bleeding is more likely to be associated with gastric
or duodenal ulcers in this setting, rather than gastritis.

Household agents containing potentially corrosive acids and alkalis

Toilet bowl cleaners
Sulfuric acid (80%)

/

Drain cleaners
Sodium hydroxide (1 0-1 00%)
Household ammonia
Ammonium hydroxide (3-1 0%)
Automatic dishwasher detergents
Sodium tripolyphosphate
Sodium metasilicate
Sodium silicate
Sodium carbonate
Oven cleaners
Sodium hydroxide
Bleaches
Sodium hypochlorite (3-6%)
Sodium silicate (15-17%)
Sodium carbonate (60%)

Automobile battery fluid

Sulfuric acid (25-30%)
Swimming pool sanitizers
Calcium or sodium hypochloride (70%)

From Hawkey CJ, Hudson N. Gastroenterology. Mucosal iniury caused by drugs,
chemicals and stress. Philadelphia: Saunders, 1995.

30 /

ErrarncnNcy MnucrNr,:

to saponification of

Tnn Conn CunrucuLUM

these tissues and

a deeper burn.

Given its acidic environment, the stomach is less prone to
alkaline injury than is the esophagus.
Swallowing of a corrosive substance with gastric
injury causes severe epigastric pain with retching and
vomiting of blood or necrotic tissue. Patients with any
stridor, hoarseness, or shortness of breath pose an immediate airway risk and should be considered for immediate
intubation. Patients complaining
dysphagia and
odynophagia are likely to have esophageal burns.

of

The immediate complications of a corrosive gastritis
include hypovolemia, as with any severe burn, and gastric

perforation with peritonitis.

A

metabolic acidosis can

occur with ingestion of a large amount of acid. Patients
who survive a caustic ingestion face the long-term complications of strictures that may become symptomatic
weeks to years postingestion.
ED management of patients with corrosive gastritis
should include IV hydration, chest and abdominal radiographs looking for evidence of perforation, and admission. Insertion ofa nasogastric tube is contraindicated in
alkali ingestions due to the risk of perforation. It is controversial in large acidic ingestions, as some authors feel
it is worth the perforation risk to remove the acid from the
stomach to prevent severe systemic acidosis. Emetic
agents as well as the administration of "neutralizing"
acidic or basic compounds is contraindicated. Corticosteroids, given in the hopes of preventing stricture formation, remain highly controversial. The empiric use of
broad-spectrum antibiotics in the absence of perforation
is of unproven benefit, yet recommended by many
authorities.

Drug-Induced Gastritis

TABLE 1-8. Medications associated with gastric mucosal
tnlury
Antibiotics
Nalidixic acid

Sullonamides and derivatives
Erythromycin
Pivampicillin

Antiinflammatory drugs
NSAIDS

Corticosteroids
Colchicine
Chloroquine
Elements
Fe+
K+

Gold

Hypnotics
Chloral hydrate
Meprobamate
Miscellaneous
Ethacrynic acid
Ethanol
Mebendazole
Mucolytic agents
Prostaglandins
Reserpine
Salicylates
Sulfasalazine
Sulfinpyrazone
Xanthine (and catfeine)

From Eisenberg MM, Fondacaro PF, Dunn DH. Gastroenterology. Applied anatomy and anomalies of the stomach.
Philadelphia: Saunders, 1 995.

in these patients when treating minor pain.
Some authors advocate primary prophylaxis against
NSAID-induced gastropathy with synthetic prostaglanminophen,

dins, such as misoprostol, or H2 antagonists.
Peptic Ulcer Disease (1.5.3)
Peptic ulcers are defects in the gastrointestinal mucosa
extending through the muscularis mucosae, caused by the
action of the acid and pepsin present in gastric juice. An
estimated half million new cases are diagnosed each year
in the United States, with approximately 15,000 deaths per
year attributed to peptic ulcer disease (P[ID).The lifetime
prevalence of PUD in the United States has been estimated
at llo/o to l4Yo for males and 8o/o to llYo for females with
an increased prevalence among lower socioeconomic
classes. These numbers are likely to increase in the future

Several medications have been associated with gastric
mucosal damage leading to gastritis and ulceration (Table
1-8). Medications are believed to cause mucosal injury
either directly, or by reducing the mucosa's resistance to
the damaging effects of stomach acid, or by increasing
hydrochloric acid output. NSAIDs, including aspirin, are
believed to be the most common offending agents in this

increasing use of NSAIDs. Peptic ulcers are found in the
stomach and in the duodenum. Ninety-five percent of peptic ulcers in the duodemrm are located in the first portion.

category.

under the broad heading ofpeptic ulcers.

Little is known about the exact incidence of mucosal
damage caused by NSAIDs. It appears to be most common in elderly women, perhaps because these are the

A breakdown of the usual mucosal defense mechanisms is believed responsible for the majority of peptic
ulcers. Colonization of the gastrointestinal mucosa with
Helicobacter pylori and NSAID use (including aspirin)
are felt to be the two main risk factors. It has been estimated that roughly 25Yo of chronic NSAID users will
develop PUD. Other risk factors include smoking, a history ofchronic renal failure, hepatic cirrhosis and chronic

patients for whom these medications are most commonly
prescribed. NSAIDs may cause acute or chronic mucosal
injury, and their damaging effects appear to be increased
with the addition of corticosteroids.
Patients with presumed drug-induced gastritis should

discontinue the oflending agent if possible. Caution
should be used by emergency physicians when prescribing NSAIDs, especially in elderly patients. It may be wise
to try alternative firstline analgesics, such as aceta-

due to an increasing proportion

of elderly patients

and

While some clinical differences exist between the two
ulcer types (Table l-9), they will both be discussed here

pulmonary disease, Zollinger-Ellison syndrome, and
radiation therapy. Ethanol consumption, diet, corticosteroid use, and psychogenic stress all remain controversial as possible causes of PUD.

AsooNarNAL eNo GesrnoINTESTrNAr
TABLE

1-9.

Symptoms of gastric and duodenal ulcers
Gastric
ulcer
(Y")

Symptoms
Pain/discomfort
Features of the pain
Primary pain
Epigastric
Right hypochondrium
Left hypochondrium
Frequently severe
Within 30 minutes of food
Gnawing pain
lncreased by food
Clusters (episodic)
Relieved by alkali
Food relief
Occurs at night
Not related to food or variable
Radiation to back
lncreased appetite
Anorexia
Weight loss
Nausea
Vomiting
Heartburn
Nondyspeptic symptoms
Fatty food intolerance
Bloating
Belching

100

67
6
6

Duodenal
ulcer
(%\

53
5
16
1

0-40
56

34

20-31

46-57
24-61

25-36
1 9-45
49-59

19

54-70
38-73
19

25-57

27-59

2

49
59

From Soll AH. Gastrointestinal disease. Gastric, duodenal
and stress ulcer. Philadelphia: Saunders, 1993.

Epigastric pain is the primary complaint in two-thirds
of PUD patients, and the vast majority will give a history
of some dyspepsia. The pain is frequently described as
"burning," nonradiating, and occurring two to three hours
after meals and at night. Relief is frequently obtained

with food or antacid use. Physical examination

may
reveal some epigastric or upper quadrant tenderness and
heme-positive stool. It should be noted, however, that it is
not possible to diagnose PUD with any accuracy by history and physical exam alone.

Definitive diagnosis

of PUD involves the use of

endoscopy or contrast radiography and is beyond the scope

of this text. Diagnostic workup of patients with symptoms
suggestive of PUD in the ED should focus on the potential
complications, as discussed below. The differential diagnosis to consider includes nonulcer dyspepsia, gastroesophageal reflux, neoplasm, mesenteric ischemia, pancreatitis,
hepatobiliary disease, and ischemic heart disease.
Treatment of presumed uncomplicated PUD is contro-

versial. While

all agree any potentially

those patients who must remain on NSAID therapy. If
outpatient antiulcer medication is started in the ED, it is
probably best to consult with the patient's primary care
physician (if possible) or to at least arrange close followup for the patient.
The majority of uncomplicated PUD patients may be
discharged from the ED. Reasons for admission include
suspicion of any of the complications discussed below.
Approximately l0% of PUD patients will present with a
serious complication as the initial manifestation of their
illness. This is especially true for elderly patients.
Hemorrhage

8

41-72
55
48

logue. Sucralfate and bismuth are less popular "protective

61-86
7-17
3-5

32-43
22-53

2-48

famotidine being the most commonly prescribed), the
H*/K*-adenosine triphosphatase (AIPase) inhibitor
omeprazole, and misoprostol, a prostaglandin E ana-

antacids (Mylanta or Maalox) are relatively inexpensive
antiulcer medications. All of these medications will give
approximately the same ulcer cure rate after 6 to 8 weeks
of use, with misoprostol being especially efficacious in

39-86
20-63
50-88
21-49

36-87

31

100

13
16

/

barrier"-type ulcer medications available. Finally,

68
20
24

DrsorusRs

ulcer-causing

medications and social habits should be discontinued (if
possible), differences of opinion exist as to whether outpatient antiulcer medications should be started in the ED.
Several medications now exist for treatment of PUD
including the Hz antagonists (cimetidine, ranitidine, and

Hemorrhage

is the most common complication of

PUD, occurring in approximately l5oh of ulcer patients.
Hemorrhage usually occurs in older ulcer patients, with
the peak incidence being in the sixth decade. Endoscopic
studies indicate that approximately 50% of upper gastrointestinal bleeding (UGIB) is from peptic ulcers. PUD
accounts for approximately 560/o of deaths from UGIB.
Major bleeding from peptic ulcers is arterial in origin.
Hematemesis or melena or both will be present in more
than 95o/o of patients. Hematochezia may be present if
bleeding is rapid. Most PUD bleeding is painless. If a significant amount of upper abdominal pain is present, perforation should be considered since a small percentage of
perforations will have a significant amount of UGIB.

Diagnostic workup for any UGIB should include

a

complete blood count and coagulation profile. It should
be noted that a significant drop in hemoglobin may not be
present in acute bleeds before fluid resuscitation. Insertion of a nasogastric tube and aspiration is routinely performed; however, this has been shown to be of little value
in predicting active bleeding. Nevertheless, return of
"coffee grounds" or frank blood helps establish the bleeding as being of upper intestinal origin.
The differential diagnosis to consider in any patient
with evidence of UGIB includes gastritis, gastric or
esophageal varices, Mallory-Weiss tears, esophagitis, and
duodenitis. History and physical exam alone are usually
not helpful in determining the exact source of UGIB.
ED interventions for any patient with UGIB should
include insertion of at least one large-bore I! two in any
patient with signs of instability. Blood for type and crossmatch for packed red cells should be sent to the blood

32 /

Err,rnncnNcy

Mnorcnn: Trm Conr Cunnrculurvr

bank, while type O negative red cells may be used

if

needed before the cross-matched blood is available. Correction of any existing coagulopathy should be attempted.
Ice water lavage through a nasogastric tube has been

proven unbeneficial. Lavage with tap water is frequently
done in an attempt to "lavage the stomach to clear" thus

indicating a cessation of bleeding. Administration of
intravenous H2 antagonists has been shown to be of some
benefit in preventing rebleeding.
Endoscopy should be considered for all patients with
UGIB. The timing of this procedure remains controversial. In addition to locating the site of the bleed, several
endoscopic therapeutic modalities such as laser therapy,
thermal probes, and injection sclerotherapy are now
available. Surgical intervention is indicated when continued life-threatening hemorrhage cannot be stopped by
endoscopic methods. Angiographically guided embolization may be an option in those patients who are poor surgical candidates.
Any patient with evidence of significant UGIB should
be admitted to the hospital. Those patients with hemodynamic instabiliry repeated episodes of hematemesis or
hematochezia, age over 60, a failure to clear with gastric
lavage, or significant cardiac, pulmonary, or renal disease
should be admitted to an ICU setting. From l0% to 32o/o
of patients admitted to the hospital because of UGIB
caused by peptic ulcers will rebleed.

Perforation (1.5.3.2)
Perforation is the second most common complication
7Vo of ulcer patients. Perforation
occurs when the ulcer extends through the muscle wall
and serosa, establishing a communication between the
lumen and the peritoneal cavity. Pyloroduodenal perforation occurs six to eight times more frequently than gastric

of PUD, occurring in

perforation. Spillage of gastric or duodenal contents
causes a chemical peritonitis that quickly progresses to
bacterial peritonitis.
Patients frequently complain

contrast material through a nasogastric tube may be done

to aid in the diagnosis. Paracentesis may be helpful in

a

few select cases.
Treatment in the ED consists of fluid resuscitation,
correction of electrolyte abnormalities, nasogastric suction, and administration of broad-spectrum antibiotics
covering both aerobes and anaerobes. Surgical intervention is indicated in almost all cases, though some studies
have shown similar outcome results in young patients
treated nonoperatively. The overall mortality for perforated peptic ulcers is from 60/o to l|oh.

Pyloric Stenosis
Pyloric stenosis with resultant gastric outlet obstruction occurs in approximately 2oh of PUD patients.
Penetration
Penetration describes the erosion of an ulcer through
the entire thickness of the stomach or duodenal wall without leakage of digestive contents into the peritoneal cavity. The ulcerative process is contained by fibrous adhe-

sions to adjacent structures. Penetration occurs most
commonly with posterior wall ulcers.
The pancreas is the most common site for penetration
by both gastric and duodenal ulcers. Other less commonly penetrated organs include the liver, spleen, and
kidney. Duodenal ulcers may penetrate into the inferior
vena cava and aorta, usually with catastrophic results.
Most patients with penetrating ulcers have had longstanding symptoms, and present with a change in the pattern of their usual ulcer pain. They frequently describe a
change in their pain from episodic to constant, with new
referral of the pain to the midback. Ultrasound and CT
may aid in the diagnosis.
Tirmors (1.5.4)

of an abrupt

onset of

severe upper abdominal pain that progresses to symptoms

of diffuse peritoneal inflammation. Posterior wall gastric
ulcers may perforate into the lesser peritoneal space,
which results in a more localized inflammatory reaction
and more obscure symptoms. Physical exam frequently
reveals an acutely ill patient who remains very still to
avoid any peritoneal irritation. There is diffirse abdominal
tenderness, often most pronounced in the epigastric area,
with many patients having a classic "board-like rigidity"
of the abdominal musculature. Bowel sounds are absent
in approximately two-thirds of cases.
Demonstration of free air on an upright chest x-ray or
left decubitus abdominal film is diagnostic. However, this
finding is present in only 650/o Io 80% of cases. Insufflation with 250 cc of air or instillation of a water-soluble

Both benign and malignant tumors may arise in the
stomach. Benign tumors are usually in the form of gastric
polyps. Most remain clinically silent, with a rare few
causing obstructive symptoms. Approximately 95Yo of
malignant gastric tumors are adenocarcinomas arising
from the gastric epithelium with lymphomas, carcinoid
tumors, and sarcomas representing the other 5%.
Metastatic disease to the stomach may be confused with
a primary tumor. Tumors known to metastasize to the
stomach include melanoma, lung, breast, and" most frequently in AIDS patients, Kaposi's sarcoma. For the purposes of this text, the term gastric cancer will be used in
reference only to gastric adenocarcinomas.
Gastric cancer is the second most colnmon cancer in
the worl4 having been surpassed in frequency by lung

1995. SELECTED READING Boland CR. A chest x-ray looking for pulmonary metastases should be done in all patients with concomitant respiratory complaints. Chile. Fordtran JS. While this is not a frequently performed study in the ED it can often be ordered as an outpatient in coordination with follow-up. and the use of food refrigeration. 1993. eds. Also controversial is a possible protective effect of a diet high in fresh vegetables and dairy foods. Schaffirer F. Textbook of gastroenterology. Philadelphia: Saunders. In: Spiro HM. significant bleeding. Schafftrer F. ed. Gastric ulcer. chemicals. In: Sleisenger MH. . the offspring of immigmnts to the United States will have approximately the same risk as the native population if raised here. Scheiman JM.28319 4. early satiety. Organic causes of obstruction are generally treated with surgical management. Clinical gastroenterologlt New York: McGraw. Abdominal pain is frequently the first complaint' Patients may complain of a vague upper abdominal fullness or a steady. Infrequently. Once the specific small bowel disease is diagnosed. also referred to as mechanical obstruction. While the small intestine pathophysiology is complicated there exist some common signs and symptoms of specific small bowel disorders. Factors associated with an increased risk ofgastric cancer include tobacco and alcohol use. Schaffirer R Berk JE. There has been a dramatic and unexplained decline in the incidence of gastric cancer worldwide in the past 30 to 50 years.1.H lll. Ulcer complications and their nonoperative treatment' In: Sleisenger MH. Other complaints may include vomiting. severe epigastnc pain. or heme-positive stool. Unfortunately. Classic signs of distant metastases such as umbilical nodes (St. Diverticula. eds. In: Haubrich WS. Berk JE. definitive treatment and final disposition of the patient is addressed. SMALL BOWEL (1.6. and Ireland being at exceptionally high risk. hernias. Berk JE. 1995. Philadelphia: Saunders. The incidence of gastric cancer decreased by 67% in the United States from 1950 to 1979. supraclavicular nodes (Virchow's nodes). In: Spiro HM. 199 5 . The current annual incidence of gastric cancer in the United States is less than 5 cases per 100. and stress. Mechanical Organic obstruction. Physical exam may reveal cachexia.6) Motor Abnormalities (1. and therefore close follow-up Obstruction (1.94:204. Of note. Spiro HM. 1993 . Clinical gastroenterology. Gastroenterology.rrNAr AND GASTRoINTESTINAL DIsonoeRS cancer in the 1980s.to 7O-year-old age group. or any evidence of metastatic disease. Webb WA. Gastrointestinal disease. Hudson N. Management of foreign bodies of the upper gastrointestinal ft act. The vast majority of patients with gastric cancer will not be diagnosed in the ED. Gaslrointestinal disease Philadelphia: Saunders. hernias. New York: McGraw-Hill. and occupations involving excessive exposure to dust. 1995. Diagnostic workup should include eval- uation for anemia and liver dysfunction. eds Gastroenterology. Spiro HM. There is a definite geographic predilection. (Krukenberg tumor) rarely occur. Tumors of the stomach. with immigrants from Japan. 1993. China. bloating.AeloN. and prior gastric surgery appear to be at increased risk.561-581.1) Disorders of small bowel motility are classified into organic and functional obstruction causes. Dunn DH. with the largest number ofreported cases in the 50. and rupture. Eisenberg MM.478485. Applied anatomy and anomalies of the stomach. The physician should consider any alternative diagnosis and be alert for potential complications of each small bowel entity. an epigastric mass. Gastroenterology. Duodenal ulcer. Definitive diagnosis is usually made with endoscopic tissue biopsy. Gastroenterology 1988. intestinal metaplasia. making it one-fifth as prevalent as colon cancer. ed.1) Abnormalities of small bowel function will frequently result in visits to the ED.656-699.698J 12. Mary Joseph's nodes). Patients with chronic atrophic gastritis. Eliciting and interpreting symptoms and signs. eds. ed. most noticeably in indus- trialized nations. Wolf SG.251-282. pemicious anemia. Graham DY. In: Haubrich WS. In: Haubrich WS. Gastric cancer is rare under the age of 30. Functional causes of obstruction are generally managed medically.3-10. Doublecontrast radiography is frequently used to evaluate patients with epigastric complaints. Hawkey CJ. hepatomegaly. 1993 .1494-1522. Gastric cancer is more colrunon in lower socioeconomic classes. Much controversy exists as to whether gastric ulcers are a risk factor for gastric cancer. Gastnc cancer is usually asymptomatic in its ear$ stages and even in advanced stages has nonspecific symptoms. eds. a diet high in pickled vegetables. Indications for admission include severe anemia or malnutrition. In: Yamada T. and smoked foods and nitrates. or frank anorexia. patients present with symptoms from metastatic disease such as ascites from liver involvement or dyspnea secondary to malignant pleural effirsions. Males are affected at a ratio of approximately 2:1.6. Philadelphia: Lippincott.000 popula- tion. Philadelphia: Saunders. Fondacaro PF. vohulus. Mucosal injury caused by drugs. Philadelphia: Saunders. usually results from adhesions. Hematemesis or melena may occasionally occur. most physical findings are the result ofextensive disease. Harford W! McArthur KE. Fordtran JS. A high index of suspicion is needed to detect gastric cancer in the ED. intractable pain or vomiting. The emergency medicine physician should promptly recognize these suggestive characteristics and conduct initial management and further confirmatory analysis. salted fish and meats. or an ovarian mass / 33 is important in all suspected cases.

frequently attempting to relieve the pain by changing positions. and trauma. appendicitis. severe electrolyte imbalances (especially hypokalemia). Crohn's disease. has a variety of intraabdominal etiologies. In contrast to mechanical obstruction. Distention becomes more evident with the more dis- tal the level of obstruction. uremia. A possible history of an underlying precipitating medical condition should be investigated. and CAI scan.2. Abdominal radiography images will detail distended gas-filled and air-fluid loops in the small bowel. Supportive care includes nasogastric suction along with replenishment of fluids and electrolytes as necessary. intraabdominal vascular accidents. The patient may present as restless. and anxious. The syndrome can also be the result of Whipple's disease. Adynamic Functional obstruction. diabetes mellitus. and parasitic infections. or in association with postoperative abdominal surgery. Malabsorption (1. functional obstruction patients may show serum electrolyte imbalances and hemoconcentration on laboratory analysis. tachycardiac. Patients present with diffirse colicky abdominal pain. hyperlipemia. along with disaccharidase deficiencies. severe infections. exposure of the peritoneum to irritants. Similar to mechanical obstruction. fluid and electrolyte correction. There may be associated vomiting and obstipation. or renal abnormality. The most common site of occurrence is the distal portion of the duodenum. primarily of fats and fat-soluble vitamins. 6. Structural Disorders (1. Dehydration may develop secondary to vomiting or third spacing of fluid in the bowel. Examples of maldigestion conditions are pancreatic or biliary secretion deficiencies. Visible and audible peristalsis may be observed. Ultrasonography images of the abdominal aorta may show the aneurysm location in relation to the renal arteries. or the longer the duration of obstruction. The treatment of functional obstructions is conservative medical management and treatment of the primary underlying condition. pancreatitis. Computer-aided tomography images give a better degree of aneurysm diameter size and indicate if any rupture has occurred. The patient is restricted from any oral nourishment until normal intestinal function returns.34 / EuoncnNcy Mnucwn: Tun Conr CunrucuLUM tumors. Other laboratory abnormalities may reflect the underlying cause of the ileus. or renal colic. hypertension.6. Adynamic ileus usually results from external trauma. or strictures. and weakness. Physical examination of the abdomen reveals generalized distention and nonlocalized abdominal tenderness. 2. 2) Malabsorption syndromes of the small intestine are caused by the malfunctioning of infected intestinal mucosa. such as an increase in amylase or lipase with pancreatitis. gallbladder. Differential diagnosis should consider any possible cause of acute abdominal pain. . Prompt surgical intervention and resection is the specific treatment for aortoenteric fistula. ultrasound. Abdominal angiography will greatly demonstrate the source of the bleeding site in the gastrointestinal tract. Acute abdominal radiologic series will characteristically show gas and fluid-filled loops in the small bowel. Peritoneal signs are generally absent. which becomes more persistent with increasing distention. Predisposing factors include atherosclerosis. Adhesive bands are the most common cause of small bowel obstruction. The loss of mucosal microvilli results in disaccharidase deficiency. Noninvasive imaging studies for an aortoenteric fistula include plain abdominal roentgenogram. Anticholingeric medications altering the sympathetic tone may cause adynamic ileus. without signs of peritoneal irritation and borborygmus. intussusception. obstipation. 1) Aortoenteric fistula occur primarily postoperatively when an abdominal aorta aneurysm erodes into the enteric tract.2) Aortoenteric Fistula (1. Electrolyte disturbances or hemoconcentration secondary to persistent vomiting and dehydration is common. and administration of preoperative sur- gical prophylactic antibiotics. Lateral abdominal x-rays may reveal an abdominal aortic aneurysm outlined by sclerotic plaques. There are a variety of small bowel absorption etiologies including celiac and tropical sprue. such as perforation. smoking. the mild abdominal pain of functional obstruction is continuous rather than colicky.6. The signs and symptoms vary according to the extent of small bowel involvement and the progression of the disease. may be present. also referred to as adynamic or paralytic ileus. Patients often complain of vomiting. whereas maldigestion conditions are the result of intraluminal abnormalities in the breakdown of nutrients by the gastrointestinal tract. Surgical intervention is the definitive treatment of mechanical obstruction. Management in the ED includes nasogastric suction to relieve abdominal distention and vomiting and possibly reduce aspiration. Sprue syndrome is indicated by motor abnormalities and impaired nutrient absorption. Moderate generalized abdominal tenderness. particularly lactase deficiency. Sprue syndromes are characterizedby severe weight loss and nutritional deficiencies.

rrNAL AND GAsTRoTNTESTTNAL Drsonnnns / 35 Tropical sprue patients have a history oftravel to tropical climates with symptoms sometimes appearing years after travel. The symptoms are initially characterized by explosive watery diarrhea. frothy. Acute appendicitis is the most common nontraumatic surgical located between the surface absorptive cells and the lamina propria. increased flatulence. all in response to the breakdown of lactose. The diarrhea can be exacerbated by a high-fat diet. Localization ofthe source of bleeding from the lower intestine involves endoscopic visualization. celiac sprue responds very well to a gluten-free diet. if required. usually bright red rectal bleeding in a child. Folic acid should be administrated for several weeks to reverse the deficiency. Meckel's diverticulum inflammation may also trigger intussusception or simulate acute appendicitis. Barium radiologic studies of the small intestine demonstrate a dilated lumen with flattened mucosal lining. Appendicitis is one of the more common presentations of an acute surgical abdomen to the ED. fats. and pale in color. Vitamin and electrolyte replenishment should be considered in celiac sprue as needed. which cannot be broken down in celiac sprue patients. and water. and intestinal obstruction or volvulus. Unlike tropical sprue. flatulence. Celiac sprue causes absorption abnormalities in the fat-soluble vitamins. The patient will complain of indigestion. Vitamin replenishment should be considered if the tropical sprue is long standing. The diet should also be high in calories and proteins and low in fat. localization ofthe source ofthe bleed. The gold standard in diagnosing Meckel's diverticulum is with isotopic scanning (red cell scintigraphy). Inflammatory Disorders (1. due to the poor fat absorption. cholesterol. 2. cheilosis. A small percentage of discomfort. phosphorus. assessment of volume loss and fluid resuscitation. This protruding appendage or dilation can be located anywhere within 100 cm of the ileocecal valve along the antimesenteric border of the small intestine. The mucosal lining of the small intestine sim- emergency in children. The highest incidence of occurrence is in male patients between ages l0 and20. will become fewer. The vermiform appendix is a slender blind-end tubular structue extending from the proximal portion of the cecum. Patients with dermatitis herpetiformis frequently have symptomatic celiac sprue as well.6. if required a milk challenge trial or abstinence may assist in Meckel's Diverticulum (1.AsroN. 6. and prothrombin will be decreased. third. There may exist a latent phase of remission. early surgical evaluation. however. Tropical sprue responds very well to folic acid and broad-spectrum antibiotics. and the stools become more solid. and dry rough skin. Serum protein. Symptoms generally consist of abdominal bloating. iron. mimicking peritonitis. Laboratory analysis may reveal a mixed picture of hypochromic anemia (macro or microcytic). The diagnosis is often made clinically. carbohydrates. The hallmark presentation of Meckel's diverticulum is a persistent. Tropical sprue appears to behave like an infectious process. arteriography. distention. The diagnosis of Meckel's diverticulum is generally made clinically by excluding other causes of the symptoms. cutaneous hyperpigmentation. with the symptoms returning later in adulthood. The initial approach to the patient is threefold: first. since their use will increase the patient's appetite and improve the absorption ofnutrients by the gastrointestinal tract. exploratory surgery or barium contrast x-ray studies of the small intestine. the etiology is unclear. Laboratory analysis reveals microcytic hypochromic anemia. The diarrhea ply lacks the enzyme lactase. signs and symptoms of peritonitis may develop. Corticosteroids may also be necessary for severely ill patients. Symptoms generally begin in early childhood. which may aggravate the condition. required for the breakdown of lactose. patients have been found . Meckel's diverticulum are present in 2o/o to 3% of the population and is the most frequent congenital malformation of the gastrointestinal tract. 6. and diarrhea. Initially. 1) Appendicitis is the inflammation of the vermiform to have a collagenous layer appendix. If the ulcer perforates the intestinal lining. Acute appendicitis is usually a result of bacterial infection secondary to appendiceal lumen obstruction. confirming the diagnosis. proteins. intussusception. Physical examination may reveal abdominal distention and mild tenderness. angular stomatitis. Pancreatic enzymes are normal. A suction biopsy may be indicated to eliminate other etiologies such as cancer or lymphoma if the patient is unresponsive to a gluten-free diet. calcium. Meckel's diverticulum presentation can vary considerably. abdominal cramps. foul smelling. The patient will describe the greasiness of the stool. episodes Vitamin-deficiency symptoms can develop. Frequently the presence of gastric mucosa in the diverticulum may result in ulceration. the diet should lack foods containing lactose. However.3) Acute App endicitis ( 1. such as glossitis. and weakness. There will be increased fecal fat content. 3) Meckel's diverticulum is the congenital remnant of the omphalomesenteric duct. This diet lacks the polypeptide linkage. The most common disaccharidase deficiency is lactase deficiency. painless. 3. second.

this finding is infrequent. and lymphoma. No current medications are proven effective in reducing reexacerbations of Crohn's. perforation. These medications have significant side effects that limit their availability. also referred to as regional enteritis or terminal ileitis. or malabsorption may develop due to the damage of the intestinal wall. Toxic megacolon or intestinal perforation are rare complications of Crohn's. If recognition of appendicitis is delayed. 3. The initial abdominal pain is vague and diffuse.36 / ErrrencrNcv MrorcrNn: Tsn Conn CunrucuLUM The physical examination is the key to diagnosing appendicitis. flatulence. hemorrhage. the inflam- matory process is of a nonspecific granulomatous disease. Regional Enteritis/Crohn's Disease (1. 6. and pelvic signs and symptoms. There is no cure for Crohn's disease. Physical examination often reveals tenderness or a mass in the right lower abdominal quadrant. Bowel obstruction must also be high on the differential diagnosis in any acute abdominal pain presentation to the ED. which is restricted to the large intestine (colon and rectosigmoid) and nonsegmental distribution. malaise. especially symptoms. Rectal examination may reveal occult blood in the stool. the complications include abscess formation. Pregnancy test. Complications of Crohn's disease are commonly divided between intestinal and extraintestinal manifestations. Sulfasalazine. These complications carry a higher morbidity and mortality. These generally have a higher occurrence in Crohn's disease patients with colonic involvement. Radiologic images of the abdomen may assist in ruling out bowel obstruction or perforation. ovarian cyst. however. 2) Crohn's disease. anemia. With increased inflammation the abdominal pain will become more distinct. urinary analysis. A rectal and pelvic examination are mandatory in all abdominal patients. Rebound tenderness with guarding will become more pronounced in the right lower quadrant. The immunosuppressive drugs also aid in tapering the dose of long-term steroid therapy. The presence of a fecalith in the right lower quadrant on the plain abdominal film strongly suggests an appendicitis. Corticosteroid therapy effectively suppresses the inflammatory response of the bowel and systemic manifestations. . and eventually focused in the right lower quadrant. sharper in nature. The underlying etiology of this disease remains unknown. with nausea and vomiting. Laboratory evaluation can aid in ruling out alternative with tenderness in the right lower quadrant. The antibiotic sulfasalazine is structurally related to sulfur and aspirin drugs. Immunosuppressive therapy of 6-mercaptopurine (6MP) and its active metabolite azathioprine is useful for the closure of enteroenteric or enterocutaneous fistulas and abscesses. Prophylactic preoperative antibiotic administration may be preformed in the ED. Crohn's disease is characterizedby an insidious onset of exacerbations and remissions of the variable signs and symptoms. or perirectal abscesses. is a chronic recurrent segmental inflammatory process of the gastrointestinal tract. intussusception must be considered. Medical treatment is very similar to that of ulcerative colitis and is empirically aimed at relieving and avoiding the exacerbation of mainstay of ED management of the acute appendicitis patient. Patients with Crohn's disease generally complain of intermittent colicky abdominal pain. Histologically. Obstruction. Patients' common presentations frequently involve anorexia. In infants. and pelvic inflammatory disease. Sulfasalazine has a better effect on the disease's involvement in the large than in the small intestine. These findings are in contrast to the inflammatory process of ulcerative colitis. The Crohn's disease clinical presen- cultures are required. infectious diarrhea. but most frequently involves the distal ileum and the right colon. and weight loss. Peritoneal signs may later be accompanied by signs of a low-grade fever and leukocytosis. and peritonitis. fistulas. Differential diagnosis of Crohn's disease can be challenging given the various presentations of the patient's diagnosis. Periods of severe diarrhea may be separated by intervals of constipation. similarly to steroids. Crohn's disease can involve any segment of the intestinal tract from the lips to the anus. The topical form of 5-ASA is useful for Crohn's disease cutaneous involvement in the distal colon and rectum. Other diagnoses to consider at initial presentation include appendicitis. does not enhance the relief from the acute exacerbations of Crohn's disease. Differential diagnosis of acute appendicitis includes ectopic pregnancy. low-grade fever (or rarely spiking with chills). Sulfasalazine is cleaved in the colon to its active metabolite 5-aminosalicylate acid (5- ASA). Abdominal pain may be evaluated using the psoas sign (extension of the right hip) or obturator sign (pain on passive rotation of the flexed right hip). Intestinal complications of Crohn's disease include anorectal ulceration. Anorexia. generally periumbilical. adnexal torsion. The slow release of 5-ASA enables the primary effect to occur in the lower gastrointestinal tract. fissures. is a common associated symptom. The inflammatory process will show discontinuous involvement of "skip lesions" of the bowel. Treatment lasts for 2 to 4 weeks and then is tapered off as symptoms permit. Prompt surgical intervention is the tation will often initially mimic inflammatory large bowel process of ulcerative colitis. administration of sulfasalazine and antidiarrheal medications may relieve mild exacerbations of Crohn's disease. However. Bowel sounds may be hyperactive.

persists for I to 3 days.4) troenteritis. dfficile. Shigella secretes shiga toxin. stools with no puss. malaise. jejuni is similar in structure to V cholerae. E. Common bacterial species affecting the small intestine are Staphylococcus aureus. The incubation period from infection to clinical symptoms for Staphylococcus. low- nated meat products. which usually begins 2 to 3 days after exposure. Clarification of the patient's stool description is very helpful for detecting any signs of blood or mucus indicative of an invasive agent. watery with mucus. dfficile-induced diarrhea frequently follows broadspectrum antibiotic administration that wipes out the nor- mal flora of the gastrointestinal tract and causes pseudomembranous colitis. Attempts at specific vaccine protection against all four pathogenic serotlpes of rotavirus have been unsuccessful. Their outbreaks are generally associated with contaminated food and water. coli species. The remaining organisms have a longer incubation period in the gastrointestinal tract. The diarrhea can last from2 to 12 days.1) associated vomiting. Transmission is commonly via the fecal oral route. V cholerae secretes an exotoxin choleragen. Treatment for the rotavirus infections is supportive. a powerful exotoxin that promotes binding and invasion into the Signs and symptoms of rotavirus infection include persistent watery diarrhea and vomiting. and may include Viral (1. Illnesses induced by Norwalk and Norwalk-like viral agents account for up to 35oh of all acute diarrheal outbreaks in the world. S. enterocolilica causes bloody diarrhea by enterotoxin. enteritidis has hundreds of serotypes that may cause diarrhea. S. The gramnegative rod has a polar flagellum that facilitates motility. Bucterial (1. and vomiting.6. dysenteriae causes large volumes of bloody diarrhea with mucus. The symptoms. The history of other household members with similar symptoms is highly suggestive of common food poisoning contamination. a special request fot C. These agents cause diarrhea either by direct intestinal invasion or by exotoxin stimulation of the intestinal tract. E. culexamination. Yersinia enterocolitica. The volume of diarrhea can be severe. The cholera infection is described as severe rice watery stool samples. Occurrences are more prevalent during the winter months. nausea.4. causing hemorrhagic colitis and grade fever. The degree of symptoms may vary with any of the viral agents from acute viral gastroenteritis diarrheal illness to extraintestinal manifestations. coli. Poor food preparation. abdominal cramps.rrNAL AND GAsTRoINTESTINAL DIsononRs / 37 Infectious Disorders (1. which is also part of the normal intestinal flora. Vomit ing is more prevalent with Norwalk than with the Norwalk-like viruses. The treatment is supportive only. Salmonella enteritidis. commonly associated with travelers' diarrhea. The most common presenting complaint is diarrhea with abdominal discomfort. to proliferate and secrete exotoxin. Other possible differential diagnosis for gastroenteritis should be considered for viral or parasitic infection' An . and Vibrio arc brief. Major complications involve the possibility of bac- teremia and dehydration.4. The gram-positive S. Exo- toxin release disturbs the electrolyte balance in the intestinal lumen and leads to an osmotic diarrhea. Yersinlc is self-limited diarrhea and requires no treatment unless it invades the blood. Patients must maintain an adequate level of hydration. Frequently. Shigella dysenteriae. Diagnosis is made by antibody-specific identifications of hemolytic uremic syndrome. The 0157:H'7 strain of E. and fever. or a fecal to oral transmission will often result in a gas- intestinal mucosa. The diarrhea is described as voluminous. coli has been indicated in contami- Viral infections of the small intestine generally occur worldwide and can affect any age range. and sensitivity. and Clostridium dfficile. Diagnosis is again by enzyme-linked immunoassay and radioimmunoassay identification in the stool specimen. V cholerae is identified by examining the stool specimen under dark field microscopy. and frequently lasts less than a week. dfficile is thought responsible for the diarrhea. Vibrio cholerae. dfficile toxin is required by the lab.6. The physical examination is generally unremarkable. a contaminated food source. qureus triggers diarrhea by exotoxin release and is the most common cause of food poisonlng. Campylobacter jejuni. The two most common viral agents causing infectious diarrheal syndromes are rotavirus and the Norwalk virus. Rotavirus has been associated with the development of necrotizing enterocolitis in neonates. This allows C. headache. If C. Escherichia coli. The common clinical findings associated with viral infections of the small intestine include persistent diarrhea.AsooN. while not as severe as rotavirus. Campy- lobacter-induced illness usually begins as fever and headache followed by bloody loose diarrhea and abdominal cramps. C. Y. Direct intestinal invasion causes bloody diarrhea. causes diarrhea by both direct invasion and exotoxin release.6. C. offending agent in the stool Confirmatory diagnosis ture. polymorphonuclear leukocytes will be seen on the Gram stain with invasive infl ammatory causing organrsms.2) Numerous bacterial agents can infect the small intestine. is made by isolating the Gram stain. Recent traveling is frequently associated with the source of diarrhea.

and lack a true digestive tract of their own. The larvae will invade and deposit in muscle tissue. If C. lumbricoides. the helminth eggs will trigger an immune reaction and may be distributed throughout the body. Generally. japonicum is common to Eastern Asia. The trophozoite permits movement by the cytoplasmic projections called pseudopodia. Tapeworm infection generally results from ingestion of a contaminated intermediate host meat. Tapeworms may become quite long (several meters) in size. americqms and S. The schistosome penetrates through skin and invades the venous system. The proper preparation of meats greatly reduces infections by tapeworms. Mature helminths do not generate a strong immune response and may live for years in their human host. Parasitic (1. dfficile toxin is highly suspected" treatment regimens consist of either metronidazole (Flagyl 500 mg po tid x 3 days) or vancomycin(125 mg po qid x 3 days). Protozoa replicate by both sexual and asexual reproduction. Antispasmodic and antibiotic agents are not indicated in patients unless symptoms are severe and protracted. This migration causes perianal irritation and itching. Treatment for intestinal nematodes is with any one of the following agents: mebendazole (Vermox 100 mg po bid x 3 days). stercoralis larva travel directly to the lung alveoli. Serum analysis reveals an eosinophilia and increased creatinine phosphokinase. mansoni). These pseudopodia guide direction ofthe protozoa and allow it to surround and engulf food.6. americanis and S. larvae through unprotected skin. or pyrantel pamoate (11 mg/kg single dose max The intestinal roundworms I gram). Once the cyst form of the protozoan is ingested. Diagnosis is aided by examination of perianal tape to detect for the presence ofeggs. vermiculans (pinworm) and Z trichiura (whipworm) do not invade the intestinal tract mucosa. Giardia lamblia.38 / ENmRcsNcy MnorcrNs: Tur Conn Cunnrcuruvr elderly patient with gastrointestinal bleeding and a nor- mal stool must be investigated fuither to determine the source ofbleeding. Complications include invasion of the liver. and blood cultures should be obtained. All tapeworm infections are treated with praziquantel or niclosamide. Complications of this infection may cause blockage of the portal system. Diphyllobothrium latum (fish). thiabendazole (Mintezol 22 mglkg po bid x 3 days). C estodes (tapeworms ) are hermaphrodite s. Unnecessary treatment with these drugs will often prolong the carrier state of the individual. The female E. abdominal cramping. and therefore do not cause a genenlized eosinophilia. mansoni is found in South America and Africa. vomiting. Empirical treatment for severe diarrhea of suspected bacterial etiology includes initiating fluoroquinolones (Cipro 500 mg po bid x 3 days) while awaiting stool cultures. Trichuris trichiura (whipworm).3) Parasitic infections of the small intestine are classified parasites as helminthic and protozoan. Bacterial infections of the small intestine are treated with supportive rehydration and replenishment of electrolytes. albendazole (400 mg po single dose). vermicularis infections are caused by ingestion of N. Nector qmericanis. Solid foods are restricted and only oral fluids are administered. However. Protozoa are free-living. The patient infected with the schistosome will frequently complain of skin irritation and itching at the penetrarion site. The intestinal Platyhelminthes flatworms include trematodes (flukes) and cestodes (tapeworms). Diagnosis is accomplished by identification of helminth eggs or larva in the stool. protozoa transform between two structures. ver- micularis (pinworm) usually migrates to the perianal area at night to lay her eggs. Children frequently have hand-tomouth reinfection. The larvae migrate to the hepatic portal venous system. If the source of the possible contamination is from a public facility. Praziquantel is the commonly used drug for treatment of the helminths. and Is ospora belli. and surround the veins of the intestinal system. single-celled eukaryotic cell organisms with cellular organelles and cytoplasmic membrane. T trichiura. it transforms back to a more motile form called the trophozoite. The sizes of protozoavary . (Nematodes) include Ascaris lumbricoides. Tapeworms live and replicate in the digestive tract of their host. Enterobius vermicularis (pinworm). N. The tapeworm continuously sheds eggs into fecal material. A. The main infectious trematode is Schistosoma Qaponicum and. the physician should noti$u the local health authorities. which include trematodes (flukes) and cestodes (tapeworms).4. T. stercoralis infections result from penetrating filariform eggs. weight loss. Assessment of fluid status is necessary. There are four medically important protozoans that can cause diarrhea infection: Entqmoeba histolytica. which enter the gastrointestinal tract for excretion. and. The worms mature in the gastrointestinal tract. The Z spiralis infection is traced to the ingestion of encysted larvae in the contaminated pork meat and is termed trichinosis. clinical presentation of helminth infections include diarrhea. Severe infections result in malabsorption. E. Examples include Thenia solium (pork). while S. and bile ducts. Any type of helminthic infection causes a eosinophilia response from the host. Strongyloides stercoralis. If comorbidity or bacteremia is suspected. In general. and fever. The schistosome lays its eggs. saginate (beef). S. Helminthic include Nemathelminthes (roundworms) and Platyhelminthes. and Trichinella spiralis. the patient should be hospitalized for intravenous antibiotic. gallbladder. where they are coughed up and swallowed. and E. Cryptosporidium.

steatorrhea. The diagnosis of carcinoid syndrome is confirmed by urine levels of 5-hydroxyindoleacetic acid (5-HIAA). The watery diarrhea can be protracted with evacuations up to 15 L a day. approximately 2000 cases occur yearly in the United States. lqmblia infection is with metronidazole (Flagyl 250 mgpo tid x 5 days). several diagnostic studies may be employed. and the prognosis is very poor. The protozoa Cryptosporidium parvium (cryp- tosporidiosis) and Isospora belli (isosporiasis) are more common diarrhea infectious causes in immunocompromised individuals. The clinical course in immunocompetent patients is self-limited. vomiting. G. and is more common in Tumors (1. low-grade fever. However. and anorexia.6. Most individuals are asymptomatic carriers. histolytica generally causes bloody diarrhea. recurrent abdominal pain and diarrhea. Instead the diarrhea is described as very foul-smelling greasy stools.6.6. Radiation and or chemotherapy is reserved for tumors that have advanced past the bowel wall. Improving sanitary conditions is also part of preventatrve treatment. The diagnosis by identification ofan oocyst is often difficult because of the sparse amount found in stools.1) and Ischemic Colitis (1. Since the G. in immunocompromised patients this protozoa organism is treated using trimethoprim with sulfamethoxazole (Bactrim DS po qid x l0 days then bid for 3 weeks). Approximately 5% of the United States population are infected by Histolytica. These include upper gastrointestinal radiologic series and endoscopy for biopsy of abnormal pathology. The organism coats the wall of the small intestine and interferes with fat absorption. an active final metabolite of 5-hydroxytryptophan. fluid" and electrolyte replenishment. Treatment of E. Carcinoid syndrome of the small intestine is rare and usually does not develop until after metastases. Treatment of G. This may subside and the immunocompromised patient may suffer frequent periods of recurrence. Supportive measures include nutrition. histolyticq infections is with metronidazole (Flagyl 750 mg po tid x l0 days). There are no direct signs or symptoms to suggest the presence of small intestine neoplasms.6. causing malabsorption. who may pass the infective form (cyst) of Histolytica by fecal-oral transmission. dyspnea and wheez- ing. Tumors of the small intestine are extremely rare. Transmission of protozoa is generally by the fecal-oral route. The earliest manifestations of small bowel tumors are subtle and may vary from persistent peptic ulcer disease to occult gastrointestinal bloo4 malabsorption. Infrequently the diarrhea may recur or become protracted for months. lamblia do not invade the mucosa. With carcinoid tumors the metastases are generally too widespread for the benefit of surgical resection. Vascular Disorders (1.6. Generally the infected patients are asymptomatic. Their discovery is usually the result of a secondary presenting complaint. lamblia has also been documented in wildlife as a common cause of camper's diarrhea. Carcinoid tumors develop from argentaffin cells and frequently occur in the distal small bowel. histolylica ingests the normal bacterial flora of the intestine wall and sometimes invades the intestinal mucosa.AsnoNarNAL AND GASTRqTNTESTTNAL DrsoruBns / 39 from 5 pm to 2 mm. If cancer of the small intestine is suspected. The suspicion of small bowel cancer is increased with hereditary or preexisting factors such as long-stand- E. Carcinoid syndrome can result from carcinoid tumor cells that secrete 5-hydroxytryptophan. G. The symptoms of abdominal cramping and severe diarrhea are generally self:limited in the immunocompetent patient. The trophozoite form of E.5) unsanitary conditions and Third World countries. lamblia (giardiasis) affects approximately 5% of the United States population. they do not cause bloody diarrhea. Adenocarcinomas are the most common cancer of all the small intestine tumors. This invasion causes bloody diarrhea and abdominal pain. Abdominal ultrasound may be required for jaundice secondary to tumor mass obstruction of biliary outflow common bile duct. Diagnosis is made by identification of a cyst or trophozoite in the stool specimens. The flagellated trophozoite adheres to the small intestine wall. I. There is an increased incidence in the long-standing Crohn's disease patient.6. the result of drinking from contaminated streams. The tumor is slow growing but the prognosis is poor. or intestinal obstruction.6) Mesenteric Ischemia (1. The definitive treatment for either benign or malignant tumors of the small intestine is surgical resection. Adenocarcinomas generally occur in the proximal small bowel. CAT scan imaging of the abdomen is required for staging of the neoplasm. Currently there is no effective treatment regimen for Cryptosp oridium-induced diarrhea. Outbreaks occur as a result of poor sanitation conditions contaminating community drinking water. and symptoms of right-sided valvular heart disease.2) Gastrointestinal ischemia is more prevalent in elderly patients with a previous history of vascular disease. and weight loss. These secretions result in the systemic manifestations of paroxysmal flushing. ing Crohn's disease. belli infection generally causes abdominal cramps. such .

should be obtained immediately. Fordtran JS. Mahogany stools (partially digested blood) or bright red blood per rectum frequently denote a lower gastrointestinal (LGI) source of blood loss but can occur with a brisk and massive UGI bleed as well.288: 1663. The ischemic episodes can resolve very quickly or may progress to cause bowel necrosis. allowing convenient defecation. the abnormalities seen on barium studies may remain for a few days. The rectum has a separate arterial and venous system and is discussed in the next section. After the patient's ischemic episodes subside. Webster DP. et al. Whipple's disease: a multisystem infection. Long-acting vasodilators may be beneficial. Arch Virol 1978. Exploratory abdominal surgery is indicated for the suspected infrequent complications of extensive infarction or bowel perforation. et al. Schneider CBN. . If bleeding continues. Shaffer N.132: 9l 0. gross structure that constitutes the final portion of the alimentary canal. The epidemiology of appendicitis and appendectomy in the United States. It can manifest in a variety of ways from guaiac positive stools with or without anemia to massive acutely life-threatening hemorrhage. Differentiating acute appendicitis from pelvis inflammatory disease in women of child bearing age. Obscure gastrointestinal haemorrhage of small-bowel origin. similar to that seen with Crohn's disease. Newer surgical techniques allow for ileocanal anastomoses so that many patients who have undergone colectomies do not have ileostomies. SELECTED READING Addiss DG. Flewett TH. et al. Bayless TM. In: Sleisenger MH. Gore RM. et a'1.40:1201. with the presence of acute ischemic colitis. and the rapidity with which it is lost determines the form that the blood takes as it passes out through the rectum and anus. 4th ed. A residual stricrure may develop at the ischemic site. Barium contrast images may demonstrate edema of the mucosal folds.11:569. and neoplasia are commonly encountered (and often overlapping) colonic disorders. Vascular diseases of the bowel. Silen ML.214:230.7) advanced atherosclerotic lesions compromise blood flow to the vessels of the intestinal mucosal wall. Visible bleeding routinely prompts patients to seek medical attention. An attempt to quantitate the amount of blood lost should be made through questioning. As in all gastrointestinal bleeding.. to resuscitate the patient immediately. There may be some associated nausea and vomiting and. et al. Approximately 12 cm of the distal colon is designated the rectum.40 / EnmncnNcv MporcrNs: Tnr. Woode GN. Ashley CR. The location of the bleeding site. McPherson GAD. irritable bowel syndrome. extends to the anus. with aching abdominal pain usually occurring shortly after a meal. It is important to remember that the colon is not a vital organ and many individuals lead long and productive lives after colectomy." Pediatr Clin North Am 1993. Hemorrhoidal bleeding is the most common form of lower gastrointestinal bleeding. 1988. Cheche S. Fowler BS. Sequence and genome organization of a human small round-structured (Norwalk-like) vints. and averages l 5 m in length. Knox DL. Mesenteric angiography may reveal areas of vascular deficiency to the intestine. Ann Surg 1991. Acute ischemia episodes generally resolve on their own. N Engl J Med 1991. Primary and recurrent Crohn's disease: experience with 1379 patients.300:920. Philadelphia: Saunders. It begins at the ileocecal junction.325:12009. Mental . Treatment of suspected intestinal ischemia requires surgical evaluation for possible salvage ofbowel necrosis and arterial bypass graft. Science 1993:'259:516. Caul EO. Patients with chronic ischemia have a tendency to have an increased volume of stool and may develop malabsorption of nutrients and fat. Patients may give a history of similar episodes occurring intermittently for weeks. The typical ischemic colitis patient is often a poor surgical candidate. Vital signs. Gastrointestinal disease. The LARGE BOWEL (1.Br Med J 1994. direct observation is helpful. This section reviews common problems associ- Patients with acute ischemia may show rebound tenderness and rigidity on physical examination secondary to irritation of the peritoneum. becomes semisolid. the volume of blood lost. constipation. The right lower quadrant "revisited. ated with the colon. Lambden PR. eds. The colon absorbs up to 70%o of the water from the fecal stream so that liquid stool bloody diarrhea. Celiac sprue (medical progress). diarrhea. Initial management consists of supportive measures including antibiotics. Smaller amounts of bright red blood per rectum in a hemodynamically stable patient suggests a colorectal source. colitis. Bleeding.57:1. The distal colon and rectum also serve as a fecal reservoir. Hemingway AP. Ballantyne GH. and if not. Am J Emerg Med 1993. Bleeding Bleeding is a common presentation of colonic pathology. Tracy TF Jr. Chronic lowgrade blood loss may portend a worse outcome eventually. diverticulitis. Thompson JN. Michelassi F. Melena (digested blood) often occurs as a result of upper gastrointestinal (UGI) bleeding but can result from a proximal colonic bleed of lesser volume and slower transit time. Conn CunnrculuM as coronary artery or peripheral vascular disease. Trier JS. obstruction. the first step is to determine whether the patient is hemodynamically stable. NEngl J Med 1979. The colon. but evaluation and diagnosis are frequently delayed when bleeding is occult. or large intestine. Grendell JH. The rotaviruses. including orthostatic blood pressures. is the hollow tubular lntestinal ischemia clinical onset is very rapid.4zr J Epidemiol 1990.

Both conditions may be suspected while definitive proof remains frustratingly out of reach. the colon should be prepared using a standard oral lavage solution. If possible. are not indicated in the evaluation of acute LGI bleeding. and when possible. AVM bleeding is painless and usually self-limited. inflammatory bowel disease. Subsequent endoscopy may be required to determine the precise reason for the hemorrhage. Arterioles in the mucosa encounter sharp angles at the openings ofthese outpouchings. symp- tomatic anemia will generally require admission for transfusion. Even when they detect potential pathology they do not demonstrate that the lesions are actually bleeding. Angiogra- Drsonnnns / 4l tis. and at times as recurrent gastrointestinal bleeding of obscure etiology. Causes of colonic bleeding include diverticulosis. resulting in ischemia with tissue loss and bleeding. and gross ongoing hemorrhage. Diverticulosis is common in Western societies with refined diets low in fiber. The patient's coagulation status should be assessed and an effort to correct any coagulopathy detected should be considered. massive bleeds with no warning. gastric lavage with room temperature water is recommended. such as barium enemas. Arteriography may suggest AVMs. or both. Such patients may never be aware that they have been bleeding. find the specific bleeding site. they usually do so because they have outgrown their neovascular blood supply and tissue necrosis with sloughing results. endoscopy may reveal that a patient with recent colonic bleeding has responsible either diverticula or AVMs. they obstruct the views of both the angiographer and the endoscopist. Likewise. Weight loss. or who has undergone repairs of such aneurysms. Arteriovenous malformations are aberrant connections between arterioles and venules that largely bypass capillary beds. Clinicians should not be misled by "normal" hematocrit readings during any acute bleeding episode. The distal duodenum is the most frequent site for these fistulae. an effort can be made to diagnose the underlying problem. and symptoms of anemia are common complaints heard from patients suffering from colon cancer. phy and endoscopy have lessened the need for exploratory surgery in this setting. and self-limited. neoplasia (benign and A rare cause ofgastrointestinal bleeding that should not be overlooked is that which results from aortoenteric or ilioenteric fistulae. Angiography is recommended. and ischemic colitis. Blood transfusions should be considered in the settings of significant anemia (significance may vary due to comorbid conditions). Chronic bleeding in stable patients and small amounts of bright red blood per rectum associated with bowel movements can be handled definitively during follow-up after the ED visit. shock. A patient with aortic or iliac artery aneurysms. Their pathogenesis remains a matter of speculation. When the patient is hemodynamically stable and the bleeding is self-limited. In ongoing massive GI bleeds (both upper and lower) arteriography is used to localize the site of the bleeding. and hypotension suggest major blood loss. painless. Diverticula are herniations of the mucosa and submucosa through the muscularis propria that result in outpouchings of variable size in continuity with the colonic lumen. . bright red or mahogany in color. A patient can exsanguinate acutely despite a "normal" hematocrit. with hypotension and an UGI bleed suspected. When colorectal neoplastic lesions bleed. They may be congenital or acquired. Once resuscitative measures have been started. should be considered at risk for such an occurrence. If a patient is experiencing melena.AND GAsTRoTNTESTTNAL confusion. to stop it via embolization of the culprit artery. but without blood" argues against an active UGI bleed. Luminal contrast studies. In the case of massive ongoing bleeding in an unstable patient. Significant. infectious coli- tract may be involved. Bleeding is often brisk. or bright red blood per rectum. abdominal pain. arteriovenous malformations (AVMs). They can present in a variety of ways including occult bleeding. radiation colitis. Furthermore.Asoor\dtNAr. Similar to diverticular bleeds. cool clammy skin. and control it directly if possible. Occasionally they serve as the lead point for intussusception wherein colonic mucosa is pulled into the more dis- tal lumen. but without active bleeding during the study there is no proof they are actually for the hemorrhage. The plasma volume can take 24 hours to equilibrate after large blood volume losses. it is generally advisable to prepare the colon properly for endoscopic evaluation rather than attempt emergent or urgent unprepared studies that ultimately prove to be suboptimal. Ongoing larger volume bleeding requires an aggressive diagnostic approach beginning in the ED. Lavage water returned with bile staining. Anorectal bleeding is discussed elsewhere. mahogany stools. but if no visible bleeding site or adherent clot is detecte4 the diagnosis will remain "likely" while not actually confirmed. but this can be arranged subsequently in a controlled seuing. Anoscopy in the ED may confirm hemorrhoids but follow-up should be arranged to make certain that they stop bleeding and that they represent the sole source of the blood loss. Fluid resuscitation is indicated with any significant bleeding. Bleeding is often occult but can become massive if a major vessel is disrupted. surgery may be indicated. but other portions of the GI malignant). temporarily self-limited "herald" bleeds before potential exsanguination. Colonoscopy may be attempted in the setting of an active bleed. The unprepped colon with retained stool and blood can obstruct the endoscopist's view. It is thought that bleeding occurs when sheer forces cause arteriolar rupture at the edges of a diverticulum. These life-threatening conditions may present with smaller. Surgery may be the definitive corrective action once the problem has been diagnosed.

Anticholinergics. travel and immobility. the patient can usually be managed with increased dietary bulk and occasional laxatives. Hyperactive bowel sounds are often noted earlier in the course with diminished or absent bowel sounds when ischemia or infarction ensues. and alternating diarrhea and constipation are common manifestations of IBS. anorectal disorders. a family history of constipation. intercurrent illness. although only about 5%o of the population actually seeks medical care. Constiputio n (1. but is not enough for a definitive diagnosis. and Hirschsprung's disofcolonic gan- ease (a congenital disorder in which lack Obstruction of the lumen of the colon can occur as the result of an intraluminal mass. weight loss. thumb-printing (with ischemia). Unfortunately. as well as a chronic course. 7. opiate narcotics. mechanical obstructions. Obstruction (1. 2. and calcium channel blockers are coflrmon offenders. alumina-based antacids. and the specific details of the problem per the patient. If simple measures do not work. Although the ED can offer attempts at short-term symptomatic relief.1) Irrituble Bowel Syndrome (1. thyroid function tests. and constitutional symptoms. Treatment of an anal fissure. colonic inertia. Patients presenting with changes in bowel habits of recent onset should not be given the diagnosis without a thorough evaluation for other causes. which is often considered functional in nature. abdominal cramping.1. and variable bowel sounds. blood glucose. or external mass compression. such as adenocarcinomas of the prostrate. Urgent abdominal x-rays reveal dilated bowel loops. The last is the rarest. Two or three million United States medical visits per year result from constipation. Cathartic laxative use on a regular basis may lead to neuromuscular degeneration in the colon. This will be discussed below. Longer standing cases may be accompanied by nausea and the vomiting of feculent material. Most such visits are not emergent. Intravenous fluid resuscitation should be started promptly and surgical consultation sought urgently. Some tumors.7. The history and physical examination as well as abdominal x-rays usually suffice. Colonic obstruction presents with abdominal pain. for example. proctoscopy. A single visit to the ED may prompt suspicion. results in generalized obstruction to forward flow of the fecal stream. bloating. A careful history and physical examination should seek to elicit a medication profile. Adhesions. In the ED constipated patients must be dis- tinguished from those who are obstructed. diarrhea./or proctoscopy. or difficulty with stool passage.4) cate. Although IBS prompts many visits to health care providers. increased stool firmness. or even changes in daily schedules that disrupt stooling habits. Others will not defecate for days or even weeks prior to seeking care. referral to a gastroenterologist for more extensive evaluation is recommended. A barium enema would be more cost-effective unless there is concomitant bleeding. IBD. hernias. It is also common to see the symptoms (especially cramps and diarrhea) resolve when the patient sleeps. 1) The irritable bowel syndrome (IBS) may affect as much as a third of the population. Oversensitivity to bowel distention and disordered bowel motility are theorized to be the basis for the syndrome. It can occur concurrently with other conditions. suggest the diagnosis. diabetes mellitus. can grow into the colon and either bleed or obstruct. and free intraperitoneal air ifthere has been a perforation. air-fluid levels. If the history physical examination. bloating. it still remains largely a diagnosis of exclusion. l. Some individuals become concerned with mild increases in stool solidity or after missing a single bowel movement.42 / EunRcrNcy MnorcrNp: Ttrn Conr Cunxrculurvl Motor Abnormalities (1. con- stipation. it can probably do the most for patients with IBS by ensuring that they are referred for follow-up to physicians familiar with IBS who will provide the appropriate long-term glion cells leads to lack of proper motor function) are organic causes for the syndrome of constipation. Rarely extracolonic tumor bulk will be great enough to obstruct the colon. 7. When there is perforation broad-spectrum antibiotics are also neces- . for example. obstipation. Soft but solid stools are generally passed painlessly and with minimal straining from once every 3 days to three times per day. could lead to correction of resultant constipation. it is never fatal. Severe constipation. Dyspepsia. and barium enema are not revealing. 7. 1. and is therefore not recommended. 1. Short-term. decreased or absent defecation and passage offlatus. and vohulus (a twisting of the bowel with subsequent luminal compromise) are common causes of colonic obstruction. Irritable bowel syndrome. including ED usage. certain medications. l. 3) Constipation refers to decreased frequency of bowel movements. The variability of patient perception as to what constitutes constipation is impressive. Colony masses are most often tumors. as well as looking for signs of systemic illness and localized disease. Lack of bleeding.7. although investigators have proposed diagnostic criteria. kinking of the colon itself with a pinching off of the lumen. intussusception. A barium enema or colonoscopy will rule out obstructing lesions. hypothyroidism. Medications. is a common cause of chronic or recurrent constipation. Painful defecation should prompt anoscopy and. although bezoars can occasionally obstruct the ileocecal valve area. self-limited constipation may result from changes in diet (usually decrease in dietary bulk).

Parasitic colitis in the United States generally means E. young patients with fibromuscular dysplasia of the major intestinal arteries will suffer ischemic events. Gay bowel syndrome is a term. Bowel rest. C. Careful attention should be paid to searching for symptoms and signs of IBD that are extraintestinal. nausea. fever. The onset of severe abdominal pain fol- lowed by bloody diarrhea is the classic presentation. and vomiting are common presenting symptoms. fever. Patients who present to the ED with symptoms and signs of colitis should have a thorough history and examination performed. and broad-spectrum antibiotics (including anaerobic coverage) are the mainstays of therapy for diverticulitis. C. D iverticulitis (1. I ) Diverticulitis is a common inflammatory lesion of the colon originating from diverticula. Sicker patients can be evaluated by CAT scan. Abdominal pain (often in the left lower quadrant) with fever. radiation. histolyticc. skin lesions. and larger.Asno\dINAr eNn GesrnorNTESTrNAr DrsoRorRs sary. The etiologies of colitis include infectious agents (including C. Typhlitis is the much rarer condition in which the inflammation involves the serosa of the colon principally. dfficile is a facultative anaerobe that can cause syndromes ranging from mild diarrhea to toxic megacolon and shock. abdominal pain and cramps. which may or may not be bloody secondary to frank mucosal disruption. the term implies that the lesion involves the mucosa or arises from it. Gonorrhea. The amount of bleeding that results from colitis depends on the intensity generally of the mucosal disruption and / 43 the surface area involved. usually in therapeutic settings. anorexia. will often perforate. and inflammation of ocular structures are seen in IBD patients as well. 7. Ischemic colitis occurs most often in individuals with significant atherosclerotic disease. and extraintestinal manifestations including arthritis. Contaminated food and water may spread bacterial infections. The precise reason for localized inflammatory lesions arising from diverticula is unknown. however. hence so is diverticulitis. and idiopathic inflammatory bowel disease (IBD) (Crohn's colitis and ulcerative colitis). Diverticula either bleed or become infecte4 but not both. On occasion. This surgical emergency is accompanied by serious constitutional symptoms that can include shock. although the resultant diarrhea may or may not be bloody. Colectomy is usually required. In general. becomes paralytic. and vomiting usually precede bleeding from colitis. those institutionalized due to developmental handicaps. ischemia. Laboratory analysis must include a complete blood count with differential. and all patients with proctocolitis should have their sexual practices reviewed while being evaluated. Infectious colitis may occur in outbreaks involving several people or more. cholangitis. although the latter is much less common. fever. being used less often more recently. Symptoms of colitis include diarrhea. prodromes are common with colitic bleeding. Unlike diverticular or AVM- related bleeding. In Western societies diverticula are more common in the left colon. Radiation enterocolitis requires prior exposure to radiation. and other venereal proctidites are seen in greater numbers among sexually active homosexual males. that refers to the sexually transmitted proctitis that occurs with anal intercourse. Perforations. Most often complete bowel obstruction requires operative decompression. Some abscesses can be drained percutaneously if they do not respond to conservative measures. weight loss. but occasionally as the result of an industrial accident. Colitis (1. The colon dilates. nausea. parasites. and is seen most frequently among homosexually active men. Surgical management may require more than one step if there has been significant peritoneal contamination.7. nausea. Particular attention should be paid to . and those who have traveled to areas where parasites are endemic. Occasionally a volvulus. malaise. dfficile should be suspected in patients with colitis who have received antibiotics up to 8 weeks prior to presentation. Antibiotic-related diarrhea may involve the overgrowth of bacteria that leads to diarrhea. Diarrhea. Partial bowel obstruction can present with paradoxical diarrhea as mentioned above. Ulcerative colitis presents as bloody diarrhea (unless an extraintestinal presentation occurs first). It can range from occult bleeding to massive life-threatening hemorrhage. They are not confined to this population. hydration. Children may experience failure to thrive. Abscesses can develop with luminal obstruction and/or perforation with generalized peritonitis. A rare complication of colitis is toxic megacolon. Malaise. 2. can be reduced endoscopically or by the administration of an enema. strictures (especially with significant obstruction).3) Colitis refers to inflammation of the colon. Mild diverticulitis can be evaluated with a water-based contrast enema. and guaiac positive stools are common signs. IBD usually leads to recurrent episodes of active colitis with diarrhea with or without bleeding. and vomiting. Increasing dietary bulk is suggested as a means to forestall the development of diverticula and their complications. refractory abscesses require surgical resection. Crohn's disease may cause bloody or nonbloody diarrhea or manifest chiefly as abdominal pain or weight loss. Endoscopy suspected diverticulitis due to the risk of perforation. The is relatively contraindicated in microbiology mirrors that of the gut flora. especially one involving the sigmoid colon. It involves small vessel ischemia. Abdominal tenderness. Muscular hypertrophy of the colonic wall adjacent to diverticula and diverticulitis can cause further luminal compromise. dfficile). and if untended.

Diverticulitis. IBD is managed with S-aminosalicylates and steroids. sexual practices. Stool studies and endoscopy may be considered at such times.325(14): 1 008-1 0 I 6 RECTUMANDANUS (1. It lies retroperitoneal. C. Screening regimens have been developed to prevent the development of frank colon cancer. Rarely. Hyperplastic polyps have no malignant potential and are usually found incidentally during endoscopy or contrast radiologic studies.7. Histologic review is required to determine the significance of colorectal neoplastic lesions. Adequate fluids and antidiarrheal drugs maintain adequate volume status and minimize symptoms. and inferior hemorrhoidal arteries. histolytica. guaiac positive stools. Reinus JF. Metronidazole is used for C. it refers to more frequent stooling. Endoscopy may be required when ischemia is suspected but should be performed by a fully trained endoscopist. Podolsky DK. in extreme cases. SELECTED READING Although diarrhea is a prominent symptom of colitis.000 cases of colon cancer per year occur in the United States alone. metabolic derangement.ndrome. dfficile and E. culture and sensitiviry. Diarrhea is technically defined as the passage of greater than250 g of stool per day. As above ications the patient might be taking that could cause diarrhea. Elective endoscopy is the means by which the tissue is sampled" although surgery may be required for lesions unreachable or unresectable by endoscopic technlques. . Tumors (1. However. Diarrhea may also occur paradoxically as a result of a partial obstruction with "over- flow" incontinence. 150. Viral gasrroenteritis N Engt J Med I99l: 32s(4):2s2-264.304: J 1166-1169. Self-limited viral infections are a common cause of diarrheal illnesses in children and adults. Freeman SR. and gaseous waste. Radiation coli- tis is usually an insidious disease with a frustrating response to therapeutic attempts. Inflammatory bowel disease (two parts). Moriarty KJ.Ischemia requires supportive medical care and often. or a combination of these symptoms. Bobak DA. massive bleeding requires surgery. Stool should be sent for white blood cell counts (WBCs). but familial syndromes occur at earlier ages. 329(26):1940-t945. These are not performed in the ED. Volume depletion should be corrected and hemorrhage managed as needed. Practically. surgical care. Diagnosis and treatment of constipatron.20(l):4449. Antibiotics are usually unnecessary in bacterial infectious diarrhea unless there is systemic illness. The type and size of the underlying adenoma determine subsequent malignant potential. Milder cases of colitis may be handled in the outpatient setting as long as medical care is readily available. Relief of the obstruction restores normal bowel function.lr'Ez gl J Med 1991. Br Med 1992. Lynn RB.8) The anorectum is the most distal portion of the lower GI tract. serious hemorrhage. and (if the history is suggestive) ova and parasite examinations. Crit Care Clin 1995. The irritable bowel syndrome. it has many causes. evidence of sepsis. and comorbidities. Ellis DJ. and. Lower intestinal hemorrhage. Greenberg HB. It serves as the conduit for colonic solid.325(5 ):327 -j40.. Med Clin North Am 1993. Most colon cancers form in previously benign adenomas. middle. I 1(2):369-389. Stool studies should be sent as appropriate. parasitic. enemas. is supplied from the portal and systemic vascular distributions through the superior. Treatment is aimed at the underlying cause. Significant volume depletion. although adjuvant chemotherapy after surgery in stage C improves 5-year survival significantly. 325(13):928-937." In the ED it should be determined if volume or blood loss (or both) will require hospitalization. and is innervated by the pudendal nerve and the autonomic nervous system.5) Colonic neoplasia is very common in the United of the world.orcrNn: Tsn Conn Cunnrculurvr food and water consumption. Irritable bowel sy. Friedman LS. Increased disease activity in patients with IBD may represent such infections. Self-limited colitis (especially with a positive stool culture) does not require an invasive workup. Falchuk ZM. liquid. difficile toxin titers. Bleday R. Obstipation may require manual disimpaction. Surgical removal affords the only true hope of cure. originating at the terminus of the sigmoid colon and ending at the outside world. greater stool volume.77(5): 1149-1167. greater liquidity of the stools. Over States and other developed nations Blacklow NR. N Engl J Med 1993. Patients with IBD are not immune to bacterial. or a rectal adenoma found on proctoscopy should prompt a referral as well as education of the patient as to the importance of follow-up. Certain fam- ilies are genetically prone to developing adenomas and adenocarcinomas of the colon. McNally PR. Attention should be paid to any medpathology. and vol- untary control of this expulsion is by the internal and external anal sphincters (motor level S2-S4). unexplained anemia. the health of surrounding individuals. 1991. Most carcinomas occur in people over the age of 50. N Engl J Med t 99 1 . Flexible sigmoidoscopy is often useful for the diagnosis of other types of colitis. surgical decompression. and ischemic colitis warrant admission. Juvenile polyps have little or no malignant potential but may bleed and result in their disclosure. past similar histories. and clostridial infections. Guenant RL. . Colonic diarrhea is usually lower volume and higher frequency than that caused by small intestinal it may be bloody or "bland. travel. Bacterial and protozoal gastroenteritis. Comp Ther 1994.44 / EnrncnNcy Mr.

The sentinel pile is a region of swollen excess skin superficial to the crater of the chronic anal fissure and given the similariry of appearance. Deep chronic fissures. Anorectal Fistula (1. such as foreign bodies.8. and those away from the midline require surgical referral. which will impair recovery.3) Hemorrhoids are defined as varicosities of the venous plexus. Cases in which the appearance of an anal fissure occurs other than in the midline should be referred for evaluation of other etiologies such as inflammatory bowel disease (see below).8. progressive pain and tenderness during abscess formation. The use of topical ointments is to be discouraged as they may retard healing. The most frequent complications of anal fissures are infection and stricture. quiescent period after cutaneous healing. syphilis. In the ED any persistent local abscess should be incised and drained. such as with sitz baths. It also is the most common anorectal pathologic process in infants and children. the pain may persist for some time postdefecation. Bleeding from internal hemor- . itching. leukemia. diet. Anal fissures are generally the result of excess distention of the anus and are most typically the result of either the passage of large hard stool or the insertion of large objects. A probe can be passed through the origin to assist in definition. when present. as the anal sphincters may go into spasm secondary to pain. as they are one of the three sites of portal-systemic anastomosis. With more chronic disease. They are classified with regard to their position of origin with respect to the pectinate line. Examination during the fistulous phase will reveal the draining anocutaneous tract. those with complications. Anterior fissures. Internal Internal hemorrhoids generally do not thrombose. tuberculosis. Management is elective outpatient surgical repair. Care must be taken in the prescription of analgesics to avoid the side effect of constipation. An anal fissure is a linear tear of the anal canal occurring in the midline. paroxysmal forceful coughing. which may be palpable during digital rectal examination. systemic pain control may be required.1. The patient usually presents following sharp pain associated with the passage of stool.1) Anal Fissure (1. and discharge.Asoo\. Occasionally they may provide a cyclic history of discharge. The patient with prolapse may notice bleeding. The hemorrhoids that emerge from the skin distal to the pectinate line are covered with squamous epithelium and are known as external hemorrhoids. Infection of anorectal fistulae is common and they are particularly prone to abscess formation. The patient with internal hemorrhoids is often asymptomatic. straining with stool. have a history of resolved anorectal abscess. Good hygiene. Those that arise from the submucosal space proximal to the pectinate line are covered with columnar epithelium and are defined as internal hemorrhoids. resulting in Iimitation of further examination. Small amounts of blood may be seen in superficial fissures with greater amounts in deeper craters. thereby completing the cycle. or fistula in ano. and back to the foul-smelling discharge associated with fistula in ano. is the most common source of painful rectal bleeding. are most commonly seen in women. In cases where the tub soaks and sitz baths used for hygiene are not sufficient to reduce inflammation. also referred to as fissure in ano. Anal fissures have been reported following episodes of diarrhea. Other predisposing etiologies include inflamma- GASTRoTNTESTTNAT DrsonnrRs / 45 tory bowel disease (see below) and tuberculosis. and surveillance for infection are also very important in the care of the patient with an anal fissure. a discharge may be seen. Particular care must be taken to ensure a gentle examination. which lies in the wall of the anal canal. and hepatic dysfunction (internal only). Hemorrhoids (1. itching can occur. and the history of pain with intercourse may be elicited.1. Treatment includes the use of bulk laxatives and stool softeners to normalize stool consistency. Acute anal fissures are generally very shallow and not associated with a sentinel pile.8. Hemorrhoids are the most common cause of minor rectal bleeding. 2) The anorectal fistula. prolonged sitting. The majority of cases. Significant cellulitis. Prior perianal surgical intervention may induce greater risk for fissure.1) An anal fissure. purulent drainage with abscess rupture. particularly in the immunocompromised warrants admission. Antibiotics are not felt to be of benefit in uncomplicated cases. The majority of cases in the midline are found posteriorly. Fistula in ano should not be confused with other fistulae including vagino-cutaneous and diverticular-cutaneous fistulae. increased intraabdominal pressure.8. Patients typically complain of a discharge staining undergarments. 1. The anal mucosa is not innervated with pain afferent fibers and thus internal hemorrhoids are painless unless they prolapse and cause anal distention. and does not present until bleeding or prolapse occurs. Etiologic factors may include pregnancy. 800/o. is an abnormal tract connecting the anal canal and the skin. and neoplasms.rNAr AND Structural Disorders (1. often confused with an external hemorrhoid. Deaths from sepsis arising from ano-cutaneous fistulae are reported. Profound internal hemorrhoids are noted with portal hypertension.

The procedure for exci- sion of thrombosed external hemorrhoids described in Table l-10. lifting. thereby reducing their potential benefit. (2) true rectal prolapse type I. they do afflict all age groups. covered with skin. The presentation of the mass may follow Valsalva. or sepsis. cauda equina syndrome. Asymptomatic internal hemorrhoids may be discovered during anoscopy. stab incisions are associated with a higher rate of infection Removal of clot(s) with pickups and/or tangential pressure Packing of the region with gauze or Gelfoam followed by generous padding and tape Adequate analgesia. Procedure for incisional therapy of thrombosed external hemorrhoids Proper positioning and exposure Local infiltrative anesthesia. in which only rectal mucosal tissue is passed through the rectum. manifested by intussusception ofthe upper rectum into and through the lower rectum. The ED therapy of internal hemorrhoids consists of conservative measures such as bulk laxatives. small amounts of bleeding. Care should be taken to avoid liquidization of stool as this is associated with cryptitis.8. and easily visible. elliptical incisions are preferred. True rectal prolapse occurs as a result of laxity of the pelvic fascia and muscles of the pelvic floor. occurs most commonly in children under 2 years of age or in association with the more severe internal hemorrhoids. In the event of prolapse of an internal hemorrhoid. although excision of thrombus provides enhanced comfort and symptomatic relief. Rectal prolapse can be divided into two classes----external and internalbased on the position of the prolapsed tissue. Patients with extremes of age. 1. Recurrent true rectal prolapse is . and itching. but triangular or linear incisions are acceptable. on toilet tissue. It is also an infrequent complication of multiple sclerosis. which may progress to abscess. select narcotics that are less constipating Frequent warm sitz baths Good hygiene Bulk laxatives Appropriate referral Rectal prolapse. Excision is felt to be of greatest benefit in the patient who presents in the first 48 hours following the onset of symptoms. orprocidentia. sclerosing injection. External hemorrhoids are purple in color. to reduce risk factors for development. or limited mucosal prolapse. history of heavy bleeding. it does little to improve the time course of the disease and does not warrant the enhanced risk of infection. Rectsl Prolapse (1. sitz baths. linear incisions are likely to seal early and rethrombose more quickly. where all layers of the rectum are extruded. Conservative measures in the treatment of nonthrombosed external hemorrhoids are as follows: normalization of stool consistency. is the extrusion ofrectal tissue distal to its normal position. and mental illness. Internal hemorrhoids should not have excisional or incisional therapy even if thrombosed. and in the bowl. tabes dorsalis. is fully Some recent authors have suggested that. or difficult passage of hard stool. External rectal prolapse may take one of three forms: (1) limited mucosal prolapse. excisional therapy. or false procidentia. reduction in the ED is mandated to prevent strangulation and mucosal ulceration. This is most commonly seen in nulligravid women. and may be more prominent in the upright position. Nonprolapsed internal hemorrhoids may or may not be palpable on digital rectal examination. The definitive treatment is surgical. a fullness in the region. but is not mixed with formed stool. The patient with an external hemorrhoid will complain of severe pain. fistulae. External itories are painful to place and are placed proximal to the site ofpathology. Many external hemorrhoids do rethrombose after excision. gums. External hemorrhoids should be treated with conservative measures. they may experience a discharge. and cryotherapy. straining. It may occur as a complication of hysterectomy or lower GI tumor and may also be seen in children with paraplegia and myelomeningo- cele.46 / EnrnncsNcy MrorcrNr: Tnn Conr CunnrculuM rhoids is noted on the surface of stool. or signs of anemia such as pale skin or loss of color in palmar creases. Nonconservative measures in the treatment of thrombosed external hemorrhoids include incisional therapy. or loss of rectal sphincter control with resultant involun- tary flatulence or defecation. and behavior modification. such as with bulk laxatives. or conjunctiva should have determination of their hemoglobin and hematocrit in the ED. Less commonly. with larger hemorrhoids a ring block may be required Skin preparation and cleansing lncise over the hemorrhoid directed radially to the anus only through the cutaneous layer. and (3) true rectal prolapse type II. Topical agents are of limited value and should be avoided in most cases. This is thought to occur as a result of combined weakness of the anal sphincter and the cross-linkage between the submucosal and mucosal layers of the distal rectum. Anal suppos- TABLE 1-1O. True rectal prolapse may also present in young adulthood as a consequence of the congenital absence of mesentery. unless they are thrombosed. Of these modalities only incisional therapy is appropriate for the ED. Patients with rectal prolapse most commonly present with a complaint of a painless mass that they may suspect is a hemorrhoid.4) Although external hemorrhoids are most common in young adults. False procidentia. rubber band ligation. coupled with weakness of the anal sphincters.

direct visualization. but as a manifestation of secondary syphilis. gentle reduction. Secondary syphilis is treated with 2. Sur- / 47 by digital rectal examination. Following removal of an anorectal foreign body. abdominal pain. This is typically performed for the purpose of enhanced sexual arousal. and the emergency physician should ensure appropriate follow-up and of endoscopic evaluation. ischemia secondary to strangulation of tissue. which is a manifestation of syphilis.ns associated with ulceration of the anterior anal mucosa. As the nature of inserted foreign bodies is quite variable. and retained or broken rectal thermometers. Even less frequent are iatrogenic foreign bodies such as lost endoscopic or enema equipment. or objective findings on abdominal examination may need admission for observation. Parks retractors. and careful proctosigmoidoscopy to exclude the complications of perforation and laceration is mandated. Patients should be counseled to spend 2 to 3 hours in a sitz bath or tub in order to wash off excess podophyllin and minimize the risk of local burns. Prolonged presence of anorectal foreign bodies is associated with abscess formation.4 million units benzathine penicillin G by intramuscular injection.or sexual partner-initiated. Any patient with clinical or radiographic evidence of perforation is an operative candidate and requires urgent surgical consultatron. The use of analgesics and sedation may be required in some cases. Patients with fever. particularly when the patient is anxious or the object is large. and other suction devices. and that they are wetter lesions. Postrecovery radiographs to exclude intraperitoneal gas. Patients may complain of mass and some may experience anal pain or itching. so too is the technique and tools used for the removal of lower GI foreign bodies. Agents that increase GI motility are not appropriate as they may result in obstruction or retrograde propulsion of the foreign object proximally in the GI tract. and peritonitis secondary to perforation. Perianal Warts Foreign Body (1. Valsalva. Internal rectal prolapse has a female predominance and may present with complaints of pelvic or rectal fullness. The presence of rectal prolapse should alert the clinician to the possibility of associated carcinoma. inability to withhold flatulence or defecation. balloon catheters and tubes. gical consultation and referral is necessary. many patients with genital condylomata may also harbor other sexually transmitted disease and thus patients should be appropriately examined. flexible and rigid sigmoidoscopes. obstetric suction extractors. and treated if indicated. or retained stool. and to return for A stool softener such as docusate (Colace) should be employed to prevent constipation. Refractory and more advanced cases require surgical care. External rectal prolapse can most generally receive ini- tial treatment in the ED with simple. or lifting. a period of observation for sequelae is required. The definitive treatment in the majority of cases is surgical. ring forceps. it can be accomplished by passing a hollow instrument past the item. their more rigid texture. forming an occlusive seal with the adjacent mucosa.1.8. Repeat treatments every 7 to 14 days may be required for eradication. The range of presenting symptomatology includes anxiety. anorectal discharge. Prior to removal. The infection in rare cases may also invade the rectal mucosa. screened. although occasionally accidental or assaultive in nature. as evidence of perforation. back pain. probes affixed with glue. Potential devices as suggested in the literature would include standard or neonatal obstetric forceps. are indicated.5) Rectal foreign body. abscess formation. but the patient may try to conceal this history from all health care workers until they are seen by the emergency physician. Bimanual examination. Treatment for minor cases of perianal papillomata involves topical treatment with 25% podophyllin. There is generally a known history of instrumentation or insertion. is usually self. and radiographic evaluation may be helpful in some cases. Condyloma lata are also sexually transmitted. bleeding. rectal spasms. tenaculum forceps. On physical examination they may be differentiated from condyloma acuminata by their low horizontal plane. or pain.AsooN. vaginal specula. particularly in children and in the elderly. from the human papillomavirus. pain. rectal spasms. Should the prolapse have been prolonged with the rare complication recurrences. and studies of sexual partners reveal a 25o/o coinfection rate. and condy- loma latum. the nature and position of the foreign body must be defined Perianal warts are of two main categories-condyloma acuminatum. and the emergency physician should be careful to evaluate this area and document the quality of the observed mucosa. pressure. A small subset of ingested foreign bodies will lodge as they attempt to make the turn to leave the rectum and pass through the anus. . then prompt surgical evaluation in the ED is required. In some cases it will be necessary to release a relative vacuum to facilitate removal of objects. anoscopes. Condyloma acuminata are often sexually transmitted. Penicillin-allergic patients may be given a lO-day course of either erythromycin or tetracycline.{lNAr AND GASTRoTNTESTTNAT Drsonnr. Should this be necessary. Both sedation and local infiltrative anesthesia of the anal sphincter may facilitate the removal of foreign bodies. spoons. Patients should be counseled prior to discharge to avoid straining.

eds. papillae hypertrophy and infection spreads to adjacent crypts. It has been postulated that cryptitis may be a precipitant for several etiologies dis- cussed above. 7) Anorectal abscesses are classified according to their location and extension. The different types.1) Proctitis is a general term relating to both inflamma_ tion and infection of the anal canal. Acute anorectal disorders. Brown. Infectious Proctitis Cryptitis. The perianal abscess typically presents with perianal pain exacerbated by passage of stool or Valsalva. Specific etiologies include infectious proctitis. but with progression. The diagnoses of fistula in ano and Crohn's disease should be considered in any patient with recurrent perianal abscesses. immuno_ compromise. (From Cabot EB. exam.8. and radiation proctitis.48 / EunnceNcy MnucrNB: THs Conn CunnrculuM Perianal Abscess (1. Sugarbaker DJ. traumatic proctitis. are perianal abscess. .2. Classification of anorectal abscesses by location.?HTj. anal fistulae. A significant percentage of patients with Crohn's disease present with this manifestation as their first indication of disease. patients who have inci- sion and drainage require packing changes and surveillance for healing and the complication of fistula development. tender rectal fullness should cause one to doubt the diagnosis of perianal abscess. Even in cases where spontaneous draining occurs during the count.8. formal incision and drainage is required to mini_ mize the risk of recurrence.2nd ed. The majority of patients are afebrile and do well with incision and drainage in the ED." The patient with a submucosal abscess will complain of an uncomfortable sense of incomplete evacuation. Patients with constitutional complaints. Abscesses of the anorectum are encapsulated accumu- lations of infectious and inflammatory material. -E coli. A proximal. The infection can spread locally to the contralateral ischiorectal space. The supralevator abscess may not be palpable to all examiners due to its cephalad position. Only the perianal abscess is well suited for ED incision and drainage (I & D). and those anal infections that only occur in immune deficient hosts. pain and possibly bleeding may ensue.horseshoe abscess.: antibiotics such as cefoxitin (Mefoxin) prior to I & D. which may reveal asymmetric fullness or firmness. Emergency medicine. Cryptitis is the infection of the superficial Intermuscular Ischiorectal FlG. In advanced cases erosions ofthe crypts form and papillae may hypertrophy to the point of prolapse.T rtlt. general anal infections.n*. External examination is usually normal.2) Proctitis (1. forming a . As inflammation increases. This process may be best appreciated by bimanual rectal examination. S. 1-2. and supralevator abscess. namely anal fissures. Gluteal asymmetry or cellulitis may be noted on inspection. 6. Inflammatory Disorders (1. The treatment for any abscess in incision and drainage. ischiorectal abscess. grarrulomatous proctitis. Patients with ischiorectal abscess are often febrile. Boston: Litile. 1. 1. Figure l-2 depicts these various abscesses and their locations. Bacteroides.lJ. submucosal abscess. On digital examination a proximal tender mass will be appreciated. in order of frequency.The greatest difficulty with ED I & obtain adequate local o limit the procedure ary to incomplete initi s or with immuno de f i c i ency . Proteus. Aghababian RV. or cellulitis should be considered for admis_ sion and parenteral antibiotics. Infectious proctitis can be divided further into the specific syndrome cryptitis. 1992.1532. 8. and perianal and anal abscesses. Streptococcus. fever. and anaerobes are commonly encountered. ln: May HL. Colonic flora are the predominant organisms of these polymicrobial collections. The anorectal abscess cannot be palpated a significant distance proximally during digital rectal examination. Fleisher GR. They often complain of an nondescript pain the buttocks. Early infection is asymptomatic.) mucosal pockets that are formed as a result of the normal contraction ofanal sphincters. 1. venereal proctitis. with peimission. Findings are confirmed by anoscopy..

Anorectal syphilis presents with the chancre of primary syphilis. and staining of undergarments. sprays. Such patients may not yet be aware of their HIV infection. Mycobacterium avium-intracellulare. Cqndida Drsorunns in other locations. women. perianal abscesses. discussed elsewhere. The initial presentation is usually with bleeding. is a relatively rare cause of anal canal infection. the perianal chancre may be exquisitely tender. Herpes infection of the anorectum presents with the same painful vesicles seen elsewhere on the body. manual disimpaction. lymphadenosis. and systemic antiviral therapy (e. Adenopathy of the inguinal chain is often present as well as pain in the lumbosacral dermatomes. as might be caused by lubricants. Examination may be normal or may reveal mucosal irritation and a purulent discharge. The organism lives in the anal canal and lays eggs that develop into larvae on the perianal skin. and sup- positories. Trichophyton species albicans. and the clinician must consider that a patient presenting with an atypical anorectal infection may have more significant pathology' Traumatic Proctitis Traumatic proctitis occurs as the result of repeated minor insults such as rectal prolapse. however. The most common organism in venereal proctitis is Neisseria gonorrhea. Such can be found using the "Scotch tape" test. Granulomatous Proctitis Granulomatous proctitis may occur with either ulcera- tive colitis or Crohn's disease. Warm soaks. good hygiene with tub soaks and sitz baths. unlike chancres in other locations. Treatment consists of a 2l-day course of doxycycline. Acquired immune deficiency syndrome (AIDS) proctitis from atypical pathogens in patients with AIDS is becoming common. Complications include rectal stricture. Traumatic proctitis can also result secondary to chemical irritation. Anal fistulae are commonly found in patients with Crohn's disease involving the anorectum. Primary infection may also demonstrate with anorectal inflammation. It is typically asymptomatic.to l4-day period. may also plague the anal region. and rectal irrigation are thought to enhance healing. Erythromycin is preferred in the pregnant patient. Lymphogranuloma venereum infection with dramatic inguinal adenopathy. and is discovered on anoscopy where an ulcer is noted on the anterior anal wall. In most instances the treatment is similar not identical to that recommended for the same organism if when found / (LGV) is a specific syndrome of Chlamydia trachomatis General Anal Infections may also infest the anorectum. Venereal Proctitis Venereal disease found in the anorectal region is in general the result ofanorectal intercourse. Anorectal discharge or a perianal papule may be seen. and staining of undergarments. These will likely have been preceded by innocuous pruritus and discomfort. a biopsy to exclude malignancy must be obtained. Pinworms are caused by infection with Enterobius ver- micularis and the patient usually complains of perianal itching with a nocturnal and morning predominance. acyclovir) are appropriate. Secondary syphilis is seen as condyloma lata. and cytomegalovirus.g. or anal intercourse. As with anal ulcers from other etiologies. Radiation Proctitis Radiation proctitis usually presents 4 to 5 months fola course of local anorectal ionizing radiation.AsnoNarNAL eNo GesrRorNTESTrNAr Treatment consists of normalization of stool consistency with fiber and stool softeners. Potential opportunistic organisms include herpes simplex type I. 49 Chlamydia anorectal infection is often the cause of "nonspecific proctitis" and is characterized by discomfort. and discharge. sitz baths. Gonococcal proctitis has been found in l0% of homosexuals and presents with mild discomfort. as well as in the natural course of the disease where vesicles progress to ulcers and craters over a l0. may present to the ED with one or more of these etiologies. although cases of contamination from vaginal or urethral discharge are documented. Patients with HIV and active herpes should be admitted for IV antiviral therapy.. and only variations in treatment are discussed in this section. although a frequent cause of perineal infection in infants. Erythromycin and sulfa are options in the allergic patient. Most patients present to the ED with known disease. A purulent discharge and irritation of the mucosa may be seen on examination. It generally heals with reversal of the precipitant. inflammation. The patient should be counseled as to the risks of transmission and superinfection. Individuals infected with HI! but who have not yet met the diagnostic criteria for AIDS. and fistulae. but watery lowing . Lice. a sensation of incomplete evacuation. Incontinence and impotence may also be present. Symptomatic treatment with analgesics. This phenomenon has been contributory to the usage of the term gay bowel syndrome. More advanced cases require surgical referral. and diabetics.

personal history of breast or uterine carcinoma. Tumors (1.7 4(6):1 49 | -l I 293-1 308. when identified and referred early. familial polyposis. ureterosigmoidostomy.2nd ed. Anorectal abscess-fistulae.50 / Err. pelvic irradiation. many of which are indistinguishable from more benign lesions.7 4(6) : | 43 3-l 464. Any nonhealing or suspicious lesions should be referred for excision and biopsy. Thrombosed external hemorrhoids. brittle anal canal. In: Roberts JR. are preventable causes of death. Anal fistol^ Br J Surg 1992. or obstruction may follow. SELECTED READING Bassford R. Bowen's disease. a feeling of a need to evacuate.rnncnNcy MnlrclNc: THe CoRE Cunnrculurvr stool or constipation. It should be noted that tumors of the anal canal are more aggressive. Am Fam Physician 1993 .4s (4): 17 87 -17 9 4. Examination will typically reveal a swollen. Modesto VL. and associated with greater morbidity and mortality than their perianal counterparts. Kaposi's sarcoma. Glauser JM. Rectal strictures may be found. Surg Clin North Am 505. Phitadelphia: Saunders. Seow-Choen FS. Tumors of the anorectum. and inflammatory bowel disease. Less frequent etiologies include basal cell carcinoma. Anorectal trauma and foreign bodies. Rosen L. extramammary Paget disease. 199 1 . painful rectal spasms. melanoma.8. Sexually hansmitted diseases and anal manifestations of AIDS. Hedges JR. eds. Fry RD. Surg Clin North Am 1994. The majority of anorectal malignancies are squamous cell tumors (70%) and adenocarcinomas.74(6): 1994. . Clinical procedures in emergency medicine. epidermoid carcinoma. and others. earlier to metastasize. Leukemia may present with an anal leukemic infiltrate.7 04-'l 07 . Surg C I i n N orth Am 199 4 .79(3):197-205. Treatrnent ofcommon anorectal disorders. tender. The most common presentation for anorectal tumors is that of bleeding and pain.3) There are several tumors of the anorectum. Gottesman L. Nicholls RJ. and it is imperative that the emergency physician do an appropriate visualization and evaluation for every anal and perianal complaint. Risk factors for anorectal tumor are family history of lower GI cancer.

2) . Acquired: Venous (2. Vahular Heart Disease (2. Restuccia Cardiovascular Disorders (2.2. DeStefano Diseases of the Circulation.8) G.0) .1) P.1) . Myocarditis (2. Goodman Diseases of the Circulation. Cardiomyopathy (2.2.7 ) Gury S.2.3) Richard A. Setnik and Arshad Khan Hypertension (2.10) Robert L.1 1) 51 .4) P"ggy E.2). Brown. Meredith and Charles K.1) John T. Gough and E.6) David P. Craven Congenital Abnormalities of the Cardiovascular System (2.5) John T. Richard Braen Primary Tumors of the Heart (2. Pathophysiology (2.9) Robert L. Meggs Myocardial Manifestations of Systemic Disease (2. Meredith Diseases of the Pericardium (2. Counselman Treatment Modalities (2. Goodman and Amy A. Hunt.3) Michael K.Jr.2.5.5. Brown Endocarditis (2. Brown and William J.4) . Lymphatics (2.3) John E. Counselman Cardiac Transplan tation (2. Richard C.6) Francis L.2. Kerr and Charles K. Diseases of the Conduction System (2. and Francis L.5. Hightower and Charles K.2.CHAPTER 2 Cardiovascular Disorders Marc C.Jackson Allison. Brown Ischemic Heart Disease (2.ggy E. Acquired: Arterial (2. Brown Cardiac Failure (2.

Cardiac causes of cyanosis relate primarily to partial or complete failure of the circulatory system to transition from fetal to neonatal function. approximately 400. As the lungs expand after birth.52 / EunncrNcy MnucrNr: THr Conn CunnrcuI-uM CARDTOVASCULAR DTSORDERS (2. In addition. After birth. This is the single most common cause of cyanotic cardiac disease in the newborn. which during intrauterine life has been kept open by prostaglandin. This relatively common cause of cyanosis accounts for about 10% of all congenital heart disease. the pulmonary artery arises from the left ventricle and receives oxygenated blood from the pulmonary venous return. Nearly all patients will present with cyanosis within 24 hours of birth. Cyanosis itself is a physical sign that is characterized by the slate-blue color of the mucous membranes. the fetus is oxygenated via the maternal cir- Tricuspid Atresia. neonates with severe congenital heart disease. The following sections discuss the most common complaints and disorders with which the emergency physicians are presented in their practice. Cyanosis will usually be present when the oxygen saturation is less than 85% or when the amount of deoxygenated hemoglobin in the blood is greater than 5 gidl. In the normal infant it is functionally closed in 12 to 24 hours and is permanently sealed with thrombosis and intimal proliferation by 3 weeks. . Examples of Cyanosis Producing Lesions Transposition of the Great Vessels. A general rule of thumb is that in the first 24 to 48 hours infants with pulmonary causes of their cyanosis will have greater respiratory distress and be more tachycardiac and tachypneic than those with pri- Tetralogy of Fallot.1. In the United States 1. the earlier the presentation. Cyanosis This is the most common presenting complaint in culation through the placental vessels. with the greater the stenosis. the practicing emergency physician has at his or her disposal many diagnostic and therapeutic interventions that simply did not exist a few years ago. aortic override. In his or her armamentarium are multiple medications and procedures that can be employed to open blocked coronary arteries.1) Congenital Disorders (2. right ventricular outflow obstruction. PATHOPHYSTOLOGY (2. Children with tetralogy have a large ventricular septal defect. Since most emergency physicians will only occasionally see a patient with a congenital cardiac disorder. The placental-umbilical circulation is disrupted and the pulmonary circulation must almost immediately begin replacing it as a source for oxygenation. From there a small percentage goes to the pulmonary circulation while the majority crosses the ductus arteriosus and enters the descending aorta for systemic distribution. nail beds. the current economic climate demands that the emergency physician limit interventions and admissions to only those patients who absolutely require it. rapidly closes. Timely. definitive diagnostic testing often does not exist. stabilize the irritable myocardium. The color is due to an excessive amount of deoxygenated hemoglobin in the blood. Most congenital defects leading to cyanosis will present in the neonatal period. it may be helpful to approach the subject via the presenting complaint. either a patent ductus arteriosus or an atrial or ventricular septal defect. In this disorder there is no direct connection of the right ventricle to the right atrium. In addition. the cardiovascular system must rapidly transition to support aerobic metabolism of the infant. The ductus arteriosus. assist the failing ventricle and help prevent recurrent episodes. In patients presenting to the emergency department (ED). there is a connection between the circulations. More optimistically. Cyanosis . . life-threatening disorders can be confused with and may overlap with less serious conditions. Before birth. and it may be difficult to determine which is predominant.000 people suffer sudden cardiac death from dysrhythmias. the pulmonary vascular resistance falls dramatically.5 million people experience acute myocardial infarctions (AMIs) each year and of these 40% wrll die. the aorta arises from the right ventricle and receives deoxygenated blood from the systemic venous circulatron. mary cardiac disorders. The outline follows the core content curriculum outline set forth by the American College of Emergency Physicians. Oxygenated blood is sent from the right ventricle into the pulmonary vein. and skin. The most common configuration of the great vessels is the following: . making difficult the task of sorting the serious from the benign. and right ventricular hypertrophy.0) Cardiovascular disease is one of the most common and challenging problems to confront the practicing emergency physician. The amount of pulmonary outflow obstruction determines the presentation of the patient.1) Congenital heart disease occurs in approximately 8 to 10 per 100 live births. in a newborn is usually secondary to cardiac or pulmonary disease. Blood enters the left-sided circulation from the systemic circulation via an atrial septal defect.

and hypoplasia of the proximal aorta. Occasionally. surgical repair is usually successful. With alarge VSD. which is always fatal. Cyanosis is in relationship to the amount of admixed oxygenated and deoxygenated blood. This allows increasing left to right shunting in those patients with intracardiac defects. the abnormal flow associated with a VSD is more likely to be heard. Patient Ductus Arteriosus. This is a malformation of the tricuspid valve. once the ductus closes cardiovascular collapse is rapid. it is not surprising that most murmurs are due to defects in the septal walls or abnormalities of the valvular apparatus. Right to left shunting supports the systemic circulation. Aortic Stenosis This entity also becomes critical when the ductus occludes. Although there are usually signs of abnormality such as cyanosis. Examples of Congestive Heart Fqilure Ventricular Septal Defect. These lesions usually close . the fall in pressure in the pulmonary circulation will be slowed and the murmur's appreciation delayed. the ductus arteriosus fails to close. Congestive Heart Failure (CHF) Most often. for reasons that are usually unclear. the more likely it will be found early. critical aortic stenosis. where the descending aorta is significantly narrowe4 and in the related interrupted aortic arch syndrome. Murmurs A murmur heard in the first 24 hours of life has a l\Yo to l5oh chance ofbeing due to a congenital cardiac disorder. This anomaly is associated with a continuous. patients presenting with congenital causes of CHF do so after the first 2 weeks of life and usually in a less dramatic fashion than patients with cyanosis or collapse. In this disorder a single artery arises from the heart. Trisomy 2l is associated with a huge percentage of congenital cardiac disorders. mitral stenosis. Since murmurs are heard with turbulent or abnormal blood flow. supplying all of the circulation. and tachycardia soon after birth. machinery-like murmur. Usually they present when the ductus closes. Coarctation of the Aorta In this disorder. tachypnea. The prognosis is directly tied to the adequacy of the left ventricle. This defectranges in severity from mild to severe. If the left ventricle is sufficient to support the systemic circulation. consists of a tiny left ventricle. In general these children will not have progressed well after birth with poor feeding and weight gain as well as tachypnea. heard over the second left intercostal space. As the pulmonary outflow resistance drops. Many small defects will close spontaneously and no intervention is needed ifthe child is thriving. This defect consists of a common atrioventricular valve. Atrioventricular (AV) valve regurgitation may be present. Atrioventricular Septal Defect. primum atrial septal defect. Ventricular Septal Defect (VSD) The smaller the defect. Most frequently the underlying cause of collapse is due to systemic outflow obstruction. the patient usually presents in shock. In the normal neonate pulmonary vascular resistance gradually decreases. and AV canal defect is the most common single entity. A variable percentage of patients with this anomaly will be cyanotic due to a right-to-left shunt through an atrial septal defect. the infant can initially appear well. Patients will be symptomatic due to left-to-right shunting of blood. Tbtal Anomqlous Pulmonary Venous Connection. C ardiovascular C ol lap s e Cardiovascular collapse or shock is a true medical emergency that requires prompt therapy to resuscitate and stabilize the patient. Those with severe obstruction tend to be difficult to manage.CeRolovescut-AR DTsoRDERS Truncus Arteriosus. Quite / 53 often associated intracardiac abnormalities such as ven- tricular septal defects are present. Ebsteinb Anomaly. Hypoplastic Left-Heart Syndrome This syndrome. Congenital disorders leading to collapse usually are manifest in the first week or two of life. When the ductus closes. The degree of symptoms each patient experiences is due to the amount of pulmonary outflow obstruction that is present. Patent Ductus Arteriosus This is the classic machinery murmur. The valve is usually stenotic or incompetent. Patients with minimal or no obstruction to pulmonary flow do uniformly well. and ventricular septal defect. requiring surgical repair depending on the size ofthe defect and the general health ofthe child. This occurs when the pulmonary veins drain into the systemic venous system.

totally occluding the vessel with the resultant thrombus. it can also be seen in patients who have experienced viral. and third. structural abnormalities of cardiac valves. Dilated Cardiomy op athy This is the most common of the cardiomyopathies. The etiology can be idiopathic or secondary to a wide variety of toxic.. Aortic Stenosis This condition is very common. dysrhythmias. or hypertrophic. Although the average emergency medicine physician will only rarely encounter patients with these defects.2) Cudiomyopathy Myocardium The myocardium is the muscular pump of the heart and its dysfunction leads to significant changes in normal cardiovascular function. Failure Cardiac failure implies inadequate myocardial function. although the diminished ventricular compliance leads to diastolic dysfunction. or the plaque may rupture. Ischemia Ischemic cardiac dysfunction is brought on when the oxygen supply is inadequate to the demands of the myo- Cardiomyopathies are usually classified as dilate4 restrictive. In turn this damage causes accumulation of lipids and macrophages. some of the more common are amyloidosis.g. Multiple syndromes and diseases lead to restrictive cardiomyopathy. and great vessels that impede normal cardiac filling and emptying. Fabryis disease (glycolipid . Generally seen in patients who have experienced ischemic events. can lead to failure. however. Ischemic heart disease kills over 650. or some other insult to the myocardium. or plaque rupture. but both may be operative in any patient.1. thrombus. The endothelium of the coronary vessels is damaged in some way such as disruption in normal flow as occurs at branch points. The latter is more comnon. and Toxoplasma gondii. At some point. This can occur when the flow is disrupted by spasm. toxic. and Trypanosoma cruzi. Acquired Disorders (2. systolic function is usually preserved. but unless it is severe it usually does not present in infancy. endocardium. ifthey have not by I year. Lessened or absent contractile force or a loss of coordination of contraction can lead to dysfunction. Infectious etiologies include human immunodeficiency virus (HIV). Pompeis disease (an accumulation of glycogen due to deficiency of cr-glucosidase). The etiology of cardiac failure can be on the basis of three major categories: first. alterations in organization or conduction of cardiac contraction. metabolic.54 t EurnceNcv MrorcrNn: Tsn Conn Cunnrcuruna spontaneously. Ischemia can be brought on by spasm of coronary arteries or by arterial occlusion from atheromatous plaques. second" primary dysfunction of the myocardial contractile unit leading to inadequate pump action. Systolic dysfunction leads to heart failure. These are usually systolic ejection munnurs. logical approach to the patient with potential car- diac malformation will allow him or her the greatest opportunity to correctly diagnose and treat these challenging patients. either the occluded vessel lumen is insufficient to supply adequate blood to the myocardium.000 Americans each year. These also will often close spontaneously and only rarely require surgical repair. The process of atheromatous accumulation usually develops over years. Classical findings for dilated cardiomyopathy are perivascular and interstitial fibrosis. pericardium. The above represent some of the more usual presentations of the most common congenital cardiac defects. or with increased oxygen demand as is seen with exercise or hypoxia. heard best at the upper left sternal boarder. coxsackie virus. Restri ctiv e Cardiomy op athy This is characterized by replacement of normal myocardium with a fibrotic material. cardial cells. they Atrial Septal Defect (ASD) Most children with ASDs are asymptomatic. Interestingly. or infectious insults. Ischemic damage to the myocardium occurs when the delivery of oxygenated blood is insufficient to the demands of the working cardiac cells. are unlikely to do so. Alcohol and antineoplastic medications are typical of cardiac toxins leading to dilated cardiomyopathy. e. a reasoned. Coordinated functioning of the myocardial contractile elements is basic to normal cardiac output. Smooth muscle proliferation and further accumulation of lipids and macrophages is encouraged by growth factors elaborated by the macrophages and platelets. leading to aggregation of platelets.

this differs greatly whether it develops acutely or chronically. and hypertrophic cardiomyopathy. It is in this aggregation that bacteria can lodge and multiply. The pulmonic is implicated less frequently. This pressure can be transmitted back to the atria. Acute regurgitation can be seen with ischemic damage to the papillary muscles or chordae. and" in patients with prosthetic valves. Hemodynamically. leading to cardiac failure. Other agents implicated in causing myocarditis include rickettsial diseases such as Lyme disease and Rocky Mountain spotted fever. The common pathophysiologic thread is an abnormality of cardiac endothelium. Rarely it is associated with connective tissue diseases such as Ehlers-Danlos slmdrome. the left ventricle dilates and hypertrophies. or relative laxity of either the chordae tendinae or papillary muscles. trypanosomiasis. and age-related degeneration. This exacerbates the regurgitation and a vicious cycle ensues. rarely. acute aortic regurgitation causes markedly increased left ventricular and diastolic volume with a concomitant rise in diastolic pressure. Valvular The two valves most commonly involved in causing clinical symptoms are the aortic and mitral.Ceuovascut-A. Symptoms range from none in the majority of cases to congestive heart failure. The acute form ofaortic regurgitation is quite different from the chronic version. and toxoplasmosis. maintaining more normal hemodynamics for a time. and. / 55 and increased myocardial oxygen demand. sudden death. patients with mitral valve prolapse are at an increased risk of endocarditis. Common etiologies of acute aortic regur- gitation include trauma. some groups are at increased risk such as intravenous drug users and patients with prosthetic heart valves. The most common virus causing heart muscle infection is coxsackie. Mitral Valve Prolapse This is probably the most common cardiac valve abnormality. arrhythmias. and. platelet aggregation occurs. rupture of chordae tendinae.R DTsoRDERS accumulation due to an error of glycosphingolipid metabolism). With the obstruction to left ventricular outfloq ventricular hypertrophy is seen. myocarditis is present when the myocardium itself is infected. death. The results of this infection carry significant morbidity and mortality for the patient: abscess formation. syncope. This can be due to anomalies in the mitral annulus. rheumatic heart disease. Aortic Valve The aortic valve usually has three cusps. chest pain of unknown etiology. Acutely. with an incidence of 5oh to l3%. Although the majority of persons with this condition will be asymptomatic. resulting in compensatory increased peripheral vascular resistance. Myocarditis As the name implies. similarly. Aortic Regurgitation Endocarditis Although cardiac infections are relatively uncommon. If the abnormality exposes colla- gen-containing connective tissue. prosthetic valvular dysfunction. Abnormality in any of these components can lead to valvular dysfunction. The most common etiology of such an infection is viral in nature. congestive heart failure. infective endocarditis. with the left coronary artery originating behind the left posterior cusp. valvular destruction. congestive heart failure. Attached to these are the chordae tendinae and the papillary muscles. rarely. This allows for preservation of cardiac output but at the cost of decreased coronary artery flow Like aortic regurgitation. The relatively stiff left ventricle suffers decreased forward output. In the chronically regurgitant aortic valve. compensation of the left ventricle has no time to happen and left ventricular failure occurs. relatively secure from the patient's immune system. This in turn can lead to ischemia. resulting in pulmonary congestion. Aortic Stenosis Mitral Regurgitation Causes of aortic stenosis include congenital. The abnormality present is billowing of the mitral cusps into the atria with systolic ventricular contraction. Mitrul Valve The normal mitral valve consists of two cusps. hemochromatosis (abnormal iron deposition). Loffler's endocarditis (accumulation of eosinophils). valvular stenosis. redundant cusp tissue. valvular incompetence. and aortic dissection involving the aortic root. embolization. and sudden death. infective endocarditis can lead to . Salmonella. fungi.

even with massive distention of the pericardial sac. From there. two mechanisms predominate: abnormal automaticity and reentry. fluid accumulation. As the fluid accumulates. the pericardial sac. or fungal. intrapericardial pressures begin to rise. viral. if there is insufficient time for the pericardial space to. This dilatation can predispose the patient to atrial fibrillation and left atrial thrombus formation with the attendant risk of systemic embolization. uremia.56 / ElmncnNcn MtoIcINn: THe CoRE Cunnlculutr. mitral regurgitato left atrial overload and failure. Anything that potentially can irritate the pericardium can lead to chronic pericardial Pulmonic Vulve of causes. with life-threatening pulmonary edema. Some of the more common etiologies for such noncompressing cardiac effrrsions are uremia. this fall in cardiac output is not seen. setting up a circular pattern of depolarization. the pressure gradient rises across the valve. When discussing arrhythmias. hypertension. As the area of the valve decreases. located high in the right atrium. malignancy.t In the acute form. accommodate. Atrial Arrhythmias Atrial fibrillation and flutter as well as most supraventricular rhythms are reentrant tachycardias involving the AV node. The returning impulse can then be transmiued down the normal pathway again. or interstitial fluid. Trauma. Reentry occurs when conduction occurs down a normal pathway and then is routed back to an area that has just been depolarized due to accessory or bypass paths. The ability of the left ventricle to compensate is important in determining the outcome. In some conditions this can change as the pericardial space becomes a reservoir of fluid. Pericarditis Acute inflammation of the pericardium has a multitude 2-l. In some individuals. cardiac output is impaired. Because of this. are slowed at the atrioventricular node. Pericardial Effusion or Tamponade. medications. which typically contains only a small amount of flui4 can become a collection site for flui{ bloo4 gas. Abnormalities of the pulmonic and tricuspid valve can be seen with congenital connective tissue diseases and with infective endocarditis. Pericardium The pericardium consists of two layers of tissue that reflect back on themselves. pulmonary congestion is seen. The right-sided system is a low-pressure system. there may be extra or accessory pathways short-circuiting the above conduction scheme. In the chronic form. The pericardium can be the site of an infectious process. Such conditions include trauma. If they rise to levels approach- ing intraventricular pressures. either bacterial. are retransmitted through the HisPurkinje system and thence to the ventricles. Mitral Stenosis TABLE 2-1. such as occurs with ischemia. and medications. minimizing pulmonic congestion. Initially the heart compensates with increasing stroke volume. mitral regurgitation develops slowly and the left atrium dilates. This in turn causes left atrial enlargement and pulmonary As the stenosis becomes critical. right-sided valvular lesions are in gen- Conduction System eral less critical than left. ldiopathic Radiation Drugs Viral Acute Ml Trauma Tuberculosis Neoplasm Myxedema Bacterial infections Uremia Autoimmune disease ventricles are unable to This is most commonly seen in patients with a history of rheumatic heart disease. ischemia. In addition. and varying neural impulses affect the rate and rhythm of the heart. and neoplasms. The two surfaces of the pericardium usually contain only a small amount of fluid. These can be congenital or arise due to myocardial damage. but with continued pressure rise the fill adequately and cardiac out- put falls. Some of them are listed in Table Etiologies of pericarditis The normal cardiac electrical impulse originates in the sinoatrial (SA) node. If the fluid accumulates more slowly and compensation does occur. Abnormal automaticity is the result when the SA node is superseded as the pacing site by other cardiac tissue. rapidly lead tion can acute regurgitation. infec- tion. autoimmune disorders. Wandering atrial pacemaker and multifocal . Multiple factors can impact the smooth operation of the heart's electrical system. which is worsened if the left ventricle is compromised due to ischemia or previous dysfunction. impulses traverse the atria.

ACQUIRED (2. Patients hospitalized with cardiac failure have tripled over the past two decades and it is now the most common diagnosis in patients over age 65 years. The elas- ticity and compliance of the heart diminish with time. The valves are often the site of extensive calcium deposits. but less than ordinary physical activity results in fatigue. Cardiovascular clinics. All of these etiologies result in decreased cardiac output along with decreased peripheral perfusion and associated maladaptive compensatory mechanisms. idiopathic cardiomyopathy. other illness. and genetic fortune (or misfortune) serve to make for quite diverse cardiovascular health in the aged population. Unable to carry on any physical activity without discomfort. palpitation. palpitation. Cabalka AK. Comfortable at rest. Some persons are vigorous and without significant disease until very late in life. The conduction system is not spared. slurred QRS complexes associated with ventricular rhythms. dyspnea.000 new cases are diagnosed annually with an estimated 2 to 3 million Americans suffering some degree of cardiac failure. often seen in the elderly. Cardiovascular consequences ofthe aging process. their exercise capacity TABLE decreases. and cardiac output. good health care habits. Cardiac evaluation of infants. DISEASES OF THE MYOCARDIUM. or anginal pain. Maron BJ. What are the changes caused by aging alone? Morphologically. Up to 50oh of persons older than 56 have such cardiac deposits. Emergency management of cardiovascular disease. pediatr Ctin North Am 1990:37(1):1. Systolic function appears to be fairly well preserved even into very advanced years.3) As the life span of the population increases. diastolic function is not nearly as well preserved. The Effects ofAging on the Heart (2. By contrast.1) Cardiac failure is one of the most common presentais encountered in emergency medicine. Evaluation of the cyanotic newborn.35-47. Fibrous infiltration of the sinus node and the normal conduction pathways can lead to various degrees of heart block. Amyloid is deposited in the heart in increasing numbers as people age. Level of activity. 1993. the first year of life. Despite all of this. functional deterioration. Slight limitation of physical activities. is not just a byproduct of diminished cardiac function. In: Lowenthall DT. New York Heart Association (NYHA) functional classification of heart failure No limitation of physical activities. Marked limitation of physical activity. The aortic valve seems to be affected earlier and to a greater degree than the mitral valve. phlladelphia: Davis. survival rates are exceedingly low with the 5-year survival for men being 40Yo and 55Yo for women. Driscol DJ. Philadelphia: Davis. . or anginal pain. Rudolph A. Geriatric cardiology. but ordinary activity results in fatigue. the heart weight increases. Kessler KM.41(5):991. Chakko S. The most common causes of cardiac failure are coro- nary artery disease. Rudolphb pediatrics. as the person ages. For patients with cardiac failure who display symptoms at rest [NewYork HeartAssociation (NYHA) class IVl. inactivity and Class I Class ll Class lll Class lV other diseases play major roles.2. palpitation. Coronary artery disease is more common in the elderly. it is imperative that the emergency physician be familiar with all aspects of cardiac failure. In addition. These may lead to valvular stenosis or regurgitation. Geriatric cardiology. or anginal pain. these changes have some effect on the heart. Functionally.Cenorovescut-AR DrsoRDERs atrial tachycardia are examples of rhythms that are atrial in origin and are due to abnormal automaticity. lgth ed. In: Lowenthall DT. Comfortable at rest. The conduction is quite abnormal and results in the wide. / 57 SELECTED READING R\ ed. Changes with aging as reflected in noninvasive cardiac studies. As people age. Therefore. Boston: Butterworth-Heinemarur.1. 2-2. A seemingly less compliant and distensible ventricle appears to have a prolonged 1991 . Ordinary physical activity does not cause undue fatigue. and hypertension. maximal heart rate. Burton DA. New York: Appleton & Lange. Geriatric cardiology has to concern itself with the changes brought about by aging itself and the changes caused by living with underlying diseases longer. ed. filling time and increased need for the atrial kick for complete filling. Lewis JE. ed. 1994. Symptoms of cardiac insutficiency or angina at rest. Others have relatively rapid decline in function and health. interest has grown in what effects aging has on myocardial struc- ture and function.2) Cardiac Failure (2. Discomfort increases with any physical activity. dyspnea. Left ventricular wall and septum increase in thickness with aging. Aghababian Ventri cul ar Arr hy t hmias Ventricular fibrillation and tachycardia are poorly tolerated and are usually due to reentry. Pediatr Clin North Am 1994. 1993. Approximately 400. This is in itself not due to aging but to living with a condition for a longer period of time. Cardiovascular clinics.25-34. There is a wide range of function and capabilities in the elderly. The ventricular cavities diminish while the atrial enlarge. and vital capacity all diminish. the mortality is 50% within I tions that year (Table 2-2). dyspnea.

58 / EnnncrNcv MnorcrNr: Tnn Conn CunnrculuM However. In chronic failure. Cardiac failure refers to the physiologic focal point of the heart's inability to maintain adequate cardiac output in relation to the physiologic needs of adequate tissue perfusion. or dilatation. Heart rate is determined by sympathetic outflow. The function of the renin-angiotensin-aldosterone axis in cardiac failure is to increase intravascular volume and augment preload. The relation between preload and cardiac performance can best be expressed by a ventricular function curve relating the car- diac output to left ventricular end diastolic pressure as illustrated in Fig. These two adaptations increase the LVEDP and increase In mild failure this increased filling in a compensatory increase in cardiac output to the point where the ventricleis function is maximal on the Starling curve. and afterload. Physiologic adaptations to mild failure include an increase in venous tone and an expansion of intravascular volume.. the myocardial cells undergoing remodeling in which the length and volume of individual myocytes are increased. In mild cardiac failure. the sympathetic nervous system. : . which leads to renal conservation of sodium and increased water retention. The most sig- nificant compensatory adaptations are neurohormonally activated and are the renin-angiotensin-aldosterone axis. effects J Increased Afterload (Decreased cardiac output) Increased Preload (Increased fi lling pressures) Ren in-an giotensin-aldosterone axis. 2-2. myocardial performance is also a function of heartrate. . there exists a complex continuum of pathophysiologic changes occurring throughout the body to compensate for the progressive cardiac failure. ultimately resulting in increased left ventricle workload. Of importance to note is that cardiac failure is a syndrome and not a specific disease. an increase in left ventricular size. cardiac output is decreased secondarily to impaired myocardial contractility. Therefore. pericardial pressure. Aldostemne \ t't \ Increased Increased water md sodium retension FlG. As cardiac failure profilling pressure. Ventricular function curve depicting cardiac output in relationship to left ventricular end diastolic pressure based on Frank-Starling principles. 2-1. Cardiac Output Mild Heart Failure Moderate Heart Failure Low cardiac output symptoms Pathophysiology Left Ventricular End-diastolic Pressure (mm Hg) Cardiac In cardiac failure. Angiotensin II plays a major deleterious role. contractiliry and electrical conduction. increased left ventricular afterload. Extracardiac Although this chapter's primary focus is the cardiac system. It increases vasoconstriction of peripheral arterioles. this specific syndrome is complex and involves not just cardiac failure but also a series of pathophysiologic circulatory derangements that exacerbate the heart's failure. The effect is frequently a tachycardia with increased gresses there is an increasing degree ofdysfunction. as outlined in Fig. 2-1. which increases afterload.. Preload refers to the ventricular volume at the end of diastole and is often expressed as left ventricular end-diastolic pres- sure (LVEDP). cardiac output is decreased as a result of impaired myocardium. hypertrophy. maintains stroke volume and cardiac output as the ventricular ejection fraction decreases. Stroke volume is determined by preload. This increase in ventricular size is the principal cardiac adaptation to failure. By definition cardiac output is a function of heart rate and stroke volume. This volume physiologically loads the ventricle for contraction. stroke volume. and amount of venous return to the atrium. Autonomic tone is frequently increased in cardiac failure resulting in tachycardia.I ltngiotensbll\ secretion I Aldosterone .2-2. and pressures are associated with a cardiac output. Left ventricular enlargement and increased filling pressure result in increased ventricular wall stress with an elevated myocardial oxygen demand and increasing decrease filling Physiologic Angiotensinogen Cardiac effects of (Renin) + Angiotensin (Converting Enzy-") az I . Sympathetic outflow is increased in cardiac failure. myocardial contractility. This action is accomplished by an increase in aldosterone. and the atrial natriuretic system. The net product is a progressive decrease in cardiac output to the point of being unable to meet the metabolic demands of other organ systems. pressure results FlG. Factors that can affect preload include intrathoracic pressure. Both a decrease and increase in preload will change stroke volume evoking compensatory mechanisms.

Afterload is increased primarily by arteriolar vasoconstriction. venous hypertension fiugular venous distention and hepatojugular reflux). beriberi. anemia. Increased afterload also results in increased left ventricular wall tension and elevated myocardial oxygen consumption. angiotensin-converting enzyme inhibitors. peripheral edema. stroke volume decreases and pulse pressure narrows. Definitive treatment is accomplished by treating the underlying pathology. Both adjuncts are effective in overcoming the decrease in pulmonary compliance associated with pulmonary congestion. and is frequently seen in ischemic heart disease. The wall tension stimulates myocyte remodeling and altered ventricular wall morphology. Paget's disease. A reduction in cardiac work load is achieved by reducing the level ofphysical activity and reducing afterload. so do those of the myocardium. As tachycardia progresses. One way this intervention is most effectively achieved is with continuous positive airway pressure through a tight-fitting mask or positive endexpiratory pressure if the patient is intubated. Atrial natriuretic peptide released from the atria has been shown to temporally counteract the effects of fluid retention and vasoconstriction. . its effects are very minor and short lived in comparison to other adaptations present in cardiac failure. increasing the renal excretion of sodium and water. hyperthermia. the retention of sodium and water is an important compensatory mechanism for increasing preload. as the bodyis metabolic and oxygen demands increase. The increase in sodium and water retention compounds the increasing ventricular filling pressure and ventricular wall tension. with the hallmark being systemic hypoperfusion with widespread end-organ dysfunction. Underlying etiologies include thyrotoxicosis. exacerbating the degree offailure causing the clinical presentation. Reduction in fluid retention is best achieved through the use of diuretics and dietary sodium restriction. and vasodilation. prazosin. The electrocardiogram can be extremely variable. and vasoconstricting agents may be utilized if vasodilation is acute or severe. interventricular conduction delays and blocks. These patients frequently experience dyspnea with activity or rest. / 59 end-stage valvular heart disease. Left-Sided Failure High Output (2. Renal underperfusion and resultant sodium and water retention lead to pulmonary congestion as the cardinal manifestation of low-output failure. Initial treatment is aimed at restoring myocardial perfusion by controlling the rate of tachycardia and maximizing oxygen delivery to the myocardium. Pharmacologically this action is best achieved by use of nitrates for venodilation and calcium channel blockers for arteriolar dilation. Principal clinical characteristics are impaired peripheral circulation with subsequent mental confusion. and pulsus alternans. the time interval for diastolic filling decreases and stroke volume decreases with a subsequent decrease in myocardial perfusion. The focus of low-output failure is left ventricular dys- function. Low Output (2. this increase results in elevated systemic vascular resistance. cardiac output and contractility are initially increased. Nocturia is common. Afterload reduction is best accomplished by vasodilation of both the arteriolar and venous systems.CenDrovescut-{R DTsoRDERS myocardial oxygen consumption and increased peripheral vascular resistance. a protodiastolic gallop or 53 on cardiac auscultation. of paramount importance is the utilization of supplemental oxygen as one goal to maximize the level of oxygen available to the failing myocardium.2. Intravascular volume may need reduction with diuresis if chronic. however. The result is eventually myocardial failure secondary to ischemia. leading to further sodium and water conservation. Agents with combined venous and arterial dilator effects include nitroprusside. decreasing the volume of retained fluid. and improving contractility. In this specific condition. The increased peripheral vascular resistance results in an increase in both afterload and preload.1) By definition. weakness. As the derangement advances. and phentolamine. and paroxysmal nocturnal dyspnea. Physical findings are consistent with those of pulmonary congestion and left ventricle failure: rales on lung auscultation. In the acute setting. However. and pregnancy. arteriovenous fistulas. early sepsis. widened pulse pressure.1. congenital heart disease. decreasing renal blood flow. Treatment is primarily directed at the underlying type of heart failure.2. Typically. and the cardiomyopathies. Atrial natriuretic hormone is felt to have no significant impact on the progressive course ofcardiac failure. Nev- ertheless. The chest radiograph invariably shows cardiomegaly and evidence of pulmonary congestion.2) Low-output failure characterizes most forms of heart failure. displaying acute ischemic changes. generalized fatigue. orthopnea. and sodium and water retention. these patients present with an associated tachycardia.1. angiotensin-converting enzyme inhibitors are the most important. The net outcome is a maladaptive response that steadily exacerbates the failing myocardium. However. resulting from a redistribution of venous blood in the supine position. high-output cardiac failure is a hyperdynamic circulatory state in which there is a failure to maintain cardiac output and a concomitant decrease in peripheral vascular resistance. Of the later agents. Treatment is directed at optimizing myocardial oxygen utilization by reducing the myocardial work load and enhancing oxygen availability. or various arrhythmias. hypertensive heart disease.

The subsequent alveolar hypoxia contributes to further pulmonary hypertension by causing pulmonary vasoconstriction. digitalis reduces the cardiac response to sympathetic tone and prolongs the refractory interval of the atrioventricular node. The potassium-sparing diuretics. ascites. a calcium channel blocker. furosemide. and R:S ratio in V I of more than I . first-pass radionuclide angiography. Other inotropic agents include epinephrine. further augmenting preload reduction.3) In the strictest definition.60 / EnrncrNcy MBnrcrur: Tne Cons CunrucuLUM Diuretics reduce preload by reducing intravascular vol- 50%. Traditionally. The classic electrocar- diographic findings of chronic cor pulmonale demonstrate right-axis deviation. spironolactone and triamterene. A negative inotropic agent. and an R: S ratio in V5 and V6 of less than l. If significant venous congestion is present. the most definitive tests are those of two-dimensional echocardiography. orthopnea. However. These facts make it a common presentation that is often not considered in the acute presentation of the COPD patient. The term cor pulmonale was introduced more than 50 years ago to describe the cardiopulmonary state whereby the right ventricle is enlarged and impaired secondary to pulmonary hypertension. hepatomegaly. Diltiazem. and peripheral edema. there is often a delay between the onset of the disease and the specific diagnosis as the physical findings occur late in the process. the incidence of cor pulmonale in patients with chronic obstructive pulmonary disease (COPD) is approximately l0o/o Regardless of the inciting etiology. dlltiazem is employed in the rapid conversion of supraventricular tachycardia to sinus rhythm. this process has been thought of as either chronic or acute with differing eti- ologies and pathophysiologic processes occurring in each. furthermore. Without treatment. Right-Sided Failure Cor Pulmonale (2. also prolongs atrioventricular node conduction and controls the ventricular response to atrial fibrillation. the pulmonary hypertension associated with chronic cor pulmonale is a result ofan increased resistance to blood flow throughout the pulmonary vasculature. norepinephrine. hepatojugular reflux. Cor pulmonale is only exceeded in prevalence by coronary artery disease and hypertensive heart disease. and reactive polycythemia. Alveolar hypoxemia is the strongest known stimulus for pulmonary vasoconstriction. In addition. Inotropic agents are the mainstay for augmenting myocardial contractility. Treatment of chronic cor pulmonale is directed at relieving pulmonary hypertension. hypoxemia is present with associated dyspnea. The chronic aspect of this disease accounts for up to of all patients with cardiac disease. acting directly on the loop of Henle. The pathologic lesion is one of medial hypertrophy and intimal hyperplasia of the pulmonary arterioles and small arteries. The most commonly used diuretics to achieve this result are loop diuretics. cardiogenic shock is present. The result of these physiologic changes is an increased demand for right ventricular output. tricuspid insufficiency. dobutamine. dopamine. ethacrynic acid. The diagnosis of chronic cor pulmonale is difficult because signs and symptoms are often nonspecific in the early course ofthe disease process. and syncope. Typically. The occurrence of venous con- gestion predominates and is manifested by jugular venous distention. but must be used with caution in those patients with heart failure. However. Other diuretic classes that are useful include the thiazides and the potassium-sparing agents. an S: summation gallop may be heard. the interstitial fibrosis that accompanies pulmonary hypertension is irreversible. COPD is the leading cause of chronic cor pul- ume through increased excretion of sodium and water at monale. and bemetanide. Not only does supplemental oxy- . Thus. the reserve of the right ventricle is exceeded and right ventricular failure occurs with its characteristic findings. Historically the use of digitalis glycosides have been and continue to be the first choice as an inotropic agent. In addition. In short. Overdiuresis can occur when these classes are used together. and amrinone. Furosemide has been shown to provide a degree of venodilation. 1. inotropic agents such as dig- italis move the ventricular function curve upward increasing stroke volume and contractility for a given preload. the net effect being the control of the ventricular response in arrhythmias such as atrial fibrillation. an increase in pulmonary blood volume. cor pulmonale refers to right heart failure and hypertensive pulmonary disease. 2. dizziness. As these physiologic derangements continue. fatigue. Management is thus directed at relieving the hypoxic pulmonary vasoconstriction through the use of supplemental oxygen. Cardiac auscultation reveals evidence of right ventricular hypertrophy with an increased P2 component of Sz and a rightsided S+. or the need for rapid stabilization is paramount. can potentiate the diuresis achieved by the loop diuretics. These agents are typically of benefit when the degree of failure is severe. the level of the renal distal tubule. Chest radiographs when viewed in succession from a number of studies may reveal right ventricular enlargement and the characteristics of pulmonary hypertension. right ventricular dilatation and hypertrophy occur as an adaptation to the increased pulmonary aftery pressure. and cardiac catheteization. P pulmonale. chronic cor pulmonale is part of the natural course of pulmonary interstitial fibrosis and the sleep apnea disorders. resulting in a precipitous decrease in preload" further aggravating the degree of failure as the body compensates to counteract this iatrogenic insult.

thrombolytic therapy. Electrocardiogram findings. and improved oxygenation to other organ systems. Invariably. AV node ischemia is present secondarily to occlusion ofthe right coronary artery and various degrees ofAV nodal block are present with associated bradyarrhythmias. In addition. tachypnea. and therapy. and clear lung fields on auscultation. . McMurray JJV Diagnosis and management of heart failwe. Right-sided precordial leads will demonstrate ischemic changes in leads V3R through V6R. Br Me d J 1 99 4. decreased right ventricular afterload. as nitrates and diuretics may result in a precipitous drop in blood pressure. this involves inotropic support. This preload augmentation may require substantial amounts of IV fluids. The use of nitrates and diuretics may be detrimental as right ventricular preload needs to be maximized. and increased right ventricular myocardial oxygen demand. Dargie HJ. and diuresis as in isolated left ventricular failure.102'. increased work load. jugular venous distention. sudden dyspnea. During acute right ventricular infarction. and infiltrative diseases involving the right ventricle. Treatment after considering the appropriateness of thrombolytic therapy versus emergent coronary angioplasty is directed at augmenting the preload of the left ventricle and maximizing oxygenation of the right ventricular myocardium. the presentation is typically that of significant hypoxemia. may consist of a right ventricular strain pattern encompassing an 31 Q3 T3 pattern. dilated cardiomyopathy. the initiating pulmonary congestion substantially decreases oxygen saturation levels. thus aggravating existing myocardial ischemia and failure. The principal event is a sudden elevation ofright ventricular filling pressures as the outflow of the right ventricle is obstructed. chest pain. the improved right ventricular performance. The most common electrocardiographic finding is that of tachycardia with nonspecific ST:-segment changes. the diagnosis can be made by considering the pertinent historical and physical findings in addition to arterial blood gas analysis demonstrating a significant Aa gradient. Chest 1992.590s-595s. The major determinate of low cardiac output in patients with right ventricular infarction is a decrease in the left ventricular preload. and diuretics can alter electrolytes or increase pulmonary vascular resistance by hemoconcentration from excessive diuresis. In these severely hypoxic patients. heart transplantation. The result is increased right ventricular filling pressures. The goal of supplemental oxygen therapy is to achieve an arterial pOz of more than 60 mm Hg or an arterial Oz saturation of greater than 90%o. and inotropic support. a ventilation perfusion lung scan is required in most cases as may be pulmonary angiography. and cardiac output. other modalities of treat- presentation ment including digitalis. digitalis can induce arrhyhmias.nrovescur-AR DTsoRDERS / 6l gen therapy decrease the degree ofpulmonary hypertension by decreasing the hypoxic-vasoconstrictive effect on pulmonary vasculature. Typically isolated right ventricle infarction and pulmonary embolism present acutely. treatment is directed at primarily restoring left ventricular function. as pul- monary congestion develops. tricuspid and pulmonic valvular insufficiency. hypotension. though in no way specific. Definitive treatment may consist of lung transplant or combined heart-lung transplant depending on the etiology of the pulmonary hypertension. LVEDP.16:182-190. This fact is not surprising given the hemodynamic considerations. pulmonary hypertension. lung compliance decreases. and sodium restriction may be helpful. Other Considerations of Right-Sided Failure The most common cause of right ventricular failure is left ventricular failure. preload and afterload reduction. tachycardia. Clin Cardiol 1993. their use is controversial. diagnosis. Treatment is directed at stabilization with aggressive correction of hypoxemia. the interventricular septum. However. Swan-Ganz catheter monitoring should be strongly considered in these patients. sudden onset ofsyncope. Chatterjee K. which contributes a substantial part of right ventricular performance. Cardiogenic shock: elements ofetiology. the presentation is typically that of chest pain with the standard electrocardiographic changes consistent with inferior ischemia. or embolectomy. acute pulmonary thromboembolic disease. In the setting of acute pulmonary embolism. However. Typically.308 :32 l-328. stroke volume. supplemental oxygen therapy is the mainstay of treatment for chronic cor pulmonale. Frequently. diuretics. Becker RC. Definitive therapy may consist of anticoagulation. SELECTED READING Alpert JS. In part this occurrence is due to both ventricles sharing a common wall. Pathogenesis of low output in right ventricular myocardial infarction. though thromboembolic disease may have an insidious presentation. The clinical presentation is that of hypotension. In short. In turn. Aortic balloon pump augmentation maybe needed" and if the patient is an appropriate candidate with endstage dysfunction. Although. it also results in improved myocardial oxygenation.Cer. which determines left ventricular filling. In biventricular failure. Right ventricular infarction is present in 20o/o to 40%o of inferior myocardial infarctions. This decreases pulmonary intravascular volume. augmentation of cardiac output with fluids. or of pulmonary embolism can be insidious and difficult to diagnose. Acute Right Ventriculqr Failure Other causes of right ventricular failure include isolated right ventricular infarction.

Postgrad Med 1992. hypertension. When tricuspid regurgitation is present. Hypertrophic cardiomyopathy is often identified by left ventricular hypertrophy with preservation of contractile function. a degree of mitral regurgitation is often heard and less frequently tricuspid regurgitation. intraventricular thrombi are present.62 / EunncoNcv MruclNn: TsB Conn Cunnrculul. Chest radiograph displays left ventricular enlargement. pulmonary edema. Pathophysiology of heart failwe. Physical examination often reveals rales on pulmonary auscultation and an S: and S+ on cardiac auscultation. Therapy is the same as for congestive heart failure and is symptom oriented. diuretics to relieve preload. patients with DCM present with congestive heart failure. In addition. vasodilators and angiotensin-converting enzyme inhibitors to decrease afterload and preload.13:73s-81s. Pulmonary hypertension and cor pulmonale. Most importantly. Traditionally these diseases have been classified into three distinct types-dilated. Palevsky HL Pulmonary hypertension and chronic cor pulmonale. The principal characteristic is that of myocardial dysfunction in the absence of myocardial ischemia. Anticoagulation is employed when intracavitary . and is one of the most common conditions affecting the heart following ischemic heart disease and eases hypertensive heart disease. South Med J 1 993. D ilated C ardio the left ventricle. there is electrocardiographic evidence of left ventricular enlargement. The management of heart failure: a matter of definition? Cardiovasc Drugs Ther 1993.7:661469. hypertrophic.r Fishman AP. Physical activity is restricted to avoid exacerbation of severe symptoms. and evidence of pulmonary venous congestion. Of these three distinct types of cardiomyopathy the dilated variant is most comnon. Harley A.2\ pathologic process involving are usually patent and the cardiac valves are normal. characteizedby dilation of all four chambers of the heart and associated left ventricular failure. and secondary cardiomyopathies in which the underlying pathologic process is known. Int Med 1994. with atrial fibrillation most common. The result is a markedly reduced ejection fraction and increased endsystolic volume. valvular disease. fatigue. congestive heart failure is frequently noted. The coronary arteries Clinically. Characteristically the ECG in dilated cardiomyopathy has high voltage ratios of the R wave in V6 to that of leads I to 3.'2:315-341. a pulsatile enlarged liver is noted on abdominal examination. because of the turbulent blood flow through the ventricles. This classification is most useful to the emergency physician. treatment implications of right versus left ventricular impairment. restrictive cardiomyopathy. decreased left ventricular ejection fraction. The focal point of the dilated cardiomyopathy (DCM) is that of left ventricle failure. Cor pulmonale. Most often though. Often there is a component of left ventricle hypertrophy. Patterson JH. Pharmacotherapy 1993.33:363165. Vandiviere HM. C Cardiomyopathy defines a group of myocardial disin which there is notable derangement in myocardial function. Clinical Features ardio myop athy (2. but there frequently exists a degree of overlap among the three principal types. is beneficial for its negative chronotropic effects. The most common symptom is dyspnea with exertion followed by orthopnea. reveals dilation Therapy Specific treatment of idiopathic dilated cardiomyopathy is unknown as the specific cause is not known. and peripheral edema. in addition to improving diastolic relaxation and thus improving myocardial oxygen utilization. Frequently. paroxysmal nocturnal dyspnea. High output heart failure as a cause of pulmonary hypertension. Sherman S. Okura H. is characterized by rigidity of the ventricular wall and associated diastolic dysfunction. Beta-blockade. Pulsus alternans is often present with severe left ventncular failure. but the degree of wall thickening is often inconsequential to the extent ofdilation. This functional classification is most useful when describing the cardiomyopathies. Heart Dis Stroke 1993. and restrictive-based on the type of pathophysiologic functional abnormality present. This group has often been classified according to primary cardiomyopathies in which the underlying the myocardium is unknown. Arrhythmias are the second most common manifestation of dilated cardiomyopathy and a wide variety of both atrial and ventricular arrhythmias may be present. Because of the left ventricular systolic dysfunction.2. and B-adrenoceptor blockade. and elevated systolic and diastolic volumes. The ECG frequently demonstrates sinus tachycardia when failure is present. there is a high association of dilated cardiomyopathy with viral myocarditis. Adams KF. or pericardial disease.86:2s7-2s I 0. Takatsu Y. Two-dimensional echocardiography ofall four chambers. Pharmacologic interventions consist of digitalis glycosides to increase myocardial contractility. a corresponding increase in cardiac silhouette. there is impaired contractility and decreased myocardial oxygen utilization. As a result of the dilation of myop at hy Pathophysiology The dilated variant is most common and characteristically there is dilation of all four chambers of the heart with the ventricles dilating to a greater degree than the atria. The least common variant.9I(6): 227 -236.

however.Cerurovescut-AR DrsoRDERs / 63 thrombi or thromboembolic disease is present. palpitations. Interestingly. Ventricular outflow obstruction occurs in approximately 25Yo of patients with HCM. Commonly there is disproportionate involvement ofthe interventricular septum as opposed to the left ventricular free wall. there is dias- tolic dysfunction of the left ventricle with associated impairment of ventricular filling and elevated filling pressures. further defining two distinct types of HCM: those with outflow obstruction and those without ventricular outflow obstruction. the murmur is decreased by squatting and passive leg raising. Abnormal Q-waves are found in the inferior and lateral leads. Systolic function of the left ventricle is preserved as evidenced by the frequent finding ofnormal cardiac output and ejection fraction. is the most common symptom followed by ischemic chest pain. hence the term septal Q-waves.5o/o. dyspnea. left ventricular ejection fraction has been the best predictor of mortality in dilated cardiomyopathy. Other factors associated with an increased risk of sudden death include a family history of sudden death. The clinical spectrum of HCM is extremely broad. the incidence of left ventricular outflow obstruction is high and the most important predictor for sudden death is nonsustained ventricular tachycardia. 25%o to 50% display supraventricular tachycardia. In symptomatic patients. The ECG is almost always abnormal. syncope. Other . Paroxysmal nocturnal dyspnea. accounting for up to 80% of sudden cardiac death. Often. The symptomatology is directly related to the diastolic impairment of the ventricle. with severe functional limitation. ischemic cardiac pain. which increase left ventricu- lar filling. Pathophysiology At the cellular level. In these adult patients with HCM. Nonsustained ventricular tachycardia is the most significant rhythm disturbance as it is a harbinger of sudden death and should be treated aggressively. In turn. The mortality is substantially higher in patients with an ejection fraction of less than20o/o than in patients with an ejection fraction of 30Yo. A dramatic presentation in young patients. Anther cofirmon abnormality is ventricular amhythmia occurring in approximately 75%o of the adult patients. Historically. and sudden death. making definition very difficult. and base of the heart but not the neck. The physiologic result is a marked decrease in ventricular compliance.loh. Valsalva maneuver increases in intensity by decreasing left ventricular filling. and have improved survival rates. marked ventricular wall thickening. and heart failure. The ischemic chest pain results from an imbalance between the oxygen demands of the markedly enlarged myocardium and the resultant diastolic dysfunction. Often a harsh and diamond-shaped systolic murmur is present. 12 to 35 years ofage. Pharmacologic treatment of ventricular tachy- because of a lack of symptomatology and the fact that the cardia has neither decreased the incidence of sudden death nor improved survival. is one ofsudden death often associated nonsustained ventricular tachycardia on Holter monitor- ing. end-diastolic and end-systolic volumes are normal. Of this subset. nonobstructive form predominates in approximately 75Yo of the patients with HCM. while atrial fibrillation occurs in only 5o/o to l0o/o of patients. and occur in 20oh to 50o/o of patients with HCM. Physical examination may reveal evidence of mild cardiomegaly with an apical systolic thrill and heave. especially exertional dyspnea. It must be stressed that oxygen therapy is the principal cornerstone of management. and symptoms appear later at 40 to 50 years of age. Most patients remain asymptomatic until midlife. The radiation pattern is toward the lower sternal border. the presence of ventricular outflow obstruction has no association with the occurrence of sudden death. These Q-waves are a result of depolarization of the abnormal septal myocardium. Ventricular tachycardia is the single most common event resulting in sudden death in these patients. whereas in patients with known heart disease it is estimated at 0. Commonly there is an 54 present corresponding to the systolic apical impulse. Prevalence in the general population has been estimated at O. Patients who have received an automatic implantable cardioverter-defibrillator do with physical exertion and often heralded by syncopal episodes. the principal feature of HCM is one of circular arrays of myocytes and abnormal arrangement of large cardiac muscle bundles in the area of hypertrophy. Disqualification from athletics is strongly recommended for patients with HCM because of the strong association with sudden death and vigorous physical activity. orthopnea. ST:segment and Tlwave abnormalities are the most common finding followed by evidence of left ventricular hyperhophy. Correspondingly. and dizziness occur much less frequently. Clinical Findings The clinical presentation of HCM is extremely variable and a number of patients with HCM go undetected. and a brisk carotid upstroke. axilla. However. The first and second heart sounds are normal. Hy p ertro p hi c C ardio myop at hy Hypertrophic cardiomyopathy (HCM) is a genetically transmitted cardiac disease of autosomal dominant expression. Marked T-wave inversion is not infrequent in the precordial leads. the central feature is asymmetrical left ventricular hypertrophy without ventricular dilation in the absence of other cardiac or systemic disease.

However. Ifthere is outflow obstruction. and left ventricular hlpertrophy. this is most often seen as asymmetrical septal hlpertrophy. the rarity RCM frequently makes identification of the exact etiology difficult. oventricular conduction. mitral valve prolapse. most importantly. The chest radiograph is variable. alter ati- At the cellular level. and inhibit sinus node automaticity. Other echocardiographic features are a small left ventricular cavity. At the organ level. Causes of secondary RCM are the infiltrative diseases of amyloidosis. decreased rate of mitral valve closure. This diastolic intraventricular pattern is no longer considered absolute requirement for the diagnosis an of RCM. the use of calcium channel blockers is not without some risk. patients with RCM present with exercise . family history of sudden death. The net result of this left ventricular diastolic dysfunction is the inability to increase cardiac output according to demand and in spite of a compensatory tachycardia. nondilated left ventricle with normal contractility. often described as a dip and plateau or square root pattern because of the rapid rise and sudden leveling offof the intraventricular pressure during diastole. in addition to endomyocardial fibrosis and Loffler's endocarditis. Other antianhythmic death. Typically there is only a mild to moderate increase in cardiac silhouette. Echocardiographic findings often show the cardinal manifestation of left ventricular hypertrophy. This pressure differential is exacerbated by phystantly there tioned only to be avoided. and dynamic left ventricular outflow gradient. In the past. Calcium channel blockers are the next line of therapy as they appear to increase left ventricular diastolic filling. and partial closure of the aortic valve during systole. Clinically. mitral regurgitation. prophylactic administration of B-adrenergic blockers or verapamil is recom- The prognosis for HCM is variable. a Therapy Therapy is stratified among asymptomatic and symptomatic patients. They increase myocardial contractility and thus can exacerbate myocardial oxygen demands. They can induce hypotension. a narrow ventricular outflow tract is seen. history of syncope. The most cornmon symptoms are dyspnea and between RCM and constrictive pericardial disease where both the right and left ventricular diastolic pressures are equal. However. Re strictiv e C ardio my op athy Restrictive cardiomyopathy (RCM) is the least common of the cardiomyopathies. Specifically. Nonpharmacologic treatment consists of surgical excision of a portion of the hypertrophic septum or mitral valve replace- ical activity and is extremely useful in differentiating ment. yet no definitive evidence exists that surgery significantly prolongs survival. indicating a more benign course than previously thought. intolerance. Their role is limited to the small select group of patients with HCM who have atrial fibrillation with a rapid ventricular response and no outflow obstruction. Verapamil has been shown to improve the exercise tolerance in patients who have failed to improve with beta-blockade. The problem is one of marked diastolic dysfunction with elevated ventric- ular filling pressures and normal end-diastolic volumes. there is an absence of in symptomatic patients. Clinical factors thought to result in an increased risk of sudden death are young age of onset. Impor- is often a diastolic pressure difference between the right and left ventricles of at least 5 mm Hg in RCM. and. Treatment of arrhythmias is of paramount importance as nonsustained ventricular tachycardia is a prelude to sudden in low doses has often been cited to the risk of sudden death. restrictive cardiomyopathy typically demonstrates myocyte hyperhophy or interstitial fibrosis or both. reduced septal motion during systole. Some authorities recommend an implantable cardioverter-defibrillator if the Clinical Findings response to medical management is ineffective. The cardiac silhouette can appear normal in size and configuration or may show marked left ventricular enlargement. but recent prospective studies have indicated a lower mortality of lYo. Cardiac catheteization often reveals decreased left ventricular compliance. Although RCM is the only cardiomyopathy without accepted diagnostic criteria. nonsustained ventricular tachycardia. Amiodarone decrease agents have not been shown to reduce the incidence ofven- tricular tachyarrhythmias.64 / ErurncrNcv MrucrNn: Tsr Conr CunnrcuI-uM less common abnormalities are those of an abnormal axis and nonspecific P-wave abnormalities. Nevertheless. hemochromatosis. beta-blockade has been used extensively as the first agent. and abnormal diastolic function. several studies have defined this specific disease as heart failure in the presence of a nonhypertrophic. Pathophysiology Beta-blockade decreases myocardial oxygen demand by increasing ventricular compliance and blunting the innate chronotropic action of the myocardium. Primary RCM may be a genetic disorder with dominant inheritance and incomplete penetrance. Digitalis glycosides are men- significant coronary artery atherosclerosis. and sarcoidosis. mended. In asymptomatic patients who have a family history of sudden death. normal or increased posterior wall motion. The annual mortality has often been reported tobe2%oto 4%o. restrictive cardiomyopathy was strictly characterized by the left ventricular pressure tracing during diastole. valvular heart disease.

Stewart Jl McKenna WJ. or both. Hypertrophic and Restrictive Cardiomyopathy Borggrefe M. Momiyama I Mitamura H. Wilmshurst Pl Wendon JA. Sadoul N. This accounts for approximately 650. As with the other cardiomyopathies. Sudden death in idiopathic dilated cardiomyopathy. Echocardiography frequently demonstrates normal systolic function and a normal-sized left ventricular cavity. Prognosis in hypertrophic cardiomyopathy observed in large clinic population. ECG characteristics of dilated cardiomyopat\ -r E/e c trocordiol 1994. Marian AJ. special attention is given to infiltrative etiologies. Lehmann MH. intraventricular conduction defects. Davies MJ. Determinants of oxygen supply and demand Oxygen demand SELECTED READING Dilated Cardiomyopathy Di Lenarda A. Contractility Wall stress (preload and afterload) Heart rate Oxygen supply Diastolic pressure and duration Coronary vascular resistance . Digitalis glycosides and calcium channel blockers are contraindicated in amyloidosis. Slade AKB. or 54.27 :323-328. Management of arrhythmias in hyperhophic cardiomyopathy. Pedersen WR. Sole MJ. Cardiovasc Drugs Ther 1994. Kimura M. Computerized tomography and magnetic resonance imaging may be employed to help differentiate between constrictive pericardial disease and restrictive myocardial disease. Chen X. Roberts R. Alkylating agents are often employed in the treatment of amyloidosis. Br Heart J 1994. Diuretics can decrease preload and vasodilators may affect afterload but only at the risk ofinducing hypotension. Therapy / 65 Larsen L. Often there is an increase in left ventricular mass and infrequently an increase in the left ventricular wall thickness. AMI. Am J Cardiol 1993.Cenuovescut-AR DTsoRDERS fatigue.90:31153117. McKenna WJ.8:95-99. therapy in primary RCM is symptom directed. Hypertrophic cardiomyopathy: an introduction to pathology and pathogenesis. These TABLE 24. Maron BJ. In advance diseased right ventricular failure is present with an enlarged pulsatile liver. Outcome with implantable cardiovert-defibrillator therapy for survivors of ventricular fibrillation secondary to idiopathic dilated cardiomyopathy or coronary artery disease without myocardial infarction. Markham J. Natural history of hypertrophic cardiomyopathy.3) toward enhancing the diastolic function of the left ventricle. Haffajee CI. The role of the ICD in patients with dilated and hypertrophic cardiomyopathy. If amyloidosis is present. Half of these deaths are in patients under 65 and over 507o ofthese deaths occur before the individual arrives at the hospital. variant angina. ten Cate FJ. although a normal cardiac silhouette is not infrequent.000 deaths per year from ischemic heart disease (IHD). Molecular basis of hypertrophic and dilated cardiomyopathy. Sudden death in idiopathic dilated cardiomyopathy: role of ventricular arrhythmias. Digitalis glycosides can enhance contractility. Vos J. Often these patients display elevated pulmonary and systemic pressures. Management of hypertrophic cardiomyopathy.72(suppt):s46-s5 1. Katritsis D. Pathophysiologlt Clinically the spectrum of IHD can be divided into subsets ofdisease: chronic stable angina. Heart Dis Stroke 1993 . Jugular venous distention is present and accompanied by an inspiratory increase in venous pressure (Kussmaulis sign). Block M. Pulmonary auscultation may display rales consistent with pulmonary edema.l 6: 105 l-1 05 9.9: 337-343. Cardiac auscultation reveals an 53. Chest radiograph may show a mild to moderate increase in cardiac silhouette depending on the degree ofprogression of the disease. 9:344-348. Siu S. et al. Secoli G. Tamburro R Wilber D. Primary restrictive car- diomyopathy: clinical and pathologic characteristics. ascites. et al. The prognostic significance of nonsustained ventricular tachycardia in hypertrophic cardiomyopathy. however. Two of the most important aspects of therapy are arrhythmia control and minimizing conduction disturbances. and peripheral edema or anasarca. et al. Curr Opin Cardiol 1994. and sudden cardiac death. Am J Cardiol 1993. J Am Coll Cardiol 19911'18:1230-1235. for secondary RCM.72: 91 l-9r5. Texas Heart Inst J 1994.2. PACE 1992:15:616426.3 million individuals suffer from nonfatal acute myocardial infarction (AMI). Foale R. These defects are a result of the interstitial fibrosis frequently pathognomonic of restrictive cardiomyopathies. Br He art J 199 4. Chelation therapy with deferoxamine is an important adjunct in the treatment of hemochromatosis. Circulation 1994. Br Heart J 1 994. Restrictive cardiomyopathies. as is steroid improve. Atrioventricular conduction defects. Curr Opin Cardiol 1994.21:6-15. Am Heart J 1992. Spirito B Bellone P. Changing mortality in dilated cardiomyopathy. Goldenberg IE. Kofilard MJ. Treatment is oriented Ischemic Heart Disease (2. The ECG can display a vaiety of nondiagnostic findings. Perkan A. Dilated cardiomyopathy. Spyrou N. Of all deaths in the United States approximately 45Yo are due to cardiovascular disease.72:s2-s3. McKenna WJ. and mitral regurgitation is commonly noted. As therapy in sarcoidosis. Significant toxicity can result when using these agents as they bind to the amyloid fibrils.2:203-208. et al. Waldstein DJ. Steinman RT. Lessmeier TJ.7 2 :sl0-s12. unstable angina. PAC E 1993 . Saumarez RC. a granular or sparkling pattern is seen in the left ventricular wall. 72:939-943.124:1035-1045. Chest pain of ischemic etiology is an infrequent presentation. as cardiac output can substantially Annually 1. digitalis is only of limited benefit since contractility is minimally impaired. and low precordial voltages are common.

lasting usually 5 to l5 minutes. or stress. or reflux Herpes zoster. which is classically localized to the retrosternal area and radiates to the neck. emotion. Cocaine causes myocardial ischemia by increasing myocardial oxygen demand while decreasing coronary blood flow through vasoconstriction. hypertension. ST:segment elevation is usually noted with chest pain. aortic dissection.3. AV block. 2. 2) Chest pain is the most common cocaine-related medical problem. 3. both of which form plaques. ASCAD is the focal narrowing of the large and medium-sized coronary arteries due to intimal proliferation of smooth muscle cells and deposition of lipids. Complications include dysrhythmias.T wave inversion occurs less than half the time.1) episodes. Unstable IHD occurs when myocardial blood flow fails to satisfz myocardial oxygen demand resulting in ischemia. constitute acute ischemic coronary syndromes (AICS). heaviness. left ventricular hypertrophy. disruption of atheromatous plaque. but no transmural infarction (new Q waves) is noted. angina into three subsets distinguished by pain syndrome: (1) recent onset exertional angina. divides unstable output and hypotension cause decreased flow across the fixed obstruction. to consider factors in those patients with a history of angina that have potentially exacerbated their stable state. and bundle branch blocks are associated with these attacks. which is described as increasingly more severe. spontaneous pneumothorax. The differential diagnosis is included inTable 24. autoregulation increases coronary blood flow. mitral valve prolapse Pulmonary Pulmonary embolism. or exposure to cold). Troponin indicating the presence of microinfarcts. it is felt that variant angina is caused in part by spasm of the epicardial coronary arteries alone or in combination with coronary artery disease. These changes may reduce the supply and produce ischemia with or without an increase in demand. squeezing.2. Presently. premature atherosclerosis. ST and T wave change s (66% with ST depression and 33o/o with ST elevation) may occur up to several hours after the episode. ventricular septum or papillary muscles.66 / EuBncrNcy MnorcrNn: TABLE 24. Serum enzyme levels show minor elevation without definite serial changes. acute myocardial infarction (AMl). and relieved by rest or sublingual nitroglycerin. In normal Unstable angina represents a clinical state between stable angina andAMI. pneumonia. Stable Myocardial Infarction Stable angina is characterizedby episodic chest pain. or down the inside of one or both arms. Causes of myocardial ischemia and determinants of myocardial oxygen supply and demand are listed inTable 2-3. pericarditis. Cocaine Induced (2. or sharp discomfort. and shoulders. tachyarrhythmias. and tachycardia. These attacks tend to recur at similar times and are most prevalent at night. Similarly. enhancement of platelet aggregation. as increased demand is needed. Classification proposed by Conti et al. There are multiple causes of chest pain in addition to IHD. (2) chest pain with changing pattern. or increased requirement for nitroglycerin. Chest pain increases with severity and/or duration from normal anginal pain. jaw. gastric peptic ulcer disease. ECG shows changes including ST:segment depression. Elevation of cardiac enzymes does not occur since the myocardium is not injured. myocarditis. the fixed lesion prevents the increased flow and oxygen delivery necessary with severe anemia and the increased inotropic states of myocardial hypertrophy and tachycardia. Boerhaave's syndrome. longer in duration. chronic pulmonary obstructive disease Gastrointestinal Esophagitis (including esophageal ref lux). (3) chest pain occurring at rest. emotion. The typical patient with cocaine-associated myocardial infarction is a young tobacco-smoking male with a history of repetitive cocaine usage. Fixed obstruction or stenosis of coronary blood flow prevents normal coronary blood flow and any increase in coronary blood flow needed to compensate for increased demand. It is important individuals. and ST:segment elevation is seen less commonly. Unstable angina is thought to be due to the progression in severity of atherosclerosis.. . Decreased cardiac including discontinuation of prescribed medications or a new underlying medical problem. rupture of the ventricular free wall. occurring within 4 to 8 weeks previously. is found to be elevated in about one-third of the I Angina (2. or hemorrhage into nonoccluding plaques with subsequent occlusion developing over hours to days. The majority of IHD is due to atherosclerotic coronary artery disease (ASCAD). esophageal spasm. Cardiovascular Tnr Conn Cunruculurvr Differential diagnosis for chest pain Angina. chest wall pain (coPD) Other Variant Variant (Prinzmetalb) angina occurs primarily at rest. in situ thrombus formation. asthma. coronary artery spasm. It is commonly described as a pressure. This is usually caused by exertion or stress (heavy meals.

Treatment with aspirin is controversial. Cocaine additionally has a local anesthetic (quinidine-like) effect similar to other type Ia antidysrhythmics and tricyclic antidepressants. Serum Enzymes with Cocaine-Induced AMI. For treatment of a wide complex tachydysrhythmia secondary to cocaine toxicity. Retrospective studies of cocaine users with chest pain have found that the incidence of myocardial infarction ranges from 0 to 3lo/o. limits the size of AMI. aspirin. Thrombolytic agents do carry the risk of intracranial hemorrhage or dissection in severely hypertensive patients. prospective clinical trials. an unopposed cr-adrenergic-mediated vasoconstriction can occur. Continuously rising enzyme concentrations are more likely to occur in patients with cocaine-induced AML Treatment Treatment of cocaine-induced AMI is patterned after the treatment of IHD. Sodium bicarbonate is felt to reverse cocaine-induced QRS prolongation. Other associated symptoms may include dyspnea. Though not widely accepted. the ECG is abnormal 1n 56o/o to 84o/o of patients. Additionally. Some authors recommend that with new ST:segment elevations and no improvement with the above therapy. Use of a low dose (e.qR Drsononns and bradycardia secondary to inferior MI. Theoretically. P ro gno s is /Di sp o s iti o n Because of the difficulty in identiffing patients with cocaine-associated chest pain who are at low risk for myo- . nausea. some authors feel it should be administered to prevent the formation of thrombi. approximately 50% of cocaine intoxicated patients have elevations in the semm creatine kinase concentration myocardial band (CK-MB). there have been no welldesigned. Though mainly used for their anxiolytic effects. increase the likelihood of seizures. and may rep- resent a safe alternative for patients whose ventricular arrhythmias immediately follow cocaine use. anxiety. or qualiry plus associated symptoms. Clinically.. Administration of p-adrenergic blockers is not recommended. With cocaine-associated chest pain.Cenuovescur. J-point and ST:segment elevation often make the identification of ischemia difficult due to early repolar- ization or left ventricular hypertrophy. which may prompt unnecessary administration of thrombolytic agents to patients without AMI who also have a greater potential for intracerebral hemorrhage.g. avoids the hypotensive effects of the drug while maintaining its antiischemic effects. and decrease survival. reverses cocaine-induced coronary -artery vasoconstriction. Additionally. The use of thrombolytic agents is controversial.The frequency ofAMI was approximately 60/o in two prospective studies. skeletal-muscle injury. it is reason- able therapy in the of traditional contraindications. symptoms of chest pain location. This increase can occur in the absence ofAMI. Parker and his colleagues suggest intra- venous administration of bicarbonate in patients with cocaine-induced MI. Those patients who continue to have severe chest pain after the administration of oxygen. Diagnosis Electrocardiogram (ECG). Others feel that to give the patient thrombolytic absence although thrombolytic agents may be safe. benzodiazepines also diminish cardiac toxicity by reducing blood pressure and heart rate. lidocaine should be used with caution due to its association with an increased incidence ofseizures. These authors cite the overall mortality from cocaine-associated AMI. and reduces infarct-related complications in patients with myocardial ischemia unrelated to cocaine. Calcium antagonists have no proven benefit in AMI unrelated to cocaine. Nitroglycerin reverses cocaine-induced coronary artery vasoconstriction. however. are predictive of myocardial infarction. Calcium antagonists or phentolamine should be considered as second-line therapy. causing severe hypertension and coronary vasoconstriction that could lead to intracranial hemorrhage and increased cardiac ischemia respectively. however. hyperthermia. randomized. increased motor activity. or thrombolyics. while others feel it must be avoided in those patients who are at risk for subarachnoid hemorrhage. fail to control heart rate. verapamil does reverse cocaine-induced coronary -artery vasoconstriction. Patients with cocaine-induced myocardial infarction in one study are as likely as not to present to the hospital ED with a normal or nonspecific ECG that has led to the discharge of up to l5o/o of patients with cocaine-induced AMI. increase blood pressure. Whether or not they are undergoing infarction. and rhabdomyolysis. dizziness. I -g) p-adrenergic blockers can also produce profound hypotension due to their negative inotropic and type Ia antiarrhythmi c effects. Their use has been found to exacerbate cocaineinduced coronary vasoconstriction. benzodiazepines. they should not generally be recommended. palpitations. relieves symptomatic chest pain. thus decreasing myocardial oxygen demand. and nitroglycerin may be treated with either low- / 67 dose phentolamine or verapamil. and the clinical benefit of thrombolytic therapy in this context has not been studied. young patients may demonstrate a pseudoinfarct pattern (early repolarization) on ECG. Cocaine causes complications in nearly all organ systems. Benzodiazepines are the first-line treatment for cocaine-intoxicated patients with chest pain. which is extremely low in patients who reach the hospital alive. duration. Cocaine withdrawal may also cause myocardial ischemia. Phentolamine. an ct-adrenergic antagonist.

therefore. and initial cardiovascular complications.: Tun Conn CunrucuLUM cardial infarction. Silent coronary artery disease is significant IHD without clinical symptoms and is found in 2. morbidiry and mortality are determined by the amount of infarcted tissue. Late complications can be predicted in the first 12 hours after arrival in those with diagnostic ECG ischemic changes. they are diagnostic in only 25o/o to 50o/o of patients subse- . vomiting. Auscultation of the heart may reveal a tran- sient S+ or apical systolic murmur indicative of mitral regurgitation. Q wave infarctions tend to be larger. A high index of suspicion must be taken particularly with diabetics. questioning should be directed toward cardiac risk factors to more quickly distinguish cariogenic chest pain from other causes (Table 2-5). The classical presentation is an individual who presents with severe substernal chest pressure that lasts longer than 15 minutes. the elderly. jaq or medial aspect of one or both arms. damaging more myocardial tissue. radiates to the neck. Presently.68 / ErrmncrNcy MnorcrNr. dyspnea. it is recommended that patients with the above findings should be admitted to monitored beds. multiple factors have been felt to AMI. 4%o to 12% wlll have lifethreatening ventricular arrhyhmias. platelet aggregation and thrombosis at the site of preexisting narrowing. Prognosis. a low index for admission should be held for patients with cocaine-induced AMI. The elderly are more likely to present with nonspecific symptoms. weakness. During the initial interview. Non-Q wave infarctions possess a lower in-hospital mortality rate. most patients are hospitalized. (2) differentiating acute ischemic coronary disease from nonischemic causes of chest pain so as to avoid unnecessary costly hospitaliza- tions. alcoholics. the time period from onset of symptoms to initiation of therapy is the key to improved outcome. apd (3) identiffing those patients with AMI who would be discharged inadvertently from the ED. and post-coronary Although ECGs are used extensively in the ED. or with no pain in comparison with younger patients. Of particular concern with these individuals is extension of the infarct into a transmural infarction. Acute Pathogenesis Like unstable angina. coronary artery spasm. Patients with cocaine-associated chest pain have a l-year survival of 98%. the use of ancillary studies for the evaluation of ED patients with chest pain has focused on three key issues: (1) early iden- tification of those with AMI to reduce time to definitive treatment (percutaneous transluminal coronary angioplasty or thrombolytic therapy) and minimize the extent of myocardial infarction. Non-Q wave AMI accounts for 30% to 40% of AMIs. or syncope. dizziness. including coronary artery embolism. resulting in higher peak serum CK- MB levels and lower ejection fractions. This distinction is used to discern whether acute ischemia is confined to the subendocardial area (manifested by ST segment depression) or involves the transmural wall (manifested by presence of Q waves and usually ST-segment elevation). plaque fissuring. Those diagnosed with silent TABLE 2$. Ischemia leads to infarction affecting lead to both electrical depolarization and contractility of the myocardial cell. Electrocardiogram and Interpretation AMI usually have vague complaints of discomfort. yet are more likely to be complicated by recurrent infarction or subsequent angina. Duration of ischemia determines the extent of infarction. Diagnosis and Ancillary Tbsts Precisely differentiating these IHD syndromes (a. Long-term mortality tends to be equal after about 3 years. diaphoresis. progression of the atherosclerotic process to the point of total occlusion. Pathophysiology AMI can be divided into Q wave and non-Q wave MI.5%o to l0o/o of middle-aged individuals.k. and is associated with nausea. Atypical presentations can include abdominal pain or vague chest discomfort. Major risk factors for ischemic heart disease Age Family history (Ml in first-degree relative age <55) Smoking Hypercholesterolemia Hypertension Diabetes mellitus Male gender Morbid obesity Cocaine artery bypass graft (CABG) patients. elevated CK-MB. and subintimal hemorrhage within an intimal plaque. syncope. AICS) may require the use of sophisticated diagnostic tools and prolonged observation. Overall approximately 6%o wlllhave AMI. considering that approximately 6% of these patients have myocardial infarction. Unfortunately. and 5Yo to 7o/o wlll have chronic heart failure. Clinicql Features There is no single presenting symptom uniformly diagnostic or specific to IHD. Overall. the physical examination in all types of IHD may be deceptively normal.a. Overall. dyspnea. epigastric pain. nonretrosternal chest pain.

and give results within minutes using immunologic techniques. which is even more disturbing. Serum Markers segment depression or elevation of less than 1 mm. or hypotension with distended neck veins and clear lung fields) Identifuing AMI candidates for reperfusion as soon as possible in the ED has become a priority. The inverted T wave of ischemia is symmetrical (left half and right half are mirror images). up to 4% who have AMI are released unintentionally from the ED. and AVF (R or L coronary artery) Q's or ST elevation in Vr. patients have been admitted for at least 24 hours in order to be ruled out for AMI. Routine assays indirectly measure CK and CK-MB concentration by determining enzymatic activity. Due to these factors an estimated 2o/o to 4oh of ED patients with AMI are undiagnosed while others are inappropriately included or excluded from aggressive reperfusion therapy. however.9. 55 out of 64 had AMI. Localization of ischemia can be identified by the leads in which it occurs (Table 2-6). Q waves remain for a lifetime and are no indication of the acuity of an infarct. T waves are normally in the same direction as the QRS and often become inverted because of ischemia or infarction. Isolated (noninfarction) ischemia may also be located by those leads where T wave lnverslon occurs. and aVF) lsolated ST-segment elevation in lead Vr or ST-segment elevation in lead V1 or ST-segment elevation in lead Vr > Yz Symptoms suggestive of RV ischemia (e. and Vq (left anterior descending coronary artery) ST segment elevation greater than 1 mm in lead Vsn and/or V+n quently diagnosed with AMI. A normal or nonspecific ECG does not exclude ischemia and should not negate the need for hospital admission. Serum CK-MB. performed at least 6 hours apart. mirror test Q's or ST elevation in I and AVL (circumflex coronary artery) Q's or ST elevation in ll. Traditionally. Vs. RV infarction occurs in about 60% of patients who suffer an inferior MI and becomes hemodynamically significant in approximately 10% of left ventricular inferior wall and right ventricular AMI. significant hypotension after nitroglycerin. The most frequent ECG findings in chronic IHD are nonspecific ST andT wave changes. A significant Q wave is I mm wide (. and T wave flattening or inversion. Q waves indicate infarction. Due to the variable normal serum levels of CK-MB. have only a 2Yo chance of having AMI. not the quantity or mass of enzyme. T wave inversion indicates ischemia. 80% had a positive ED serial CK-MB enzyme study within 3 . Additional leads in conjunction with the standard l2-lead ECG attempt to improve sensitivity in the identification of right ventricular and posterior AMIs associated with inferior AMIs. Newer assays of CK-MB directly measure enzymatic mass. its presence in noncardiac muscular tissues. a variety of non-Q wave infarction.04 sec) or greater than or equal to one-third the amplitude of the QRS complex. Non-Q wave infarction is suspected with significant ST:segment elevation alone. Ischemia reverses the sequence TABLE 2-7.Cerurovescur-AR DISoRDERS TABLE 2-6.. Serum markers may have the potential to rapidly identify candidates for aggressive therapy and address the unintentional discharge of AMI patients from the ED. a single CK-MB determination is not reliable in eliminating the diagnosis of AMI.In90%o ofpalients. However. Clinical signs and symptoms and ECG manifestations are not sufficiently specific to distinguish noncardiac chest pain from necrosis. the accurate diagnosis of AMI in the early hours remains difficult. lll. lll. and its delayed entry into the serum (3-6 hours). lndications for 1S-lead ECG ST-segment depression or suspicious isoelectric STsegments in Vr through V3 Borderline ST-segment elevation in leads Vs and Vo or in leads ll. Unfortunately. ST segments return to baseline with time. not activity. The l5lead ECG may better identifu the extent of injury in patients suffering from an inferior AMI and thereby have therapeutic implications for the emergency physician (Table 2-7). ST:segment depression can represent subendocardial infarction. Rapid CPrK. administration. epigastric pain. indicates an acute transmural infarct. patients with no ST:segment elevation on their initial ECG and two consecutive negative CK determinations. ST:segment elevation indicates an acute process an4 with associated Q waves. These are usually defined as ST: / 69 of repolarization. Usually T wave inversion is noted in the same leads as acute infarction (ST elevation and Q waves). and aVF All inferior Mls (ST-segment elevation in leads ll. Gibler and associates found that of the patients with nondiagnostic ECGs. In a multicenter study. Vz. As few as llo/o of patients hospitalized with suspected acute myocardial necrosis are eventually confirmed to have AMI. the right coronary artery supplies the inferior wall of the left ventricle as well as the right ventricle. Localization of infarction using Q waves and ST elevation Posterior Lateral lnferior Anterior Right ventricular Large R with ST depression in Vr and Vz. lll. let alone from transient myocardial ischemia. causing it to occur in the endocardialto-epicardial rather than the normal direction.

did not assess the application of cardiac enzyme measurement for patients under consideration for discharge from the ED. an MB2:MBl ratio of 1.5 or more in samples collected 6 hours after AMI were 96% sensitive compared to 48o/o for the conventional plasma creatine kinase assay. has distinct differences in the subunit amino acid composition and can differentiate cardiac from skeletal muscle immunologically. For recognizing AMI and myocardial ischemia. The advantage is that it is a relatively noninvasive procedure that can be obtained quickly. a structural component of cardiac muscle cells. It is taken up by myocardium in proportion to blood flow. preventing the use of MB subforms for early diagnosis of infarction. increases in troponin I do not occur even when plasma levels of CK-MB are increased with severe acute or chronic skeletal mus- cle injury unless associated cardiac injury is present.70 / EvrncrNcy MntlcrNr: Tun Conn CunnrculuM hours of presentation. and renal failure. Green et al. proved that myoglobin concentration was as specific as CK-MB concentration (93% in both cases). availability of trained personnel to interpret the image. found that serum myoglobin elevation at 3 hours identified all 21 patients with AMI. It is also elevated in skeletal muscle trauma. in a prospective study. Additionally. Outpatient treatment of stable . found that perfusion defects persist in patients with angina for several hours after resolution of symptoms.6% negative predictive value for no AMI (94% specificity). Bakker and colleagues. but do not rule out ischemic heart disease.. it also had the highest falsepositive rate. The decision to discharge a patient is based on the history and an assessment of the patient's potential for suffering a cardiac event if sent home. the nuclear imaging studies described suggest high sensitivity and specificity. these studies suggest that the new rapid CK-MB assays may assist the emergency physician in identifying some patients with unsuspected AMI and inadvertent discharge from the ED. and the study's cost may limit their use. CK-MB determination was eventually positive in 19 of these 21 patients. sensitivity was 100% and specificity was 83oh to 92o/o in patients with active chest pain and a nondiagnostic ECGs. Nuclear Imaging. not solely on a laboratory result. The troponin complex. providing a specific tool for diagnosis of AMI. Myoglobin has been evaluated as an indicator for myocardial injury. This may be useful for patients presenting to the ED with chest pain suggestive of myocardial ischemia. Immunoturbidimetric myoglobin assay has been introduced requiring only 2 to l0 minutes to perform. myoglobin.5 hours after admission in comparison to CK-MB at 4 hours after admission. is modified by the plasma enzyme car- It boxypeptidase-N. however. CKMB was positive in only three individuals. Troponin complex consists of three protein subunits (! I. Treatment of Ischemic Heart Disease Treatment of IHD can be divided into both inpatient and outpatient therapy. According to Puleo and associates. but with nondiagnostic ECG. Presently. Myoglobin. Addressing this issue directly. Brogan et al. however. found negative predictive values of 100%. decreasing accuracy with time. found in a l-hour observation period that an increase in serum myoglobin of 40 ng/ml increased the sensitivity of the myoglobin assay forAMI in ED patients from 73o/o to 9lo/o. in a small study of 59 patients. these ancillary tests should not prevent timely treatment of individuals with a history and symptoms consistent with AMI.. found that troponin T had the highest sensitivity for prediction of AMI. Serum levels can be elevated within I to 2 hours after symptom onset. In studies by Hilton and Varetto. According to Adams et al. although further research is needed. Technetium-99m is a radioisotope that is more readily available than thallium-2O1 because it is generator produced. They reported a 99. initially. Rapid determination of MB subforms may become important for the early determination of AMI in the ED. but when noted in serum is a sensitive indicator of muscle damage. normal serum levels of CK-MB. Myoglobin is a cellular oxygen-carrying protein normally located in all muscle tissue. Serum markers currently are an adjunct to clinical evaluation. Cost. Areas of transient ischemia from stenosis or spasm do not actively take up thallium and will therefore appear as an area lack- ing isotope on the scamed image. but myoglobin had a sensitivity of l00o/o at 1. or prevent admission to unmonitored beds. and troponin shed light on the absence of myocardial infarction. MB Subforms. factors such as the availability of radionuclides. and overall poor availability limit its use. Kilpatrick et al. This study. obtainable assays lacked adequate sensitivity to detect the individual MB subforms in normal plasma. inability to distinguish old from new infarct. However. CK-MB exists as single form in tissue (MB2). Thallium-2Ol is a nuclide that following intravenous injection distributes into myocardial tissue and is therefore dependent on coronary blood flow and the ability of myocardial cells to extract the thallium. In summary. They suggest that measurements of troponin I provide information comparable with that from echocardiography in clarifuing the presence or absence of cardiac injury when elevations of CK-MB occur. Cardiac-specific troponin in serum is measured using monoclonal immunoassay. Until recently. Myoglobin from skeletal muscle is indistinguishable from myocardial tissue and lacks specificity for myocardial infarction. peaking at 4 to 5 hours after AMI. Studies have suggested that in those patients presenting within 6 hours thallium201 can identifu AMI with 100% sensitivity. It is used to identifyAMl and reversible ischemia. and C) each with different structures and functions. kchnetium-99m. yielding its subform MBl. Varetto et al. Gibler et al. Troponin. shock states.

then IV heparin is necessary to pre- vent reocclusion. increasing collateral blood flow. and cardiac monitor and pulse oximeter placed. and a 46oh reduction in nonfatal stroke rates. then 100 mg/d Atenolol 1-4 g IVP over 5-20 min Magnesium Morphine 2-5 mg every 5-1 5 min 1-4 g IVP over 5-20 min 2-5 mg every 5-15 min orally angina includes correction of modifiable risk factors and drug therapy.4 mg tablets sublingually given every 3 to 5 minutes. reduce reinfarction. sublingual Nitroglycerin. a 49o/o reduction in nonfatal reinfarction rates. Its antithrombotic activity complements the antiplatelet activity of aspirin to prevent progression of ischemia to AMI. or the mean arterial pressure decreases by l0%. Selective agents such as esmolol and metoprolol preferentially inhibit Br receptors of the heart at low and intermediate doses. if tissue-type plasminogen activator (t-PA) is to be given or primary percutaneous transluminal coronary angioplasty (PTCA) is to be conducted. If chest discomfort continues after three doses. Medications used in the ED inpatient setting listed in Table 2-8. Current recommendations by Sirois for the use of heparin in the treatment ofAMI are as follows: heparin is indicated if no thrombolytic agents are given. and decreased heart rate and thus decreased myocardial oxygen demand. must be ruled out.Cenorovescur-A. Adequate therapy is 160 to 325 mg qday. A non-rebreather mask.000-unit IV bolus. Nonselective padrenergic antagonists have been shown to be useful in the treatment of angina.or 5 mg lV every 5 min x 3. heparin has been found to reduce reocclusion and reinfarction (20 to 30%) and mortality rate (16 to 2lo/o). Becommended doses for AMI treatment adjuncts Agent Nitroglycerin. More importantly. The major complications of and contraindications to nitrate therapy (SL or IV) are hypotension and marked bradycardia. It should not be used with a systolic blood pressure of less than 90 mm Hg. then 10 units/kg/hr infusion or 5000 units bolus then 1000 units/hr Beta-blockers Esmolol Metoprolol 500 pg/kg lV over 1 min. For patients with unstable angina or AMI. are Oxygen. then a continuous infusion of 1. then 50 mg every 6 hr orally 5 mg lV every 5 min x 2. and decrease mortality due to increased coronary artery blood flow. In the Second International Study oflnfarct Survival (ISIS-2). Aspirin. and pneumonia. reduce the incidence of ventricular fibrillation. The latter usually consists of nitroglycerin. and heparin is contraindicated due to subsequent increased risk of hemorrhage. It can be increased in increments of 5 to l0 ug/min at 5. Additionally. and calcium channel antagonists. In those patients with unstable angina or AMI who do not respond to aspirin. Many institutions use an initial 5. The majority of patients respond to infusion rates of 50 to / 77 200 ug/min. particularly thoracic aortic aneurysm.R DrsoRDERs TABLE 2-8. but the dose and route of administration remain controversial. which inactivates thrombin and factor Xu. aspirin alone exhibited a23o/o reduction in mortality rates. The initial infusion rate is 10 to 20 tg/min. Nitroglycerin Nitroglycerin (NTG) helps relieve the pain from myocardial ischemia by dilating epicardial arteries. It works by catalyzing antithrombin III. A rapid antithrombotic effect due to inhibi- tion of thromboxane and cyclooxygenase-dependent platelet aggregation is produced by aspirin. intravenous Aspirin Heparin 0. The size of infarct may be reduced with supplemental oxygen. and will improve ventricular remodeling and reduce infarct size and mortality. Hlpotension usually will respond to small boluses of normal saline. pneumothorax. Heparin.000 units an hour. The recommended weight-based dose of heparin is an initial bolus of 80 units/kg followed by a constant infusion rate of l8 units/kg/h.to l0-minute intervals until chest discomfort resolves. p-adrenergic antagonists. and reduce overall mortality. or endotracheal intubation should be strongly considered if supplemental oxygen fails to correct significant hypoxemia. it has been found to have antiplatelet effects. the individual should simultaneously be examined while oxygen is given. Initial dosing should be based on weight to ensure consistent and adequate anticoagulation. and decreasing left ventricular preload. p-Adrenergic blockers should be considered when symptoms of chest pain are not resolved or are poorly responsive to NTG therapy. continuous positive airway pressure. Trials have shown conclusively that beta-blockers decrease infarct size. then 50 pg/kg/min titrated max dose of 200 pg/kg/min. Additionally. no added benefit has been shown if streptokinase is used. The role of heparin in the treatment of AMI has been controversial.4 pg every 5 min x 3 doses Begin at 10 pg/min and titrate as needed 160-325 mg/day 80 units/kg bolus. The greatest beneficial effect is achieved when beta-blockers are started early in ofAMI. but only moderately useful in patients with unstable angina or AMI. the management . However. They have also been found to decrease cardiac rupture. Detection of other causes of chest pain. aspirin has been found to prevent reocclusion and reinfarction. Supplemental oxygen should be provided to all patients with AMI. decreased myocardial contraction. Beta-Blockers. intravenous access is established. an intravenous NTG drip should be initiated (50 mg NTG in 250 ml dextrose 5% in water) and titrated until pain subsides while keeping systolic blood pressure greater than 90 mm Hg. Treatment should be directed toward pain relief with initial administration of NTG 0.

dlltiazem may be considered. Pain and anxiety reduction to leads decreased circulating catecholamines and decreased myocardial irritability. The dose of esmolol is 500 ug/kg intravenously over I minute followed by an intravenous infusion at 50 rgikglmin titrated to a maximum dose of 200 ug/kg/min. however. Indications for its use in patients with AMI include more than six premature ventricular contractions (PVC) per minute. performing PTCA after failed thrombolysis has shown mixed results. nifedipine was found to increase mortality and therefore is not recommended. Patients with AMI who stand to gain the most are those who are not candidates for thrombolytic. aspirin. however. bradycardia. In patients with unstable angina who do not respond to aspirin. are important. Dllliazemmay be given as a bolus of 25 mg IV over 5 minutes followed by a l5-mg/hr infusion. relative reduction in mortality . Thrombolytic Therapy Cessation of blood flow to the canine myocardium initiates necrosis in approximately 20 minutes. magnesium therapy was delayed more than 12 hours. neither diltiazem nor verapamil has been shown to decrease mortality. of other interventions were uncontrolled. Potential wave AMI. and intravenous esmolol . It is unclear how much of the observed reduction in mortality can be ascribed to magnesium alone. Though the mechanism is unknown for this reduction in mortaliry some feel it may be due to a direct cardioprotective effect. hypotension and variant angina. Addition- ally. intravenous beta-blockers such as esmolol. Magnesium. Morphine. mortality decreased by 23%o and 300/o. Initially. atrioventricular block. if readily available. within 18 to 48 hours. or beta-blocker therapy. obstructive lung disease.Indications and contraindications are shown in Tables 2-9 and2-10. is a one-time dosage of I to 4 g given IV over 5 to 20 minutes. the effects sium. and ventricular fibrillation. it is my opinion that expedient comparison of old ECGs and a portable chest radiograph to rule out dissecting aneurysm. The use of calcium channel blockers is controversial in unstable angina and AMI. with complete transmural necrosis occurring between 3 and 6 hours. ventricular tachycardia. therefore decreasing myocardial oxygen demand. The ISIS-4 trial showed no benefit from magneure and a 24o/o reduction however. The routine use of prophylactic lidocaine has been shown to have no added benefit and may increase mortality rates. leading to a reduction in cardiac work by reducing both preload and afterload. When pain from myocardial ischemia is not otherwise rapidly controlled by other methods. or atenolol should be considered. respectively. This is especially true in patients with tachycardia and/or hypertension. Streptokinase. Morphine blocks central sympathetic efferent discharge. generally contraindicated in patients with asthma. the latter two respond well to fluids and atropine. its prophylactic use should be discontinued. The usage of the first two is by far more common. respectively. and bradycardia. In most cases. and insulin-dependent diabetes mellitus. Metoprolol and atenolol can also be used. Magnesium. intravenous nitroglycerin. or delayed for 5 to 14 days. A g g res s iv e Rep erfu s i o n Th e rapy Aggressive reperfusion therapy (ART) includes thrombolytic agents or PTCA. the use of magne- sium resultedina25%o reduction in left ventricular fail- in 28-day mortality rates. congestive heart failure. when considered. None of these combined strategies has been shown to be more eflective than thrombolysis alone. Currently three thrombolytic agents are available: r-TPA. the decision to administer thrombolytic therapy should be made based on the clinical presentation and the initial ECG alone. metoprolol. 2 to 5 mg IV boluses of morphine every 5 adverse effects include respiratory depression. either concurrent. Calcium Channel Blockers. Lidocaine. The Gruppo Italiano per lo Studio della Sopralvivenza nel 'Infarto Miocardico (GISSI-I) showed patients treated after 6 hours had no significant reduction in mortaliry while those treated within I hour of symptom onset had a of 50%o. closely coupled PVCs (R-on-T). This is the major factor in decreasing both early and late nonarrhythmic mortalify after AMI. A decrease in mortality of two to three patients per 100 treated and a reduction in relative mortality of 22Yo in comparison with nonthrombolytic management versus placebo were found in pooled results of five major randomized trials. therefore. Beta-blockers are. In two placebo-controlled megatrials of mortality (GISSI-I and ISIS-2). bursts of three or more PVCs. ART strategies focus on the combination of thrombolytic therapy and PTCA.72 / EnrncnNcv MnorcrNn: THn Conn CunnrcuI-uM intravenous NTG. hypotension. multiform PVCs. streptokinase. Although diltiazem has been shown to decrease early reinfarction and recurrent angina in patients with non-Q- to l5 minutes should be used. In small studies of unstable angina and AMI patients. intravenous heparin. immediately within 90 minutes. Minimizing infarct size is associated with improved residual left ventricular function. Though some authors feel that these alone should be the only decision criteria. In the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). The time from symptom onset to initiation of treatment has been consistently shown to be the most important factor in reduction of mortality. and intravenous heparin. and urokinase. Morphine is contraindicated in patients with significant bradycardia or hypotension. in patients with AMI randomly assigned to IV streptokinase (SK) or compared with placebo within 6 hours of symptom onset.

for patients 76 Yr and older. Controversy surrounds the clinically of high-grade residual stenosis after successful thrombolysis (75 to 80%). patients with inferior AMI. this is not a contraindication for use of other agents) Major surgery or trauma more than 2 weeks before Puncture of noncompressible vessel Prolonged or traumatic cardiopulmonary resuscitation Hemorrhagic retinopathy Recent gastrointestinal or genitourinary bleeding (within 10 days) Bacterial endocarditis Recent transient ischemic attack Known left heart thrombus Active peptic ulcer disease History of chronic.5o/o to l. The prehospital Myocardial Triage and Intervention Trial (MITD group from Seattle showed a mortality rate from AMI of 1. SK costs approximately $100 to $300. and a 0. Arrhythmias are commonly observed and are neither dangerous clinically nor consistent markers of TABLE 2-1O. arteriovenous malformation or neoplasm Active internal bleeding.000 patients. The 1988 Anglo- Scandinavian Study of Early Thrombolysis (ASSET) placebo-controlled trial demonstrated a significantly lower mortality of 28oh for patients treated with t-PA within 6 hours of symptom onset. and is clot-specific. the decision to administer thrombolytic agents should be made on an individual basis Symptoms 12-24 hr Non-Q-wave AMI ECG ST-depression Cariogenic shock Unstable angina relevant superiority / 73 of t-PA considering the similar patency rates (70o/o vs 7 5oh) at 3 hours versus the statistically significant increase in hemorrhagic stroke rates of those who receive t-PA. Initially. immediate reocclusion (15 to 20%). studies found a superior ability of t-PA to open arteries at 90 minutes compared with SK.r\R DTsoRDERS TABLE 2-9. Early administration is the most critical determinant of response to and outcome with thrombolytic therapy. Recombinant t-PA (t-PA) activates the fibrinolytic system. however. Unfortunately. patients with a longer duration of pain. and those individuals with pulmonary edema and AML Due to the potential for allergic reactions. while t-PA costs $2200 to $2500. uncontrolled hypertension (diastolic >100 mm Hg).0o/o incidence of intracranial bleeding. reocclusion in approximately l5Yo to 20oh of patients. those hav- ing a first AMI. failure to achieve artery patency (15 to 40o/o). Megatrials addressing mortality directly compared t-PA and SK randomized to more than 100. lndications for thrombolytic therapy Probable harm lndications Chest pain of >30 min and <12 hr duration ECG ST-elevation (>1 min >2leads) Anterior. Cost differences are substantial. Howeveq further trials have shown benefit in older patients. and poor results in certain subgroups. both have a high-grade stenosis rate. has no allergic side effects.Cenorovescur. Recombinant t-PA. SK is not recommended to be readministered for a period of 5 days up to 6 to 12 months after previous use. such as gastrointestinal Bleeding disorder or anticoagulation Aortic dissection or pericarditis Pregnancy Recent head trauma Previous use or allergy to streptokinase (SK therapy should not be repeated within 6-12 months. those with anterior AMI. and those with no or few signs of heart failure. including hemorrhagic cerebral vascular accident. Thromb o lyti c C omp li cations Complications of IV thrombolytic therapy include the inability to open 20Yo of occluded coronary arteries. inferior or RV AMI New bundle branch block LV dysfunction Chest pain and ECG changes persist after administration of sublingual nitroglycerin Age <75 yr. those younger than 65 years old. continued presence subgroup analysis could only prove a benefit in patients treated within the first 6 hours after pain onset. Only small absolute differences were found between thrombolytic agents. treated or untreated Any other reason that would result in a signilicant bleeding hazard . which persists after thrombolysis. The most common reason for exclusion is symptoms without ECG ST:elevation. catalyzingthe conversion of plasminogen to plasmin. 120 ) diastolic Major surgery or trauma less than 2 weeks before or spinal or intracranial surgery within 2 months Cerebral aneurysm. in terms of lives saved and major complications. Contraindications to thrombolytic therapy Absolute Relative Hemorrhagic cerebrovascular accident within last 6 months Uncontrollable acute hypertension (>180 systolic. serious bleeding complications (3%). t-PA has the shortest half-life. patients treated after 70 minutes had a more "normal" AMI mortality rate of 9o/o. though both agents result in recanalization of infarct-related coronary arteries. or to patients with a history of a recent streptococcal throat infection.2%with initiation of treatment within 70 minutes. Thrombolytic therapy limitations include limited applicability (only 15 to 25oh eligibility).

A normal or nonspecific ECG does not exclude ischemia nor should it negate the need for treatment and hospital admission. the most prevalent is loss of critical left ventricular muscle mass secondary to AMI. the time to initial balloon inflation has been less then 60 minutes from presentation. such as oxygen. and most importantly. and reducing mortality. and no increase in hospital costs were noted. judgment. Nearly 70% of these patients will have severe multivessel coronary . If the projected time to PTCA is longer than 60 minutes and the patient meets eligibility criteria. In many patients. The benefit of magnesium has not yet clearly been determined. The ED observation unit charges range from $1. is the loss of myocardial pump function resulting in poor perfusion to the rest of the body. morphine. only 18% of hospitals perform PTCA. This provides a rapid" cost-effective way to rule out AMI for large numbers of people. preserving myocardium. lower rates of death and recurrent ischemia. Rapid return to baseline or normalization of the ST segment suggests opening of the occluded vessel. it is most important for the emergency physician to recognize and admit patients with AMI and unstable angina. Primary PTCA appears to be the best overall strategy for ART for those who are ineligible or poor candidates for thrombolysis and when it is available in less than 60 minutes. the elderly. in the ED it is usually guided by physical examination and clinical parameters. a more rapid method of ruling out or ruling in AMI in the outpatient setting is more likely to be used" not only to decrease hospitalization. 7 4o/o of patients were ruled out in the ED observation unit and were released home. which are frequently overlooked in routine ED management despite all of their advantages and benefits. then thrombolysis should be considered and is indicated. and left atrial myxoma. are treatment adjuncts that are universally available. the history. Patients with multivessel disease. Although treatment is urgent and optimally guided by hemodynamic monitoring. More important Disposition An undiagnosed AMI is the fourth most common clinical entiry but ranks first with respect to monetary awards for malpractice suits against emergency physicians. Patients with AMI who do not experience a decrease in ST:elevation may therefore be candidates for PTCA. These should be considered in all patients without specific contraindications. Additionally. Mortality rates range from as low as 30%o with aggressive reperfusion strategies to as high as 80% to90Yo if untreated.000 to $2. reinfarction.74 / EuencrNcy MnorcrNr: THr Conn CunrucuLUM reperfusion. clinical assessment. and those who have undergone previous bypass surgery. Routine use of antiarrhythmics is not recommended universally. and death.3. For cardiogenic shock it is clearly the treatment of choice. Such decisions continue to be based on risk factors.000. those in cariogenic shock. short-stay treatment and diagnostics for patients with chest pain. As managed care progresses. In three randomized trials. Additionally. PTCA PTCA is probably superior to thrombolysis in patients it can treat the underlying fixed obstructed coronary artery lesion in addition to relieving the acute thrombosis. and trained staff must be on call 24 hours a day with cardiothoracic surgery backup. PTCA is more with AMI because effective in preventing reocclusion of the infarct-related artery. 8Yo to 30% of patients have unfavorable anatomy upon angiography. Etiology Although several etiologies are possible.3) Cardiogenic shock is a dramatically presenting entity that. In all published studies to date. myocarditis. At two institutions that use ED chest pain observation units. The average observation stay was l2 to 18 hours. it affects virtually every organ system and is a leading cause of inpatient mortality after AMI.000. but also to target patients expected to benefit most from aggressive therapy. For patients with AICS. Many hospitals use ED observation units to deliver low-cost. and betablockers. These effects are particularly evident in patient subgroups with increased risk of bleeding complications. aspirin. Cardiogenic Shock (2. do worse with primary PTCA. Conclusion The standard of care is now reperfusion therapy for all patients who meet eligibility criteria. Most importantly. Studies of primary PTCA have shown it to be effective in obtaining infarct-related artery patency. less in-hospital complications. whereas the hospital bill for inpatient evaluation was in excess of $5. The time constraint is a major limitation of primary PTCA. no intracranial hemorrhage. 2. Another 24oh were admitted with changes in their ECG. changes in the CKMB levels. recurrent unexplained symptoms. A small or negligible change may indicate lack of reperfusion.1%. depending on time of arrival and whether stress testing was done after the period of observation. heparin has a clear role. simply defined. the "miss" rate for sending home a patient with AMI was less than 0. and it has a lower incidence of recurrent ischemia. acute valvular failure. however. including cardiomyopathy. or positive stress thallium testing. nitroglycerin.

Presentation Patients with cardiogenic shock are typically older. Clinically these patients have the classic signs of shock: cyanosis. All cardiac sounds. Tachycardia causes increased myocardial oxygen con- sumption that worsens preexisting ischemia and decreases the time during which left ventricular filling occurs. massive pulmonary embolism. Vasoconstriction augments preload" which initially improves ventricular function. resulting in decreased stroke volume. pulmonary edema. and the classic ECG findings of AMI. or peripheral edema if underlying ventricular dysfunction is chronic. Pericardial tamponade may have the classic findings of Beck's triad (JVD. however. papillary muscle rupture. impedes ventricular ejection. leading to worsening ischemia. and cardiac index is depressed below 2. wheezing. acute mitral insufficiency. or free wall rupture will also lead to cardiogenic shock. and right ventricular diastolic collapse. Ischemia and/or loss of contractility leads to poor cardiac output and activation of the B-adrenergic and reninangiotension systems to improve vital organ perfusion. aortic catastrophes. Definitive diagnosis is made echocardiographically with evidence of a large pericardial effusion. may be obscured by abnormalities of breathing or external noise within the ED. accessory muscle usage.Cenorovescut-AR DTsoRDERS disease. septal rupture. Cardiac examination may reveal an abnormal apical impulse or thrill. but may show cardiomegaly or a normal or small heart shadow if acute. If Swan-Ganz moni- toring capability is available. they manifest pulmonary congestion resulting in tachypnea. Tachycardia. making examination difficult. anda systolic blood pressure less than 90 mm Hg.2 Llminlm2. which decreases coronary filling and oxygen delivery in the face of accelerated myocardial oxygen demand. above 18 mm Hg. Pathophysiology Although simply defined cardiogenic shock is a complex mixture of myocardial dysfunction and neurohormonally mediated attempts to correct the situation. and circumstances precipitating the collapse may be essential in determining the etiology. More commonly the fluid accumulates less rapidly and patients appear agitated and tachypneic with hypotension. past history. Mechanical complications of AMI such as right ventricular infarction. Physical examination will reveal all or some of the previously described findings with cardiogenic shock. and salt and water retention result. ventricular aneurysm. or risk factors for pulmonary embolism. a major determinant of cardiac output. Poor underlying left ventricular function with a superimposed smaller infarction-induced loss of muscle produce the same result. medication usage. Loss of approximately 40o/o of left ventricular muscle will result in cardiogenic shock. dyspnea. Major entities to be considered in the patient with chest pain and hypotension include pericardial tamponade. weak pulses. The presentation is dramatic and diagnosis may be obvious ifAMI is noted on the ECG in patients with these symptoms. and rales or wheezes on lung auscultation. The lungs will remain clear or much less congested than expected. Afterload increases with vasocon- Diagnosis Diagnosis can be easy with shock. right atrial compression. decreased mental status. and right ventricular infarction. but may shift ventricular function detrimentally on the Starling curve and worsen pulmonary congestion. In cardiogenic shock. but the emergency physician usually does not have this luxury in the ED and must depend on history. or have underlying conditions such as congestive heart failure or diabetes. The holosystolic murmur of acute mitral insufficiency or the harsh murnur of ventricular septal rupture may be present. physical examination. have sustained an acute anteriorAMI. and often negates any gains made in ventricular hemodynamics. Otherwise. / 75 striction as well. cool and clammy skin. Additionally. increased contractility. vasoconstriction. filling pressures and cardiac output can be measured. Chest radiograph classically reveals a "water bottle" heart shadow in chronic tamponade and absence of pulmonary vascular congestion. pink frothy sputum. The net result is a vicious cycle: poor systolic function leads to poor diastolic function and worsening systolic function. History may reveal previous ischemic heart disease. Medications that depress ventricular function or affect compensatory mechanisms will may cause a tenuous situation to deteriorate into the shock state. Further attempts by the body to compensate perpetuate the cycle and ultimately result in multiple organ failure and death if left untreated. and muffled heart sounds) if fluid accumulation is rapid. jugular venous distention (JVD). During ischemia the left ventricle has difficulty compensating and malfunctions further. an S: or S+ gallop or both. decreased urine output. Aortic catastrophes must be immediately suspected when a history ofhypertension or connective tissue disease accompanies tearing chest pain radiating to the back. Hemodynamic monitoring is the most precise method of diagnosing cardiogenic shock and guiding therapy. have previous ECG evidence of AMI. and a few ancillary studies to initiate therapy. and often above 25 mm Hg. known aortic aneurysm. pulmonary capillary wedge pressure or left ventricular filling pressure is elevated. ventricular rupture. . decreased blood pressure.

5 to 5. loss of the aortic knob. Nitroglycerin is begun at 5 to l0 mcg/min and titrated upward in 5. care must be taken not to induce or worsen an existing tachycardia. negating improvement. Physical examination may reveal JVD. and preload and afterload should be judiciously reduced without worsening the imbalance in myo- cardial oxygen delivery and utilization. are most commonly utilized.0. and other findings of dissection (displacement of the trachea or esoph- or aortic calcification).to 3mcglkg/min increments every 5 to 10 minutes guided by blood pressure and peripheral perfusion is indicated for patients with systolic blood pressure greater than 80 to 90 mm Hg. hepatojugular reflux. The increased intrathoracic pressure may impede venous return and decrease preload resulting in decreased cardiac output and negate any benefit.to 7. ECG classically shows the Sr Q: T: pattern.5-mcg. Dopamine may be used alone or in conjunction with dobutamine for patients with systolic blood pressure less than 80 to 90 mm Hg.76 / EurncrNcv MnlrcrNr: Tur Conn CunrucuLUM A pulsatile abdominal mass. Right ventricular infarction usually presents with chest pain and ECG evidence of inferior AMI. but tachycardia with nonspecific ST:segment or T:wave changes is most common.to l0-minute intervals.5-mcg/kg/min range and carefully titrated upward in 1.0-mcg/kg/min range that are dose dependent.to 1S-mcg/kg/min range. while CT will delineate other mediastinal pathology and aortography identifies the arterial anatomy.. while minimizing their disadvantages. a fluid bolus should be administered and the patient examined frequently for response and to detect pulmonary edema.5. Definitive diagnosis is made by computed tomography (CT).to 50-mcg/min range. Although dobutamine is not known to produce tachycardia.5 mcglkg/min and rapidly advancing by 2.to 10minute intervals. and a shift to a more favorable hemodynamic state. Hemodynamic central monitoring should be strongly considered before instituting these agents as hypotension. Bi-PAP is being studied as well. and clear lungs on auscultation.to 5.5. apical pleural cap tants' preference. The left ventricle receives poor filling pressure with which to produce cardiac output. while noncardiogenic or right ventricular causes are sought. increased ejection fraction. The patient will continue to deteriorate unless specific interventions occur. The combination of dopamine and dobutamine is recommended at lower doses (both in the 5. Chest radiograph may reveal mediastinal widening.5. and worsening ischemia can be precipitated. begin with 2. Massive pulmonary embolism causes acute hypoxemia and affects the right ventricle directly. Should positive end-expiratory pressure be used. transesophageal echocardiography (TEE). unequal blood pressures. or acute neurologic deficits may be noted. in doses approaching 10 mcg/kg/min the Br effects intensify. Nitroprusside is begun in the 0.0. Ideally. loss of pulses. Chest radiograph is without pulmonary congestion and may demonstrate the uncommon findings of pulmonary infarction (Hampton's hump) or vessel cutoff with enlargement of the pulmonary outflow tract (Westermark's sign). Performance of the VrR and V+R leads in conjunction with the l2-lead ECG is essential for making the diagnosis. Nitroprusside and/or nitroglycerin. This author has noted that response can be expected in the 2. or usually the combination. However. Dopamine produces positive inotropic effects in the 2. Dobutamine infusion beginning at 2.to 2. Complete right-sided ECG may be beneficial.0 to 2. If the lungs are clear. Physical examination will reveal clear lungs unless heart failure is preexisting. hepatomegaly. dopamine is similar to norepinephrine and has only deleterious vasoconstrictive effects in the setting of cariogenic shock. Intervention Evaluation and treatment must occur simultaneously and with a sense of urgency.to 7. Physical examination reveals hypotension and dypsnea with minimal pulmonary findings unless congestive heart failure is preexisting.0 cm HzO and reassess the patient carefully. Response is usually noted in the 10.&g/min range) to provide the beneficial effects of both. Restoration of coronary perfusion with myocardial systolic and diastolic function is the ultimate goal. this therapy will reduce both preload and afterload" causing improved diastolic filling. Nitroprusside does have the potential for decreasing coronary flow by inducing widespread arterial dilatation at low .5-mcg/kg/min range. or aortography. In doses approaching 20 mcglkglmin. Contractility must be improved. Hypotension may occur as the right ventricle cannot supply the needed left ventricular filling pressure. If pulmonary congestion is improved and if systolic blood pressure has improved to approximately 100 mm Hg. then vasodilator therapy can be very carefully begun to improve pulmonary congestion by reducing preload and afterload. All are very sensitive and specific and the decision may rest with availability and the consulagus. causing tachycardia and cr-mediated vasoconstriction that will increase both preload and afterload.to 10-mcg/min increments at 5. Findings of rales or pulmonary edema indicate the need for inotropic support and discontinuation of the fluid bolus.0-mcg/kg/min increments at 5. Endotracheal intubation and 100% oxygen delivery alone may be adequate. TEE is portable. Oxygenation with 100% oxygen is crucial and delivered by either endotracheal intubation and positive end-expiratory pressure or continuous positive airway pressure (PAP) techniques. Favorable response is usually noted in the 7. decreased coronary blood flow. Nitroglycerin used by the patient may exacerbate the hypotension and is a clue to the presence of right ventricular infarction.

and ST:-seg- ment elevation persists beyond 2 weeks following AMI. pseudoaneurysm. In the early stages. True Ventricular Aneury sm Treatment Surgical removal ofthe aneurysm and or anticoagulant therapy is indicated when there is refractory heart failure events. Severe shock states unresponsive to these pharmacologic measures will require consultation for placement of a ventricular assist device to temporize until a revascular- necrotic tissue. Most patients are minimally symptomatic. It is a complication of AMI resulting most often from rupture of the ventricle. It is emphasized that hemodynamic monitoring should be instituted prior to use of these agents. 3. This process begins within hours of a transmural infarc- tion and progresses over the first week. and predisposi- tion to recurrent ventricular arrhythmias and sudden death. The wall reported have resulted from complications of the pseudoaneurysm. or an aneurysm producing refractory or recurrent lifethreatening arrhythmias. Normal contractile energy is expended and virtually wasted by passive systolic out- of the aneurysm. however. neurysm. If the emergency physician has angiography and surgical support readily available. cardiomegaly. have documented the efficacy of any treatment to prevent embolic 2. but surprisingly the frequency of clinically recognized systemic embolism is low (2%o to 5oh). No controlled studies. Pseudoaneurysm A pseudoaneurysm is rare. a noted bulge is noted on the left heart border on a chest x-ray (CXR). A ventricular aneurysm causes the heart to have a mechanical disadvantage. revascularization. unlike the true aneurysm. if not. the congestive heart failure.Cenorove. Aggressive reperfusion therapy in eligible candidates is indicated in the setting of AMI with shock because ischemia is the presumed cause of the acute left ventricular dysfunction. progressive accomplished. densely fibrotic and may even calcify. rupture of a true aneurysm is rare. Most often it is noted with anterior AMI involving the left ventricular apex. noncontractile outpouching of necrotic tissue that stretches. then emergent PTCA is recommended. the anterolateral wall. is composed of pericardial adhesions and is devoid of myocardial tissue and coronary arteries. then thrombolytic agents should be utilized and arrangements made for expeditious transport to a facility where more aggressive reperfusion can occur or continue. or free-wall rupture. A true ventricular aneurysm is a circumscribed. This includes ventricular aneurysmectomy. Clinical suspicion can be confirmed by two-dimensional echocardiography (2-DE) or a radionuclide ventriculogram to differentiate a true aneurysm from a pseudoa- Disposition Patients should be transferred expeditiously to critical invasive hemodynamic monitoring can care units "l'here optimally guide pharmacologic therapy. Diagnosis Diagnosis should be considered when early or late severe hearl failure develops. A high frequency of associated mural thrombosis (15% to 77o/o at necropsy or surgery) is also noted.scur. or bacterial endocarditis. Patients may develop angina pectoris. the aneurysm contains left of cardiac surgery. appropriate consultation for placement of a ventricular assist device can be made.AR DTsoRDERS / 77 doses. The rupture and resulting hemopericardium is contained by circumferen- . Ventricu lar Aneurysm (2. Both the GISSI 2 and the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-1) trials noted a lower mortality rate (55-650/o) with streptokinase than with rt-PA (63-78%) in those patients presenting in cardiogenic shock. 4) Infarct expansion represents fixed. Survival has not been ward bulging improved with these devices unless revascularization is aneurysm may cause malalignment of papillary muscles with consequential mitral regurgitation and congestive heart failure (CHF). and the septum. but carries the drawback of requiring cardiothoracic surgical capability on standby. PTCA in small and uncontrolled studies has decreased mortality to 30oh in this setting due to the overall improvement in reperfusion. thins. Additionally. and expands. Additionally. chest trauma. regional thinning and dilatation of the infarct zone and is caused predominantly by the slipping of necrotic myofibrils. but eventually its walls become more izalion procedure can occur. permanent. Infarct expansion further predisposes to development of a true ventricular aneurysm. Nearly 75o/o of pseudoaneurysm cases transmural Chronic left ventricular aneurysm occurs in l0% to 38% of patients who survive acute transmural AMI. embolic events or a diffuse or dyskinetic left ventricular apical impulse may help in diagnosis. and a revascularization procedure can be done. and mitral valve repair or replacement if the papillary muscles are involved. Unlike pseudoaneurysm.

78 /

EnsncrNcy MsucrNn,: THE Conn CunrucuLUM

tial

adhesions between the pericardium and the epicardium. Although the precise incidence is not known, a
retrospective review by Catherwood et al. detected a
pseudoaneurysm in 0.5% of patients referred for cardiac
catheterization.

Diagnosis

Dalen JE, Gore JM, Braunwald E, et al. Six- and twelve-month follow-up
of the phase I Thrombolysis in Myocardial Infarction (TIMI) tnal. Am J
C ard io

I

1988;62:

I

79-l 85.

Dole WP, O'Rourke RA. Pathophysiology and management of cardiogenic
shock. Curr Probl Cardiol 1983;8:1-72.
Dykewicz MS, McGrath KG, Davison R. Identification of patients at risk
for anaphylaxis due to streptokinase. Arch Intern Med 1986;146:305.
Gibler WB, Gibler CD, Weinshenker E, et al. Myoglobin as an early indicator ofacute myocardial infarction. Ann Emerg Med 1987;16:851-856.
GISSI-2 (Gruppo Italiano per lo Studio della Soprawivenza nel ,Infarto

Miocardico) Effectiveness of intravenous thrombolytic treatment in

Clinically,

pseudoaneurysm may be silent or manifest
a true aneurysm. Patients with a pseudoaa

similarly to
neurysm may have worsening congestive heart failure,
recurrent ventricular arrhythmias, cardiomegaly, an
abnormal bulge on the cardiac border, systolic and dias-

tolic murmurs, and persistent elevation of the ST segment
on the ECG. Howeveq a pseudoaneurysm, unlike a true
aneurysm, is susceptible to free rupture in approximately
one-third of these patients with an invariably fatal outcome. Free wall rupture is estimated to occur in 1.5%o to
8% of transmural AML Rupture usually occurs within 5
days afterAMI. Conformation of clinical suspicion can be
made by 2-DE, radionuclide ventriculography, or invasive

cardiac catheterization and left ventricular angiography.

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ENDOCARDTTTS (2.2.4)

Etiology
While bacteria are, by far, the most common infectious
in endocarditis it must be remembered that any
organism can be the causative agent. Cases ofendocardiagent

/79

TABLE 2-11. Common pathogens in
endocarditis
Native valves
Staphylococcus aureus
Staphy lococc u s epide

Streptococcus

r m i d is

vi ridans

Enterococci
Group A p-hemolytic streptococcus
Streptococcus bovis
lV drug abusers/immunocompromised
Staphylococcus aureus
Pseuomonas
Serratia
Haemophilus
Gram-negative bacteria
Fungi
Prosthetic valves
Staphyl ococcu s e p id e rm id i s

Staphylococcus aureus
Streptococcus vi ridans
Fungi (Candida and Aspergiilis)
Gram-negative bacteria
Group D streptococcus

tis have been reported secondary to viruses, fungi, and
rickettsiae. With HIV and the rise in immunocompromised patients, these atypical organisms are becoming
more prevalent. A list of the more common offending
organisms is shown in Table 2-11.
Presentation
Endocarditis has a bimodal age distribution reflecting
valve replacement and the increase in AIDS and IV drug
usage. The older population, over age 50, is more likely
to have endocarditis after valve replacement or from
undiagnosed valve disease existing in an asymptomatic
phase. A younger population is more affected by congenital defects, IV drug abuse, and HIV
The incidence of endocarditis with a prosthetic valve is
0.5oh to 4Yo a year. The overall recurrence rate of endocarditis is 2.5%o to l7o/o but IV drug abusers (IVDAs)
have a 4lo/orecwrence rate.
The presenting symptoms of endocarditis are frustrat-

ingly vague and nonspecific. Intermittent fever (85%),
malaise (95%), dyspnea, chest pain, cough, headaches,
and anorexia are commonly reported. Rarely, there will
be neurologic complaints and/or focal CNS deficits from
emboli. In more severe cases the patient will present with
rigors, fever, chills, petechiae, hypotension, or a sepsis
syndrome. Symptoms start subclinically and progress in
severity. The mean time of presentation from onset of
symptoms is 20 days.
Endocarditis is a diagnosis easily missed if symptoms
are mild and it must always be kept in the differential.
Patients with any risk factors or a murmur presenting

80 /

ErurncpNcy MnorcrNn: TsE Conr CunrucuLUM

with fever must have this diagnosis considered and the

etations or emboli. Empiric treatment without a known

appropriate consultation or referral arranged.

organism is usually required in such cases.
ECG is usually normal unless there is extensive myocardial damage, such as from an abscess. Chest radiography is also usually noncontributory except in cases of
right heart endocarditis. Septic emboli from right heart

Pathophysiology
The pathophysiology of endocarditis is fairly simple.
People are bacteremic for short periods of time each day.
Simple acts such as brushing teeth or chewing hard
candy, as well as invasive medical and dental procedures,
introduces bacteria into the circulation. In a normal host
these bacteremic episodes are of no concern. In patients
with damaged heart valves from trauma, inflammation,
high-flow lesions, orprevious cases ofendocarditis, normal laminar flow is disrupted, allowing bacterial deposition on the irregular valves. There they flourish, worsening the valvular damage and producing the hallmark of
endocarditis, the vegetation.
Damaged valves act as foreign bodies allowing bacte-

ria

increased adherence and physical shielding from
blood flow that protect them from normal body immune
defenses. Bacteria are shed into the bloodstream, causing
the intermittent fever, other general systemic symptoms,
and characteristic physical findings and ancillary results.
Valvular damage may be severe, sometimes causing valve
rupture and acute insufficiency. Vegetations can interfere
with normal valve function, producing either stenosis or
insufficiency, or may dislodge, becoming systemic or
CNS emboli. Abscess formation at the site of vegetation
or distal emboli is common.
Diagnosis
The diagnosis of endocarditis is usually a coupling

of

clinical and laboratory evidence. Physical signs ofendocarditis are helpful when present but are absent in many
patients, especially early in the disease course. A new
regurgitant murnur is often hear{ but in IVDA patients
this is often absent or very minimal and easily overlooked. More than 50% of the patients will have vascular
lesions of septic emboli including petechiae, splinter
hemorrhages, Osler nodes, or Janeway lesions. Roth
spots, whitish spots on fundoscopic examination, thought
to be from microemboli, are present in less than l0% of
patients.

Laboratory evidence

is

largely nonspecific. Most

patients will have a leukocytosis with a shift and an elevated erythrocyte sedimentation rate. Microscopic hema-

turia is common (40 to 50%), from renal microemboli,
and is an important finding in a patient at risk.
The most productive test is the blood culture. In bacte-

rial endocarditis, properly obtained blood cultures are
almost always (80 to 90%) positive and will help guide
therapy. In cases of atypical bacterial or fungal endocarditis, blood cultures are rarely positive and the diagnosis is sometimes made on histologic examination of veg-

lesions, especially

in IVDA with S. aureus

infections,

will

appear as multiple pulmonary abscesses or areas of
pneumonia.
Echocardiography is useful in diagnosis when vegetations can be visualized but a negative examination does
not rule out endocarditis. Vegetations may be too small,

be missed on exam, or not formed yet on the grossly
infected and inflamed valve.

Intervention/Disposition

Appropriate treatment

is

depends

on the clinical

appearance of the patient. In the early stages, with mild
symptoms or fever alone, the main goal should be making the diagnosis so appropriate antibiotics can be insti-

tuted. Minimally, three blood cultures from different
sites over the course of I hour should be drawn prior to
administration of any antibiotic. In severe cases with
hemodynamic instability, antibiotics should not be withheld prior to blood cultures. For antibiotic coverage see
Table 2-12.
Indications for surgery in an active case ofendocarditis include vegetations greater than 10 mm in size, CHF,
infection uncontrolled by parenteral antibiotics, fungal
infections, abscess formation, or recurrent emboli.
Endocarditis in patients with prosthetic valves should
always have early consultation with a cardiothoracic surgeon.

Obviously, the emergency physician will not have the
results of blood cultures to guide therapy. Patients with
prosthetic valves or history of IV drug use who present
with fever should be admitted and treated for presumed
endocarditis until the blood cultures prove otherwise. All

TABLE 2-12. lnitialtreatment of endocarditis
Native valve
Penicillin G 20 million units lV (continuous or divided
q4h)
or
Ampicillin 3.0 g lV q4h plus nafcillin (oxacillin) 2.0 g lV
plus gentamicin 1.0 mg/kg q8h lM or lV
lf penicillin allergic
Vancomycin 1.0 g lV q12h plus gentamicin 1.0 mg/kg
q8h lM of lV
Prosthetic valves/lV drug abuse
Nafcillin 2.0 g lV q4h plus gentamicin 1.0 mg/kg lV q8h
plus rifampin 600 mg po qd or
Vancomycin 1 .0 g lV q12h plus gentamicin 1 .0 mg/kg
q8h plus rifampicin 600 mg po qd

Ce-mrovnscur-AR DTsoRDERS
TABLE 2-13. Antibiotic prophylaxis for endocarditis
Dental/upper respiratory procedures
po dosing
Amoxicillin 3.0 g t hr prior to procedure and 1.5 g
6 hr post or
EES
800 mg 2 hr prior to procedure and
400 mg 6 hr post or
Erythromycin 1.0 g 2 hr prior to procedure and 500 mg
6 hr post or
Clindamycin 300 mg t hr prior to procedure and
150 mg 6 hr post
lV dosing
Ampicillin 2.0 g lV/lM 30 min prior to procedure and
1.0 g 6 hr post or
Clindamycin 300 mg lV 30 min prior to procedure and
150 mg lV/po 6 hr post or
Vancomycin 1.0 g lV over t hr, starting t hr prior to
procedure; no repeat dose needed
Gl/GU procedures
po dosing
Amoxicillin 3.0 g t hr prior to procedure and

l.5gGhrpost

lV dosing
Ampicillin 2.0 g lV + gentamicin 1.5 mg/kg lV (not
exceeding 80 mg) 30 min prior to procedure, then
amoxicillin 1.5 g po 6 hr post or repeat lV dose 8 hr
after first dose or
Vancomycin 1.0 g lV over t hr, starting t hr prior to
procedure + gentamicin 1.5 mg/kg (not exceeding
80 mg) t hr prior; may repeat gentamicin 8 hr post
Pediatric dosing
As per above regimens with total dose not to exceed
adult dose; repeat doses half initial
Ampicillin/amoxicillin 50 mg/kg
EES/Erythromycin 20 mg/kg
10 mg/kg
Clindamycin
2.0 mg/kg
Gentamicin
20 mg/kg
Vancomycin

other patients need to be evaluated on an individual basis,
weighing the predisposing risk, clinical symptoms, and
ability for follow-up should cultures be positive.
Patients at risk should also be treated with antibiotics
prior to any dental or medical interventions likely to
cause bacteremia. Many of these procedures are com-

monly done in the ED, and antibiotic prophylaxis may
easily be overlooked or forgotten. See Table 2-13 for
commonly used doses.
SELECTED READING
Bayer AS, Ward JI, Ginzton LE , et al. Evaluation of new clinical criteria
for the diagnosis of infective endocarditis. Am J Med 1994;96:

2tt1l8.

Gersony WM, Hayes CJ, Driscoll DJ, et al. Bacterial endocarditis in
patients with aortic stenosis, pulmonary stenosis, or ventricular septal
defect. Circulation 1993;87 (2):12l-126.
Gibler WB, Aufderheide T. Emergency cardiac care. St. Louis: Mosby,
t994.

Lukes AS, Bright DK, Durack DT. Diagnosis of infective endocarditis.
Infect Dis Clin North Am 1993;7(1):1-8.

/ Bl

VALVULAR HEART DISEASE (2.2.5)
Valvular heart disease may produce virtually all of
the symptoms of congestive heart failure and myocardial ischemia. Furthermore, valvular dysfunction can
result from other cardiac disorders, and it should be
considered more frequently than it is. The emergency
physician (EP) can play a critical role in its prevention,
need of early intervention and treatment, prevention of
complications, and acute management of its end-stage
pathology.
Rheumatic fever is a major cause of valvular pathology. Prevention with appropriate evaluation and treatment of streptococcal pharyngitis is important for the EP
to consider.
An important task of the EP is to recognize valvular
pathology early, as most valvular lesions have an asymptomatic phase lasting several decades. With the current
capability of echocardiography to visualize valves and
monitor flow and pressures, coupled with advanced surgical valve replacement or repair techniques, early recognition is critical. Patients can be identified, followe4 and
referred for surgical intervention before irreversible cardiac damage has occurred. Young patients in the asymptomatic phase often have no primary physician and present to the ED for unrelated reasons. The EP should
ideally listen for muffnurs and other signs of asymptomatic valve pathology on all patients so that appropriate
referral can be made.
The EP should also be aware of antibiotic prophylaxis
in patients with valvular lesions (see Endocarditis,
above). Many procedures commonly done in the ED
will cause a transient bacteremia and place the patient
with altered valve morphology at risk for endocarditis.
Patients with dental injuries or about to undergo abscess
incision and drainage (I&D), anoscopy, or other invasive procedures should be questioned about past history
of heart problems as well as screened for murmurs.

Appropriate prophylactic antibiotics should be given.
Timing of administration is crucial for adequate coverage.

When the valvular pathology remains unrecognized
until it causes systemic symptoms or collapse, the EP's
duty is to resuscitate, stabilize, and recognize valvular
etiology. End-stage valvular pathology mimics or coexists with many other disease processes; unlike many
processes, valvular changes can be treated with surgery.
The EP can significantly reduce mortality with appropriate intervention and referral.

Valvular lesions vary widely in presentation. They
may be stenotic and obstruct the outflow of blood; they
may be incompetent and allow retrograde regurgitant
flow; or they may be a combination of both. Multiple
valves may be affected. Lesions can cause a slow, gradual increase in symptoms over many years; or they may
decompensate, acutely causing a previously "healthy"

trauma. 'Atypical" symptoms are common. but systolic blood pressure will increase to reflect increased blood flow while diastolic pressure will fall. Diseases that dilate the aortic wall include Marfan syndrome. idiopathic spontaneous rupture. turning chronic AI into acute AI. and in-hospital mortal- ity approaches 50%. patients the symptoms of will experience dyspnea and fatigue. This is from the widening of the aortic annular ring with vasoconstriction. and cystic medial necrosis of the aorta. diaphoresis. As pulmonary hypertension and edema worsen. Diagnosis Patients with acute AI may remain compensated for some time or present in extremis. Most lesions can be diagnosed accurately based solely upon history and physical examination. While echocardiography and cardiac catheterization are the gold standards in diagnosis and evaluation ofvalvular pathology. palpitations. Patients will have sudden dyspnea. orthopnea. pale extremities. Pathophysiology In acute AI. tertiary syphilis. and mixed stenotic and regurgitant pathology. the body compensates The top three causes of aortic insufficiency (AI) are endocarditis (active or healed). but the basic pathophysiology is essentially the same. rarely.2. and chest pain. resulting from the slow destruction of the leaflets or dilatation of the aortic annular ring. Cardiogenic shock from acute AI is very refractory to treatment. Both rheumatic heart disease and congenital unicuspid and bicuspid valves cause progressive scarring of the leaflets. Most patients die within 5 years after onset of angina and within 2 years of congestive heart failure. As end-organ perfusion drops. . rheumatic heart disease. and increased stroke volume. ankylosing spondylitis. usually from infective endocarditis. Sudden dilation of the aortic root from aortic dissection will also cause acute AI. systemic lupus erythematosus (SLE). prosthetic valve dysfunction. Acute AI occurs with the sudden failure of valve leaflets. Presentqtion Acute AI has fairly dramatic presenting signs and symptoms. Chronic AI is progressive. postural dizziness. These elevated pressures are transmitted backward. edema. as well as signs ofdecreased cardiac output such as hypotension. 5. and sudden death are common as the noncompliant hypertrophied left ventricle compresses the coronary arteries and small vessels with resultant ischemia. and congenital.82 / ElrpncrNcv MrrrcrNn: Tnn Conn CunrucuLUM person to go into cardiogenic shock. and evidence of right-sided heart failure. 1) Etiology pulmonary hypertension and edema. The increased stroke volume (SV) maintains effective CO temporarily. Antibiotic prophylaxis is recommended for all patients with AI. widening the pulse pressure. Mild AI is commonly seen in all patients over 80 years old. ascites. The effective cardiac output (CO) drops precipitously and tachycardia results. People are usually asymptomatic until their third or fourth decades of life. Complications of AI include endocarditis and aortic root rupture. with age. or past medical and family history. After symptoms appear the 5year survival drops to 75o/o. Chronic AI has a much more indolent. which increases afterload and worsens regurgitation. angina. neck or abdominal pain from excessive stretching of the carotids and aorta. and paroxysmal nocturnal dyspnea. Finally they may present with pulmonary edema. peripheral cyanosis. Those patients with disease affecting the aortic root [Marfan. angina. followed by exertional dyspnea. The regurgitation will gradually increase over many years until the compensation mechanisms fail. the left ventricular end-diastolic pressure (LVEDP) increases dramatically as blood rushes backward through the incompetent aortic valve. tachycardia. A normal apical impulse can be palpated. and. Increasing LVEDP and end-diastolic volume cause increased pulmonary pressure and a drop in CO. and rarely causes any symptomatic pathology requiring intervention. recent blunt trauma. scarred valve predisposes to bacterial deposition and endocarditis. Ventricular arrhythmias. chest pain from aortic dissection. Reiter's syndrome. Most cases (80%) are chronic. and confusion. There may be associated information depending on the etiology of the acute valve failure: fever in endocarditis. causing rapid Aortic Insufficiency (2. The blood pressure will be normal or decreased and there will not be peripheral pulse signs common in chronic AI. and hepatosplenomegaly. Ancillary tests such as ECG and CXR help in the diagnosis but are not required. Pulmonary examination reveals inspiratory rales. syphilis] are at risk for sudden root rupture. compensated course. rheumatoid arthritis. The first symptoms are exertional fatigue. They will complain of significant dyspnea and apprehension. the EP must rely heavily on physical diagnosis. The ven- tricle compensates by first dilating then by hypertrophy. Chronic AI has a more insidious presentation. The floppy. including chest wall pain from forceful left ventricular contractions. which is often refractory to all interventions. rheumatic fever.

Ifpatients show symptoms such as palpitations. Chest radiographs usually show an enlarged heart and the lung fields will range from normal appearance to frank pulmonary edema. commonly showing pulmonary edema. The murmur of chronic AI is classically a decrescendo. rheumatoid arthritis. Vasoconstricting agents (dopamine and norepinephrine) should not be used to maintain blood pressure as they will WD are seen. Duroziez's sign-a singsong bruit over the femoral arteries. Mild AI can be treated with fluid and salt restriction.Cenorovescut-A. Hypertrophic stenosis is an autosomal dominant trait with incomplete penetrance. and a normal heart size may have acute AI secondary to endocarditis. while Sz is normal or slightly decreased. Tirnnel defects are least common and consist of a congenitally narrow hypoplastic aortic outflow tract and annular ring. These patients may have a minimal or absent heart murmur. Paget's disease. Approximately 2% of the population has a bicuspid or . These patients are at increased risk for ventricu- Aortic Stenosis (See 2. blowing murmur best heard at the left sternal border in the third/fourth ICS. edema. treat as above plus vasodilators and dobutamine as in acute AI. Dobutamine is useful to increase CO but may worsen ischemia. tachycardia.2. 31 is usually normal. but more importantly to be evaluated for surgery. Valvular stenosis is also most commonly congenital. Treatment is geared toward improving forward cardiac output while heard at the left sternal border in the third/fourth intercostal spaces (ICS). or hypertrophic pathology. with sinus tachycardia and nonspecific S-T changes predominating. ECG findings usually reflect the chronic changes in the left ventricle. treatment is geared toward the severity of symptoms. The left ventricle is usually hyperkinetic with a left chest heave and an inferolateral strong apical impulse secondary to left ventricular hypertrophy (LVH).R DTsoRDERS / 83 A murmur may be difficult to hear due to tachypnea. dyspnea. increasing respiratory distress from pulmonary edema and right-sided heart failure with ascites. This condition has a worse prognosis than acute AL and pulsations in the capillary nail beds. diuretics. It may also cause abnormal placement of the mitral Int erv en t i on /D i sp o s i t i o n unicuspid aortic valve that predisposes toward later stenotic pathology. causing an idiopathic thickening of the left ventricle and outflow left bundle branch block.5. and idiopathic sclerosis.. wide mediastinum. medium pitch diastolic murmur that ends quickly as pressures equ'alize. discrete. normal heart size. A diastolic thrill may be palpable at the left sternal border. There is a widened pulse pressure. antibiotics for endocarditis.g. imize therapy. and vasodilators are the mainstays of initial treatment. and pulmonary rates. in cases of ischemia. or aortic dissection. Oxygen. Quincke's sign- lar arrhythmias and need close cardiac monitoring. mild diuresis. the diagnosis may be difficult due to the patient's critical nature. Flow may be impeded by subaortic. Conduction disturbances can be seen in cases of endocarditis. As the condition worsens. and prominent pulsations in the retinal arteries. In chronic AI. e. In acutely decompensated chronic AI. and possibly a dilated aortic root. they needed to be admitted for treatment with nitrates and diuretics. pulmonary edema. A large number of findings seen with chronic AI have been described: Corrigan's (water-hammer) pulse-a pounding. valve. rapid rise and fall of the pulse. Mueller's sign-pulsations of the ulula. The murrnur is an early phase. or aortic obstruction. Discrete lesions are 160/o of all subaortic lesions and are a congenital membranous obstruction partially blocking the outflow tract. Filling pressures and cardiac parameters should be used to max- worsen regurgitation.1) Etiology Aortic stenosis (AS) accounts for 25o/o of all vahulopathies and falls into three main types. There will be a diminished Sr as the mitral valve is closed before systole by the retrograde blood in the ventricle. and. Chest radiographs are more dramatic. Vasodilators (nitroglycerin and nitroprusside) reduce afterload and increase effective CO. valvular. DeMusset's sign-head bobbing with each systole. Patients should also be instructed about prophylactic antibiotic use for invasive procedures. ECG findings in acuteAl are minimal. rapid recognition and rheumatic heart disease. consisting of either tunnel. help LV function. Signs of LVH with strain pattern are conrmon and l0o/o of patients with chronic AI will have a reducing pulmonary edema. Other treatments should be geared toward the underlying cause. Chronic AI has a number of both peripheral and cardiac findings. Intraaortic balloon pumps will also worsen insufficiency. high-pitched. tract. Subaortic stenosis is usually congenital. Invasive monitoring should be used early because overdiuresis is common and will worsen the condition. A mid-diastolic to early systolic munnur caused by regurgitant blood forcing the anterior mitral leaflet into blood flowing from the atria to the ventricle (Austin-Flint murmur) may also be heard. and follow-up on an outpatient basis. but an S: is common. end-stage renal disease. Less common causes of AS include In acute AI. Immediate cardiothoracic surgical consultation is required. however. Of special note for the EP: IV drug abusers (IVDAs) who present with sinus tachycardia. 52 ma] be absent with the destroyed aortic valve. It is best treatment are essential for good outcome. or angina.

Presentation with symptoms of systemic or CNS emboli should include AS as a precipitating cause in the differential. and present with symptoms of dyspnea. Arrhyhmias are common with this lesion and a common cause of adolescent exertional syncope. One of the most common presentations in an older adult is new or worsening angina. In discrete and tunnel subvalvular lesions the main cause of AS is their own obstruction of the outflow tract. and ventricular arrhythmias are common. Sudden decompensation may occur if the patient suffers new atrial fibrillation (AF) as a maximally hypertrophied left ventricle may require the atrial kick to maintain cardiac output.nlar obstruction is rare. the worse the stenosis. it creates a negative pressure Venturi effect that pulls the mitral leaflet into the aortic outflow tract. and finally CHE. Additionally. even if otherwise asymptomatic. syncope. the left ventricle compensates by dilatation and hypertrophy. Older patients usually have a valr. The apical impulse is prominent and displaced inferolaterally. angina. Aortic stenosis is progressive. They also cause an increased velocity that damages the normal native aortic valve.5 cm2 is termed critical aortic stenosis. As the condition nears a premorbid state. stuttering upstroke and diminished amplitude. A systolic thrill may be palpated at the jugular notch or in the carotids. Diagnosis Signs and symptoms of AS are dependent on which type ofAS is present and its degree of progression. syncope/near- syncopal events. 51 may be normal or have a paradoxical split as the ventricular pressure causes a premature closure of the mitral valve. A left chest heave is possible in severe cases of LVH. Usually these defects are associated with other cardiac anomalies and are noted at a very early age. a discrete thickening of the proximal aortic intima.0 to 1. with 3o/o to 5%o of patients suffering sudden death per year. In IHSS there are important differences. In discrete or tunnel varieties of subaortic stenosis the murnur is identical to valvular AS. infection. Blood pressure is initially normal. less than 5%o of al7 aortic pathology. cardiac output will drop and the murmur will correspondingly decrease in intensify.8 cm2 because of the high risk of arrhythmias and sudden death. but as disease progresses the pulse pressure narrows and systolic pressure drops. these subaortic lesions have a significant valvular stenosis component. then dyspnea. First. The high flow also damages the native valves. The aortic outflow tract is normally 3 to 4 cm2. To maintain cardiac output. and sudden death. Exertional syncope occurs 3 to 4 years after onset of angina. and sudden death. Surgical repair is required when the cross section is below 0. Symptoms will worsen as the child grows and places more demand on a previously asymptomatic lesion. the anatomy of the heart is so distorted that it disrupts the tricuspid and pulmonary valves as well causes mild regurgitation. Pathophysiology The basic pathology ofaortic stenosis is obstruction of blood flow to the systemic circulation. with 50oh to 70%o of patients developing angina 2 yearc after presenting with exer- tional fatigue. A congenital web in the proximal aorta. In severe LVH. fur- ther worsening the clinical situation. The later in systole the murmur peaks. Sz is delayed and may be diminished. exertional chest pain/discomfort. CHF is responsible for 50o/oto70%o of all deaths. near syncope. Younger patients usually suffer from undiagnosed congenital lesions. congestion. Carotid pulses have a delayed. The increased LV pressures are transmitted retrograde to the pulmonary vasculature causing hypertension.ular stenosis and present with symptoms of dyspnea. An aortic valve with less than 0. and edema. mostly subaortic. but ischemia-induced ventricular fibrillation accounts for 15% to 20%o of deaths. Presentation Symptomatic presentation occurs in a bimodal distribution with median ages of 10 and 48 years. Noncompliant. and sudden death. there is a high incidence of thrombus formation. Left ventricular failure is seen within I to 2 years after development of angina and ventricular arrhythmias are very common. chest pain/angina.5 cm2. subendocardial ischemia. hypertrophic stenosis is a . A midsystolic click sometimes is heard as the stiff aortic valve snaps fully open with increasing ventricular pressure. A faint munnur may be a very worrisome sign. fever) the CO cannot be maintained and syncope is common as blood flow is directed away from the brain. In vahular AS the murmur is a harsh systolic crescendo-decrescendo ejection murrnur heard best over the right second ICS with radiation to the carotid. Idiopathic hypertrophic subaortic stenosis (IHSS) is a congenital asymmetric thickening of the left ventricle that affects the anterior mitral valve leaflet. or a general aortic hypoplasia can be present. During periods of increased demand (exercise. and endocarditis. hypertrophic myocardium requires more oxygen while simultaneously decreasing its supply by compression of the coronary arteries. symptoms are progressive with exertional fatigue.84 / EurncnNcy MtorcrNn: Tnr Conn CunrucuLUM Postvah. but lesions are not symptomatic until the opening is less than 1. AS predisposes toward thrombus formation and resulting emboli. Under conditions of high flow. By the time of symptomatic presentation. with turbulent high flow across calcified stenotic valves. Without treatment. subsequent embolization.

requiring high velocity flow. Pathophysiology In acute MI there is a sudden failure of the mitral valve. Diuresis should be avoide4 as the compensated heart may require an increased preload to maintain CO. chordae tendinae. or a history of IVDA. nonexertional. resulting in sudden severe pulmonary edema. systemic hypotension.and Marfan syndrome. Beta-blockers and calcium channel blockers help relieve symptoms but don't alter progression of disease.CarulovRscut/. left ventricular hypertrophy. the regurgitant volume is initially very small. or sudden destruction of the valve leaflet itself. If the MI is due to myocardial infarction causing papillary muscle rupture. Hypertrophic AS. Milral Insufticiency (MI) (2. there may be associated chest pain and ECG findings. In chronic MI. the cause is usually ischemia of the papillary muscles that in turns behaves like acute mitral insufficiency. Common complaints include chest pain (sharp. and ventricular ectopy. Left ventricular contraction preferentially forces large amounts of blood into the low pressure left atrium and pulmonary vasculature.2) Etiology Mitral insufficiency can either be acute or chronic. the valve becomes competent again and symptoms resolve. or in women of childbearing age who want children before valve replacement requires long-term anticoagulation. the exact opposite to valvular AS. ECG findings are usually LVH with strain. will have a component of mitral regurgitation. palpitations. a congenital condition causing a floppy mitral valve that is thought to causes of acute to l}Yo of the population. The MI are usually ruptured chordae tendinae or papillary muscle from myocardial infarction or acute leaflet rupture from infective endocarditis. Mortality in acute MI approaches 60% to 80o% even with immediate intervention. and fulminant pulmonary edema. or infection will mask symptoms of dyspnea. connective tissue disorders. dobutamine may increase CO but worsen ischemia. thought to be secondary to sterile emboli to the CNS. The difference is that with return of perfusion. Rarely. Chest radiographs usually show an enlarged heart. Similarly.R DTsoRDERS dynamic pathology. Nitrates may help angina but may worsen syncope and hypotension. anxiety. Chronic or intermittent MI presents with the symptoms of exertional fatigue or dyspnea. Serial biannual echocardiography. These procedures are normally done in younger patients as a temporizing measure until the heart finishes growing. transient ischemic attacks (TIAs). hypotension. fatigue. localized. reduce afterload (amyl nitrate). When patients become symptomatic they usually require admission for monitored diuresis. since it involves the mitral valve. MVP has been associated with endocarditis. occasionally a dilated aortic root. malignant arrhythmias. rheumatic heart disease. Balloon valyuloplasty and open commissurotomy are better tolerated in a critical patient but have an extremely high restenosis rate. or a calcified aortic valve. Very commonly ischemia or angina brought on by increased demand such as fever. the most common of which is mitral valve prolapse (MVP). Chronic MI secondary to MVP is much more atypical. Maneuvers that reduce preload (standing. hypertrophic and con- 85 gestive cardiomyopathies. Endocarditis may present with feveq hypotension. and cardiovascular collapse. with valve replacement recommended when the cross-sectional areareaches 0. and later the symptoms of pulmonary congestion such as orthopnea and short- ness Int erv enti / of breath.5. then by dilation and hypertrophy ofthe left ventri- . or increase contraction (isoproterenol) will increase blood flow and increase this murnur. The regurgitant volume may be three to four times the forward stroke volume. and of limited duration). Presentation Acute MI presents with dyspnea. pulmonary congestion or edema. prosthetic valve. Rarely. for the above maneuvers will decrease the murmur. and cerebrovascular embolic events. Females outnumber males 2:l and familial tendencies have been documented. dizziness. Valsalva). In intermittent MI. Valve replacement is definitive treatment.2. however. symptoms are intermittent and do not correlate with the severity of prolapse on echocardiography. and syncope. the presentation of chronic MI is the sequela of systemic or CNS emboli. antibiotic prophylaxis. treatment is mainly avoidance of strenuous exercise. exercise. from rest or nitrates. and sudden death. Mortality is influenced greatly by comorbid disease and left ventricular function. Cardiac output is first maintained by fluid retention.8 cm2 or the pressure gradient across the valve exceeds 50 mm Hg. usually due to the detachment of the ruptured papillary muscle. In a calm ED setting the murmur may be soft to nonexistent. tachycardia. Only a fraction of patients are symptomatic. Chronic MI can be caused by multiple processes. and close follow-up. o n/ Tre at m e n t In the early stages of asymptomatic or mild AS. Other causes of chronic or intermittent MI include papillary muscle affect up ischemia. possible ischemia. MVP has also been associated with migraines.

Half of an patients present with a gradually worsening course of dyspnea. There may be only a faint murmur or no murmur at all. Mitral Stenosis (See 2. Presentation Usually symptoms begin in the fifth decade of life. or hemoptysis. It is thought to be a congenital defect causing a redundant. and loss of the posterior hilar window on lateral views from LAE. Valsalva) will increase the intensity of MVP's classic midsystolic click (the leaflet snaps as it prolapses) and subsequent late systolic murmur. As congestion worsens. Those with significant ECG changes or regurgitant flow should be referred to a cardiologist. Treatment is limited to diuretics and fluid and salt restric- tion. and confusion. or focal neurologic defects consistent with embolic events. Untreated. Diagnosis Acute MI usually presents in a state of cardiopulmonary collapse. these symptoms generally worsen until patients present with CHF.5. Dobutamine is helpful but may worsen ischemia. Beta-blockers and calcium channel blockers have been used in some patients to alleviate symptoms. Chronic MI may be mil( presenting with only mild dyspnea or exertional fatigue. The pansystolic murmur is often masked by tachycardia.2) Etiology Almost all (90 to 99%) cases of isolated mitral stenosis (MS) are the result of rheumatic heart disease. It is common for patients to be asymptomatic during examination. even if the blood pressure is being supported. Radiographs show an enlarged left ventricle. CHF is fulminant. Very rarely others occur including infectious endocarditis. tachypnea. The other half present with new-onset atrial fibrillation. and. The latent period between the episode of rheumatic fever and development of symptoms averages 20 to 25 years. . Early consultation with a cardiothoracic surgeon is essential. more respiratory complaints occur. There may be a diminished late carotid upstroke. AF may precipitate hypotension. The ECG may show left-sided ischemia but no evidence of LVH or left atrial enlargement (LAE). LVH with strain. nor do they progress in severity. congenital malformations. If symptoms worsen. AF. An Sr and S+ are common.2. Mitral valve prolapse. Reassurance is usually effective. MVP is an exception to many of the basic rules of valve pathology and the exact pathogenesis remains unclear. In chronic MI. floppy mitral valve. asymptomatic or mildly dyspneic patients can be referred for outpatient management. Emergent cardioversion or rate control with diltiazem is appropriate. pulmonary congestion.). There is a harsh pansystolic murmur heard best at the apex with radiation to the axilla and back. Atrial fibrillation (AF) is very common in later stages of this process. ECG often shows ectopy and prolonged Q-T intervals. The increased left atrial pressure transmits to the pul- monary vasculature causing hypertension and edema. rapid airway and hemodynamic support is needed as well as oxygen and afterload reduction with nitroglycerin and nitroprusside. conduction blocks. Maneuvers that decrease end-diastolic volume (standing.r cle. idiopathic annular ring calcium deposits. The symptoms are intermittent in nature and usually provoked by stress. Radiography shows a normal cardiac silhouette and severe pulmonary edema. These measures improve forward flow and myocardial function. as well as nonspecific S-T changes in the inferior and lateral precordial leads. Onset of AF may precipitate heart failure as the left ventricle may require the atrial kick for adequate cardiac output. and left atrial myxomas.86 / Err4rRceNcy MrorcrNn: THr Conn Cunnrculul. The left atrium dilates in response to the increased pressure. findings of endocarditis. Associated chest pain is thought to be from stretching of the papillary muscle. Often MVP is associated with other connective tissue diseases such as Marfan and Ehler-Danlos syndromes. Like MI. Chest radiography is usually noncontributory. A left parasternal heave and thrill are common with ventricular hypertrophy. etc. Patients may present with a variety of symptoms such as chest or abdominal pain. and evidence of cardiac atherosclerosis (Q waves. is rarely in need of treatment. Hypotension is severe and refractory. Rarely. palpitations. MS is also very prone to thrombus formation and subsequent embolization. Intraaortic balloon pump is helpful in augmenting cardiac output. MVP requires valvular replacement. This valvulopathy is progressive with an 85% mor- tality 20 years after onset of symptoms. rales. Patients with MVP often have an abnormal body habitus such as pectus excavatum or scoliosis. Most cases of MVP are not problematic. ECG findings include LAE. this murmur is also heard best at the apex with radiation to the axilla and the back. ischemia. Int ery enti on / D i sp o s i t i o n In the setting of acute MI. the patient will need admission for diuresis and improvement of ventricular function. Like most valvular diseases chronic MI is progressive and will eventually lead to left or biventricular heart failure. pulmonary edema. Surgical valve replacement is definitive. while it may cause many disconcerting symptoms to the small subset of affected individuals.

2. Any symptoms that patients experience are usually the result of pulmonary hypertension or underlying cardiac pathologies. commissural fusion. When valvular cross section become one-half normal. The maximally dilated atrium is also very prone to arrhythmias. which produces valvular incompetence and regurgitant flow. risk of thrombus formation is extremely high. These later procedures have much lower restenosis rates in MS than in aortic stenosis. atrial ectopy. and. As the disease progresses. Significant hemoptysis may require intubation and blood with fever. systemic symptoms begin to develop. mitral stenosis. Other causes include congenital malformations. From 9% to 20o/o of MS patients suffer from embolic CVAs. it is PI in conjunction with a left-sided vahular lesion (MI. The left atrium dilates progressively as compensation until the predominant left heart failure becomes biventricular as the load on the right ventricle increases. Those vahular lesions will cause significant derange- ments requiring intervention long before severe.3) Etiology- The most common cause of pulmonary insufficiency (PI) is pulmonary hypertension with subsequent dilation of the pulmonary annular ring. Chest radiography usually shows the loss of the posterior hilar window on lateral views from LAE. the S1 opening snap may disappear as the valve becomes too stiff to open quickly. Atrial flutter and fibrillation is poorly tolerated in these patients. Venodilators and diuretics should be avoided or used very cautiously as the ventricle may require high preload pressures for adequate filling. Hemoptysis occurs from dilated bronchial venules bursting under the high pressure. IV diltiazem is indicated for rate control. The damaged mitral valve is also extremely susceptible to endocarditis from transient bacteremia. treatment should be limited to antibiotic prophylaxis for procedures. Sometimes a palpable diastolic thrill may be felt at the apex. Acute pulmonary edema is noticeable immediately. dyspnea. Rightsided heart failure produces signs such as JVD. rheumatic fever. Sometimes calcification of the mitral leaflets and annular ring can be seen. balloon vahuloplasty. Int erv enti on /D i sp o s i t i o n Since rheumatic heart disease is overwhelmingly the primary cause of MS. There is a diminished or absent apical impulse from an underfilled left ventricle. or syncope. or commissurotomy. loss of mobility. followed by IV digoxin. and edema. transfusions. Pathophysiology Pulmonary hypertension directly causes a gradual dilatation of the valvular ring. ECG is notable for LAE. With the stenotic mitral valve obstructing blood flow from the left atrium. Proper evaluation and treatment of streptococcal pharyngitis will largely prevent MS from occurring. 5. Onset of AF predisposes to acute decompensation. Pulmonary Insufficiency (2. Usual symptoms are fatigue. With the dual problems of stenosis with its blood stasis andAF. causing pulmonary hypertension. left ventricular hypertrophy. Cardioversion should be avoided unless absolutely necessary due to the risk of emboli. or AS) that precipitated the pulmonary hypertension. and infective endocarditis usually from IV drug abuse or tuberculosis. MS gives a characteristic early diabolic opening snap as the stiff valve leaflets open. ascites. and a low-pitched. MS. AF is also extremely refractory to conversion to a sinus rhythm. PI becomes . Isolated PI is very rare and rarely causes any significant symptoms in the low pressure right heart system. shortness of breath. More commonly. pressure rises.Cenuovescur-qn Drsorunns / 87 Pathophysiology In asymptomatic or very mild MS. Other Rheumatic fever causes an inflammatory reaction in the mitral valve leaflets resulting in thickening. and atrial fibrillation. AF with rapid ventricular response can cause significant cardiovascular collapse. diastolic decrescendo rumbling murmur best heard at the apex. Extra care must be taken to ensure prophylaxis during procedures and to consider endocarditis when patients present medications may mask worsening symptoms that should alert the patient and the primary care provider to a worsening condition and the need for valve replacement. and in later stages atrial fibrillation is more common than not. Late in the disease right axis deviation and right ventricular hypertrophy are noted. Diagnosis In the early stages of MS physical examination findings are subtle. Presentation Isolated PI is tolerated for may years without significant pathology or progression. the first step in its treatment is the prevention of rheumatic fever. The heart needs a long diastole to allow adequate blood to pass through the narrowed opening into the left ventricle. COPD. in 75o/o of cases.

2. much like IVDA. and papillary muscle damage. Diagnosis The physical examination of a patient with pS is characteristic. high-pitched crescendo-decrescendo systolic ejection murmur. And since the most common cause of right heart failure is left heart failure. evaluation for TI is often a search for left heart pathology.ular. and infection. body responds with right ventricular dilatation and hypertrophy. Vasodilators should be avoided as a decrease in pre- load may precipitate hypotension. patients should be monitored with serial ECGs. There may be a faint systolic murmur as blood is ejected across the damaged valves. best heard at the left second ICS. If the patient has moderate to severe symptoms. and antibiotic prophylaxis is recommended. treatment is based on the other cardiac abnormalities.. Tricu spid In s uffic ie n cy (2. and valve replace- ment should be considered if right ventricular pressure exceeds 70 mm Hg or if the gradient exceeds 50 mm Hg. dyspnea. Pathophysiology PS obstructs the blood flow from the right ventricle into the pulmonary artery. tricuspid insufficiency (TI) is a result of right ventricular dilation and failure. trauma.3) Etiology Like aortic stenosis. and syncope. The murmur of PS is classically a harsh. exercise. The pulmonary vasculature is normal. infectious endocarditis.2. pulmonary hypertension is treated with diuretics. prolapsed leaf syndrome. hypoxemia. An early right parasternal lift and a systolic thrill felt in the left second ICS and suprasternal notch are caused by RVH. ECG will show evidence of RVH with strain. The murmur will increase with inspiration (Carvallo's sign).5. endocardial cushion defects. In rare cases. blowing crescendo-decrescendo diastolic murmur at the left second ICS. Diagnosis Physical findings are subtle. Often PS is found only during the evaluation of other. The lesion is graded as mild when the pressure gradient is <65 mm Hg. moderate from 65 to 120 mm Hg. Sudden death has been reported in patients with PS. There may be an early opening snap as the stiff pulmonic valves open and 52 is widely split as the right ventricle maintains pressure longer and delays pulmonic closure. and embolic bacterial pneumonia. Arrhythmias and sudden death have been reported. more serious congenital defects. valvular replacement is required. which has a variety of causes. In severe cases there may be right ventricular hypertrophy (RVH) with a corresponding right chest heave. In severe cases. Int erv enti on /D i sp o s i t io n Isolated PI is usually well tolerated and no intervention is required. or supravalvular. Unlike aortic stenosis. To maintain cardiac oueut the critical. Other causes include rheumatic heart disease. These symptoms are exacerbated by high-output states such as fever. Pulmonary Stenosis (See 2. Chest radiography is usually normal or shows changes consistent with pulmonary hypertenslon. 4) Etiology Most commonly. the obstruction in pulmonary stenosis (PS) may be infravalvular. In te rv en ti o n/D i sp o s it i o n Treatment in the asymptomatic and mild early phases should be withheld so as not to mask symptoms. and severe if >120 mm Hg. treatment is supportive with oxygen and possibly pressor sup- port.88 / ErranRcnNcv MrorcrNn: Tsn Conn Cunnrcurutr Endocarditis can become problematic. PS in all positions is usually the result of congenital defects. Endocarditis can complicate this righfsided lesion and patients may present with fever. Chest radiography will show right ventncular enlargement and dilation of the pulmonary arrery if the lesion is supravalvular. More commonly. congenital valve deformity. ECG may be normal or have evidence of RVH in severe cases. Vasodilators are helpful but should be given very cautiously as hypotension is common if preload drops too far. but usually the only evidence of PI is a high-pitched. so ECG monitoring is Presentation PS usually remains asymptomatic for many years but eventually causes fatigue. as well as fluid retention to increase preloadind augment forward flow. valr. IV drug abuse is particu- larly prevalent in tricuspid pathology as injected particu- . 5. A prominent a-wave in the jugular veins is noted.

Diagnosis There are prominent signs of right-sided venous hyper- tension such as jugular venous distention with a pronounced c-v wave. and long-term anticoagulation are required. rumbling decrescendo diastolic murmur can be heard at the left fourth and fifth parasternal spaces. hepatosplenomegaly. Of secondary concern is the increased risk of endocarditis. This increases the venous pressure with its associated symptoms. Chest radiography shows altered right heart outlines from RAE and RVH. become sy. ECG shows RAE. and ascites are common. endocarditis is often the presenting complaint in patients with TS. When the patient suffers fromAF. predisposing to AF and other arrhythmias. Int ery enti on /D i sp o s it i on In the asymptomatic or mild phase patients may be discharged with close follow-up. however. RVH. If the mitral or aortic valves are affected as well. and a soft. and commonly atrial fibrillation. dyspnea.rnptomatic. usually results from endocarditis secondary to IV drug abuse or rheumatic fever. Right atrial dilatation occurs to increase forward flow. The intensity of the sound will increase with deep inspiration (Carvallo's sign). ECG shows evidence of RAE and atrial arrhythmias. More serious symptoms need inpatient evaluation . Chest radiography shows an enlarged right atrium and possibly a dilated superior vena cave. Pulmonary architecture will remain normal unless there is mitral or aortic comorbidity. With a stifftriis obstructed to the right ventricle. correction of the pri- mary lesion takes precedence.4) Etiology Tricuspid stenosis (TS) is an uncommon entity. In cases where the TI is the result of left heart pathology. Pathophysiology Pathophysiology With RVH the tricuspid annular ring dilates slowly causing an increasing stream ofregurgitant blood into the central venous circulation. / 89 Presentation Presenting symptoms are a result of increased systemic venous pressure. Isolated rheumatic involvement of the tricuspid is rare. Carvallo's sign. Diagnosis ture. peripheral edema. A low-pitched. More severe cases need the addition of diuretics and evaluation for valve replacement. these often dramatic symptoms will predominate. Tricuspid Stenosis (See 2. ascites. Rarely does TS cause a problem. Patients with TS exhibit signs of right-sided venous hypertension. and increased heart rates will directly decrease cardiac output. which with rapid response and other tachycardiac states are very poorly tolerated by patients with TS.2. In cases of TI secondary to left heart problems. and if found premortem. is common. and salt and fluid restriction. The valvular cross section of the normal valve is 7 cm2 and patients rarely become symptomatic until the stenosis is <1. especially AF. with normal pulmonary vascula- orthopnea. a palpable right ventricular heave. an accentuation of the murmur with inspiration. cuspid. usually mitral and aortic pathology coexist and predominate. Coexistent aortic or mitral disease usually presents symptomatically much earlier. The atrium contracting against the obstructed valve has the pressure wave deflected up the superior vena cava. and causes the right atrium to dilate. I n t erv e n t i on /D i sp o s iti o n Salt and fluid restriction is the treatment of choice for mild cases. The lowpressure right heart system needs a long diastole for adequate stroke volume. or digoxin in the chronic phase. fVD and large jugular a waves may be present. especially AF.Cenuovescur-AR DrsoRDERs late and bacterial contaminants impact first against the tricuspid valve. there may be the presenting symptoms of fatigue. rate control with diltiazem in the acute phase. and hepatosplenomegaly. valve flow This predisposes to atrial arrhythmias. ascites. causing thejugular findings. peripheral edema.5 cm2. Since the most common cause of TS is IV drug abuse. blowing holosystolic munnur best heard over the left sternal border of the xiphoid. TS can. and and peripheral edema. Common complaints include Presentqtion Symptoms are usually those of rightsided venous overload such as painful hepatosplenomegaly.5. and TS is found during their evaluation.

Erythema marginatum is painless. the diagnosis is made by recognizing fulfilling the Jones criteria. New research is now finding similar proteins in GABS and on native heart valves. Close evaluation for any left heart valvular pathology is with history or laboratory evidence of streptococcal pharyngitis should be assumed to be RF and treated mandatory. The erythrocyte sedimentation rate (ESR) is nonspecifically elevated and constitutes a minor crite- rion. Rheumatic fever (RF) is more commonly a problem in developing countries. so most patients will need inpatient admission for digoxin loading and anticoagulation. Arthralgias Elevated ESR or C-reactive protein Prolonged PR interval on ECG History of previous rheumatic fever I nt erv e ntio n/D i sp o s itio n The best treatment for RF is to prevent its occurrence. although outbreaks are still group A B-hemolytic streptococcal (GABS) infections of the pharynx. but the incidence of RF approaches 3o/o of all untreated epidemic GABS outbreaks. the latency between strep pharyngitis and onset of symptoms averages 18 days but ranges from I to 5 weeks. Jones criteria for rheumatic fever Major GABS infection. For those that do.90 / EN{uncrNcy MsorcrNs: Tnr Conr CunnrculuM by echocardiography with possible surgical intervention. and wrists) and has pain out Minor Fever Diagnosis As stated above. commonly used in EDs and clinics. Diltiazem is recommended for initial rate control. Chorea consists of random. Up to one-third of all patients do not recall having pharyngitis in the weeks preceding the onset of symptoms of RF. Additional signs and laboratory findings are outgrowths from these. reported. elbows. and remain the hallmark for both presenting symptoms and diagnosis of RF. revised in 1965. is usually difficult to convert to sinus rhythm. rheumatic heart disease (RHD) is uncommon in the U. The Jones criteria (Table 2-14) were established over 50 years ago. purposeless movements usually ofthe upper body and face. Carditis may be found in up to 40o/o of patients. Presence of two major or one major and two minor criteria TABLE 2-14. fever is usually present. Rate control of AF is critical. All other phys- Rheumatic Heart Disease direct result The migratory polyarthritis usually affects the larger joints (knees. It is frequently the only symptom and may be seen with carditis. ECG may show a prolonged PR inter- val and chest radiography may show evidence of pulmonary congestion or edema and alteration of cardiac size and shape. myocardium. Presentation Carditis Polyarthritis Chorea Erythema marginatum Subcutaneous nodules Plus evidence of recent ical and laboratory findings can be negative. pericardial effirsion. due to the widespread use of antibiotics. Treatment with antibiotics up to 7 to 9 days after GABS pharyngitis has been show to prevent development of RF. rheumatic fever/heart disease was a leading cause of death in children and the most common cause of heart disease in adults over 40 years. are . nontender lumps usually on bony prominences. ankles. RF and its subsequent valvular complications are a of of proportion to physical findings. Subcutaneous nodules are pea-sized. joints. and may present as chest pain. Carditis may and present as a new murmur. While a third of all patients don't recall a pre- ceding pharyngitis.either a positive throat culture or positive ASO titers Pathophysiology The exact mechanism of pathology remains unknown but its relation to GABS infections. and skin. or heart failure. although both younger and older patients have been described. And as one would expect. Rapid strep tests. or congestive heart failure. but for some unknown reason is not seen with arthritis.. and the almost uniform presence of antibodies to valve and joint connective tissue in affected serum suggests a hyperimmune response. and throat cultures done on presentation of RF are usually negative. The dilated right atrium accordingly. dependent on its severity. Children between 4 and l8 years ofage are at the highest risk of GABS infections. Up to half of all patients may also have mild proteinuria. Current evidence suggests that antibodies to GABS cross-react and incite damaging inflammation affecting native connective tissues. dyspnea. Etiologlt Prior to the invention of antibiotics. Now. antistreptolysin antibody (ASO) titers are usually elevated for 4 to 6 weeks and indicate recent GABS infection.S. Isolated cases of strep pharyngitis and all cases of streptococcal skin infection have not been associated with RF. nonpruritic erythematous circles found on the trunk and proximal extremities.

and others indefinitely regardless of the initial severity. or feelings of fatigue. and uniformly fatal worsening of their corrAi_ tion. No treatment has yet been shown to reduce the time course or degree of pathology. Following recovery from RF. however. mucosal bleeding. Patients should be admitted for supportive and pain control measures. clarithromycin. either in an open or closed position. With modern valves. some until age 35. Failure in the open position causes acute insufficiency. Acute valve failure. In cases ofcarditis both glucocorticoids and salicylates have been used with mixed results. paravalvular leak. and the ability to monitor the ology with echocardiograPhY. Besides the risks from open heart surgery there are the complications of acute valve failure. Eradication of any GABS should be started with parenteral benzathine penicillin (same dose as for pharyngitis. and some second. painful swollen joints. Some recommend until age 18.2 million units in adults) or a full l0-day course of penicillin V 250 mg. Hemolysis may present with orthostasis. may precipitate sudden cardiovascular collapse. ity are reduced substantially. Throat cultures are much more sensitive but much less useful in ED set- tings since results will not be known for several days. each should be The mechanical valves fall into either the caged ball or tilting disk varieties. valve degeneration. Clinical judgment as well as ability to follow-up should guide EPs in whether to treat pharyngitis with antibiotics. as stopping early has been associated with treatment failures and development of RF. qd for l0 days).000 units for children under 25 kg. pro_ gressive. The caged ball (Starr-Edwards) consists of a metal cage with a floating ball that forms a one- way valve. jaun- dice.Canorovnscur_AR DrsoRDERs insensitive in finding GABS. is early recognition of valvulopathies and intervention prior to irreversible damage. but no evidence exists as yet as to whether they prevent RF. Penicillin allergic patients may take erythromycin estolate 20 mglkg divided bid or erythromycin ethylsuccinate (EES) 40 mg/kg divided bid for 10 days. patients should always be instructed to complete the full l0-day course ofantibiotics. despite all medical management. Presentation The patient's initial complaints will depend on the valve involved and method of failure.and third-generation cephalosporins in treating GABS pharyngitis. Valve replacement is not without risks. Disadvantages are the required need of long- . Prosthetic Valves Etiology The development of prosthetic heart valves in the 1950s revolutionized the treatment of valvular heart dis- largely replaced known. New evidence has shown effectiveness of azithromycin. mech cific embo va or al focal neurologic symptoms are highly suggestive of this etiology. and 1. and problems stemming from long-term anticoagulation. while failuri in the closed position acutely blocks forward flow beyond the valve. This is usually dosed tid or qid. Complications from anticoagulation are varied but may present with easy bruising. thrombus formation. Pathophysiology There are two main categories of prosthetic valves. making follow-up difficult. ecific complicaneed close follow-up with serial physical examinations and echocardiography to watch for developing valvular disorders before irreversible myocardial changes have occurred. Key to this success. Before that. patients need prophylactic antibiotics since repeat infections with GABS and RF sequelae occur and are usually more severe. patients had a well-documented. endocarditis. The literature addressing length of prophylaxis is unsettled. Treatment for acute RF is mainly supportive. Current / gl ease. but evidence has shown bid dosing is effective but has the danger of treatment failure if even only one or two doses are missed. The tilting styles but door. g to 10 years. Their The advantage of mechanical valves is their extremely long life span of 20 years compared to tissue valves. A positive result allows for treatment but a negative result is not helpful and a culture must be done to rule out GABS infection. hemolysis. The treatment consists of either a single IM benzathine penicillin injection (600. or mental status changes in the case of spontaneous CNS hemorrhage.

20(10):569-574. and hemolysis by the mechanical action of opening and closing. incompetent valve. accounting for as many as 50oh of reported cases. nevertheless. Valve replacement patients with fever or other findings must be assumed to have endocarditis. and hemolysis is rarely a problem. year). Diagnosis is made clinically by considering symptoms and auscultating a new mu{mur.93 (6): 83-88. Acute hemolysis should not be presumed to be valve-related except during the immediate postoperative period. Homografts are human cadaver heart valves. Kronzon I. but close outpatient follow-up is mandatory because increased hemolysis is sometimes an early sign of valve failure. and thrombus formation present as acute valvular insufficiency or stenosis in the affected valve. imaging. Possible complications from anticoagulation should be investigated with appropriate clotting studies. predisposition for thrombus formation (2 to 3o/oper.75:1028-1032. Pedian'Ret 1994:15(12):490493. I nt em e ntio n/D isp o s itio n All patients with signs or symptoms suggestive of valve dysfunction must be assumed to have it until will need appropriate supportive and admission for monitoring. or formed thrombi. In proven otherwise. and sudden death. Aortic/mitral obstruction and coarctation of the aorta. Clinically significant hemolysis is suspected with jaundice. Currie PJ.In addition. are a short life span requiring replacement at 8 to 10 years and the risk ofearly degeneration and valve failure. hemodynamic support and emergent cardiothoracic surgery consultation are required. Starling MR. the causes of myocarditis are numerous and extremely variable (Table 2-15). The changing and unnatural history of valwlar regurgitation. Am J Cardiol 1995.06% to 5. Prognosis of patients with heart failure and unoperated aortic valvular regurgitation and relation to ejection fiaction. Patients with valves from the affected batches may opt for elective replacement.6) (See 13. being detected in 63% of the patients with DCM who undergo endomyocardial biopsy. SELECTED READING Aronorv WS. Evaluation of heart murmurs. Postgrz d M ed 1993 .4o/o.1 5 (I) :22-27 . Howard J. Waller BF. elevated LDH.l l(4):617-641. Tissue prostheses are either homografts or heterografts. as intracranial hemorrhage or embolic disease may be present. Disadvantages. or valve replacement if warranted. Carr Opin Cardiol 1994. and help in differentiating prosthetic valvular pathology from mimics such as pulmonary embolism and acute myocardial infarction.3) Myocarditis is an infrequent etiology of cardiac disease. Biological prostheses require no long-term anticoagulation beyond the initial postoperative stage. Am J Cardiol 1994. Follman DF.92 / ErvmncnNcv Mnorcrur: Tsr Conn CunnrculuM term anticoagulation. Fess S. Endocarditis is diagnosed by physical examination positive coupled with blood cultures. Pathology of mitral valve stenosis and pure mitral regurgitation. Acute valve failure. CIin C ardio I 1992. Ahn C.89(6):123-136.9:152-157. Myocarditis (2. significant arrhythmias. Recognition and management of acute aortic regurgitation. The low incidence of myocarditis in the population is borne out in several postmortem studies showing a range of I .17:395402 Zuppiroli A. They are usually not acceptable for younger patients. Patients with symptomatic chronic hemolysis may be treated with blood transfusions and discharged home. Pathology of aortic valve stenosis and pure aortic regurgitation. Postgrad Med 1991 .e. et al. Howard J.74:286J88. Aortic valve disease. Emergent echocardiography or fluoroscopy may be required to visualize a stuck. Ann Thorac Surg 1992. et al. Rahimtoola SH. Diagnosis Complications with prosthetic valves are a common occurrence with devastating consequences. Valvular heart disease. and peripheral smear showing red cell fragmentation consistent with mechanical' disruption. it is often associated with serious sequelae consisting of cardiac failure. Rinaldi M. The most common etiologic agents are the Enterovirus genus.2. C lin Cardiol 1994. et al. falling hematocrit. Waller BF. Management of heart failure in valve regurgitation. et al. a correctable cause of congestive heart faih:.3. Compr Ther 1994. Harris JP. Lieberman EB. However. Baxley WA.2:217-221. Heart Dis Stroke 1993. and heterografts are porcine or bovine valves or pericardial tissue that are preserved and grafted onto artificial stents for transplantation into human hosts. Blood cultures should be drawn and the patient admitted for IV antibiotics until culture results are known. Thrombus formation. Rahimtoola SH. myocarditis has a high association with dilated cardiomyopathy (DCM). paravahular leak. Fess S. Carabello BA. catheterization. Of special note is that the Bjork-Shiley valve has been associated with an unacceptably high rate of metal strut breakage and acute failure. however. Blood cultures should always be drawn and antibiotics started on all patients with prosthetic valves presenting with fever. Narural history of mitral valve prolapse. Clin Cardiol 1994. Devlin WH.53:19I-199. Bashore TM. Kramer-Fox MS. identifying and treating acute and ckonic disease. is still a risk at loh to 2o/o ayear.2. while less than mechanical valves.17 :1 50-156. with coxsackie virus being responsible for the majority of cases seen in the United States and Europe. They measures severe cases with unstable patients. Aortic regurgitation. Outcome of valvular heart disease with vasodilator therapy. . Cardiol Clin 1993. Other causative viral agents include poliovirus and echovirus. Cranial CT is mandatory with mental status changes or focal neurologic deficits.

rse. tachycardia. and a decrease in intensity of 51. palpitations.tes. and cardiac failure along with systemic involvement.ocytes occurs with autoimmune activity directed against car diac myo sin. Typically the time interval between the onset of viral illness and cardiac involvement is 2 weeks. exacerbating the clinical presenta- tion.CerurovesculAR DTsoRDERS TABLE 2-15. with new onset of cardiac abnormalities. Leukocytosis is a common finding along with an elevated erythrocyte sedimentation rate. an 33 if congestive heart failure is present. Echocardio- graphy demonstrates impaired systolic and diastolic function. cyanosis. Cardiac involvement is often focal but may be diffi. Clinical Findings The clinical features of myocarditis are extremely variable. cytotoxic T lymphocytes infiltrate the myocardium and mediate destruction of host myocardial cells in a virus-specific manner. The two defining characteristics of myocarditis are myoc)'te necrosis and interstitial mononuclear cell infiltration. but with pericardial involvement or cardiac dilation an increase in cardiac'silhouette is seen. the total QRS amplitudes are significantly decreased in the acute stage. particularly infants. The ensuing ischemic damage compounds the immune mediated response. commonly present with a fulminant course. Viralinduced myocyte necrosis predominates in the acute stage. Fungal Aspergillosis Histoplasmosis Candidiasis Actinomycosis Blastomycosis Cryptococcus Chemical Lead Arsenic Carbon monoxide / 93 and dyspnea to cardiac failure and sudden death. respiratory distress. Peripheral edema may be present in cases of severe myocarditis with accompanying congestive heart failure. Pediatric patients. The pathogenesis of the disease is not well defined yet is recognized to have two stages. Streptococcus Meningococcus Clostridium Legionella Rickeftsia sp. and a recent history of viral infection. Their symptomatology con- Pathophysiolog. pyrexia. regardless of age. dyspnea at rest and on exertion. Myoc ardial autoantibodie s re sult from myosin released from lysed myoc). Further destruction of the ml. Further complicating the pathogenesis further are reports finding damage to the coronary vessels with luminal obliteration and thrombus formation. Finally. Often a sum- Radiation therapy degree Systemic disease Systemic lupus erythematosus Connective tissue diseases Sarcoidosis lnflammatory disorders mation gallup is noted with biventricular involvement. ranging from the nonspecific symptoms of fatigue sists of pyrexia. involving both ventricles along with the pericardium. Etiologies of myocarditis Viral Coxsackie A and B Echovirus Adenovirus lnfluenza Varicella Poliomyelitis Mumps Hepatitis B Epstein-Barr Cytomegalovirus Herpes simplex Protozoan Malaria Schistosomiasis Trypanosomiasis Toxoplasmosis Medications Acetaminophen Lithium Doxorubicin Catecholamines Cocaine HIV Bacterial Diphtheria Salmonella Mycobacterium sp. An important note: 40% of patients with any viral infection may have electrocardiographic changes suggestive of myocardial involvement (Table 2-16). On pulmonary auscultation a pleural rub is frequently heard. Both left and right bundle branch blocks may occur and may remain for months. Tachycardia is a frequent finding and is classically out ofproportion to the of pyrexia. particularly congestive heart failure. In addition. In the chronic stage. Chest radiograph initially reveals a normal cardiac silhouette. The electrocardiographic findings progress serially and can often help to differentiate acute myocarditis from acute myocardial infarction. ECG characteristics of myocarditis ST elevation without reciprocal ST depression Decreased QRS amplitudes Abnormal and transient Q waves (septal Q waves) Transient Mobitz type I second-degree AV block Progression to Mobitz type ll second-degree AV block Third-degree AV block Bundle branch blocks that may persist for months . There should be a high index of suspicion for myocarditis in any patient. It is suspected that the majority of cases of myocarditis are sub- clinical and go unrecognized. a decreased ejection fraction. A directed history will often reveal an antecedent or concurrent viral infection. and precordial chest pain consistent with pericarditis. The most common presenting symptoms in the adult are fatigue. This autoimmune activity persists long after viral particles are no longer detected. and is prevalent in neonatal myocarditis. Cardiac auscultation often demonstrates a pericardial rub. ST:segment elevation without reciprocal ST:depression is one of the most common findings in acute myocarditis. the conduction system of the heart is involve4 displaying a wide array of conduction defects. Transient findings consist of abnormal Q-waves that quickly resolve along with second degree or higher atrioventricular block. and an apical murmur consistent with mitral regurgitation may be heard. or a pericardial TABLE 2-16. and with severe failure pulmonary rales are present.

the emergency physician needs to be astutely attuned to the presentation and management of the various aspects of this increasingly prevalent disease process. Pathophysiology The pericardium is composed of two distinct layers. and treatment of myocarditis. Fricker J. clinical manifestations.r effirsion. pencardial effirsions have a relatively high occurrence rate in congestive heart failure (14%). which surrounds the visceral pericardium. these agents may have a role in the later stage of myocarditis. In addition. A potential space exists in which l0 to 15 cc of pericardial fluid is normally present. Active viral myocarditis: application of current knowledge to clinical practice . Nakashima H.31:951-956. This increase in pressure primarily affects the right atrium and right ventricle. Cyclosporin has been shown to be deleterious in mice with acute myocarditis. the pericardial space allows for the accumulation of 200 cc of fluid before intrapericardial pressure rises to a significant level. If the increase in pericardial fluid is gradual. However.121:942-947. Beta-blockers should be avoided because they increase the extent of myocyte necrosis and mortality. connective tissue disorders. Poole-Wilson PA. Heart Stroke I 992. an angiotensin-converting enzyme inhibitor. hemorrhagic.90:330-339. Martin AB. Annu Rev Med 1994. Viral isolation from body fluid cultures is supportive of the diagnosis. providing a rapid and sensitive method for myocardial and body fluid viral identification. and lyme disease has made a significant contribution to the occurrence of pericardial disease. This fluid functions to reduce the friction between the layers of the pericardium as the myocardium contracts. Serial electrocardiographic findings in acute myocarditis. yet only 30% of patients with clinical myocarditis have unequivocal endomyocardial biopsies. Nonsteroidal antiinflammatory agents are contraindicated in early myocarditis because they also enhance myocardial necrosis. Given in acute myocarditis. I : I 3 5-140.rsions occur in l2%o of patients with known cardiovascular disease andthat l5Vo to 20o/o of patients with HIV have pericardial effirsions. Honda ! Katayama T. Am Heart J 199l. The efficacy of immunosuppressive therapy with corticosteroids and cyclosporin is controversial. these patients have an allograft rejection rate more than twice that of recipients who do not have myocarditis as the underlying cause ofcardiac failure. Pathology 1992. Viral myocarditis. Isolation of the virus from the myocardium is incontrovertible evidence of myocarditis. Incidence of McNulty CM. and the fibrous visceral pericardium. and virus specific immunization. In part this is largely due to patients with neoplastic disorders. Clapton WK. As pericardial fluid increases. Bourne AJ. or a combination. Interestingly. Smith NM. Intern Med 1994. Webber S. Sympathomimetic agents should be used with caution since they can cause toxic myocarditis. has been beneficial when there is significant left ventricular failure and symptoms of congestive heart failure. the rise in specific infectious diseases such as HI! tuberculosis. Inflammatory heart disease: pathogenesis. Given the incidence of pericardial disease. purulent.3) Pericardial diseases are becoming more frequently recognized in emergency medicine. Tilles JG. a collagenous-parietal layer. Anticoagulation with coumadin or heparin is initiated given the increased incidence of thromboembolic complica- tions that may occur with myocarditis. Therapy Interventional treatment for myocarditis has consisted of restricted physical activity and treatment of congestive heart failure with diuretics and digitalis glycosides. and immunologic disorders living longer with advanced medical care. Recently. Similarly.94 / EuencnNcy MnucrNr: TsB Conn Cunnrculurr. antiviral pharmacologic agents. Olinde KD. Gravanis MB. Circulation 1994. which results in impairment of cardiac function.45:481490. Although there are several promising experimental protocols involving Tcell suppression. Pericardial fluid is usually serous in characteq but may be inflammatory. Acute myocarditis rapid diagnosis by PRC in children. corticosteroids have been shown to increase viral replication and enhance myocardial necrosis. DTSEASES OFTHE PERTCARDTUM (2. but it is estimated that pericardial effi. Epidemiologic data are scarce concerning pericardial diseases. Peters NS. et al. Sternby NH. none has yet shown significant benefit. valvular heart disease (21%). 2-3). in which a specific chain of viral nucleic acid is amplified. See DM. has been employed in the detection ofa specific viral agent.115:390-392. O'Connell JB. renal failure. and myocardial infarction (15%). Myocarditis-continuing clinical and pathologic confusion.lrch Pathol Lab Med 1991.33:659466. poly- merase chain reaction (PRC). Cardiac transplantation may be considered if severe cardiac failure occurs. however. which lies adjacent to the epicardium. much larger amounts of fluid can be accommodated without major impairment in cardiac function. Byard RWi The spectrum of presentation at autopsy of myocarditis in infancy and childhood. Captopril. Rev Infect Dis 1991. SELECTED READING myocarditis. the intrapericardial pressure rises in an exponential fashion (Fig. Cardiac enzymes are helpful as they demonstrate a characteristic pattern of slow elevation and fall over a period ofdays in contrast to the abrupt rise seen in acute myocardial infarction. though definitive trials are not yet available and immunosuppressive therapy has never shown proven benefit.24:129-131. which depend on systemic venous pres- .

When pericardial pressure exceeds right atrial pressure. the most common etiology is infectious.1) Although often thought to be idiopathic. and leukemia. Bacterial causes are next with Mycobacterium tuberculosis and Borreliq burgdorferi of increasing significance. In the older patient the principal etiology is neoplastic: lung cancer. Associated signs and symptoms consist of tachycardia.1) (See 13. dyspnea. nonanginal chest pain of a pleuritic quality. the etiology ofacute pericarditis is age dependent. Coxsackie A and B predominate. lymphoma. followed by echovirus. disorders. herpes simplex. At this point. Uremia is a less common cause of pericarditis (Table 2-17). tuberculosis. Following neoplasms. resulting in decreased venous refurn to the right atrium. and Epstein-Barr virus. primarily viral. if the tance occurs.Cerurovnscur-rn DrsoRnnns / 95 TABLE 2-17. Eventually.3. The net effect can be a dramatic decrease in stroke volume of the nght ventricle. it often lasts for several days and is exacerbated by positional changes. death occurs rapidly. Pericarditis (2. To maintain cardiac output. dysphagia. breast cancer. this increase is Etiology Comments lnfectious Viral Coxsackie A and B Echovirus type 4 Adenovirus lnfluenza Cytomegalovirus Epstein-Barr virus Mumps Varicella Herpes simplex Most often associated with patients less than 30 years of age High association with the immunocompromised patient Hepatitis B Bacterial Mycobacterium sp. The patient may find relief by sitting up and lean- ing forward. 2-3.3. Frequently this chest pain is precordial or retrosternal with radiation to the left shoulder and arm. collapse of the atrium occurs. adenovirus. Viral isolation is exceedingly rare. In the immunocompromised patient. Etiology of pericarditis Pressure 200m1 100m1 Volume FlG. intermittent low-grade pyrexia. systolic and diastolic collapse of the right ventricle occurs with subsequent severe hypotension. further limiting cardiac output. Systemic diseases Systemic lupus erythematosus Rheumatoid arthritis Connective tissue disorders Sarcoidosis Myxedema Uremia I nf lammatory disorders Neoplastic disorders Lung cancer Breast cancer Lymphoma Leukemia Usually young patients but of increasing occurrence Age group is often the older patient and the pericardial effusion is often chronic in character Predominantly occurring in the older patient intrapericardial pressure is not reduced quickly. especially lying supine. The historical finding that the pain is not exacerbated by physical activity is important in helping to distinguish between pericardial . As intrapericardial pressures increase right atrial transmural pressure increases. fatigue. cytomegalovirus. Borrelia burgdorferi Staphylococcus Streptococcus Gram-negative rods Legionella Rickettsia sp. In patients younger than 30 years of age. partic- ularly M. The classic presentation is that of severe. In addition.2. and influenza. rheumatoid arthritis. infectious causes predominate. sure as the major filling mechanism. the etiologies of chronic pericardial effirsions tend to be the neoplastic disorders and the systemic diseases of systemic lupus erythematous. Often this viral illness is an upper respiratory infection that typically resolves prior to the onset of symptoms. Pressure-volume curve of increasing pericardial pressure. and the connective tissue Clinical Findings Historically the patient may relate a recent viral illness in the days to weeks preceding the onset of symptoms. a compensatory tachycardia and increased systemic vascular resisin systemic resistance ultimately maladaptive and increases the afterload. Mycobacterium may be the principal agent along with varicella. However. and night sweats.

another helpful finding is significant J-point elevation. and as a diagnostic procedure in a patient with an unresolved or enlarging pericardial effi. However. there is an eventual equalization of intrapericardial and right atrial pressures. It is best heard with the bell of the stethoscope in the lower left sternal border and cardiac apex. the classic rub is triphasic with systolic. Electrical alternans is noted infrequently (Table 2-18). ethambutol. Electrocardiographic changes in acute pericarditis Concordant ST-segment elevation except leads aVR and Vr Absence of ST-segment depression except in lead aVR and often Vr PR-segment depression J-point elevation Decrease in QRS voltage when pericardial effusion is present Sinus rhythm in 90% of documented cases lnfrequently atrial fibrillation and flutter lnfrequently electrical alternans of pericardial fluid. Small effirsions are first seen as a fluid collection posterior to the left ventricle.96 / EnrnncrNcy MeucrNr: Tnr Conn CunrucuLUM pain and ischemic cardiac pain. A pericardial friction rub is often present and of significant clinical importance because it denotes inflammation of the visceral pericardium. Most often cardiac tamponade results from an increase in pericardial fluid from metastatic tumor. The net effect is a marked drop in stroke volume and biventricular output. the cardiac silhouette may be globular. Therapy Treatment for viral and inflammatory pericarditis consists of nonsteroidal antiinflammatory medication with indomethacin being recommended most frequently. Soon right ventricular collapse follows as the pericardial pressure becomes equal to the diastolic venous pressure. the patient with cardiac tamponade presents with dyspnea. At this point right atrial collapse begins to occur and becomes complete when the intrapericardial pressure exceeds the right atrial pressure. Chest radiographic findings are typically normal unless an extensive amount of pericardial fluid is present. tuberculosis requires therapy with isoniazid. Prednisone is frequently used in cases of pericarditis with associated protracted pain and a relapsing course. Bacterial and rickettsial infections may require appropriate antibiotic therapy for periods of up to 6 months. Pericardiocentesis is indicated for cardiac tamponade with rapid decompensation. rifampicin. and prednisone.rsion. viral and bacterial infections. This rub is often described as creaking leather or the sound of walking on dry snow. A pericardial window may be the treatment of choice with those patients with a chronic pericardial effi.2) Cardiac tamponade warrants special consideration because the causes of tamponade are numerous and the mortality extremely high. suspected purulent pericarditis. a narrowed pulse-pressure . Other leading causes are idiopathic pericarditis. diastolic. Echocardiography is extremely useful in demonstrating cardiac tamponade and guiding needle pericardiocentesis. if it exceeds 25oh of T-wave voltage. concluding with a return to normality. Pericardial Effusion/Tamponade (2.rsion. Other radiographic findings may include a left pleural effr. heart rate and systemic and pulmonary venous pressures are significantly increased as compensation occurs profound and progressing hypotension. As the pericardial fluid or blood accumulates around the heart. and as a complication from diagnostic cardiac procedures. configured like a Spanish water bottle. They have been described as serial changes consisting first of widespread" concordant ST:segment elevation without reciprocal depression. PR-segment depression is thought to be sensitive and specific. In turn. Pericarditis resulting from M. and presystolic components. The rub is typically transient. The principal diagnostic study used to demonstrate pericardial effirsion is two-dimensional echocardiography. lasting only a few hours to several days.rsion or bilateral pleural effirsions. Echocardiography can demonstrate as little as 17 ml TABLE 2-18. connective tissue disorders. then T: wave inversion with the ST segment at baseline. In addition. In addition. particularly cardiac catheterization. to the often Clinical Findings Clinically. relatively rapid increases in the size of the cardiac silhouette without evidence of pulmonary congestion should alert the emergency physician to a pericardial effi. and larger effirsions may be seen anterior to the right ventricle or surrounding the heart. With large pericardial effusions. It is important to note that these changes occur in only 50o/o to 70%o of the patients with documented pericarditis. Most often this rub is biphasic with a systolic and diastolic component best heard with the patient leaning forward.3. This equalization of pericardial and diastolic venous pressure results in an inability of the right side of the heart to fill with blood.rsion. as are the prolonged nature and positional characteristics ofthe pain. Sinus rhyhm is present in 90%o of the cases documented. but occasionally atrial fibrillation and flutter have also been documented. trauma. The electrocardiographic changes in acute pericarditis result from superficial inflammation of the epicardium. anticoagulant therapy. it is strongly suggestive of acute pericarditis. tachycardia. followed by return of the ST segment to baseline with later T:wave changes.

Cardiac tamponade: a clinical or echocardiographic diagnosis? Circulation 1993. etiology followed by radiation therapy and nonspecific pericarditis. Cardiac tamponade: a clinical or . requiring needle pericardiocentesis. However. 220). however. a preservation of systolic function. Typically. ventricle 97 associated decreased blood flow through the mitral valve. consisting of decreased voltage and inverted T:waves. Other causes are chronic obstructive pulmonary disease./ Treatment of acute cardiac tamponade is emergent. C linical Finding s/Therapy The clinical presentation is not unlike that of congestive heart failure. orthopnea. and elevated systemic venous pressure as manifested by distended neck veins. and regional right atrial tamponade (Table 2-19). pulmonary embolism. varying within only 4 to 5 mm Hg of each other. resulting in decreased right ventricular compliance and elevation of systemic venous pressure. The ECG changes are nonspecific. almost any ofthe etiologies responsible for acute pericarditis can cause constrictive pericarditis.Cenuovescur-AR DTsoRDERS TABLE 2-19. severe aortic regurgitation. right ventricular infarction.87: by systolic hypotension. Right atrial and pulmonary wedge pressures are approximately equal. and decreased left ventricular filling with inspiration and TABLE 2-2O. Hemodynamically there is an equal elevation of both the right and left ventricular filling pressures. left ventricular dysfunction. Definitive diagnosis is achieved with use of twodimensional echocardiography demonstrating a large pericardial effi. Depending on the etiology of the pericardial effrrsion. and constrictive pericarditis. A paradoxical arterial pulse (pulsus paradoxus) is typically found in almost all cases of cardiac tamponade. Constrictive Pericarditis Constrictive pericarditis is an inflammatory reaction involving the lining of the pericardium. the inflammatory changes are slow and extend over a period of months to years. severe asthma. However. These patients may present with dyspnea. Etiology for a lack of pulsus paradoxus in cardiac tamponade Left ventricular dysfunction Regional right atrial tamponade Positive pressure breathing Atrial septal defect Pulmonary arterial obstruction Severe aortic regurgitation echocardiographic diagnosis? Circulation 1993. Pulsus paradoxus is absent in the patient with cardiac tamponade in the presence ofpositive pressure ventilation. Evi- . An additional finding of a swinging heart may be seen on echocardiography (Table Modified from Fowler NO. pericardiocentesis may need to be repeated. there is. with permission. In the setting of constrictive pericarditis. ifechocardiography is not available. blind pericardiocentesis should be initiated since any delay in relieving the tamponade may prove fatal. There may be intraatrial conduction defects resulting in atrial fibrillation or atrial flutter. with permission. several functional abnormalities can result in the absence of pulsus paradoxus when cardiac tamponade is present. Other echocardiographic findings consist of dilated inferior vena cava without inspiratory collapse. and these patients need to be carefully monitored for recurrence of the tamponade. A paradoxical arterial pulse is defined as an inspiratory decline of systolic arleial pressure exceeding l0 mm of Hg. In addition. left ventricular compression. Intrapericardial hemorrhage is thought to be the most common. left atrial compression. paroxysmal nocturnal dyspnea. obliterating the pericardial space. Without intervention the patient decompensates: the blood pressure drops rapidly and a fatal ventricular arrhythmia is frequently the terminal event.rsion often circumferential to the heart with right atrial and ventricular diastolic collapse. however. These symptoms do not improve with diuresis as would be the case in congestive heart failure. Common echocardiographic findings for cardiac tamponade Fluid in the pericardial space anterior to the right ventricle Right ventricular collapse during diastole Left ventricular diastolic compression Right and left atrial compression Dilated inferior vena cava without inspiratory collapse Tachycardia lnspiratory increase in right ventricular dimensions lnspiratory decrease in left ventricular dimensions "Swinging heart" Modified from Fowler NO. Because the pericardial space is occlude( this process is distinct from pericarditis. Echocardiography has the unique advantage of aiding needle pericardiocentesis. Therapy 1738-17 41. Other clinical evidence consists of diminished heart sounds on auscultation and infrequently pulsus manifested alterans. increased right filling with inspiration with associated increased blood flow velocity through the tricuspid valve. pulmonary arterial obstruction. atrial septal defect.87: 1738-1741. and lower extremity edema characteristic of elevated systemic venous pressure. cardiac tamponade is not the only cause of a paradoxical arterial pulse. Both the visceral and parietal layers are involved. It should be noted that acute rheumatic fever and myocardial infarction are very rare causes.

Infrequently.98 / EuBncsNcy MnucrNn: THn Conn CunrucuLUM dence of right ventricular enlargement may be noted on ECG secondarily to localized fibrotic obstruction of the right ventricular outflow tract. Houghton JL. Am Heart J 1994. The AV node is located in the right atrium near the coronary sinus and tricuspid valve. In the majority of individuals.91 :27 3182. which is located in the right atrium at the junction of the atrium and the superior vena cava. and the differential diagnosis of restrictive cardiomyopathy must be entertained. Emergency department echocardiography in the diagnosis and therapy ofcardiac tamponade. Like the sinus node. which conduct the impulses throughout the ventricles initiating depolarization.4) To aid in the understanding ofdisturbances ofcardiac rhythm. The primary site of impulse generation in the undiseased heart is the sinus node. mediated by acetylcholine released by the vagus nerve. Abnormalities in any portion of the normal conducting system can lead to dysrhythmias. Jehle D Martin M. Upon leaving the AV node. Parasympathetic nerve endings. Magnetic resonance imaging (MRI) is also very useful in defining the extent of pericardial thickening. The first is to slow the conduction of the impulse from the atria to the ventricles. decreased flow through this artery (as seen with an acute inferior myocardial infarction) is associated with disturbances ofnormal conduction. Taylor RW. The RBB travels down the right side of the septum separating into smaller branches. Sympathetic nerve endings. J Emerg Med l99I' 9:2711. In the vast majority (approximately 90%) of individuals. reentry. Cardiac tamponade: C irculatio a clinical or echocardiographic diagnosis? 993 . with a focus on etiology. Once the discharge leaves the sinus node it travels quickly throughout both atria. Kirkland LL. Mazurek B. n 1 FowlerNO. however. Pericardial diseases. Cril Care Clin 1992. pericardiectomy can be ineffective in alleviating symptoms because of the associated restrictive cardiomyopathy that often accompanies these two etiologies. the AV node is also innervated by both sympathetic and parasympathetic nerve endings that serve to increase and decrease conduction of impulses through the AV node. pathogenesis. the impulse travels to the bundle of His located in the intraventricular septum. pathophysiology. mediated by catecholamines.237: 929-932. There are two major features of the AV node. Echocardiography is most often nonspecific but occasionally may show pericardial thickening. In this particular situation. The other specialized feature is a long refractory period. Pericarditis and myocarditis: which is benign and which isn't? Postgrad Med 1992. in those patients in which the responsible etiology is radiation therapy or connective tissue disease. Pericardial and myocardial diseases.1(2)85-94. and treatrnent. CT scanning may fail to demonstrate pericardial thickening. Definitive treatment is pericardiectomy in patients with significant symptoms. Mohanty PK. Heart Dis Stroke 1992. Ward D. Curr Op in C ardio I 1 994. The most common causes of dysrhythmias are automaticity. The rate at which the sinus node discharges is controlled by the autonomic nervous system. Computed tomographic (CT) scanning is the most useful diagnostic modality because it can clearly demonstrate the presence of pericardial thickening. DISEASES OF THE CONDUCTION SYSTEM (DTSTURBANCES OF CARDTAC RHYTHM) (2. Maisch B. The impulse moves along the anterior interatrial myocardial band directly to the left atrium. Pericardiocentesis. Lee 913-918. Tischler D. echocardiographic. new diagnostic imaging methods. it is important for the emergency physician to be familiar with the normal conduction system of the heart. Pericardial disease. pericardial biopsy becomes a necessary diagnostic adjunct. Further specialized tracts (the anterior middle. The increased refractory period helps protect the ventricles from overstimulation in situations where the rate of impulses from the atria are excessively rapid. maximizing ventricular filling. and hemodynamic signs. Pandian NG. the blood supply to the sinus node arises from a branch of the right coronary artery. thus decreasing the rate of depolarization and the frequency of discharge. or triggered automaticity. However. Chest radiographs reveal pericardial calcifications in only 40%o of the patients with constrictive pericarditis. The cardiac silhouette is typically normal or only slightly increased in size. Ptactitioner 1993. This slowing allows time for the atria to contract. Both the RBB and LBB eventually divide into Purkinje fibers.9 :37 9-388. in up to 45o/o of indi- viduals the sinus node is supplied by a branch of the circumflex aftery.8: 699-712. The emergency physician should be aware that since both the sinus and AV nodes receive the majority of their blood supply from the right coronary artery. and posterior internodal tracts) conduct the impulse directly from the sinus to the atrioventricular (AV) node. The LBB travels 2 to 3 cm down the septum before dividing into the thinner left anterior superior fascicle and the larger left posterior inferior fascicle. FowlerNO. initiating atrial contraction. hyperpolarize the sinus node. increase the rate of firing of the sinus node. respectively. SELECTED READING RI.127 Chuttani K.87 : 17 3 8-17 41 . Other cells within the AV node can serve as the pacemaker in situations where the sinus node has failed to fire or is generating impulses at too slow a rate. Diagnosis of cardiac tamponade after cardiac surgery: relative value of clinical. Automaticity refers to the potential of . The common bundle is only approximately 12 mm in length and then divides into the right and left bundle branches (RBB and LBB). the blood supply to the AV node arises from the right coronary artery.

and initiating treatment must be modified. A low threshold for obtaining repeat or serial ECGs should be maintained. the usual order of taking a history. particularfy if dysrhyhmias occur or there is a change in the patient's condition. this measurement must be corrected for heart rate. Atrial repolarization is usually obscured by the QRS complex and not identi- fied on the ECG. Of course. E lectrocardiogram (EC G) The ECG is an invaluable tool in the recognition and diagnosis of cardiac dysrhythmias and should be quickly obtained on any patient presenting with a complaint of suspected cardiac origin. Other diagnostic modalities such as laboratory testing. ventricular dysrhythmias). Factors such as description and onset of symptoms should be identified. infarction. Their use must be individualized to specific patient needs. alleviating/exacerbating factors. The height and width of the T wave is variable and is affected by multiple factors such as ischemia. The QRS complex represents ventricular depolarization and normally ranges from 0. accessory pathways). are embryologic remnants of myocardium that can conduct impulses between the atria and ventricles. or drug effects. cardiac catheteizations. echocardiography. The normal QT interval commonly ranges between 0.9. continuous cardiac monitoring of the patient while in the ED is essential. Cardiac Monitoring While the ECG is a valuable adjunct. Simultaneously with obtaining the his- tory and instituting appropriate resuscitative measures. if the patient presents in extreme distress. hypertrophy. While it is beyond the scope ofthis chapter to give a detailed explanation ofelectro- / 99 cardiography. however. As soon as the patient's condition permits. and electrolyte imbalances. . radiography. The history is usually best obtained from patients themselves.10 seconds.42 seconds. it is important to remember that it represents the electrical activity of the heart at a single point in time. Many dysrhythmias may be intermittent. The ST segment indicates the plateau phase of ventricular depolarization. drugs. and electrophysiologic examinations may all be indicated. Variation in the QT segment often represents drug toxicities or metabolic abnormalities. bypassing the normal conduction mechanism. This may be seen with damage secondary to myocardial infarction or with drug toxicities. therefore. Prolonged PR intervals may be seen with AV blocks and drug toxicities. history of previous symptoms. a history should be obtained. however. The normal duration of the P wave is less than 0. Abnormalities of the ST segment may represent ischemia. afral fibrillation/flutter. Reentry is the most common cause of dysrhythmias and is associated with myocardial damage or the presence ofan accessory pathway. medical records.20 seconds. The T wave represents ventricular repolarization. Accessory pathways. Addressing potential life threats and instituting appropriate measures adhering to the ABCs of resuscitation is indicated. performing a physical examination. a brief description of the important complexes and intervals and how they relate to conduction is indicated. The information gathered in the history and physical examination should dictate the ordering of further tests as well as guide diagnostic and therapeutic decisions. Diagnosis History and Physical Examination As with any patient encounter in the ED. The P wave represents atrial depolarization and is best identified in leads II and Vr.10 seconds. conduction delays.33 and 0. The PR interval is used to estimate the conduction time within the AV node. The presence of associated symptoms. The ECG is helpful in diagnosing specific dysrhythmias as well as identifying the presence of cardiac ischemia/infarction. and structural anomalies (ventricular hypertrophy. EMS personnel. This is done by dividing the QT interval by the square root of the RR interval. or bypass tracts. and drugs (illicit or prescribed) should not be overlooked. additional resources such as family members.Camrovescut-{R DTsoRDERS the pacing cells ofthe heart to spontaneously depolarize and initiate the impulse for contraction. cardiac stress testing. the importance of the history and physical examination cannot be overstated. junctional rhythms. drug toxicities. Triggered automaticity occurs when an ectopic pacemaker depolarizes and becomes the dominant pacemaker. The QT interval is an indication of the total time for ventricular depolarization and repola ization. This is seen with ischemia. infarction. and abnormal repolarization.12 and 0. a directed physical examination should be quickly performed. while shortened PR intervals may represent accessory pathways (WolffParkinson-White syndrome).04 to 0. as well as identification of cardiac risk factors and the presence ofpossible allergies should also be obtained. obtaining appropriate diagnostic tests. The absence of a defined P wave indicates that the impulse did not generate within the sinus node and is seen with various dys- rhythmias (e. The normal PR interval is between 0.. Prolongation of the QRS complex may represent an intraventricular conduction delay (bundle branch block) or an impulse that originated below the bundle of His premature ventricular contraction (PVC).

Transcutaneous pacemakers should be prophylactically applied to patients with significant bradydysrhythmias. Indeed" they are often the treatment of choice in certain situations. assessment/monitoring of the vital signs. Vagul Maneuvers Measures to increase vagal tone have been shown to decrease conduction and prolong the refractory period of the AV node. the empiric administration of supplemental oxygen to all patients with suspected dysrhythmias. normal P waves and PR intervals. Many dysrhythmias can be caused or exacerbated by hypoxemia. but. The success of these maneuvers in the termination of specific dysrhyth- mias is variable. thirddegree). Transdermal and transvenous pacemakers are commonly utilized in the ED in the management of hemodynamically unstable bradydysrhythmias.1) (See 13. Electrical Therapy Electrical therapies are useful adjuncts in the treatment of the energy delivered to avoid the vulnerable period during ventricular repolarization where the electrical impulse may initiate ventricular fibrillation. and unfortunately sometimes most overlooked. The process involves passing a direct current across the myocardium in an effort to depolarize Sinus Bradycardia all of the cardiac cells. gagging. continuous cardiac monitoring. C ardioversion invo lve s synchroni zation Sinus bradycardia is characterized by a decrease in the rate of atrial depolarization secondary to a slowing of discharges from the sinus node.2. Pacemakers may also be utilized to terminate certain tachydysrhythmias [supraventricular tachycardias (SVTs). Dysrhythmias (2. Both types of pacing involve the generation of a current to the heart in order to stimulate myocardial contraction.100 / EvrncoNcy MnorclNn: Tnn Conn CunnrculuM Therapeutic Adjuncts Medicutions The most common. intravenous access. These maneuvers can be valuable in the diagnosis and treatment of certain supraventricular tachycardias. tachydysrhythmias. The use of specific antidysrhythmic medications will be discussed in the context of the specific dysrhythmias. and obtaining an ECG will be applied to all of cardiac dysrhythmias. since they are generally safe and noninvasive. Defibrillation and cardioversion are utilized to terminate certain unstable patrents. whether or not they are exhibiting overt signs of respiratory distress. 2-4. such as the sinus node. Synchronized cardioversion utilizes lower energy levels and is used with unstable tachydysrhythmias when a pulse is present. the Valsalva maneuver. Defibrillation is associated with higher energy requirements and is reserved for ventricular fibrillation and pulseless ventricular tachycardia. a dominant pacemaker. "medication" used in the care of the patient with a cardiac dysrhythmia is oxygen. Potential maneuvers include carotid sinus massage.1) In this discussion of specific dysrhythmias and their recognition and treatment.4. Since myocardial ischemia/infarction may also precipitate dys- rhythmias.or trifascicular blocks in the setting of an acute myocardial infarction so that they can be quickly activated should the patient become unstable. it is assumed that the basic tenets of emergency care such as stabilization (the ABCs). bradycardia include an atrial rate less than 60 beats per minute (bpm). and oneto-one AV conduction (Fig. AV blocks (Mobitz II. 2-4). and facial immersion in ice cold water (the diving reflex). torsades de pointes]. supplemental oxygen. Transcuta- neous pacemakers have the advantage of being more eas- ily applied and initiated. is indicated. overdrive pacing allows the heart's intrinsic pacemaker to take over. can take over and transmit impulses in the normal manner. By pacing the heart at arate faster than the tachydysrhyhmia and then stopping. Sinus bradycardia. After repolarization. and patients with new bi. . they are often useful tools for the emergency physician. The ECG findings of sinus FlG.

0 mg) Epinephrine 0. is based on the patients condition. dopamine. hypothyroidism. of 3. Sinus tachycardia is a normal finding in resting heart rates of infants and small children. one-to-one AV conduction.5-1. calcium channel blockers. atenolol 5. and absence of normal P waves (the "sawtooth" flutter Sinus tachycardia. drug effects.0 mg lV. sinus bradycardia may occur in settings unrelated to pathologic processes such as during sleep. treatment should begin with transcutaneous pacing. Treatment of sinus bradycardia / 101 Sinus Tachycardis Rarely requires treatment Search for underlying causes (e. epinephrine.. for example Pathologic conditions associated with sinus tachycardia include hyperpyrexia. seda- Sinus tachycardia rarely requires treatment. acute Ml) and institute appropriate treatment. and increased intracranial pressure. If the patient is asymptomatic. lf hemodynamically unstable Transcutaneous pacemaker Atropine 0. sinus tachycardia may represent pathologic conditions or drug effects.9. Clinical manifestations vary based on the etiology. digoxin. Medications that can cause sinus tachycardia include cocaine. 1.0-3. or in conditioned ath- measures should be aimed at eliminating the underlying cause(s). 1) Atrial flutter is a dysrhythmia that usually originates in the right atria. benzodiazepines may be useful (Table 2-22). There are many etiologies of sinus bradycardia. vagal maneuvers. and usually normal P waves and PR intervals (Fig. xanthenes. TABLE 2-22. and sympathomimetics.0 mg lV (may repeat up to 15. treatment may be required with administration of beta-blockers.0 mg total dose) Benzodiazepines-diazepam 2. addressing possible pathologic causes and continued monitoring are indicated. fever) and institute appropriate treatment lf unstable or suspect ongoing cardiac ischemia Beta-blockers-propranolol 1. agents such as atropine. Furthermore.9. hypovolemia.0-2. Bz-agonists. atropine. 2-5. Although felt by some to be the result of a reentry circuit.0 mg lV (may repeat q 5 min as needed) lsoproterenol drip 2-10 mcg/min (drug of choice in patient status post-heart transplant) Dopamine drip 2-20 mcg/kg/min 2-s). if any. pulmonary emboli. ECG characteristics ofatrial flutter include a regular atrial rate ranging from220 to 350 bpm (usually around 300 bpm). beta-blockers. emotional stress. Treatment of sinus tachycardia Rarely requires treatment Search for underling cause (e.4.0 mg lV (especially useful in setting of cocaine toxicity) . Other etiologies may be the result of certain medications. hypoxia. or narcotics.0 mg lV (may repeat q 5 min to total dose Sinus tachycardia occurs when there is an increase in atrial depolarization secondary to an acceleration of discharges from the sinus node. or be physiologic. Like sinus bradycardia. epinephrine. and isoproterepol may be utilized (Table t tt\ FlG. hypothyroidism.0 mg lV. the exact mechanism is unknown.. hyperthyroidism. If a pacemaker is not immediately available. In the setting of cocaine toxicity.5-1. In the rare instance where sinus bradycardia causes hemodynamic compromise.CRnorovescur-AR DTsoRDERS TABLE 2-21. drug effects. ischemia or infarction. Atrial Flutter (2.0-5. The need for teatment. Physiologic etiologies of sinus tachycardia are exercise. The characteristics of sinus tachycardia seen on ECG are an increased atrial rate (usually between 100 and 160 bpm). Some are representative of pathologic causes such as acute inferior myocardial infarction. and congestive heart failure (both high. Initial tives. and fear. lorazepam 1. pulmonary embolus. In the setting of suspected ongoing myocardial letes.and low-output states).

hypokalemia. control ofthe ventricular response is the immediate goal. acute myocardial infarction (AMI).25 mg/kg lV (may repeat at 0. congestive cardiomyopathy.0. Vagal maneuvers or an intravenous dose of adenosine may be helpful in making the diagnosis by decreasing the ventricular response and exposing the flutter waves. and drug toxicity (digoxin).0 mg lV. The PR interval and QRS complexes are usually normal. and aVF) (Fig. In the stable patient. blood levels should be obtained prior to administenng additional digoxin as atrial flutter is a rare consequence of digitalis toxicity. Causes of atrial flutter include ischemic heart disease. if successful. 2-6). TABLE 2-23. verapamil. digoxin. they do exhibit a low incidence (20-30%o) of conversion of atrial flutter to a sinus rhythm. Clinical manifestations of atrial flutter are dependent on the etiology. When 2:1. III. and the ventricular response. atenolol 5. thyrotoxicosis. The ventricular response depends on the degree of block at the AV node. how- eveq it seldom presents in patients without underlying heart disease.35 mg/kg if no response). If the patient is tachycardiac and hemodynamically unstable.0 mg lV (may repeattototal dose of 15. If unsuccessful. the patient's existing medical condition. 2-6.0-3. vagal maneuvers or adenosine 6. Atrial flutter. reattempt at progressively higher energy levels) lf stable. Verapamil and beta-blockers should be used with caution in patients presenting u'ith congestive heart failure (CHF) as they may exacerbate rhis condition. The above agents are used primarily for rate control. Treatment of atrial flutter lf hemodynamically unstable Synchronized cardioversion 25-50 (if unsuccessful.0 mg tv)' When rate control is achieved Procainamide 50 mg/kg/day po Quinidine 1-2 tabs q po 8-12 hr aUse with caution in the setting of CHE . and the rhythm may initially be mistaken for a sinus tachycardia. If the patient is presently taking digoxin. The block may be constant (usually 2:l) or variable. myocarditis. immediate synchronized cardioversion is indicated. repeated cardioversion at progressively higher energy levels may be necessary. consider digitalis toxicity as potential cause of dysrhythmia) Beta-blockers-propranolol 1. Once rate control has been achieved.102 / EnmncrNcy MnorcrNs: THs Cons CunrucuLUM FlG.0 mg lV" Digoxin 0 4 .6 mg lV (if patient presently on digoxin. and ischemic pain. hypoxia.0 mg rapid lV push may slow ventricular response enough to establish dysrhythmia identification Diltiazem 0. but may be variable.0-5. and beta-blockers may be utilized. hypotension. Many agents such as diltiazem. the patient frequently presents with a ventricular rate of 150 bpm. Treatment of the patient with atrial flutter is based on the clinical presentation. The patient may complain of minimal symptoms such as palpitations or mild shortness of breath or may present with severe respiratory distress. a type I antiarrhythmic such as procainamide or quinidine can be administered to help convert the dysrhythmia and prevent recurrence (Table 2-23). valvular disease. The majority of cases of atrial flutter respond to low-energy cardioversion (25-50 J). waves are best seen in leads II. initial goal is rate control lf diagnosis is unclear. The possible etiologies for atrial flutter are many. If an etiology listed above is identified" measures to correct that condition should be instituted. however. may begin continuous lV infusion at 10 mg/hr Verapamil 2. pulmonary embolism.

respiratory distress. and acute alcohol intoxication (holiday heart). If the onset of the atrial fibrillation is not clear. or verapamil (Table 2-24). The ventricular rate may be faster or slower based on preexisting cardiovascular status and the presence of certain drugs.25 mg/kg lV (may repeat at 0. ischemic heart disease. Administration of heparin or warfarin for a period of I to 3 weeks prior to cardioversion will help prevent the sequelae of arterial embolism of an intraatrial thrombus. the onset of action may be slow (mean time to conversion of approximately 11 hours). and thyrotoxicosis. Starting at 100 J and escalating doses as needed is recommended.1) Atrial fibrillation results from multiple areas within the atria continuously discharging. Patients with long-standing atrial fibrillation may remain relatively asymptomatic. and hypotension are also common presentations with acute atrial fibrillation.6 mg lV (if patient presently on digoxin. As with atrial flutter. 100 (if unsuccessful.Cenolovascur-qn Drsononns FlG. reattempt at progressively higher energy levels) lf stable. and an "irregularly irregular" ventricular response usually at 160 to 180 bpm (Fig. Treatment of atrial fibrillation lf hemodynamically unstable Synchronized cardioversion. administration of intravenous procainamide may enhance success. Once rate control has been establishe4 attempts to pharmacologically convert the atrial fibrillation to a sinus rhythm may be attempted with the use of procainamide. Many agents may be used. if the ventricular rate is controlled. acute myocardial infarction. Angina. Digoxin has long been used and is effective. TABLE 2-24. but tachycardic. continuous monitoring is indicated. While the rate of atrial electrical discharges typically ranges from 400 to 700 per minute. 103 2-7. consider digitalis toxicity as potential cause of dysrhythmia) When rate control is established Procainamide 50 mg/kg/day po Quinidine 1-2 tabs po q 8-12 hr Verapamil 24O-32O mg/day (divided tid or qid)" aUse with caution in the setting of CHF.4. therefore. the treatment of choice is synchronized cardioversion. atrial septal defects. the loss of eflective atrial contractions may precipitate congestive heart failure. Diltiazem is very effective in slowing the ventricular response. Atrial fibrillation. Vz.35 mg/kg if no response). and aVF. While it is ideal to first anticoagulate patients in atrial fibrillation of chronic or uncertain duration prior to attempting conversion of the rhythm to sinus. Atrial fibrillation usually requires higher energy levels for conversion to a sinus rhythm than does atrial flutter. the clinical manifestations seen with atrial fibrillation are variable.1. often in less than l0 minutes. however. / . if the patients condition warrants. par- ticularly with a rapid ventricular response.4-0. especially digoxin. It may also be seen with pericarditis. The QRS width is usually unaffected unless aberrant conduction exists. hypertension. control of the ventricular response is desirable. 2-7). if successful. Atrial Fibrillation (See 2. The result is a lack of orderly depolarization and effective contraction of the atria. a chaotic baseline of fibrillatory waves best seen in leads Vr. This may be caused by many ectopic foci or multiple areas of reentry. quinidine. Atrial fibrillation may be constant or intermittent. If the first attempts at cardioversion are unsuccessful. If the patient is hemodynamically stable. In patients with compromised cardiac output. Characteristics of atrial fibrillation seen on the ECG include no discernible P waves. Chronic atrial fibrillation predisposes the patient to arterial embolic events (up to l5% of patients per year). may begin continuous lV infusion at 10 mg/hr Digoxin 0. attempt to control ventricular response Diltiazem 0. V3. The most corunon conditions associated with atrial fibrillation are rheumatic heart disease. decreased conduction by the AV node results in an average ventricular response of 160 to 180 bpm. it is not recommended to convert the patient to a sinus rhythm without first instituting anticoagulants.

synchronized cardioversion is the treatment of choice. consider digitalis toxicity as potential cause of dysrhythmia) Verapamil2. reattempt at progressively higher energy levels) Reentrant SVT in a stable patien Vagal maneuvers (e. PSVT usually responds to low energy levels and it is recommended to begin at 50 J. Regardless of suspected cause.704 / EunncrNcy MnorcnE. Valsalva. if the patient presents with severe distress and hemodynamic insta- bility. COPD. may repeat at 12. carotid sinus massage) Adenosine 6. Kent's bundle) that can conduct impulses into the ventricle.g. are accessory pathways located outside the AV node (e.25 mg/kg lV (may repeat at 0.0 mg for 2 doses) Verapamil2. Like atrial flutter.35 mg/kg if no response). if successful.: TFtr Conn CunrucuLUM FlG. Symptoms range from mild palpitations to severe respiratory distress. Treatment is based on suspected etiology and patient condition. Reentry SVTs can be seen in patients with normal hearts or may be associated with rheumatic heart disease. myocardial infarction. with three-fourths of those occurring in the AV node. atenolol 5. Atenolol5. Aberrantly conducted SVTs are often mistaken for ventricular tachycardia. hypotension. may begin continuous lV infusion at 10 mg/hr Digoxin 0. mitral valve disease.0 mg lV. resulting from abnormal conduction through a bypass tract or seen with preexisting bundle branch blocks. as seen in Wolff-Parkinson-White (WPW) syndrome. Wide QRS complexes may be rate related. Bypass tracts. if successful.6 mg lV (if patient presently on digoxin..4-0. or in the presence of an accessory pathway.0 mg) lf SVT thought to be secondary to digitalis toxicity Digitalism specific antibodies (Fab) Phenytoin 15. ranges between 100 and 250 bpm have been reported.0-3. pericarditis. stimulant use. Ectopic SVTs are commonly associated with digitalis toxicity.0 mg) Overdrive pacing (rarely necessary) lf ectopic SVT Digoxin 0.0 mg lV. however.0-5. 2-8).0 mg lV Diltiazem 0.0 mg lV Diltiazem 0.9. 1. Supraventricular tachycardia.12 seconds) and a slurring of the upstroke of the QRS complex (delta wave).4) Supraventricular tachycardias (SVTs) are the result of a reentry circuit or an ectopic foci occurring above the bundle of His. and alcohol intoxication.6 mg lV (if patient presently on digoxin. myocardial infarction..0 mg/kg (infuse no greater than 25-50 mg/min) Cardioversion ineffective . consider digitalis toxicity as potential cause of dysrhythmia) Beta-blockers-propranolol 1.0 mg lV (may repeat to totaldose of 15. The AV conduction in SVTs is usually 1:1. may begin continuous lV lnfusion at 10 mg/hr Beta-blockers-propranolol 1. Supraventricular Thchycardiu 2-8.0 mg lV (may repeat to total dose of 15. hypoxemia. (2. Acute paroxysmal episodes (PSVTs) are more commonly associated with a reentrant phenomenon than with ectopic foci. The ECG typically demonstrates a regular rate of 160 to 200 bpm.4.4-0.35 mg/kg if no response). Patients with WPW may exhibit a shortened PR interval <0. The other 25Yo involve the presence of bypass tracts. The P wave is often obscured by the QRS complex and difficult to identify (Fig. The QRS complexes are usually narrow even in the setting of bypass tracts. A reentry mechanism accounts for approximately 80% of SVTs.0-5. TABLE 2-25. Treatment of supraventricular tachycardia lf hemodynamically unstable Synchronized cardioversion 50 J (if unsuccessful.0 mg rapid push (if unsuccessful. and anginal-like chest discomfort.25 mg/kg lV (may repeat at 0.0-3.

variable PR and RR intervals. Phenytoin has been traditionally utilized as the antiarrhythmic of choice with varying success. it has been associated with more adverse effects. overdrive pacing may be used. it is not recommended (Table 2-25). and a ventricular rate usually between 100 and 180 bpm. and noninvasive. PACs are very common and are seen in patients of all ages in the absence of heart disease. The P' may be difficult to identiff if it occurs early enough to be obscured by the preceding T wave. beta-blockers. Theophylline and rarely digitalis toxicity are also possible etiologies. it will not be conducted Premature atrial contractions. If the SVT is thought to be of an ectopic nature (excluding digitalis toxicity). otherwise known as "wandering atrial pacemaker. verapamil is the next of choice. ECG characteristics include P waves with three or more differ- FlG. By slowing the ventricular response.Carurovescur-AR DTsoRDERS Vagal maneuvers are often helpful to both diagnose and treat SVTs. Lidocaine and magnesium may also be used. 2-9. however. are unsuccessful. MAI occurs primarily in patients with chronic lung disease. If the PAC occurs too early during the absolute refractory period of the AV node. As the initiation of the impulse is in the atria.4. Cardioversion in the presence of digitalis toxicity is generally ineffective and may precipitate more serious dysrhythmias.2) Premature atrial contractions (PACs) arise from ectopic foci within the atria. the QRS complex is usually of normal width unless a bundle branch block exists. Mu lffi c al Atria I Tac hy c ardia Atrial Ectopy (2. Due to the abnormal P wave morphologies and the irregular ventricular rate. verapamil. Treatment of multifocal atrialtachycardia Treat underlying hypoxia (oxygen. necessary. Clinical response is variable.0 mg lVa Beta-blockers-propranolol 1. and beta-blockers. and the interval to the next sinus P wave following a PAC is longer but less than fully compensatory when compared to Multifocal atrial tachycardia (MAT). With reentry SVI vagal maneuvers can terminate the circuit by increasing the refractory period in the AV node. diltiazem. the underlying rhythm is much easier identified in cases when the diagnosis is unclear. verapamil. If vagal maneuvers agent if 105 TABLE 2-26. atenolol 5.0 g lV Verapamil 2. therefore.0-3. 2-9). the tachycardia may exacerbate associated congestive heart failure. Hypoxemia associated with the chronic lung dis- ease appears to be the major initiating factor.0 mg lV. As vagal maneuvers aie generally safe. adenosine should be administered as the drug of choice. 1. . effective. Long-term antidysrhythmic therapy with either procainamide or quinidine may be ent morphologies. Rate control has also been accomplished with magnesium. However. Adenosine will produce a transient AV block that is successful in terminating approximately 90% of reentrant SVTs. Cardioversion is ineffective (Table 2-26). it is often mistaken for atrial fibrillation. Treatment is directed toward correcting hypoxemia with oxy- gen and bronchodilators. but due to its mechanism of action as a calcium channel blocker. referral to an internist or cardiologist may be indicated.0 mg lV (may repeat to total dose of 15. ECG features include an abnormal P wave (P') that occurs earlier than the next expected sinus P wave.0 mg)a aUse with care in the setting of CHF. Verapamil is as effective as adenosine. Ectopic SVT in the presence of digitalis toxic- ity warrants the use of digoxin-specific antibody fragments (Fab).0-5. and betablockers. Once the acute event has been terminated. In rare cases. bronchodilators) Control ventricular rate Magnesium sulfate 1. medications that may be helpful for rate control include digoxin. and digoxin may also be utilized if necessary. Patients with WPW have been successfully treated with radiofrequency catheter ablation oftheir bypass tracts. they should be attempted first in the stable patient." is an irregular dysrhythmia caused by multiple atrial ectopic foci. Other medications such as diltiazem. normal (Fig. The P' has a different morphology than the preceding sinus P waves. particularly hypotension. / adenosine is ineffective.

or or "blocke(" exhibiting a P' with a QRS.orcrNr: Tsn Conn CunrucuLUM TABLE 2-27. If digitalis toxicity is suspected.5-1. Treatment of junctional rhythm May not be needed in stable patient lf bradycardic and symptomatic Atropine 0. the sinus node normally serves this function. the PACs may be a precursor to SVT. Treatment of premature atrial contractions seconds. PACs have been shown to precipitate SVI atrial flutter. Clinical effects are usually minimal. Multiple etiologies include fatigue. Clinical manifestations may include CHF and worsening of ischemic symptoms. however. COPD. and betablockers are sometimes used (Table 2-27). accelerated junctional rhythms (60 to 100 bpm). Accelerated junctional rhythms are seen with myocardial ischemia/infarction. myocarditis.5 Premature junctional contractions (PJCs) occur when an ectopic pacemaker around the AV node initiates the impulse for ventricular depolarization. In situations when no impulse from the sinus node reaches the AV node for 1. Junctional rhythms may occur with severe bradycargenerate an impulse. and aVF. Premature Junctional Contractions While the conducting tissues surrounding the AV node and bundle of His above the bifurcation can serve apace- maker for myocardial contraction. P waves may be inverted (retrograde) in leads II. If the PACs trigger sustained tachycardias. The QRS complexes are usually normal (Fig. CHF. Junctional rhythm. follow. and emotional stress. tobacco) Decrease fatigue and stress If the sinus node continues to fail to if the sinus initiated impulse is blocked from reaching the AV node.106 / ElmnctNcy Mr. or be obscured by the QRS complex. procainamide.0 mg Pacemaker lf digitalis toxicity is suspected Digitalis-specific (Fab) antibodies . antidysrhythmics such as quinidine. hypokalemia. and may precede. alcohol. and atrial fibrillation. Junctional Rhythms dias. resulting in a normal-appearing QRS complex. rheumatic heart disease. Digitalis toxicity is a potential cause and if seen in this setting. Atropine may be useful to increase the discharges from the sinus node in an effort to initiate a sinus rhythm. Myocardial ischemia/infarction and distention of the atria as seen with CHF are also potential causes. the P' may be retrograde FlG. Treatment of PACs is directed toward eliminating any underlying etiology (discontinuing drugs. and digitalis toxicity. this specialized tissue can fire. repeated impulses from the tissue surrounding the AV can establish ajunctional rhythm. initiating ajunc- tional escape beat. and digitalis toxicity. it should be treated with Fab antibodies. Treatment may not be necessary in the stable patient.0 to 1. Treat underlying cause Discontinue medications (digitalis) Avoid stimulants (caffeine. avoiding stimulants). 2-10). Transcutaneous pacing should be standing by in the rare event of severe decomposition (Table 2-28). III. Some patients may note the sensation of a "skipped beat" as a result of increased ventricular filling after the PAC. 2-10. ECG findings include a P' wave of differing morphology than the sinus P wave (as with junctional rhyhms. The PR interval is often shorter than the normal preceding PR interval. The majority of PACs are conducted normally through the AV node. Junctional rhythms are usually regular and between 40 and 60 bpm.0 mg lV repeat q 5 min to total of 3. TABLE 2-28. tobacco. and junctional tachycardias (>100 bpm) can occur. particularly if the ventricular response is slow. AV blocks. caffeine.

unsynchronized cardioversion of a tachydysrhythmia is also a potential iatrogenic (digitalis. keeping in mind that the major resuscitative medications can be administered both intravenously and endotracheally. since there is no cardiac output. 2-l 1). After each medication administration. a QRS complex that is earlier than expected and usually of normal configuration. PJCs are generally asymptomatic. 4. CHE. an attempt to circulate the drug should be made through continued CPR for 30 to 60 seconds. drug toxicity or electrolyte abnormalities. Clinically. The amplitude of the baseline may vary from very coarse deflections to an almost flat line that can be mistaken for asystole. early in the course of the dysrhythmia. hence no effective contraction occurs. Premature junctional contractions. and digitalis toxic- ity. TABLE 2-29. quinidine). Treatment of premature junctional complexes Generally asymptomatic Treatment is directed at alleviating precipitating causes (CHF. digitalis toxicity) and occur anytime in relation to the QRS complex). the patient be without pulse or blood pressure. 5) Ventricular fibrillation (VF) results from multiple areas within the ventricles spontaneously depolarizing and contracting. Furthermore. airway control and support (ideally through endotracheal intubation and bag-valve-mask). the above resuscitative measures should be started and medications given. The patient will will be apneic. cardiopulmonary resuscitation (CPR). Treatment is directed at correcting any underlying causes and continued observation for the appearance of other dysrhythmias (Table 2-29). Ventricular f ibrillation. The ECG displays an erratic baseline without defined P waves. VF may occur without warning (sudden death) with or without associated acute myocardial infarction. and a fully compensatory pause before the next sinus beat (Fig. 1. The initial three defibrillations should be delivered at 200 J. also be the result of trauma. Ml. QRS complexes. . The treatment of choice for VF is immediate defibrillation. ineffective agonal respirations may be present. cause. PJCs are rare in an undiseased heart. however.200 Io 300 J. hypothermia.Cenuovesculq-n DrsonorRs FlG. or T waves (Fig. a shortened P'R interval. the patient should be 2-12. There is no organized ventricular depolaizalion. and intravenous access should be initiated. 2-12). VF may FlG. Etiologies include myocardial ischemia/infarction. and 360 J. / 707 2-11. electric shocks. If a defibrillator is not immediately available. Iatrogenic causes include direct myocardial stimulation during transvenous pacemaker or central line placement. At this point. Ventriculsr Fibrillation (2. The ventricle appears to quiver and produces no cardiac out- put. Ifthe patient does not respond to the initial defibrillation.

VF is often a preterminal rhythm.0 mg) or high dose (b. several resuscitative drugs can be delivered via the endotracheal tube) Epinephrine 1. Therefore. 360 J) Airway control-endotracheal intubation Support ventilations-bag-valve-mask Cardiopulmonary resuscitation lnitiate intravenous access (if access not immediately available. However. however. The ECG FlG. and the decision concerning when to terminate resuscitative measures will need to be addressed on an individual basis.75 mg/kg bolus q 5 min to total dose of 3. which makes VF more susceptible to defibrillation. Sodium bicarbonate may be used to alleviate the acidosis that inevitably occurs with VF. 200-300 J. procainamide. procainamide). since the acidosis is a result of metabolic by-products of hypoxic lactic acidosis. 4. 2-13). 1. . drugs (quinidine. A QRS width of greater than 0. VT is rarely seen in the setting of a normal heart. bretylium. The first drug that should be administered is epinephrine.5 mg/kg bolus (may repeat at 0. and antidysrhythmic agents such as lidocaine.0 mg lV (may repeat q 5 min as long as the dysrhythmia persists).14 seconds suggests VT. and cardiomyopathy.0 mg/kg) Bretylium 5 mg/kg bolus (after 5 minutes may repeat at 10 mg/kg boluses q 5-30 min to total-ol 35 mg/kg) Magnesium sulfate 1. the sinus node may still be firing and depolarizing the atria. Because there is often AV dissociation. and a usually constant QRS axis (Fig. hypoxia. particularly if delivered early. Following epinephrine. and magnesium may all be utilized per the American Heart Association's Advanced Cardiac Life Support guidelines (Table 2-30). Ventricular tachycardia. In the stable patient. VT most commonly occurs in the presence of myocardial ischemia and/or infarction. It is generally thought best to assume that all wide complex tachycardias are VT. however. a P wave can sometimes be seen between the QRS complexes. there will not be a fixed relationship between the P waves and the QRS complex. and clinical presentation is of little help since both can present with similar symptomatology. it is not absolute. repeated defibrillations at 360 J should be delivered. 6) Ventricular tachycardia (VT) occurs when there are three or more consecutive beats from an ectopic ventricular focus firing at arale greater than 100 bpm. will typically display wide QRS complexes. reassessed. a usually regular ventricular rate between 100 and 220 bpm. VT is often difficult to distinguish from an SVT with aberrant conduction. Ventricu lar Tachy cardia (2. it is recommended that acidosis first be treated by hyperventilation and that sodium bicarbonate be utilized with caution.0 mg) After every medication administration. vagal maneuvers or adenosine administration are felt to be safe and may occasionally demonstrate an underlying SVT. circulate drug via CPR and repeat defibrillations at 360 J Lidocaine 1. While defibrillation is effective in some cases of VE. 2-13. It would be uncommon for VT treatment to cause harm to the patient with SVT. electrolye abnormalities. ST segments and T waves of opposite polarity to the QRS. Treatment of ventricular fibrillation lf defibrillator immediately available lmmediate defibrillations (200 J.108 / EnrnncrucyMrorcrNn: THr Conn CunnrculuM TABLE 2-3O. alkalosis. some authors recommend intermediate dose (3. Other causes include mitral valve prolapse.0 lV Procainamide 20-30 mg/min (to total dose of 17 mg/kg) Consider termination of resuscitative efforts if VF is persistent.

7) Premature ventricular contractions (PVCs) may arise from ectopic foci located in either ventricle. il successful. resulting in an abnormal P wave (Fig. Patients experiencing PVCs may be asymptomatic or may complain of palpitations. If the patient is hemodynamically stable. PVCs may occur between sinus beats without associated pauses (interpolated PVC). digoxin). the goal should be to treat the underlying ischemia and not simply to suppress the PVCs. Patients who survive episodes of VT or VF should be evaluated as to the potential need for automatic implantable cardio- defibrillators (AICDs). 2-l4).Cenotovescur-qn DrsoRnnRs / 109 TABLE 2-31. in pairs (couplets). Since the depolarization does not occur through normal pathways. which cause depolarization ofthe ventricle prior to the next expected sinus beat. may begin continuous infusion ol 2. timing. reattempt at progressively higher energy levels) lf a pulse is present. PVCs may occur alone. the resulting QRS complex is often bizarre in appearance and abnormally widened (>0. 1. drugs (stimu- lants. may begin continuous infusion of 1. Lidocaine is the first agent of choice followed by bretylium and procainamide (Table 2-31). number of ectopic foci.e.12 seconds).. Treatment of ventricular tachycardia lf pulseless. Certain nomenclature has been developed for PVCs occurring in regular patterns after every sinus beat (bigeminy). Another ECG characteristic is a missing or abnormal P wave. PVCs that occur during 2-14. if successful. PVCs seen with ischemia may represent potential instability and be a precursor ofVT orVF. Most PVCs are associated with a fully compensatory pause before the next sinus beat. The next sinus P wave is usually hidden within the PVC's QRS complex.0 mg/kg).0 mg/min The clinical manifestations of VT are varied and the treatment is dependent on the clinical presentation. PVCs are common and often occur in the absence of heart disease. hypoxemia. Since PVCs may arise from separate foci. and after every three sinus beats (quadrageminy. occasionally the PVC causes retrograde depolarization of the atria FlG.5 mg/kg bolus (may repeat at 0. Premature ventricular contractions. however. An energy level of 100 J is generally effective.0-4.O mg/min Bretylium 5 mg/kg in 50 cc NS run in over 8-1 0 min. synchronized cardioversion is the treatment of choice. If a pulse is present but the patient exhibits significant symptoms or hemodynamic compromise. the resulting QRS complexes are of differing morphologies (multifocal PVCs). and electrolyte abnormalities. if successful. however. administration of sedation andlor analgesia is desirable. the ventricular rhythm is usually irregular. and the patient is hemodynamically stable Lidocaine 1. after every two sinus beats (trigeminy).O-4. As with all cardioversion attempts. CHF. and the clinical condition ofthe patient. If the PVCs do not resolve with measures to restore myocardial perfusion. treatment may be indicated. Common causes of PVCs include myocardial ischemia/infarction. may begin continuous infusion of 2.0 mg/min Procainamide 20-30 mg/min (to total dose of 17 mg/kg). then medication administration is indicated. Due to the prematurity of the PVC. The need to treat PVCs is based on multiple factors such as their frequency. repeat dose of 5-1 0 mg/kg may be given in 10-30 min. Ventricular Ectopy (2. In the setting of acute myocardial ischemia or infarction. 4. Polymorphic Vl or VT presenting without a pulse. every fourth beat is a PVC). . is treated as VF. treat as VF (Table 2-30) lf a pulse is present but the patient is hemodynamically unstable Synchronized cardioversion 100 J (if unsuccessful. if the patient's condition permits. i.75 mg/kg bolus q 5 min to total dose of 3. or in groups of three or more (VT).

QTI nterval Sy n dro m e (2: 4.0 mg/min or immediately after the T wave (ventricular repolarization) carry a risk of precipitating VT or VF (R on T phenomena). epinephrine. TCAs. hypo/hyperkalemia. Additionally. hypovolemia. increase heart rate (pacemaker.0 mg lV (may repeat q 5 min if dysrhythmia persists) lf rate is < 60/min Atropine 0. Drugs that may precipi- tate torsades de pointes are fype IA antidysrhythmics (quinidine. electrical shocks. may begin continuous inf-usion of 1.0 mg/min Bretylium 5 mg/kg in 50 cc NS run in over 8-10 min. Epinephrine and atropine (if the rate is less than 60 bpm) are also utilized (Table 2-33). Since no electrical activity TABLE 2-33. may begin continuous infusion of 2. atropine) Lidocaine 1. lidocaine is the first drug of choice.0 mg) is present.0-4. hypoxemia. However. 8) Torsades de Pointes Torsades de pointes is an atypical form of VT in which the QRS axis appears to be constantly changing. Electrolyte imbal- ances such as hypomagnesemia. it should be noted that asystole is a preterminal rhythm that rarely responds to treatment. Pulseless Electrical Activity Pulseless electrical activity (PEA). and organophosphates. and hyperkalemia. The ECG generally demonstrates a rate of 200 to 240 bpm with the QRS axis alternating between positive and negative in the same lead.5 mg/kg bolus (may repeat at 0. 1. phenothiazines. digoxin. The patient is unresponsive and pulseless. Cessation of resuscitative measures should be considered (Table 2-34). first priority is to restore adequate oxygenation and perfusion Supplemental oxygen Support blood pressure lf significantly bradycardic. procainamide. and hypocalcemia may also contribute to the onset of torsades de pointes.110 / EnrRcrNcyMnorcrNr: Tnn Conn Cunruculuu TABLE 2-32. The appearance on the ECG may range from normal appearing complexes to chaotic. Asystole should be documented in at least two different leads because fine VF may be mistakenly identified as asystole. Other etiologic factors are myocardial ischemia/infarction. If treatment is indicated. hypokalemia. procainamide or bretylium may be utilized (Table 2-32). hypothermia. Etiologies of asystole include hypothermia. pulmonary emboli. if successful. PEA often represents profound dysfunction of the myocardium ("pump failure") and is as electromechanical dissociation generally resistant to treatment. if successful.0 mg/min Procainamide 20-30 mg/min (to total dose of 17 mg/kg). may begin continuous infusion ol 2. Asystole is the most common dysrhythmia seen in patients sustaining cardiac arrest of greater than 10 minutes. calcium channel blockers]. severe acidosis. transcutaneous pacing. repeat dose of 5-10 mg/kg may be given in 10-30 min. Torsades de pointes is felt to be secondary to a triggered automaticity mechanism. and thus there is no ventricular contraction or cardiac output. otherwise known (EMD). The ECG generally demonstrates a "flat line" (Fig. hypothyroidism.0 mg/kg). although occasionally P waves or wide. rnitral valve prolapse. Treatment is directed at the identification and alleviation of the underlying causes. and atropine are utilized. Treatment of asystole consists of addressing potential treatable causes.0 mg lV (may repeat to total dose of 3. bizarre complexes with no uniformity. In the setting of cardiac arrest associated with acute myocardial infarction. and severe bradycardias. 2-15). Potentially treatable causes of PEA include tension pneumothorax. ventricular depolarization cannot occur.5-1. . Torsades de pointes usually occurs in short bursts (<15 seconds). Treatment of premature ventricular contractions Often do not require treatment lf treatment is indicated.04. ventricular rupture. occurs in settings other than VT or VF where there is electrical activity noted on the cardiac monitor or ECG without an associated palpable pulse. and drug overdoses. Treatment of pulseless electrical activity Search for and correct underlying causes Epinephrine 1. left ventricular failure. disopyramide). cardiac tamponade. irregular complexes (agonal beats) may occur.75 mg/kg bolus q 5 min to total dose of 3. if unsuccessful. hypoxemia. myocarditis. The QT interval of the beats preceding torsades de pointes is usually prolonged. Asystole Ventricular asystole occurs when there is an absence of ventricular electrical activity. severe acidosis. drug overdoses [tricyclic antidepressants (TCAs). if successful.

0 mg lV (may repeat to total dose of 3. and sinus and AV blocks. 3) Atrioventricular (AV) blocks are divided into first. dyspnea. A first-degree AV block represents a delay in AV conduction. myocarditis.4.2-15.2) Sick sinus syndrome (SSS).0 mg) Consider termination of resuscitative measures Initial treatment consists of removing or alleviating underlying causes. The PR interval is usually constant but may be variable. and junctional tachycardias. The etiology of SSS includes rheumatologic diseases (e. Treatment of torsades de pointes Alleviate underlying causes Overdrive pacing Magnesium 1. A variety of medications (digoxin. cardiomyopathy.2.5-1. Treatment of asystole ldentify and treat potential correctable causes Transcutaneous pacemaker Epinephrine 1.4. electrolyte imbalances) can potentiate the tachy. ischemia. or drug effects (digitalis).Cenorovescur-q-n Drsonosns / lll FlG.g.0 mg lV (may repeat q 5 min if dysrhythmia persists) Atropine 0. sarcoidosis). and chest discomfort may be precipitated by the dysrhythmias.0 g lV setting may be necessary to make the diagnosis. Accelerating the heart rate to a rate greater than the torsades de pointes (overdrive pacing) is the most effective treatment. Conduction Blocks (2. As the dysrhythmias are intermittent. Magnesium sulfate has also been demonstrated to be effective (Table 2-35). The block may occur in the AV node itself or may be infranodal. First-Degree AV Block With a first-degree AV block. It is recommended that pace- maker placement be considered prior to treatment of tachydysrhythmias as the treatment may exacerbate the bradycardias. Common tachydysrhythmias include atrial fibrillation. A second-degree AV block is characterized by an intermittent lack of conduction through the AV node and is further divided into Mobitz I and II AV blocks. is a clinical entity that involves both intermittent tachydysrhyhmias and bradydysrhythmias. also known as tachy-brady syndrome. quinidine) and medical conditions (hyperthyroidism. . second. Symptoms such as palpitations. reentrant SVTs. usually a regular rhythm. all impulses are conducted. myocarditis. Atrioventric ular B lo c ks (2. one-to-one conduction of P waves to QRS complexes. The bradydysrhythmias commonly seen include severe sinus bradycardias. Asystole. pericarditis. Treatment is directed at rhythm control. 4. atrial flutter. 2. syncope.or bradydysrhythmlas. TABLE 2-34. ECG characteristics of first-degree AV block include a prolonged PR interval (>0. and normal-appearing QRS complexes (Fig. 2-16).. however.2) Sick Sinus Syndrome (2. and third degree. there is a delay in normal AV conduction. They may occur in normal individuals and are not associated with increased mortality. A third-degree AV block represents complete interruption of AV conduction (AV dissocia- tion). First-degree AV blocks may be the result of myocardial infarction. Patients often require pacemaker placement to prevent untoward sequelae from the bradydysrhythmias. rheumatic heart disease. and cardiac surgery. continuous cardiac monitoring either in the inpatient or outpatient TABLE 2-35.20 seconds).

First-degree AV block. The pulse will be irregular unless the pattern is 2:1.0 mg lV (may repeat to total dose of 3. Once the complete block occurs.2-17). FlG. The P waves and QRS complexes are usually of normal morphology. cardiac surgery. If there is associated symptomatic bradycardia. Mobitz I (Wenckebach). and myocarditis.5-1. There is usually no need to initiate treatment other than correcting underlying causes (Table 2-36).0 mg) .2-16.712 / EurncnNcy MrtrcrNn: THn Conn CunrucuLUM FlG. Mobitz I. to the dropped beat. Wenckebach's disease is often transient and intermittent. 3:2. However. Treatment of second-degree AV block. Mobitz I (Wenckebach) Generally no treatment needed. TABLE 2-36. except identification and correction of precipitating etiology The patient is typically asymptomatic. Drugs such as dig- italis. Wenckebach's is more commonly associ- I Second-degree AV block. Second-Degree AV Block. The ECG demonstrates a progressively lengthening PR interval until a P wave is seen without a corresponding QRS complex. atropine or pacing may be utilized (Table 2-37). also known as Wenckebach's disease. the PR ated with a normal QRS length than is a Mobitz II block. and propranolol can also produce a second-degree Mobitz I AV block. Mobitz II. Patients are usually asymptomatic and do not require treatment. is a condition where there is progressive delay in AV conduction until there is complete block of the sinus impulse. Second-degree AV block. Wenckebach's may occur in patterns such as 4:3. TABLE 2-37. or 2:1. consider discontinuing drugs that may have initiated the block lf bradcycardic and symptomatic Pacemaker Atropine 0.2-17. Common causes include acute myocardial infarc- tion. Mobitz It is often difficult to initially differentiate a 2:l Wenckebach from a second-degree AV block. The R-R intervals shorten prior interval lessens and the pattern is repeated (Fig. verapamil. Treatment of first-degree AV block No treatment needed.

Clinical manifestations depend on the level of the block and the resulting bradycardia. ECG characteristics include a normal P wave with more P waves than QRS complexes. . the PR interval is variable (Fig. structural damage to the AV node. Mobitz ll. If the ventricular pacemaker is located near the junction. and drug toxicities (digi- talis.CenorovRscur-cR DrsoRDrRs / 773 FlG. Third-degree AV block. If the ectopic pacemaker is located lower in the ventricles. which may maintain perfusion. or the bundle branches.2-19. Mobitz ll I ncrease ventricular rate Pacemaker Atropine 0. 2-18). the ventricular response is controlled by a ventricular ectopic focus. usually at the bundle branches and less commonly at the bundle of His. it is advisable to have transcutaneous pacing pads in place even with the stable patient (Table 2-38). Mobitz II AV blocks are usually seen in association with bundle branch or fascicular blocks. ECG findings include a ventricular response that is slower than the atrial rate and usually regular. These patients should have transcutaneous pacemakers at the bedside as they may decompensate.2-18.5-1. Since patients with Mobitz II AV blocks can precipitously decompensate. and since the atria and ventricles are being depolarized at different rates from different foci. and an irregular ventricular rate associated with a regular atrial rate (Fig.0 mg) Second-Degree AV Block. Treatment of second-degree AV block. Mobitz II Mobitz II AV blocks occur infranodally. particularly in the setting of ongoing FlG. TABLE 2-38. Third-degree AV blocks occurring at the AV node may result from acute inferior myocardial infarction. the QRS complexes are usually wide. 2-19). the intrinsic rate will more likely be slower <40 bpm) and be associated with widened QRS complexes. the rhythm is typically between 40 and 60 bpm and may have a normal QRS configuration. the bundle of His. There is a potential for the block to progress to complete heart block. a PR interval that may be prolonged from normal but remains constant. Second-degree AV block. The block may occur at the AV node. Patients with blocks occurring at the AV node may initially present with stable vital signs secondary to the junctional escape rhythm. propranolol). therefore. Since no atrial impulses reach the ventricles. an atrial rate that is typically normal with normal P waves. Third-Degree AV Block In third-degree AV block there is no AV conduction.0 mg lV (may repeat to total dose of 3. Infranodal blocks are most commonly associated with acute anterior myocardial infarction. particularly in the setting of myocardial ischemia/infarction. Treatment involves increasing the ventricular rate with either atropine of pacing. Mobitz II AV block generally represents structural damage to the conducting system below the AV node.

large R waves in leads I. initially with intimal thickening. and Vo.155(2): Wagshal AB. . Vr. aVF. All patients with third-degree AV blocks should receive an evaluation by a cardiologist to determine the need for a permanent pacemaker (Table 2-3e). American Heart Association. with subsequent intimal fibrosis and calcific deposition. Wit AL. and Vo. or all three (trifascicular) pathways. In the presence of ongoing ischemia/infarction. Smeets JL. or the left posterior inferior fascicle (LPIF). Am J Cardiol 1993. surgery. V5. aVL. genetic predisposition.12 seconds). diabetes mellitus. and a qR complex in lead AVL. Conn CunrucuLUM TABLE 2-39. Atherosclerosis/Insufficiency (2. Vos MA. Roden DM.70(10):3743. McMurray J.5. Understanding of potential causes as well as the ability to properly identifli and treat cardiac dysrhythmias are essential skills for all emergency physicians. followed by macrophage foam cell migration and phagocytosis of extracellular lipid. ECG characteristics of right bundle branch blocks include increased QRS width (>0.ll4 / ErrrencrNcy MnlrcrNr: Tnn. Arch Intern Med 1995. Mechanisms 341 (8854):1 1 of cardiac arrhythmias.72(16):It4-124 LA. Risks and benefits of antiarrhythmic therapy. 1994. Patients presenting with infranodal blocks generally necessitate emergent pacing as the intrinsic rate of their ectopic pacemaker is generally too slow to maintain perfusion. Pires 137-147. Br Med J 1994. Bundle Branch Blocks (2. Lowenstein SR. aVF. but fibrosis and stenosis eventually limit this capability. initially.309(6969):1 63 1-l 635. 5.1) Acquired arterial disease includes a variety of conditions.12):7 85-7 9 l. hyperlipidemia. including tobacco use. 1) Atherosclerotic arterial disease is a complex problem due to a variety offactors. RSR' in lead Vr. 1994. Patients presenting with cardiac Aghababian R\ ed. Reiter MJ. Dallas: American Heart Association. Emergency management of cardiovascular disease. Ventricular arrhyhmias in heart failure. however. N Engl J Med 199 4.. Wellens HJ. Choice and chance in drug therapy ofcardiac arrhyhmias: technique vs. Huang SK.74(4): 401404. vascular flow characteristics. The intra-intimal depositions cause compromise of the lumen. J Emerg Med 1996. Li HG. some compensatory dilatation can occur to maintain lumen size.14(1):39-51. Am J Cardiol 1994. two (bifascicular). and ultimately hemorrhage. Waldo AL. and congenital conditions. hematoma and thrombus formation. LPIF blocks pre- with a normal QRS duration.33 I (. SELECTED READING ischemia/infarction. small r and deep S waves in leads II. deep S and small R in lead I. R wave in lead I greater than that in leads II or III. with intimal erosion and plaque fissure.2. are commonly encountered clinical entities in the ED. Boston: Butterworth-Heinemann.s) Arterial (2. sent Left bundle branch blocks (LBBB) have the following ECG findings: a wide QRS (>0. Singh BN. Gorgels AP. Textbook of advanced cardiac life support. Due to the smaller caliber of peripheral vessels. the left anterior superior fascicle (LASF). a normal QRS width. Atropine and catecholamines may be utilized as needed. patients with these blocks are at increased risk of developing thirddegree heart block and should be treated with pacemakers. The block may involve one (unifascicular). Summary Diseases of the cardiac conduction system. Bifascicular and trifascicular blocks are associated with severe heart disease. Blocks involving the LASF demonstrate QRS axis of<-45 degrees. Lancet 1993. Treatment of third-degree AV block I ncrease ventricular rate Pacemaker Atropine 0.12 seconds). V5. RankinA. Management of cardiac arrhythmias with radiofrequency catheter ablation.5-1.0 mg lV (may repeat to total dose of 3. QRS axis >110 degrees. Halperin BD. their involvement tends to be more symptomatic than major vessel disease. R wave in lead III greater than that in lead II. Zardini M. problems due to inflammatory disease. thrombosis. Treatment of heart failure and atrial fibrillation and arrhythmias.4) Bundle branch blocks can occur in any of the three major ventricular conduction pathways: the right bundle branch (RBB). Arterial lesions develop gradually. and a qR complex in lead III. myocarditis. Am J Cardiol 1992. spasm. Effect of adenosine or adenosine triphosphate on antidromic tachycardia. Bundle branch blocks may be the result of ischemia. Paroxysmal supraventricular tachycardias. and Vl] and no q waves in leads I. or emboli may also require urgent or emergent evaluation. Although the greatest number of conditions are related to atherosclerotic disease. [I. Morillo CA. deep S waves in the inferior leads. 1. drug-specific responses in evaluation of efficacy. hypertension. et al. DISEASES OF THE CIRCULATION.4. pacing is preferred in the unstable patient. valvular disease. and wide S waves in leads I. cardiomyopathy. and aging. and Vo. manifested as cardiac dysrhythmias. Vs. 89-l 1 93. ACQUIRED (2.0 mg) dysrhythmias may demonstrate little to no clinical effects or may present with lifethreatening symptoms.

An ABI of 0. More proximal symptoms imply a more proximal site of atherosclerosis. In all patients with peripheral vascular disease. It is defined as calf pain that occurs only when walking. or calf. As with coronary artery disease. hip. or nor- mal compared to surrounding areas. Before medical treatment for claudication should be considered. The strongest risks for arterial occlusive disease are tobacco smoking. aggressive intervention. requiring early. thigh. glucose and cholesterol control. and gradual improvement of exercise tolerance. color changes may occur from venous distention. if a small blood pressure cuff is used.9 or less should be considered evidence of arterial occlusive disease and an ABI 0. approximately 20% to 25o/o of these patients eventually develop acute arterial occlusion. the ABI is usually greater than 0. including cessation of smoking. hypercholesterolemia. or chronic arte- rial occlusive disease (AOD). to augment the slowly decreasing flow from the primary vessel. are usually involved. rather than an isolated extremity. and to the other extremities. or arterial stasis from hypotension. Ifonly one arterial segment is diseased. depending on the degrees of vascular compromise and compensatory vasodilatation. and an increased likelihood of males to seek medical attention for these disorders. infection. but one should note whether the temperature change occurs gradually or whether there is a sharp demarcation of temperature change. In addition. Dermal atrophy. is present in approximately 15o/o to 20%o of patients over the age of 55. ulceration. Claudication is a chronic manifestation of limb ischemia. It is essential that the examination of the patient include a careful cardiovascular assessment: a cardiac examination. or gangrene. This variability may be due to higher incidences of male smokers.8.. thrombosis of a previously compromised area. and there may be factitious elevation of blood pressure in patients who are obese. with a gender ratio of 2 to l0:1. Arterial Insufficiency Lower extremity arterial insufficiency. Skin temperature will increase proximally. The role of medications in the treatment of claudication is controversial. multiple organ systems. palpation of all peripheral pulses. or hemosiderin deposition. and at the ankle. vasoconstrictive medications should be avoided whenever possible because of their potential to compromise blood supply to the extremities. Skin temperature may be decreased. The location of disease can be determined by checking systolic blood pressure with an inflatable blood pressure cuffat the high thigh. When treating patients with claudication. It most commonly affects the vessels of the lower extremities. Although the majority of patients with arterial occlusive disease have a stable chronic condition. the patient needs to meet the following criteria: (1) they cannot walk more than 500 m without symptoms. and the carotid and coronary vessels. with decreased hair and slowly growing. The ABI should normally be slightly greater than 1 because of decreased vascular compliance and the effects of gravity and the static fluid column. males with CAD. including peripheral disease. diabetes mellitus. Patients with claudication may present to the ED when the pain occurs with less exertion than previously. It is more corunon in males.5. or have dependent rubor ifthe blood supply is inadequate. cellulitis.Cenlrovescuran DrsoRorRs it is possible for collateral vascularization to occur around small and some medium-sized vessels. and evaluation for bruits in all major vessels. present with symptoms including claudication and rest pain. history of coronary artery dis- ease (CAD) (especially dysrhythmias or valvular disease). increased. Because of its gradual progression. as with a planned exercise walking program. The overlying skin should be examined for slowly healing wounds and areas of obvious vascular stasis. The affected limb should be compared with the contralateral limb.Diagnosis of peripheral vascular disease can be suspected based on a history of limb pain with exertion in patients with known risk factors. the aorta. blood pressure. but will decrease with increasing arterial involvement. This is an objective measurement comparing the brachial artery blood pressure to the dorsalis pedis blood pressure. (3) any medications that might worsen their claudication should be discontinued. or present as frank occlusion with ischemia. In many cases. The ankle-brachial index (ABI) should be obtained. aspirin appears to be of some benefit in slowing the progression of arterial disease in general. (2) the symptoms are present and stable for at least 6 months.5 and 0. or when the symptoms progress for a given amount of exertion. In lowflow states. A pressure gradient ofgreater than 20 mm Hg usually indicates the diseased segment. The ABI is also unhelpful in patients with severe vasoconstriction or hypotension. patients with claudication can be managed conservatively. hypertension. Patients with claudication usually have an ABI between / 175 0. above the knee. Patients with lower extremity AOD will generally present with exertional pain of the buttock. and resolves'*'ithin l0 minutes of resting. through its . Skin color may be pale from lack of blood supply. particularly smoking tobacco. cyanotic. and family history of AOD. below the knee. It may be asymptomatic. the primary goal is modification of the atherosclerosis risk factors. thickened nail plates may be present. blood pressure measurements in all extremities. Its prevalence is approximately 2Yo in patients over the age of 60 years.4 or less should be considered limb-threatening ischemia. This method is of limited use in diabetic or renal disease patients with noncompressible vessels. The main causes of acute occlusion are cardiogenic thromboembolism.

They should inspect their feet and legs often for insignificant injuries. It is suspected that atherosclerotic deposits trigger endothelial remodeling. Few patients with ruptured AAA survive to reach the hospital.2) Arterial aneurysms are outpouchings of the vessel walls due to dilatation or endothelial disruption. Limb{hreatening arterial insufficiency presents as ulceration or rest pain. embolization. Additional causes ofAAA include blunt trauma. thrombosis. or structure. therefore inhibiting platelet activation and aggregation. The main risk factors associated with the development of A AA are age over 60 years. Animal studies have suggested that deficiency of copper. and affect approximately 2o/o of the population. They are true aneurysms. This derangement of the elastin-to-collagen ratio may be a predisposing factor. since neuropathy may prevent their early detection. between the diaphragm and the renal arteries. inflammation. blood flow at rest is insufficient to meet the basal tissue demands of the limb. The optimal dose of aspirin is still uncertain. compression of surrounding structures. infec- tion. and are characteized by a fusiform shape. use of aspirin alone appears to be as effective as aspirin combined with other antiplatelet agents. infection. AAAs are the most common type of aneurysm that cause patients to seek medical care. which makes it susceptible to secondary infection. male gender. The main risk of aortic and visceral aneurysms is rupture with exsanguination. elastin concentrations may be decreased by as much as 92o/o. Clearly. may slow atherosclerosis and may be of benefit in patients with peripheral arterial occlusive disease. with increases in collagenase and elastase activity.5 to 2 times normal size) of an intact vessel wall caused by hemodynamic forces and focal weakness. which is a cofactor in the cross-linking of elastin and collagen. as little as 80 mg may be effective. involving the segment of the aorta between the takeoff of the renal arteries and the aortic bifurcation. as in coronary artery disease. Prostaglandin derivatives are being investigated for their antiplatelet effects and effects on the microcirculation. since vessels already appear to vasodilate in order to compensate for atherosclerotic disease.1. Ulceration occurs primarily in patients with diabetes mellitus. In AAAs. location. and family history. use emollients to keep the skin well hydrated cut toenails carefully to avoid ingrown toenails. but are complicated by thrombosis or embolism with distal ischemia. most patients with advanced peripheral atherosclerotic disease don t develop aneurysms. also inhibit platelet aggregation but can produce neutropenia and are much more expensive than aspirin. is also a predisposing factor. Vasodilators. although. with formation of a fibrous sac. or erosion into surrounding structures. atherosclerotic peripheral vascular disease. Aneurysm (2. MostAAAs (97%) are infrarenal. aggressive wound care.5. and beta-carotene. chronic obstructive pulmonary disease.116 / EurRcnNcyMnorcrNr: THs CoRE Cunnrculuv inhibition of thromboxane Az and its inhibition of prostacyclin. with a compensatory increase in collagen. early diagnosis and treatment are of the utmost importance in decreasing mortality. although specific agents are not yet available. such as vitamins E. Approximately 30o/o of ischemic ulcers heal with careful. Antioxidants. In these cases. since all three layers of the vessel are intact. Symptomatic AAAs result from dilatation and rupture. including hyperbaric oxygen therapy. Ruptured AAA is the l3th most common cause of death in this country. Medications affecting the microcirculation by improv- ing blood viscosiry such as pentoxi$rlline. also are more prone to aneurysmal changes. and inflammation. Anatomic Classification. They may be classified by shape. Although the majorify of patients with AAA are asymptomatic. such as ticlopidine and clopidogrel. as in Ehlers-Danlos or Marfan's syndrome. Etiology and Pathophysiology. may help improve patients exercise tolerance. The exact role that atherosclerosis plays in the etiology of aneurysm formation is unclear. In these patients. While most aneurysms are seen in the presence of other atherosclerotic disease. smoking. such as calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors. although it does not appear to have any effect on progression ofthe disease. Suprarenal aneurysms. systgmic anticoagulation may prevent thrombosis. etiology. Other antiplatelet agents. Aortic/Iliac Abdominal aortic aneurysms (AAAs) involve the subdiaphragmatic aorta. Mycotic aneurysms (infections of the aorta) are due to . of those that do. Significant blunt trauma can result in intimal tears with false aneurysm formation. The traumatized tissue heals slowly due to poor tissue perfusion. mortality is approximately 45Yoto 50o/o. C. These patients must be careful to wear well-fitting shoes at all times. hypertension. they are usually due to extension of a thoracic aneurysm. Based on current studies. and pad between the toes with cotton or lamb's wool to prevent pressure ulcers. Abnormalities of either collagen or elastin. False aneurysms (or pseudoaneurysms) occur after disruption of the vessel wall with containment of blood by sur- rounding tissue. are rare. although there is no evidence that it prevents progression of the disease. because neuropathy predisposes to minor trauma to the foot or leg. True aneurysms are irreversible localized dilatations (1. have not been shown to be ofany benefit. Peripheral aneurysms rarely rupture.

nausea. Dffirential Diagnosis. However. so failure to palpate a mass does not rule out A. its extent. and the aortic bifurcation occurs at the L4 level. When abdominal or back pain with hypotension and a pulsatile abdominal mass are present. Laboratory and radiologic evaluations of unstable patients with symptoms highly suspicious for ruptured AAA waste valuable time. although image quality is improved. The erythrocyte sedimentation rate (ESR) tends to be elevated in patients with inflammatory aneurysms. Presenting symptoms may include localized or diffirse abdominal pain often radiating to the back. and surgical consultation. Hematocrit. When palpating the abdomen. image processing takes more time than conventional CT. which is evidence of retroperitoneal hemorrhage. An electrocardiogram should be ordered to evaluate for myocardial infarction. Patients may also be aware of a throbbing sensation in their abdomen. musculoskeletal back pain. particularly in the femoral or sciatic distribution. Blood urea nitrogen @U$ and serum creatinine should be obtained to evaluate renal function.Cer. and can readily be performed in the ED. with extensive reactive fibrosis. A urinalysis should be checked ifthe patient reports flank pain. possibly due to an autoimmune reaction to atherosclerotic plaque. the presence of thrombus. the patient's past medical history. In addition to eliciting the above symptoms. Because of the variety of presentations. especially of the extremities. or may fall or be involved in motor vehicle crashes. neurologic deficits. a ruptured AAA may mimic myocardial infarction. they should be treated emergently. central monitoring. or rupturing abdominal aortic aneurysms can often be a diagnostic challenge.rd{. Serum electrolytes and glucose can be evaluated as necessary ifthe patient is diabetic or is on medications that might affect these values. and present to the ED with multiple trauma. and social history should be obtained to assess for risk factors for AAA. if the examiner's hand is placed directly anterior to the aorta. claudication or limb ischemia. diagnosis of patients with symptomatic. A careful neurologic examination. dizziness. The term inflammatory abdominal aortic aneurysm is used to describe those aneurysms in which the aortic wall is unusually thickened. it is not useful in distinguishing whether an aneurysm has ruptured. It is best at determining aortic diameter. and gastrointestinal hemorrhage. and whether the aneurysm has ruptured. surgical history family history. type and cross-match of packed red blood cells. The major vessels should be auscultated for the presence of bruits.orovescur-{R DTsoRDERS bacterial endocarditis with septic emboli. there will be increased transmission of aortic pulsations. platelet count. Unfortunately. Ultrasound is very reliable in the diagnosis of AAA. The flanks should be examined for ecchymosis (Grey Turner's sign). A careful abdominal examination should be performe4 to determine the presence of a pulsatile mass and to exclude other intraabdominal pathology. or have a history of syncope. chest. and allergy to or nephrotoxicity from contrast medium. renal colic. although mural thrombi may . syncope. medications. diagnostic studies may avoid unnecessary emergency surgery. namic stability. Spiral CT further enhances the ability of CT to identify branch vessel involvement. with staphylococcal or streptococcal organisms. and frequently thereafter if AAA is suspected. a type and screen or type and cross-match should be obtained. which is in the transpyloric plane. or neurologic deficits. suprarenal and visceral aneurysms are not palpable. rapid. A complete cardiovascular examination should be performe4 looking specifically for signs of ischemia and atherosclerosis. Computed tomography (CT) can accurately determine the presence of an aneurysm. urgency. if the diagnosis is uncertain or the patient is stable. should be performed to look for deficits due to nerve ischemia or compression. Ancillaryt Tests. limb ischemia. Obesity or hypotension may make it impossible to palpate a pulsatile abdominal mass. diagnosis is readily apparent. However. hypotensive. Initial Presentqtion Many AAAs are found incidentally on examination when patients are being evaluated for other complaints. misdiagnosis of ruptured or expanding AAA is common. Therefore. slightly below the umbilicus. Patients with syncope may appear to have a primarily cardiac or neurologic event. with accuracy approaching 100%. Rectal examination should be performed to help rule out gastrointestinal hemorrhage as a cause of abdom- / 777 inal pain and hypotension. Blood pressures should be checked in both arms and both legs to look for differential pressures. although a normal ECG does not rule out MI. and weight loss. vomiting or frank hematemesis. If patients are tachycardiac. it is important to palpate the lateral aspects of the aorta. frequency or hematuria. those patients should immediately be taken to the OR. leaking. Vital signs should be checked immediately on presentation. pressing it against the spinal column. The main disadvantages of CT include inaccessibility of the patient. Depending on the level of suspicion for AAA. jaundice. Angiography is useful for the preoperative evaluation of aortic diameter in AAA. and of the presence of a mass or fullness The most important initial assessment is of hemody. diverticulitis. or flank. The first evidence of AAA may be newonset renal insufficiency or failure. and coagulation studies should be obtaine{ and a white blood cell count should be checked if infection is suspected.It is noninvasive. although it is not pathognomonic. with fluid resuscitation. CT can also evaluate fibrotic adherence to adjacent structures or fistula formation. and a normal aorta may be falsely perceived to be an AAA. along a line drawn between the iliac crests. The renal arteries arise from the aorta at the level of Ll.

often in pregnancy due to increased splenic arteriovenous shunting. Visceral Aneurysms Visceral aneurysms usually involve the splenic. electrolytes. Symptomatic aneurysms require immediate surgical management. Mortality is high for ruptured aneurysms and surgical resection should be performed on those who are operative candidates. surgery should be consulted immediately. hepatic. MRI may be used in the outpatient setting for evaluation of AAA. whether stable or unstable. They may be detected incidentally with ultrasound or Cl but angiography is the most reliable diagnostic test. Bruits or palpable masses are rarely detectable. Symptomatic patients. Two large bore IVs should be placed and blood drawn for blood type. and commonly affect elderly males. Blood pressure needs to be monitored carefully. so that it may be confused with AAA. It is comparable to ultrasound and CT in assessing aneurysmal diameter and better at assessing branch vessel involvement. but of those. Abdominal films (flat. If the patient is hypotensive. Dilatation often results in mural . fluids should be given to maintain a blood pressure of 90 to 100 mm Hg systolic. cross-table lateral) are of limited use in the diagnosis of AAA. or atherosclerosis. to decide whether operative management should take place on the basis ofclinical diagnosis alone. and they contribute to tissue ischemia and metabolic acidosis. and an indwelling urinary catheter should be placed to monitor urinary output. and severe coronary. Management of abdominal aortic aneurysms in the ED depends on the case presentation. Treatment. unless contraindicated. Most hepatic artery aneurysms are not symptomatic. 950lo occur in pregnant females. Only 2% of splenic aneurysms rupture. Treatment should include management of infection. Ultrasoun4 CT. since the rapid decompensation and death can occur is made. or a combination of a beta-blocker and nitroprusside. The goal is to decrease stress and shearing forces on the aortic lumen. Superior mesenteric artery aneurysms are the least common visceral aneurysms. and mental status and urine output should be monitored. rapid changes in blood pressure are more likely to contribute to rupture. or renal insufficiency. require aggressive preoperative management and monitoring. and coagulation studies should be obtained. Hypertensive patients require blood pressure control with short-acting agents such as labetalol hydrochloride. any delay in surgery greatly increases risk ofdeath. Ifthere is a high suspicion of AAA. Occasionally an acute rupture may be confused with an ectopic pregnancy. and baseline CBC. Continuous cardiac and vital sign monitoring and pulse oximetry should be initiated. occasionally severe. The patient should never be left unattended. a good indicator of tissue perfusion. soon aneurysm there should be emergent surgical consultation.118 / Err. with its inherent risks. these patients should be given surgical referral on an urgent basis. Calcification of the aorta wall can be identified in -600/o of patients with AAA. Diagnostic studies should be undertaken as outlined above. cross-matched for six units of packed red blood cells. but lack of immediate availability limits its use in the emergent setting. Peripheral Arterial Unlike aortic aneurysms. The majority of these aneurysms are infected aneurysms from bacterial endocarditis. If they are truly asymptomatic. Diagnosis is often as an incidental finding on ultrasound or MRI. Contraindications to aneurysmectomy include expected life span less than 2 years. renal function. Hepatic artery aneurysms can be a result of trauma. with surgical repair after the infection is eradicated. in middle-aged males and females. and coronary artery disease will need to be addressed prior to aneurysm repair. Aneurysms greater than 6 cm in diameter are managed operatively in almost all patients. Often these aneurysms are asymptomatic but may present as left upper quadrant pain. pulmonary. An arterial line should be placed for continuous blood pressure monitoring. or superior mesenteric artery. Although they are uncommon. Symptomatic stable patients may have a slowly leaking aneurysm or a ruptured aneurysm contained in the retroperitoneal space. It also requires the use of radiopaque contrast medium. there is a small chance of rupture with exsan- guination. upright. Angiography confirms the diagnosis. but angiography confirms the diagnosis. Incidentally found asymptomatic AAAs require prompt diagnostic evaluation. Patients often complain of intermittent upper abdominal pain and the physical examination reveals a palpable pulsatile mass approximately 50% of the time. but no other relevant information can be obtained from plain films. coexisting conditions such as cerebrovascular disease. Aneurysms less than 4 cm in diameter should be followed by serial imaging every 6 months. or MRI may be obtained on an outpatient basis to confirm the diagnosis and to if decide on the best therapeutic course. Splenic artery aneurysms are the most common visceral aneurysms and occur most commonly in females. infection. symptoms may include right upper quadrant or epigastric pain.rencnuctr MerrcINr: Tns Conn CunrucuLUM lead the examiner to underestimate lumen size. Asymptomatic aneurysms greater than 4 cm in diameter may be treated operatively if the patient is otherwise medically fit. Vasoconstrictors should be avoided" since they do not treat hypovolemia. As as the diagnosis ruptures. but ifthese are not suspected" ultrasound or CT should be considered for definitive diagnosis. aneurysms of peripheral arteries seldom rupture. Asymptomatic aneurysms require surgical consultation.

thromboangiitis obliterans (Buerger's disease). They are nonblanching and may be tender. Arteriography provides definitive diagnosis of arterial aneurysms. dermal. Expansion may compress adjacent nerves. It is important to rule out other conditions that can simulate of the femoral. malaria. or toms. pulmonary. The patient should be asked questions regarding symptoms such as hemoptysis. syphilis. Early operation is advised with recurrent peripheral embolization. Lesions are more common in gravity dependent-areas and at pressure points. vessel weakening with aneurysm formation. In addition. which may result in further vessel injury inflammation and scarring. which are reddish purple. Venous obstruction is often refractory to treatment. coolness. palpation of local arterial enlargement is generally adequate for diagnosis. superficial. noma). Patients may present with chest. and the patient will eventually require a workup to identify an antigenic trigger. systemic lupus erythematosus. connective tissue disease. and rheumatoid arthritis. chest pain. There may be transmural necrosis of the walls of large muscular arteries and degradation of elas- tic fibers with scars and inflammatory infiltration. paresthesias. They almost always occur in older males with advanced atherosclerotic disease. popliteal. embolic events. Depending on location. sarcoidosis. dyspnea. Aneurysms of the subclavian artery are often due to postischemic dilatation in patients with cervical rib or thoracic outlet syndrome. It most commonly affects the skin. Acute thrombosis associated with severe ischemia is an indication for immediate surgical treatment. Small Vessel Arteritis Small vessel arteritis is often due to hypersensitivity. severity. In asymptomatic patients. also occur. Upper Extremity Aneurysms Upper extremity aneurysms are relatively rare. if possible. Lyme disease. neck. allergic drug reactions. prompt surgical follow-up is necessary.5. folloled by the femoral arteries. Emboli may cause distal ischemia. disseminated intravascular coagulopathy. or deep thrombophlebitis. Although surgical repair is often necessary. thrombosis. amyloidosis. and there may be ulceration. heavy metal poisoning. and myalgias to evaluate pulmonary cardiac. this is often difficult due to the friable nature of the vessels. although caval occlusion and aneurysms. it is important to determine if of other organ sys- tems are involved. or large vessels. which will show purpuric lesions. Industrial workers may rarely develop an ulnar artery aneurysm from repeated trauma to the hypothenar eminence. slightly raised papules approximately I to 3 mm in diameter. HI! toxoplasmosis. although the erythrocyte sedimentation rate will be often be elevated as a nonspecific Lower Extremity Aneurysms indicator of inflammation. protein C or S deficiency. There are no pathognomonic signs. aneurysms tend to be multiple. Depending on the type of arteritis. Nearly onehalf of patients with bilateral popliteal aneurysms have AAAs.AR DTsoRDERS thrombi. neoplastic diseases (particularly renal cell or lung carcicytomegalovirus.Cenorovescur. lymphoma and myelodysplasia. gangrene. med- . symptoms can include pain. thrombotic thrombocytopenic purpura. although mural thrombus may reduce the apparent diameter of the lumen. such as endocarditis. Any history of sickle cell disease. brachial. medium.1. other studies may be necessary. ophthalmic. there may be a predilection for small. the organs involved" and the presenting symp- Lower extremity aneurysms most commonly affect the popliteal arteries. Physical Examination Depending on aneurysmal location. Pseudoaneurysm formation can also occur as can perforation of the vessel wall. Some of these responses to inflammation include increased vascular permeability. and shoulder pain from acute expansion. Treatment.3) The arteritides are abnormal reactions of the blood vessels to inflammatory processes. Patients may experience claudication. it should be done when the disease is not active. or involvement of mucosal surfaces. and muscle involvement. which can embolize or progress to thrombosis. particularly Arteritis (2. Ultrasound and CT scan can provide further useful informatlon. The arteritis syndromes vary with pattern of organ involvement. resulting in pain or paresthesias. or diagnostic studies for arteritis. It is characterized by recurrent mucosal ulceration. Behget s Disease Behget's disease is a vasculitis involving both arterial and venous vessels. symptoms. Diagnostic Studies. If repair is necessary. localized edema. and intimal proliferation with thrombosis. multiple sclerosis. Systolic bruits or a palpable thrill are often present. This is most commonly manifested as recurrent. and neoplasia should be elicited. When a patient presents with symptoms suggestive arteritis. sickle cell anemia. Radial artery pseudoaneurysms are an uncommon complication of radial artery cannulation. and associated conditions. and cyanosis ofthe fingers. Localizedtrama is the most common cause. / ll9 arteritis. and ulnar arteries. and vascular involvement.

The limb distal to the occlusion is critically compromised due to little or no collateral blood flow. Diagnosis of temporal arteritis depends on several fac- tors. and tenderness over affected superficial arteries. retinopathy. It appears most frequently in Caucasians over the age of 50. fever.4) complement. the most common complications are blindness from ischemic optic neuritis and cerebrovascular accident. Doppler flow studies can be useful to determine optimal biopsy sites. after signs and symptoms have resolved and the ESR has refurned to normal. nodulariry thickening. discrepancies in blood pressure in different limbs. and depression. iatrogenic foreign bodies.40 to 60 mg a day in divided doses. should side approximately 3 to 5 cm. Prednisone can be gradually tapered Acute arterial ischemia is due to embolic or thrombotic occlusion. ized by constitutional symptoms. the other side should be biopsied. particularly alkaline phosphatase. in some cases with overlying erythema due to a local inflammatory response. or swelling may be noted. Headache is the most common symptom and may be accompanied by scalp tenderness. pallor. nonspecific inflammamay include the pulmonary and coronary arteries. but are not sufficiently sensitive nor specific for diagnoSIS. intravenous foreign bodies. the patient may develop limb claudication. but it is not clear whether they slow the course of the disease.jaw claudication. Immediate diagnosis and intervention are necessary to . The onset of temporal arteritis is often gradual with nonspecific constitutional signs and symptoms. aortic disease progresses regurgitation. No laboratory studies are pathognomonic. temporal artery tenderness. anemia. facial pain. anorexia. and circulating immune complexes. The patient should be referred to a rheumatologist for further evaluation and monitoring. arthralgias. As the with increasing inflammation and fibrosis (the pulseless phase). septic emboli.1. including malaise. Acute limb ischemia is characterizedby the five P's: pain. weight loss. and. and immunosuppressive agents may alleviate symptoms. or passage of a venous thrombus through a patent septal defect into the arterial circulation. mild elevation of liver function tests. Takayasu Arteritis Temporal Arteritis Takayasu arteritis is a chronic. This consists of prednisone. The incidence appears to be highest in populations of Scandinavian decent. Emboli (2. valvular vegetations in endocarditis. tive. Additional studies include chest x-ray. paresis. although the erlthrocyte sedimentation rate is markedly elevated. night sweats. which should reduce the inflammatory response. at least 50 mm per hour. corticosteroids. should be obtaine4 because of the high incidence of skip lesions. Other diagnostic studies are similar to those for temporal arteritis. If a vascular biopsy is done. Definitive diagnosis is made by temporal artery A segment of artery on the more symptomatic be evaluated and a sufficient specimen. such as catheter tips. electrocardiogram. but eventually decreases or is obliterated. there may be mononuclear cell infiltration. cerebrovascular ischemia. visual changes. renovascular hypertension. dilatation. such as particulate contaminants of intravenous illicit drugs. including stenosis. and echocardiogram if coronary or aortic involvement are suspected. which can show vascular irregularities. and hemoglobin or hematocrit to assess for anemia. although compromise is noted primarily in areas supplied by smaller caliber vessels or areas with little or no collateral blood flow.5. and development of collateral circulation. This disorder is most common in young females and is character- tion of the aorta and its main branches. angina. such as fever.120 / EnmncsNcv MEotctNn: Tss Conn CumrcuLUM ical therapy using anticoagulation. the patient should be started on high-dose corticosteroid therapy immediately./or visual changes. In advanced cases valve replacement and vascular replacement or bypass may be necessary. Clinically. Treatment during the acute stage involves high-dose steroids to decrease the amount of inflammation and subsequent fibrosis. fatigue. Acute arterial occlusion can occur anywhere in the circulation. Etiologies of emboli include atrial fibrillation. and skeletal mus- cle and nerve fibers are very sensitive to ischemia. If the biopsy is nega- biopsy. and aortic aneurysms. The symptoms often wax and wane regardless of therapeutic intervention. and paresthesias. pulselessness. and is often greater than 100 mm an hour. depending on patient response. usually over 6 to 24 months. Elevation and compression of affected extremities may provide symptomatic relief. and elevated serum immunoglobulin G (IgG). weight loss. which Temporal arteritis is a granulomatous arteritis of unknown etiology. aneurysms. with skip lesions similar to those with temporal arteritis. heart failure. including ESR. If untreated. Visual deficits are usually a sign of advanced disease and may be irreversible. without waiting for a definitive diagnosis. Initially the temporal pulse may be more prominent than usual. with a female to male ratio of 2 to 3:1. Other nonspecific findings include normochromic or slightly hypochromic anemia. If temporal arteritis is suspected. pulmonary hypertension with hemoptysis. Diagnosis is based on arteriography. since involvement is bilateral approximately 90% of the time.

It is manifested as episodes of blanching due to vasoconstric- .1. Contraindications to thrombolysis include patients in whom (1) the distal vessel continues to be severely compromised. are being developed.5. other factors affecting its success include duration of thrombosis. although most cases are idiopathic. severe persistent hypertension. (3) there is no future mobility. the use of thrombolytic agents for acute occlusion has been undergoing greater study. areas of hemorrhage or intraluminal thrombus may be difficult to detect unless color-coding of blood flow is used. retroperitoneal hemorrhage. arteriovenous malformation or hemorrhage. known bleeding diathe- / 121 sis. pregnancy. Spasm (2.Caxuovescur-AR DTsoRDERS prevent progression to gangrene with need for amputation. Relative contraindications include peptic ulcer disease. and surgery. hemorrhagic retinopathy. Although catheter location is the major predictor of success. The l-year survival rate of patients undergoing thrombolysis is higher than that of patients undergoing surgery. Absolute contraindications to thrombolysis include cerebrovascular accident within the past 6 months or history of cerebral neoplasm. and e-aminocaproic acid (EACA). Raynaud's phenomenon can be primary or secondary. and artifact during tomography might compromise visualization of nearby vessels. This is related to the greater stresses and poten- tial complications of undergoing a surgical procedure rather than being related to rates of limb salvage from thrombectomy/angioplasty versus thrombolysis. major surgery within the past 2 weeks. and therefore is only indicated during angiography or intra. as well as increasing their specificity. availability of these studies and of personnel to evaluate them may be limited. Thrombolysis appears to be most effective when the catheter is placed within the thrombus. It is usually bilateral and is more common in patients with connective tissue disorders or other evidence of vascular reactivity. exposure to radiation. Once thrombolytic therapy has been performed" additional agents. In acute occlusion. It affects 5% to l0o/o of the general population and is more common in females than in males. although at this point the new antiplatelet agents have not been proven to work better than aspirin. aneurysm. such as aspirin and heparin may help improve vessel patency. such as polycythemia vera or cryoglobulinemia. also have a higher incidence of Raynaud's phenomenon. If no improvement occurs in the initial I to 2 hours of infusion. thrombolytic infusion should be stopped immediately. such as surgical clips from previous operations. If any of these occur. (2) there is irreversible distal ischemia. and endocrine disorders. although at 30 days there is no difference in patency between patients treated with tPA or urokinase. and spiral CT with imagery construction in three-dimensions. and renal insufficiency (serum creatinine >2. such as hirudin and other antiplatelet agents. septic thrombophlebitis. these studies would both be compro- mised in patients with metallic foreign bodies. Bidirectional continuous-wave Doppler ultrasonography can analyze blood flow through a diseased vessel. Although duplex ultrasonography combines real-time B mode and pulsed Doppler ultrasound. although it does carry with it complications of major hemorrhage. In addition to diagramming the site of occlusion. fresh frozen plasma. such as renal compromise or allergic reactions. however. the gold standard is arteriography. angioplasty. Currently. or intravascular stents. major gastrointestinal hemorrhage within the past 3 months or active internal hemorrhage. MRI could not be done in these patients. tPA has the greatest rate of initial patency. New thrombolytics are being developed that may increase the halflife of plasminogen activators. it is unlikely that the vessel can be revascularized. Diagnostic methods used in limb ischemia depend on patient presentation.5) Raynaud s Phenomenon Raynaud's phenomenon is a relatively common vasospastic disorder ofthe hands and feet. Once the lesion has been identified" several options may exist. vascular bypass graft. including thrombectomy. and if unsuc- cessful. Other diagnostic techniques include magnetic resonance angiography.or postoperatively. and provides excellent assessment of blood flow patterns and mural plaques within the vessel. cryoprecipitate. arteriography will also help assess the presence or absence of collateral flow around the site of obstruction. trauma. Thrombolysis is less invasive than surgery. and massive gastrointestinal hemorrhage.5 mg/dl). or hemorrhage prior to the guidelines given as absolute contraindications. Patients with hyperviscosity syndromes. vascular puncture. The main disadvantages of angiography are the risks of using radiopaque contrast. and degree of underlying atherosclerosis. The primary complications of thrombolysis are intracranial hemorrhage. In addition. and (4) there exist absolute or relative contraindications to thrombolytic therapy. When comparing thrombolytic agents. These techniques are noninvasive. delays time to definitive revascularization. significant liver disease. or platelets should be administered. and its invasiveness. and if no reperfusion has occurred after 12 to 18 hours. repositioning of the catheter may be necessary. thrombocytopenia. Other anticoagulants. and there appears to be an increased incidence of bleeding complications with tPA. The previous gold standard oftherapy was surgical intervention. puncture of a noncompressible vessel within the past l0 days. such as hypothyroidism. depending on the duration and location of the occlusion. due to atherosclerosis or other microvascular disease.

5.1. Antiplatelet agents may help prevent acute occlusion. Vasodilatory agents are not useful because of vascular fibrosis. although CBC. arteriography can be performed. prostacycline. In acute attacks intraarterial nitroglycerin has been shown to be of some benefit. Fibrous and granulomatous changes in the vessel walls can result in claudication.722 / ErunncrNcy MnucrNn: THr Conn CunnrculuM tion. Sublingual nitroglycerin has not been shown to be of any use. or two ofthe three changes. with no other risk factors for atherosclerosis other than smoking. platelet count. are generally pronounce4 and it cannot be used in the outpatient setting. Smoking should be Buerger's disease (thromboangiitis obliterans) is a nonatherosclerotic. including depression. antihistamines. and will not show the calcifications or irregular plaques one would see with atherosclerotic vascular disease. in patients under the age of 50. patients may need to modify the use of these tools. emotional stress. They have considerable side effects. and ESR may help to evaluate if there is a primary underlying hematologic or inflammatory disorder. and surgical sympathectomy. . It starts distally and progresses proxi- avoided because it potentiates vasoconstriction. and therefore is not recommended in the treatment of Raynaud's phenomenon. Thrombosis (2. vascular bypass grafts. The majority of patients presenting to the ED with Raynaud's phenomenon report onset of an episode after stress or exposure to cold temperatures. The majority of these episodes last less than 15 minutes. have all been used with highly variable degrees of success and are not currently recommended. or necrosis. side effects. resuits are inconclusive. light-headedness. 5. inflammatory vaso-occlusive disorder of small and medium vessels. particularly upper limb ischemia. Drug therapy has been tried in patients with moderate to severe Raynaud's. Nitroglycerin has also been used because of its effects as a vasodilator. possibly related to tobacco smoking. aspirin. such as caffeine. rest pain. cyanosis. although they have little or no effect on disease progression. sary. although narcotics may be required for more severe pain. 7) Aneurysms of the thoracic aorta are most common in the descending aorta but may involve any segment. Cessation of smoking is the cornerstone of treatment. alcohol. If the diagnosis of Raynaud's phenomenon is made. The most important factor is patient education to prevent episodes of vasospasm. Calcium channel blockers have been used due to their vasodilatory effects. although it is necessary to use topical ointment rather than systemic agents. sympatholytic agents. Other agents. and ultimately. cyanosis during a period of deoxygenated blood flow. as are analgesics. ulceration. however. increased ctz-adrenergic receptors. and then reactive hyperemia. If a patient presents with moderate to severe Raynaud's phenomenon with tissue ischemia. with advice to keep the hands and feet warm through the use ofgloves and to keep core temperature warm as well in order to avoid peripheral vasoconstriction. In some cases job-related trauma. may contribute to Raynaud's. I. steroids. orthostatic hypotension. and mally. cold temperatures. Prostaglandins. Circulating vasoconstrictors have not been proven to act as factors in Raynaud's phenomenon in laboratory investigatlon. although conditions such as cold temperatures. should also be avoided. orthostatic hypotension. ulceration or tissue necrosis may occur. Serotonin antagonists are being investigated" but. Although not needed for diagnosis.6) Diagnosis is made based on findings of limb ischemia. can also be used. Reserpine and guanethidine. such as use of laboratory tools. Aortic Dissection (2. and ment for Raynaud's. and if this is the case. such as headache and hypotension. terbutaline. Bathing the hands and feet in warm water may help treat mild attacks. such as plasmaphere- sis. and sympathetic stimulants. and dipyridamole have not consistently been proven to be of any benefit. The etiology of Raynaud's phenomenon is uncertain. have been used for many years as treat- There are no pathognomonic tests for Raynaud's phenomenon. such as nicardopine or diltiazem. diarrhea. Patients need to be warned of side effects of calcium channel blockers. again. and symptoms may have resolved by the time the patient is seen by the physician. Sixty percent of patients with this condition have these triphasic color changes. decongestants. Verapamil has minimal peripheral activity. Sympathectomy. Nifedipine is the calcium channel blocker of choice because it also has antiplatelet activity and better peripheral vascular effects than other calcium channel blockers. wound care to minimize tissue loss or secondary ischemia is neces- acute ischemia. or amputation may be necessary in advanced stages of the disease. and increased responsiveness of vascular smooth muscle to sympathetic mediators are all thought to be contributing factors. although only approximately half respond well to medical therapy. Other treatments. and impotence. Patients should be taught to avoid abrupt temperature changes. In the majority of cases nonsteroidal antiinflammatory agents can be used. and emo- Buerger's Disease tionally stressful situations. the remaining 40% may show only pallor. such as headache. peptic ulcer disease. hyperbaric oxygen. medication or aggressive therapy is usually not required. In approximately 20o/o of the cases. with highly variable results. increased central sympathetic tone.

a high-pitched blowing decrescendo diastolic murmur heard best at the third left or second Ancillary Tests Radiographically. pathophysiology.25). Syphilitic aneurysms are now rare. and difficulty visualizing the aor- tic knob or descending aortic outline are all suggestive. prognosis is poor in untreated patients. found incidentally on a routine chest radiograph. All major vessels should be auscultated for bruits. the patient may have wheezes or decreased breath sounds. Physical signs in TAAs are more subtle than those of AAAs. As with all aneurysms. and blood pressures should be checked in all extremities. a widened superior mediastinum (mediastinal width-to-chest width ratio > 0. whereas initial management of descending TAAs is usually medical. the greater the risk of dissection. Therefore. and can dissect proximally. According to the law of LaPlace. In nonemergent patients. at or near the ligamentum arteriosum. neoplasm. Left-sided heart failure can be ease and due to congenital or acquired cardiac disease. Patients with hoarseness due to recurrent laryn- insufficiency. bounding or water-hammer (Cor- Classification is based on etiology. TAAs tend to progress. Most thoracic aortic aneurysms (TAAs) are atheroscle- rotic. If the subclavian artery is compromised. or cough. If there is bronchial compression. and lens subluxation. at a given pressure wall tension increases in direct proportion to its diameter. Aneurysms of the ascending aorta dilate the aortic annulus resulting in aortic rigan's) pulses. left-sided heart failure. dyspnea. and extend distally. as are descending thoracic aneurysms. occluding coro- nary arteries. They are not palpable. Five-year survival ranges from 15% to l9Yo. or hemoptysis from bronchial compression or erosion. Aneurysms of the ascending aorta may involve the aortic valve or coronary arteries. The neurologic examination should reveal any presence of ischemic or compressive neuropathy. as well as by nasopharyngeal bleeding or aspirated hematemesis. and for signs of AAA. . Pain associated with bony erosion may mimic or other thoracic strictures. pistol-shot femoral pulses. left mainstem bronchus depression. may prevent.Cenorovescut-A. rarely. Treatment Treatment of ascending TAA is surgical. Aneurysms of the aortic arch have the potential to occlude the subclavian and carotid arteries with limb and cerebrovascular compromise. the greater the diameter. or neoplastic chest or back pain. in a weakened vessel. Aortic regurgitation is also due to rheumatic heart dissyphilitic aortitis. tracheal or esophageal deviation to the right. kyphoscoliosis. Etiology and Pathophysiology geal nerve involvement will have unilateral vocal cord paresis or paralysis. and esophageal compression may result in dysphagia. Symptoms are often related to size and location. cysts. Surgical consultation should not be delayed in either symptomatic or asymptomatic patients. Descending TAAs may present with back pain secondary to spinal erosion. as well as risk factors. of TAA. or decrease the rate of. and the effects on adjacent structures. Overall. Initial Presentation Thoracic aortic aneurysms are often asymptomatic. expansion and risk of rupture. the patient may present with symptoms of cerebrovascular accident or limb ischemia. Dffirential Diagnosis Compressive symptoms may be caused by mediastinal abscesses. such as Marfan's syndrome or cystic medial necro- sis and. and probability of dissection. Stigmata of aortic regurgitation. for signs of Ehlers-Danlos syndrome such as joint hypermobility and bruising. Other causes include progressive degenerative diseases. Patient history may reveal the gradual onset of compressive symptoms. or neoplasms. resulting in dyspnea or chest pain. and tuberculosis. chest wall deformities. Descending thoracic aneurysms originate distal to the left subclavian artery. so signs are related more to size and location. The patient should also be examined for signs of Mar- fan's syndrome. Ascending aortic aneurysms are commonly due to medial degeneration as in Marfan's syndrome. such as arachnodactyly. which can be visualized by direct or indirect laryngoscopy. such as a widened arte- rial pulse pressure. often with use of a betablocker. Those involving the aortic arch are usually secondary to atherosclerosis. arising in the descending thoracic aorta and extending to the abdominal aorta. although not pathognomonic. involving the visceral vessels. and capillary pulsations (euincke. musculoskeletal. Thoracoabdominal aneurysms are rare. joint hypermobility.R DTsoRDERS / 723 Anatomic Classification right intercostal space. Aortography is the definitive study to verify the aneurysm. CT or MRI can provide useful information. Treatment of hypertension.s pulse). may be present. Stretching of the recurrent laryngeal nerve may cause hoarseness. syphilis. cardiac. Hemoptysis can be caused by numerous upper and lower airway disorders such as bronchitis.

The combination of hypotension. a patient may present with syncope. Anatomic Clas sifi cation Ancillary Classification is based on location of the dissection. Involvement of the aortic annulus may produce CHF and signs and symptoms of aortic insufficiency. not on the site of origin of the tear. Pain may also be reported in the epigastrium. iliac. Hypotension may result from dissection Tests The ECG may indicate chronic hypertension. These include DeBakey type III and are referred to as distal dissections. smoking. abdominal organs. and age. and rupture into the pericardium may cause cardiac tamponade. and strictures. However. When the blood supply to the brain or spinal cord is compromised" neurologic findings typical of acute stroke or paraplegia may result. Echocardiography is noninvasive. resulting in true and false lumina. If the dissection severely limits or obliterates flow to the major vessels of the brain. paraplegia. including varices. It is contraindicated in patients with esophageal disease. Blood tracks between the media and the adventitia. or congenital abnormalities. Disadvantages include . and provides detailed anatomic information about the dissection. Type A includes DeBakey types I and II (ascending only or ascending and involving the arch. quick. Risk factors associated with dissection include large aneurysm diameter. Thus. flank. DeBakey and Stan- ford. Computed tomography with contrast medium is minimally invasive with a sensitivity and specificity equal to aortography.t Thoracic Dissection into the pericardium with pericardial tamponade or hypovolemia secondary to rupture. Only intravenous contrast is necessary. All aortic dissections not involving the ascending aorta are defined as Stanford type B. image quality is adversely affected by obesiry mechanical ven- tilation. normal. visceral or renal ischemia. muffled heart sounds. tumors. or extremities. Spiral CT adds the advantages of increased scan speed and the ability to provide three-dimensional images. Chest pain may be similar to that of acute MI or pulmonary embolism. This degen- eration may be secondary to atherosclerosis. The most common catastrophe involving the thoracic aorta is acute dissection. although blood pressure can be elevated. evidence of early ischemia or infarction will be seen. or any extremity. Initial Presentation Typically. Distal extension usually occurs very rapidly because of little tissue resistance in the potential space. ECG findings indicative of myocardial ischemia are present in 10o/o to 40o/o of patients. and requires no contrast or radiation. decreas- ing the risk of nephrotoxicity. pregnancy. although communication between the two may be present. or low. or acute pulselessness in an extremity. including coronary involvement. Stanford type A aortic dissection involves the ascending aorta and is frequently described as a proximal dissection. More than 75o/o of patients have a history of chronic hypertension. Distal extension of a thoracic dissection may of with symptoms typical acute surgical abdomen. and emphysema. Pulse deficits and blood pressure discrepancies between limbs are characteristic signs. hypertension. Howeveq pulse deficits in the lower Etiology Dissection results from endothelial disruption with leakage of blood into the media. Retrograde dissection may occlude coronary arteries. These are usually noted in the upper extremities due to involvement of the subclavian arteries. easily performed at the bedside. myocardial ischemia or infarction. acute stroke.In addition. and jugular venous distention (Beck's triad) indicates pericardial tamponade. respectively) and occurs in approximately 67oh of patients.124 / EurRceNcv MrorcrNr: THn Conn Cunruculul. Medial necrosis may also occur with coarctation. Transesophageal echocardiography has replaced aortography as the gold standard for detection of thoracic aortic dissection. excruciating chest pain that radiates to the back. or cystic medial necrosis as in Marfan's syndrome. There are two widely accepted systems of classification. or femoral arteries may present simulate an acute thromboembolic disease. Pulse discrepancies from occlusion of subclavian. However. It overcomes many of the obstacles to transthoracic echocardiography. due to degenerative weakness of the muscularis layer of the aorta. abdomen. Dffirential Diagnosis The symptomatology of acute thoracic aortic dissection may mimic a number of pathologic processes. and may not be tolerated by up to 3% ofpatients. patients experience abrupt onset ofa learing. survival can be improved by early diagnosis and rapid institution of medical and surgical therapy. or heart block if the coronary vessels and conduction system are involved. and functional information. the sensitivity of transthoracic echocardiography is only -60%. widely available. extremities may occur if dissection involves the iliac or femoral arteries. Untreated patients have a mortality of over Io/oper hour delay.

Cemlovescur-{R DTsoRDERS
increased image processing time for more sophisticated
images, increased signal noise, and decreased intravascular detail. CT has the disadvantage ofpatient transfer and
restricted access to the patient while being scanned.
MRI is appealing because it is noninvasive, requires no
contrast medium, and can visualize the aorta and its
branches in detail, but its limited availabiliry high cost,
and inaccessibility to the patient limit its use in the emergent settmg.
Aortography remains one of the best methods to assess
the anatomy ofthe aorta and its branches, but disadvantages include risk of aortic rupture from catheter manipulation, and nephrotoxicity or anaphylaxis from contrast
media.
Treatment

Arterial pressures, urine output, level of consciousness, and neurologic status should be closely monitored.

Hypotension usually responds to fluid resuscitation with
crystalloid or blood products. Immediate surgery is necessary when the ascending aorta is involved in the dissection (Stanford classification type A), because of the
risks of acute aortic regurgitation and coronary sinus
occlusion. Dissections of the descending aorta (type B)
are initially treated medically and repaired later unless
evidence of continued dissection is present. Medical
treatment consists of aggressive blood pressure control
with beta-blocking agents and nitroprusside. Narcotics
and short-acting benzodiazepines may be used to alleviate pain and anxiety.

SELECTED READING
Bradbury AW, Milne AA, Murie JA. Surgical aspects of Behget's disease.
Br J Surg 1994;81(12):1712-1721.
Browne BJ, Jotte RS, Rolnick M. Raynaud's phenomenon in the emergency
department. J Emerg Med 1995;13(3):369-378.
Chirillo F, Cavallini C, Longhini C, et al. Comparative diagnostic value of
transesophageal echocardiography and retrograde aortography in the
evaluation of thoracic aortic dissection. Am J Cardiol 1994;74(6):
590-595.
Cook JB Ma AO. Medical therapy of peripheral arterial occlusive disease.
Surg Clin North Am 1995;75(4):569-579.

Curci JJ. Modes of ilresentation and management of inflammatory
aneurysms of the abdominal aorta. J Am Coll Surg 1994;178(6):
573-580.
Dapunt OE, Galla JD, Sadeghi AM, et al. The natural history of thoracic
aortic aneurysms. J Thoracic Cardiovascular Surg 1994;107(5):
1323-1332; discussion 1332-1 333.
Gloviczki P. Ruptured abdominal aortic aneurysms. In: Rutherford RB, ed.
Vascular surgery, 4th ed. Philadelphia: Saunders, 1 995; 1060-1069.
Grayor RA, Comerota AJ, Douville I et al. (the STILE Investigators).

Results

of a prospective randomized trial evaluating

surgery versus

thrombolysis for ischemia of the lower extremity. The STILE Tial. Ann
Surg 1994;220(3):25 1 166; discussion 266168.
Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative
treatment of abdominal aortic aneurysms. J Vascular Surg 1992;15(6):
1046-1056.
Kerr GS, Hallahan CW, Giordano J, et al. Takayasu arteritis. Ann Intern
M e d 1994;120(1 1):9 19-929.
Kuzu MA, Ozaslan C, Koksoy C, et al. Vascular involvement in Behget's

disease:

/ I25

8 year audit. World J Surg 1994;t8(6):948-953; discussion

9s3-954.
Laissy JP, Blanc F, Soyer i et al. Thoracic aortic dissection: diagnosis with
transesophageal echocardiography versus MR imaging. Radiology
1995;194(2):331-336.
Lavanier GL, Sacks Q Robinson ML. Acute limb ischemia. Emerg Med

Clin NorthAm 1992;10(l):103-1 19.
Mandell BF, Hoftnan GS. Differentiating the vasculitides. Rheumatic Dis
C lin Nor th Am 199 4 ;20(2) :409 442.
Mitchell MB, Rutherford RB, IGupski WC. Infrarenal aortic aneurysms.
In: Rutherford RB, ed. Vascular surgery, 4th ed. Philadelphia: Saunders,
1

995; I 032-1059.

Ouriel K, Comerota AJ. Thrombolytic therapy and the management of
peripheral arterial occlusion. In: Ouriel K, ed. Lower extremity vascular
disease. Phlladelphia: Saunders, 1995;295-320.
Ouriel K, Shortelt CK. Popliteal and femoral aneurysms. In: Rutherford

RB, ed. Vascular surgery, 4th ed. Philadelphia: Saunders,

1995;

l 103-1 I 12.
Riggs P, Ouriel K. Thrombolysis in the treatment of lower extremity occlusive disease. Surg CIin NorthAm 1995;75(4):633-645.
Roggo A, Brumre U, Ottinger LW, Largiader F. The continuing challenge
of aneurysms of the popliteal artery. Surg Gynecol Obstet 1993;
t 77(6):565-s72.
Rothrock SG, Green SM. Abdominal aortic aneurysms: current clinical
strategies for avoiding disaster. Emerg Med Rep 1994;15(14):125-136.
Rubin GD, Zarins CK. MR and spiral,/helical CT imaging of lower extremity occlusive disease. .lurg Clin North Am 1995;75(4):607-620.

Siegel CL, Cohan RH. CT of abdominal aortic anetrysms. Am J
Roentgenol 1994;163(l):17 -29.
Siegel CL, Cohan RH, Korbkin M, Alpern MB et al. Abdominal aortic
aneurysm morphology: CT features in patients with ruptured and non-

ruptured aneurysms. Am J Ro entgen o I I 99 4;1 63 (5) : 1 123-1 I 29.
Soh D-W, Shin G-J, Oh JK, et al. Role oftransesophageal echocardiography in hemodynamically unstable patients. Mayo Clin Proc 1995;70:

925-931.
Tilson MD, Gandhi RH. Arterial aneurysms: etiologic considerations. In:
Rutherford RB, ed. Vasailar surgery,4th ed. Philadelphia: Saunders,
1995;253-263.

Venous (2.5.2)
The most common venous disorders presenting to the
ED are due to insufficiency, inflammation, or thrombosis.
These are best managed conservatively, and rarely require
surgical intervention. The primary goals of therapy are to
alleviate symptoms and to prevent the complications of
ulceration, systemic sepsis, and thrombosis.

Ve n o u

s I n s ullicien cy/Varic

os

itie s (2. 5. 2. I )

Venous insufficiency is a debilitating, although not a
limb- or life-threatening, disorder. Its main presentations
include telangiectasia and reticular or varicose veins,

although cutaneous changes including ulceration and cellulitis may develop. This venous dysfunction does sometimes occur after venous thrombosis, although the stigmata may be present with no evidence of phlebitis or
thrombosis, and patients who have had venous thrombosis do not necessarily show subsequent evidence of
venous dysfunction.
Varicose veins are the most common manifestations of
venous dysfunction. Varicosities occur as a result of several factors, including venous hypertension, venous valve
insufficiency, and degree of calf muscle contraction,

126 /

EunRcnNcy MnnrcrNr:

Tnr Conr

Cunnrculurvr

which is the primary pumping mechanism to assist blood
flow from the distal venous system. Calf muscle contraction primarily augments blood flow from the deep veins.
In venous insufficiency, blood refluxes via perforator
veins to the superficial veins, which have much less soft
tissue support. Therefore, patients most likely to have
varicose veins are those with elevated venous pressure,
such as patients who stand for prolonged periods of time,
and inactive patients with decreased muscle contraction.
There also appear to be hormonal influences because of
the high incidence of varicose veins early in pregnancy,
thought initially to be triggered by progesterone, although
estrogen also relaxes smooth muscle fibers. There may
also be familial inheritance of simple dominance. Varicose veins may be due to alterations in vein wall, collagen, and/or elastin characteristics.
The most common presenting symptom is diffirse ache
secondary to stretching of or pressure on somatic nerve
fibers adjacent to dilated veins. Patients will also show
concern for the cosmetic appearance of dilate4 tortuous
veins, even if asymptomatic.
Physical examination of the patient with venous insufficiency includes careful examination of the patient's
extremities from the groin to the toes, looking for reticular veins, telangiectasia, and varicose veins, which are
most evident along the greater saphenous circulation. The
varicosities should be easily compressible with no palpable cords. There may be chronic skin changes, such as
hyperpigmentation secondary to hemosiderin deposition;
however, ulceration or cellulitis can develop in these tisSUES.

Presence of reflux can be assessed using Doppler or
duplex examination. Continuous wave Doppler ultrasound can be used to detect reflux, and is one ofthe best
ways for assessing venous insufficiency by looking for
venous obstruction secondary to thrombosis.
The initial treatment of venous insufficiency is modification ofrisk factors, ifpossible, followed by conserv-

ative therapy. The patient should be discouraged from
standing for long periods of time, encouraged to increase
calf muscle use, which enhances muscular pump action,
and evaluated for application of external compression
therapy, including support stockings, elastic supports,
elastic bandages, cast boots, or semirigid support appliances. The elastic supports should have maximal pressure

distally, decreasing more proximally to encourage flow
from the periphery to the central venous circulation.
Venous stasis ulcers require bed rest, leg elevation, and
aggressive wound care; infected ulcers and those with

surrounding cellulitis require appropriate antibiotic therapy. There are no specific medications at this time for
venous insufficiency, although methylxanthines may
improve blood cell deformability and may inhibit interleuken-2 alterations of the microvasculature. Oxypentoxifulline may also promote healing of venous ulcers,
although results ofthese studies are inconclusive.

In patients who fail external compression therapy, surgical therapy may need to be considered, including superficial venous sclerotherapy or disruption of perforating
veins. Valvuloplasty and venous segment transfer may
also need to be considered.
Thromboembolism

(2.

5.

2.2)

Thromboembolism or deep venous thrombosis (DVT)
is a common condition. Its true incidence is difficult to
determine, because the majority of cases are not clinically significant. Its diagnostic significance is due to the
risk of pulmonary embolus if a clot dislodges and travels
to the pulmonary vasculature; therefore, early diagnosis
and treatment are essential to avert this potentially catastrophic complication. Deep venous thrombosis has
many etiologies, which can be divided into clinical factors and coagulopathies. This section reviews the pathophysiology, etiologies, and epidemiology of deep venous
thrombosis, and its clinical presentation, differential
diagnosis, current diagnostic methods, and recommended
treatment.

E ti

ology and Pathop hy s i o I o gy

Venous thrombosis occurs as a result of hemostatic
abnormalities involving the vessel wall, the coagulation
cascade, or blood flow characteristics. When abnormalities of one or more of these components occur, there is a
high risk of thrombosis.
Veins are components of a low-flow system, not
exposed to significant hydrodynamic stresses; as a result,
they have a poorly developed adventitia and media. Oneway valves in the superficial and deep systems, assisted
by the pumping action from calf muscle contraction,
facilitate venous return from the periphery to the central
circulation. Proximal to the valves there is relative stasis
that increases with valve damage; vessel trauma with
endothelial damage activates the coagulation cascade
with platelet activation and aggregation, resulting in a
thrombus.

Normal blood flow is nonturbulent with little contact
between the cells and the endothelium. When blood is
more viscous, there is greater interaction between the cellular elements of the blood and the endothelium, leading
to increased risk of thrombosis. Enhancement of the procoagulable state or deficiencies of the anticoagulable
state, such as antithrombin C, protein C, and protein S
deficiencies, also result in increased thrombosis or
decreased fibrinolysis.

Most commonly, DVTs occur due to an acquired,
rather than congenital, condition. Some of these include
pregnancy, malignancy, burns, trauma, sepsis, hemiplegia, the post-operative state (particularly pelvic surgery
or orthopedic procedures), and cardiac disease. Other

Cennrqvescut-AR DTsoRDERS
contributing factors include sedentary lifestyle, the use of
estrogen-containing compounds, and a history of previous thrombotic events. Cardiovascular disease and shock
states are thought to be predisposing factors due to
hypoperfusion, resulting in stasis and thrombosis. Malignancies are well documented as creating a hypercoagulable state. Congenital or hereditary blood defects, such as
antithrombin III, protein C, protein S, plasminogen,
heparin cofactor 2, and tPA deficiencies, dysfibrinogenemia, and other hereditary coagulopathies, as well as factor XII deficiency, contribute to a hypercoagulable and
ultimately thrombotic state. Acquired blood defects, such
as polycythemia, thrombocytosis, lupus anticoagulant,
anticardiolipin antibodies, and acquired coagulopathies
also create a hypercoagulable state.

Initial Presentqtion
The presentation of deep venous thrombosis varies
greatly. Patients often present with a complaint of recentonset unilateral leg pain and swelling. There is generally
no history of trauma or infection, although there may be
a history of recent immobilization, such as recent hospitalization, a sedentary lifestyle, or a history ofprolonged
sitting, such as an automobile or plane trip. DVTs are
much more common in the lower extremities than in the
upper. The majority of DVTs occur in infrapopliteal
veins, although proximal DVTs are more likely to result
in embolization. The location of swelling depends on the
location of the thrombus, with venous congestion and
swelling distal to the thrombus. There may be localized
pain secondary to focal inflammation, although this is
nonspecific and is often present with other disorders.
Patients may present with concurrent dyspnea related
to pulmonary thromboembolism, and the first indication
that a patient has a DVT may be cardiopulmonary arrest
due to pulmonary embolism (PE). The latter is known as
the "great imitator," with some patients presenting with
chest pain, shortness of breath, tachycardia, diaphoresis,
and anxiety, although few or none of these symptoms
may be present.
Past medical history is important to determine if the
patient has had previous evidence of embolic or thrombotic events, rheumatic heart disease, ischemic heart disease, malignancies, infections, or trauma or surgery to the
pelvis, abdomen, or lower extremities. Significant family
history includes autoimmune disease, malignancy, hyperlipidemia, or coagulopathy. Other significant factors
include use oftobacco, use oforal contraceptives, sedentary lifestyle, and obesity.
The physical examination of patients with DVT is variable and often misleading. In addition to the patient's
vital signs (to assess for fever, tachypnea, and tachycardia
in particular), it is important to determine the presence or
absence of palpable cords, erythema (90oh specificity),

/

127

warmth of the extremity or part of the extremity (90%
specificity), superficial venous dilatation (80% specificity), tenderness, and the comparative size of the
extremity (taking measurements at several locations on
the extremity). The classic Homan's sign with pain of the
calf on dorsiflexion with a palpable cord in the calf has a
75Yo specificity and a40Yoto 50oh sensitivity. Stasis der-

matitis and venous stasis ulcers can be present, without
evidence of preceding or concurrent DVT. It is important
to evaluate the patient for signs and symptoms of PE,
such as sudden onset of dyspnea with tachypnea, tachycardia, pleuritic chest pain, and hemoptysis.

Dffirential Diagnosis
The differential diagnosis of DVT includes varicose
veins, muscle strain, hematoma, venous reflux, Baker's
cyst, cellulitis, lymphangitis, malignancy with venous or
lymphatic obstruction, exacerbation of rheumatoid arthri-

tis, contact dermatitis, gout, erythema nodosum, and
superficial phlebitis.

Ancillary Studies
Due to the 50oh error rate in diagnosis of DVT based
on history and physical, diagnostic studies have been
developed to improve the accuracy of diagnosis. The gold

standard

is contrast venography, with the injection of

radiopaque contrast into the peripheral veins of the
affected extremity. Flow can be assessed from a distal to
proximal direction, with visualization of the vessels and
any vascular lesions, including obstruction. Chronic
occlusion can be differentiated from acute occlusion.
Although highly specific and sensitive, it is also invasive.
Risks of this technique include inability to cannulate a
distal vein, allergy to contrast media, renal compromise
from contrast media, and potential for thrombogenesis by
the contrast media. This technique also requires the
appropriate radiology suite and staffto perform the procedure.

Studies have been developed that are less risky, with
very good sensitivity and specificity. One of the most
popular techniques is venous impedance plethysmography (IPG). This is a noninvasive test that analyzes flow
characteristics of the venous system. Recent studies
demonstrate a sensitivity of 6lYo to 9loh, a specificity of
45Yo to l00o/o, a negative predictive value of 68% to 960/o,
and a positive predictive value of 48oh to 1000/0, compared to venography in symptomatic patients. Because of
these wide variations, other tests should be considered in
patients with high clinical suspicion.
Other tests showing higher sensitivity and specificity
include Doppler ultrasound, B-mode compression ultrasound (preferably with color Doppler), fibrinogen labeling, and ascending contrast venography. Doppler ultra-

128 /

ErvmRcENcy MnorcrNr,:

Tnn ConB CuRnrculunr

sound is a noninvasive method that is considered 94%
accurate. The diagnosis is made by assessing the venous
velocity signal. It is most useful in symptomatic patients
with proximal DVT and is not sensitive in patients who
are asymptomatic or in patients with calf DVT. Real time

B-mode ultrasound is also useful for the diagnosis of
proximal DVT with a sensitivity of 90o/o and specificity
of 97% in symptomatic patients. Again, sensitivity is
decreased in asymptomatic patients or patients with calf
DVTs. B-mode combined with duplex scanning Doppler
is faster and more accurate than each of the other studies
individually. The color-enhanced Doppler flow can examine both deep and superficial veins and the color
enhancement allows venous flow assessment, with and
without compression of the vessels. Calf veins can be
assessed by this method and thrombus can be visualized,
and the age ofthe thrombus can be assessed. Its accuracy
in symptomatic patients is 73% to 92oh sensitivity with
860/o to 100% specificity. Limitations of ultrasound and
Doppler techniques also include availability of equipment and personnel to do the procedures, and risks of

interobserver inaccuracies.
D-dimer assay is currently being touted as an easy

adjunct

in the

diagnosis

of DVT. D-dimer is a fibrin

degradation product found to be elevated in patients with
DVT and PE. The blood test, using a highly specific monoclonal antibody against D-dimer, induces red-cell agglutination in the presence of elevated D-dimer levels. Early
studies suggest that a positive test is 93% sensitive for the

diagnosis of proximal

DVI

and 70% sensitive for calf

DVI with 77o/o specificity. This low specificity is due to
other conditions with elevated D-dimer levels, such as
surgery or trauma within 10 days, acute infection, pregnancy or recent delivery, active collagen vascular disease,
or metastatic cancer. Since all of these are DVT risk fac-

tors, D-dimer is currently being recommended only in
conjunction with another study, such as IPG, to improve
the positive predictive value of both studies.
There are no other specific screening studies available,
although a prothrombin time and a partial thromboplastin
time are recommended as baseline studies prior to therapeutic anticoagulation. Other baseline studies should
include hemoglobin and hematocrit, and a platelet count.
Specialized tests, such as factor assays and antithrombin
III levels, are not part of the screening procedure; however, they may be indicated in the workup for the etiology
of the DVT. Pulse oximetry, arterial blood gases, electrocardiogram, and chest x-ray should be obtained if there is
any suspicion of pulmonary embolism.

as the use

Thrombophlebitis

is currently

being

(2.

5. 2.

3)

Thrombophlebitis is usually a self-limited disorder of
superficial veins. It is localized inflammation and thrombosis of a vein, often precipitated by trauma. The majority of cases are reported after venous cannulation; vasculitis and use of oral contraceptives are also associated
with its development. Endothelial damage triggers an
inflammatory response, manifested by tenderness and
overlying erythema. Secondary infection by skin organisms such as Staphylococcus epidermidis can occur with
rare progression to suppurative phlebitis.
Complications include involvement of the deep venous
system with subsequent deep venous thrombosis and pulmonary embolism, septicemia, and postphlebitic ulcera-

tions. Diagnosis is primarily clinical, although duplex
scanning is advised to determine if the thrombus has
extended to the deep venous system.
Treatment is conservative, with use of analgesics, heat,
elevation, and elastic support bandages. Antibiotics are
not indicated unless an organism is isolated from blood
cultures, and anticoagulation is necessary only ifthe deep
venous system is involved. In cases ofextensive phlebitis,
recurrence, or suppurative disease, phlebectomy may be
necessary.

SELECTED READINGS
Baker WF, Bick RL. Deep vein thrombosis. Diagnosis and management.
Med Clin North Am 1994;78(3):685-712.
Bergan JJ. Venous stasis disease. In: Ouriel K, ed,. Lower extremity vascular disease. Philadelphia: Saunders, 1995.37 5-384.
Carter CJ. The pathophysiology ofvenous thromb osis. Prog Cardiovasc Dis

1994;36(6):439446.
Colucciello SA, Jones JJ Stewart C. Evaluation and management of deep
venous thrombosis. Emerg Med Rep 1996;17(9):89-100.
Johnson G. Superficial venous thrombosis. In: Rutherford RB, ed,. Vascular
s urgery, 4th ed. Philadelphia: Saunders, I 995; I 696-1 698.
Koopman MM. Diagnosis of deep vein thrombosis. Prog Cardiovasc Dis

1994;37

Traditional management of DVT is initial anticoagulation with intravenous heparin, followed by continued
anticoagulation with warfarin. Alternative therapy, such

agents,

mined if possible. Other treatments have included prophylactic heparinization in high-risk patients. In patients
who have contraindications or failure of anticoagulant
thenpy, an inferior vena cava filter should be placed to
prevent the occurrence of pulmonary embolism. Patients
also need to be evaluated for the risk of paradoxical
embolism, with migration of venous clot through a septal
defect resulting in cerebrovascular thromboembolism.

Markel

Treatment

of thrombolytic

investigated as are alternative heparin and warfarin regimens. The etiology of the thrombosis should be deter-

(t):1-12

.

A, Weich X Gaitini D. Doppler ultrasound in the diagnosis of

venous thrombo sis. Angi o I o gy 199 5 ;46(l) :65 -7 3.
Rosenow EC. Venous and pulmonary thromboembolism: an algorithmic
approach to diagaosis and management. Mayo CIin Proc 1995;70(I):

4549.
Weinmann EE. Salzman EW. Deep-vein thrombosis. N Engl J Med 1994;
331(24):1630-1641 .
Wells PS, Brill-Edwards B Stevens P, et al. A novel and rapid whole-blood

Ischemic changes are also rare. with recurrent prolonged episodes. The most common surgeries resulting in lymphedema are surgery of the breast. Geriatics 1995. However. or infection. The differential diagnosis of limb swelling is extensive. The main treatment for acute lymphedema is reducing the size of the limb. Depending on the etiology. however. is also used.Cenorovescur-c. Elevation is the simplest metho4 with positioning of the limb at approximately 45 degrees or more over the level of the heart. infection or inflammation. congenital vascular malformation. Anderson FA. factitious edema after prolonged application of a tourniquet. surgeries. and a thoracic problem is more likely to cause bilateral upper extremity. Systemic causes often result in bilateral exftemity swelling. graduated elastic support stockings. Some patients may have small vesicles on the skin draining clear lym- phatic fluid. Wells PS. decreased mobility due to the edema. Lymphatics (2.91(8):2184-2187. that are most likely to be seen are lymphedema and lymphangitis. Primary lymphedema may present as a familial disorder. to try to allow some of the lymphatic fluid to move to the normal limb. estrogen. trauma. less commonly. Chronic lymphedema is generally painless and progressive. as well as travel to countries where filariasis is common. rheumatoid arthritis. as in Meige's or Milroy's disease. is employed often. Ginsberg JS. Wheeler HB. Excoriation may occur. These include cardiac failure. Conservative management will usually address the acute symptomatology. it is important to determine if there is a family history to determine whether this is a primary or a secondary disorder. trauma. This can be attempted by several means.50(2):29-32. lymph node dissections. tumor invasion into the lymphatic vessels. Other causes of perceived lymphedema are urticarial manifestations of dermatitis. Heat therapy. irradiation. and monoamine oxidase inhibitors. and elas- tic bandages wrapped distally to proximally to help prevent fluid reaccumulation. and. When assessing a patient who has apparent lymphedema. due to increased vascularity.5. Most cases of lymphedema presenting to the ED are an acute exacerbation of chronic. such as stockings with sequentially inflated chambers. from distal to proximal. traumatic disruption. or prolonged positioning of the extremity in a dependent position. it can be unilateral or bilateral. which is thought to help mobilize fluid and soften the tissues. although ulceration is rare. and parasitic infection or lymphatic filariasis caused by Wuchereria bancrofti and other wormJike parasites. . using intermittent pneumatic com- pression. swelling. renal failure.R DISoRDERS assay for d-dimer in patients with clinically suspected deep vein thrombosis. or as a component of lymphatic dysplasia. and malignant melanomas of the leg. and hemihypertrophy. Extremity compression. It starts distally with proximal extension as the fluid builds up in the exkemity. including history of prior malignancies. Circulation 1995 .25(1 -2):6-26. arteriovenous fistula. abscess causing extrinsic compression of lymphatic vessels. After the initial fluid extravasation. complications such as ulceration or infection. there is eventual fibrosis and scarring of the skin with a peau d'orange snake or insect bite. The skin may appear slightly hyperemic and have slightly increased warmth. 35-36.3) Lymphatic vascular disease is not commonly seen as a presenting symptom in the ED. such as lymphatic dissection during surgi- cal extirpation of a malignancy. and some medications. Size reduction generally occurs with 2 to 5 days of continuous bed rest. DVT and pulmonary embolism: choosing the right diagnostic test for patients at isk. a congenital disorder in children associated with genetic syndromes. nifedipine. the condition of lymph fluid extravasation into the surrounding tissues. which impedes venous as well as lymphatic return. Haemostas is 1995 . The primary symptoms of lymphedema causing distress to patients are the sensation of extremity heaviness due to the accumulated lymphatic fluid. including methyldopa. with stimulation of lymphatic flow. cervical cancer. Other causes of secondary lymphedema include lymph node incision with fibrosis secondary to radiation. dependency. Lymphedema Lymphedema. gradual fibrosis and scarring in the tissues occurs so that eventually the edema becomes irreversible. occurs most commonly in the extremities. or obstruction of lymphatic vessels by a mass proximal to the lymphatic vessels. Massage of the limb can help promote drainage. The two most frequent conditions. lipedema. secondary lymphedema. This is usually secondary to an underlying disorder. although in North America and Europe surgical intervention is the most common cause of lymphedema. Filariasis is the leading cause of lymphedema worldwide. although rare. Initially. hypoproteinemia. infection with inflammation and occlusion of the lymphatic vessels. soft-tissue tumors. It is also important to obtain a medical history. hematoma. / 729 appearance. hy dr alazine. as well as possible lower extremity. myxedema. using a variety of techniques. hereditary angioedema. the adjacent limb should be massaged to stimulate its flow and then in the affected limb. allergic disorders. These include chronic venous insufficiency. Local or regional causes are more likely to cause unilateral disease. which is particularly effective in early cases. hepatic failure. it is important to remember that a localized intraabdominal process can result in bilateral leg swelling. Diagnostic methods for deep vein thrombosis.

are thought to increase macrophage activity and decrease proteinaceous fluid. Wright NB. AS. It is usually secondary to another infectious focus.4th ed. pulmonary vascular resistance rapidly ofthe lungs and a rise in arterial oxygen tension. SELECTED READING Gloviczki P. Clin 24O. MVP.22(6):392-398. TOF Aortic and mitral insufficiency. or trauma. Increased pulmonary venous return raises left atrial pressures. atrioventricular septal defect (endocardial causing defect). surgical.000 live births will be affected by CHD. and steroids have been tried with varying degrees ofsuccess to decrease the inflammation in long-standing cases of lymphedema. Other agents. This blood is then ejected into the pulmonary artery but most of it flows through the ductus arteriosus into the descending aorta. Inferior vena caval blood enters the right atrium and is preferentially directed to the left atrium via the foramen ovale. ed. diuresis is much less effective. combined with decreased right atrial pressure from cessation ofplacental flow through the ductus venosus. Over the . PDA. Rooke I Gloviczki P. half of which is delivered to the inferior vena cava via the ductus venosus while half enters the hepatic circulation. This relatively oxygen-rich blood then flows into the left ventricle and is ejected into the ascending aorta to supply the fetal upper body. and the ventricular septal defect (VSD) is the most common CHD.7 | (r):4449. insect bite. although diuretics have been used to help remove excess fluid in lymphedema of recent onset. and. with coverage of beta-hemolytic strep. 240). such as benzopyrones. Vascular surgery. ASD. mitral valve prolapse. Young JR. atrial septal defeat. aortic stenosis. Relatively oxygen-poor blood flows from the superior vena cava to the right atrium and enters the right ventricle instead oftraversing the foramen ovale. Antibiotic therapy is essential. Bourgeois P. Select syndromes and commonly associated CHD Syndrome Congenital rubella PDA Down syndrome Fetal hydantoin Fetal alcohol syndrome Marfan's syndrome AVSD. coarctation of the aorta. Famaey JP.4th ed. In: Rutherford RB. Lymphedema: introduction and general considerations. Patients should be referred to their primary care physician or a vascular surgeon for follow-up and further evaluation as needed. Up to 20%o of patients with CHD have associated congenital anomalies At birth. adulthood. COA VSD. most commonly caused by beta-hemolytic streptococci. AS PDA. where there is more fibrosis. In cases of chronic lymphedema. Beyond elevation and compression. Today early discharge from the newborn nursery is common and acutely ill neonates may present to the ED for treatment. The umbilical vein carries oxygenated placental blood. particularly ifthe patient does not have a medical. Advances in surgical and medical management of these patients result in an 85% survival into Lymphangitis is infection of the lymphatic vessels. hypertrophic cardiomyopathy COA. Studies. (Table Lymphangitis C ardiol TABLE 199 1 .. The swollen leg. Philadelphia: Saunders. or occupational history suggesting a clear-cut etiology for the edema. the patient's nutritional and immunologic status should be evaluated" and occult malignancy should be considered. CONGENITAL ABNORMALITIES OF THE CARDTOVASCULAR SYSTEM (2. MVP TGA. Approximately eight of every 1.1 883-1 888. such as cellulitis. ed. The result is functional closure of the foramen ovale. 1995. CCA. as well as staphylococci. ASD. If malignancy is suspected. tetralogy of Fallot. Vascular surgery. If there is no obvious etiology. while systematic vascular resistance increases in response to removal of the low resistance umbilical circulation.9(3):443456. the septum pridecreases in response to expansion mum is pressed against the septum secundum. Arch Dis C h i I d 199 4.1920-1927. patent ductus arteriosis. ASD. Philadelphia: Saunders. supplying the fetal lower body and returning to the placenta via the umbilical arteries. can then be performed on an elective basis as necessary. ventricular septal defect. CT may be indicated. Sem Arthritis Rheum 1993. such as lymphoscintigrams. Joos E. VSD Maternal diabetes Turner's syndrome VSD.6) Congenital heart disease (CHD) is a group of conditions in which abnormalities in cardiovascular anatomy or function are present at birth or develop during normal maturation. it will usually not be necessary in the ED setting to initiate other measures. Clinical significance and differential diagnosis. TOF.130 / EunncnNcy MnucrNn: THr Conn CunnrculuM Medications are not routinely used in the treatment of lymphedema. Nonoperative management of chronic lymphedema. Lymphatic disorders in rheumatoid arthri- tis.VSD. ulceration. Pathophysiology Fetsl to Neonstal Circulution The placenta provides for gas and metabolite exchange in the fetus and the ventricles exist in a "parallel" circuit. 1995. In: Rutherford RB. The swollen leg and primary lymphedema. AVSD. Carty HM.

resulting in either life-sustaining flow or additional stress to the circulation. In certain CHD. and should be allowed to maintain that position if possible. hypoplastic left heart. When present in children. including maternal and perinatal information. and is common in premature infants and those born and living in high altitudes. and primary pulmonary hypertension all cause chest pain. and performance in physical education. most often in the newborn nursery. Hypertrophic heart disease may be found up to 20o/o of patients when present in a first-degree relative. Infants or children presenting with cyanosis should be triaged to receive immediate care and supplemental oxygen. Fetal hydantoin syndrome is associated with an increased risk of CHD. TGA should be considered in the cyanotic neonate born to a diabetic mother. Thirty to 40%o of infants with fetal alcohol syndrome have CHD. including any presence of cyanosis and any oxygen therapy and subsequent response. atrial septal defects (ASD). course Emergency Department Evaluation Neonates who are intolerant to the changes in the tran- sitional circulation present early with cyanosis. Specific CHD predominates in certain clinically recognizable syndromes (Table 240). Cardiac and pulse oximetry monitoring should be continuous in the cyanotic child. Advanced airway management may be necessary in the critically ill with respiratory decompensation. and patent ductus artenosus are most common. with coarctation of the aorta most common. Maternal complications. Beyond 2 months. bicycle riding. is more common with ventricular septal defects (VSD). mitral valve prolapse.Cennrovescur-{R DTsoRDERS of several days. The age of onset of cardiac failure can provide a diagnostic clue regarding the underlying CHD.1) History A birth history should be obtained. A positive family history of CHD. Because extracardiac manifestations may be noted in about 25Vo of patients with CHD. substance abuse. Coarctation of the aorta and transportation of the great vessels are predominant when cardiac failure occurs between I week and 2 months of age. and tetralogy of Fallot (TOF). ventricular septal defect is the most common lesion producing cardiac failure. Children may exhibit poor tolerance of exercise compared to their peers. patent ductus arteriosis (PDA). Thus. fetal circulatory pathways persist. A growth history may reflect delays due to heart disease. coarctation of the aorta.6.g. In addition. The child with CHD often assumes a position that reduces the work of breathing (e. especially in firstdegree relatives. coupled with a careful physical examination and selected ancillary studies will help establish a diagnosis and treatment priorities. and may also have a history of syncope. the ductus arteriosis constricts and eventually becomes the ligamentum arteriosum. most commonly ventricular septal defect or atrioventricular septal defect (endocardial cushion defect). decreasing shunting and increasing flow through the pulmonary vasculature. Chest pain is usually not a manifestation of cardiac disease in the pediatric patient but circumstances surrounding the pain should be detailed as should any episodes of syncope. and in response to high oxygen saturation and bradykinins.. transposition of the great vessels. The patient with aortic stenosis may have atypical chest pain with exertion or at rest. Flexing the hips and knees increases systemic vascular resistance. decreasing pulmonary vascular resistance during the first few weeks of life influences the timing of clinical signs and symptoms from CHD that rely on relative differences between systemic and pulmonary vascular resistance to sustain life. Several historical clues can be helpful in diagnosing CHD and differentiating organic from innocent murmurs. should be elicited. dyspnea. especially ventricular and atrial septal . These changes transform the fetal circulation to the neonatal circulation and pair left ventricular outflow with the high resistance systemic circulation and right ventricular outflow with the low resistance pulmonary circulation. The incidence of CHD in infants of diabetic mothers is five times that of the general population with transposition of the great arteries (TGA) the prevalent lesion. A detailed history. The response to supplemental oxy- gen can guide the physician in determining whether or not the cyanosis is resulting from a cardiac or pulmonary cause. chest pain is rarely associated with CHD. Infants with CHD may exhibit feeding difficulties such as or diaphoresis. Forty to 50o/o of patients with Down syndrome also have a CHD. About 30% of patients with Turner's syndrome have CHD. stair climbing. one should inquire about the presence of a congenital malformation syndrome (Table 240). FamiliaVGenetically Transmitted Disorders (2. Severe pulmonic stenosis. Patent ductus arteriosis is the most frequent cardiac anomaly in rubella syndrome babies. / l3l crying is often readily noted. and in up to 30% of infants born to diabetic mothers. Cyanosis at rest may be overlooked by parents while cyanosis during exercise or easy fatiguing. From birth to I week old. Other infants with CHD typically present in the first few weeks of life. A history of squatting following exercise is characteristic in patients with tetralogy of Fallot. and specific questions should be asked regarding play habits. or medication exposures. while the emergency physician may also be confronted with an older child with an undiagnosed murrnur. knee-to-chest). such as diabetes. most frequently ventricular or atrial septal defects or tetralogy of Fallot.

More common is the innocent continuous murmur of a venous hum. tetralogy of Fallot. in which the patient's arterial PaOz is normal. A child with chronic hoarseness and a heart murmur may have cardiovocal syndrome. Physical Exuminstion In addition to the general physical examination. The infant presenting with cyanosis deserves particular attention. The management of the patient is guided by differentiating between pulmonary and cardiac causes of the cyanosis. while weight is more adversely affected in lesions producing cardiac failure. VSD. VSD ASD. tetralogy of Fallot. Atrial and ventricular septal defects and patent ductus arteriosus are most commonly associated with cardiovocal syndrome. C ardiovascular Exsmin ation Radial and femoral pulses should be palpated and compared for timing and strength. such as aortic or pulmonary stenosis or coarctation of the aorta. and the arterial pCOz comfortable at rest but have increased cyanosis with agitation. increased catecholamine release). Infants with central cyanosis are warm and well perfused with bluish conjunctivae and tongue. ventricular septal defect. PaOz. will often lessen the cyanosis unless significant intrapulmonary shunting is present. and patent ductus arteriosus. evidence ofrespiratory distress. especially in the presence of aortic regurgitation. The arterial pCOz is usually normal and there may or may not be a murmur present. Both transcutaneous oxygen saturation and arterial PaOz are low.and back. patients with pulmonary cyanosis will show improvement in their oxygen saturation. effort. Auscultation of the heart should include the precordium. Obstructive lesions without cardiac failure. which is most often in the right upper sternal area.732 / Eur. The infant with pul- monary cyanosis will have some degree of respiratory will be abnormal. or from a lesion associated with aortic runoff (patent ductus arteriosis. Ebstein's anomaly. cific attention should be given to spe- abnormalities of growth. Arterial blood pressure should be measured in both the arms and legs in any patient with suspected coarctation of the aorta. are associated with normal growth. total anomalous pulmonary venous return. caused by closure of the aortic and pulmonic valves. In the absence of . and right bundle branch block. even at rest. and clinical picture. coarctation of the aorta. Wide splitting is noted in pulmonary stenosis. Examination of the chest should begin with inspection. Pressures in the legs are normally l0 mm Hg higher than in the arms. RBBB. In response to administration of 100% oxygen. The second heart sound. a patent ductus arteriosis should be considered. and patent ductus arteriosis. atrial septal defect. total anomalous pulmonary venous return. coarctation reverses this relationship. Elevated pulmonary venous pressure is implied in the otherwise happy infant with persistent shallow tachypnea. aortic insufficiency. TAPVR. Except for aortic and pulmonic regurgitation.ncrNcv MporcrNn: Trtn Conn Cunnrcur-unr defects. more noticeably is split during inspiration due to delayed closure of the pulmonic valve from increased right ventricular filling. PS. venous hum PDA. A continuous muffnur extends from systole into diastole and indicates continuous blood flow. and associated presence of intercostal retractions or nasal flaring. murmurs occur during systole. right axilla. PS. patent ductus arteriosis. Cardiovascular examination Feature Deceased femoral pulse Prominent cardiac impulse Widely split S Continuous murmur Associated Airway Coarctation of aorta PDA. Peripheral cyanosis. which improves ventilation. When heard in the second left interspace. Since the aortic and pulmonary valves remain closed during isovolumic contraction. The patient's respiratory status should be noted. pulmonary stenosis. Cyanotic heart disease patients show little change in these parameters with oxygen administration due to shunting of blood away from the pulmonary system. anx- iety. arteriovenous malformation). pansystolic murmurs represenf blood exiting the contracting ventricle via either a ventricular systole defect or atrioventricular (mitral or tricuspid) vahular i4sufficiency. should be differentiated from central cyanosis. coarctation of the aorta. TAPVR. TOE RBBB PDA. Ebstein's anomaly. and should begin with concentration on the various heart sounds and their relation to respiration. Suprasternal pulsations can occur with aortic stenosis. TABLE 241. The hallmark of coarctation of the aorta is strong radial pulses with weak or absent femoral pulses (Table 241). and the presence of cyanosis. TOF. Infants with cardiac cyanosis will be distress. Cyanotic lesions generally impede both height and weight. right bundle branch block. ASD. aortic insufficiency. Bounding pulses can be a result ofincreased cardiac output (anemia. Crying. A prominent cardiac impulse is seen in patients with severe mitral regurgitation and large volume loads such as patent ductus arteriosis and ventricular septal defects. atrial septal defect. The venous hum murmur is louder in the upright patient and disappears with compression of the jugular venous system in the neck. Transcutaneous oximetry may be unreliable in poor perfusion states such as shock. These patients have large left-to-right shunts with pulmonary hypertension producing a large pulmonary artery that compresses the left recurrent laryngeal nerve against the aorta and trachea. including the rate.

Auscultation of the lungs should be done to search for rales and wheezes and evaluate the adequacy of ventilation. AS. The innocent murmur of newborns. and is a result of turbulence during increased cardiac output. Since murmurs of atrial septal defect and mild pulmonary stenosis can sound identical to the innocent pulmonic ejection murnur. ASD. noninvasive way to monitor the patient and the response to oxygen treatment. The presence of irregularly branched pulmonary vessels suggests systemic collateral arteries and is most often associated with severe pulmonic stenosis or atresia. cardiac silhouette. aortic stenosis. single ventricle COA. and the descending aorta will usually be on the same side as the aortic arch. transposition of the great arteries. rather than hepatomegaly. the superior vena cava will deviate to the right. VSD. and truncus arteriosis. Cardiomegaly can be seen with coarctation of the aorta. One should evaluate the pulmonary vasculature.TOF. truncus arteriosis. AS. In the cyanotic infant. and the aforementioned venous hum. Decreased pulmonary vasculature indicates obstruction to pulmonary flow. ASD. a murrnur may be present without pathologic significance. Puffiness of the eyelids. Ancillary Studies Measurement of oxygen saturation is a fast. E xtruc ardi a c E xamin atio n of congenital syndromes should be sought. Decreased pulmonary tricuspid atresia vasculature Systematic colateral arteries Severe pulmonic stenosis or atresia TOF. The cardiac silhouette may be normal or abnormal in the patient with CHD. TAPVR. Murmurs from ventricular septal defects are usually delayed for several hours to a few weeks depending on the size ofthe defect and the time at which the pulmonary vascular resistance drops enough to allow shunting to occur. A right aortic arch is characterized radiographically by transverse aortic arch situated to the right side of the a The tracheal air column will deviate to the left trachea. the innocent pulmonic ejection murmur. VSD. The infant with a cardiac cause of cyanosis will not show improvement in oxygen saturation with supplemental oxygen. double outlet right ventricle and single ventricle. or patient ductus arteriosis. Ebstein's anomaly. as approximately 20o/o of patients with CHD will have extracardiac anomalies. double outlet right Right aortic arch ventricle. as well as asplenia syndrome. In the acyanotic infant. patent ductus TABLE 242. PDA vasculature TOF. COA. the vibratory murmur is heard. the vibratory murmur. Between the ages of 2 and 7 years. limited to the left upper sternal atea. Murmurs detectable at birth are usually due to aortic or pulmonic stenosis. aortic arch. patent ductus arteriosis. pulmonary atresia. This systolic murmur has a twanging sound and lessens in the upright position. truncus arteriosis. and most patients will be cyanotic. AVSD TOF "Boot shape" TOGA "Egg on side" TAPVR "Snowman" lncreased pulmonary TOGA. total anomalous pulmonary venous return. Ebstein's anomaly. ventricular septal defect. The chest x-ray is invaluable in evaluating patients with suspected CHD (Table 242). Most normal infants have a palpable liver edge. the patient should be reexamined when causes ofincreased cardiac output such as fever or apprehension are eliminated. VSD. just below the clavicles. The lungs will appear overexposed. Patent ductus arteriosis murmurs may occur as early as 6 hours after birth. atrial septal defect. Arterial blood / 133 with normal pH and pCOz in the cyanotic infant with CHD. Cardiomegaly PDA. Patients with persistently or permanently low arterial oxygen saturation extremities. TA Acyanotic: ASD. AVSD. ventricular septal defect. rather than edema of the is a common manifestation of righrsided cardiac failure in small children. coarciation of the aorta. Tetralogy of Fallot. total anomalous pulmonary venous return.Cerutovescul{R DISoRDERS historical or physical evidence for underlying cardiac disease. The age of onset of murmurs can guide the clinician in diagnosis. and tricuspid atresia are the most common CHDs associated with this finding." is a short systolic ejection murmur present from birth to 3 months of age and it is clearly transmitted to both axillae. A right aortic arch is most commonly associated with tetralogy of Fallot (with or without pulmonary atresia). Chest x-ray findings in CHD Chest x-ray findings Associated anomaly Cyanotic: TOGA. but oximeter readings are unreliable in patients with poor skin perfusion. TA. is a more reliable sign of congestive heart The presence failure. Tachypnea. PDA. and position of the gastric bubble and liver (abdomgases are more reliable and show a low PaOz inal situs). tetralogy of Failot. increased pulmonary vasculature will nearly always be due to one ofthree lesions: atrial septal defect. such as the innocent murrnur of newborns. TAPVR. (<90%) often have red fingers and toes as a precursor to cyanosis and clubbing. fullness of the pulmonary vasculature is associated with transposition of the great arteries. TA. also termed "peripheral pulmonary artery stenosis of the newborn. but one more than 3 cm below the costal margin is abnormal. The innocent pulmonic ejection murmur is systolic.) . Atrial septal defect murmurs may not be detectable for a year or more after birth. pulmonary atresia. atrioventricular septal defect (endocardial Cushing defect.

Preterm neonates require a total loading dose of 20 mcglkg. Cyanosis increases with increased right to left shunting. followed by 25% of the digitalizing dose at g hours and at 16 hours.6. Specific ECG findings depend on the particular CHD. Patients with congestive heart failure also require admission and cardiology consultation. or angioplasty. Accurate evaluation of the anatomy and physiology is provided. and atrioventricular septal defect. while 40 mcg/kg is used from I month to 2 years of age and 3 5 mcg/kg (max 2. The classic "boot-shaped" cardiac silhouette of tetralogy of Fallot is due to an average size heart coupled with a concave pulmonary artery and decreased pulmonary markings. Most patients with mild CHD require no emergent treatment and should be referred to the pediatrician or pediatric cardiologist for continued care.0 mg) for those 2 to I 0 years old.05 to 0. Echocardiography provides noninvasive yet definitive evaluation of the patient with CHD. full-term neonates require 30 mcgkg. Acyanotic lesions can be subdivided into those with an increased volume load and those with an increased pressure load (Table 244). This is due to cardiomegaly with a narrow mediastinum. tetralogy of Fallot (TOF) is the most common cyanotic CHD. and lower gastrointestinal tract procedures. Abnormal abdominal situs suggests complex cardiac disease. an aortic arch convex to the right. MRI can be used to study function as well as structure and is the imaging modality of choice for confirming the presence of coarctation and for characterization of the lesion. hypotension. prostaglandin Ey (alprostadil) should be infused at a rate of 0. The ECG is almost always abnormal in the patient with CHD. aortic stenosis. patients with CHD require antimicrobial prophylaxis for dental. ventricular and atrial septal defects. Patients have the TABLE 243.. the less pulmonary flow. Endotracheal intubation may be required for the critically ill. persistence of a positive T wave is evidence for right ventricular hypertrophy. the greater degree of cyanosis. howeveq common side ed Pulm eflects include apnea. Transposition of the great arteries is characterizedby an.r arteriosis. fever. Cyanotic lesions can be further subdivided into those with increased or decreased pulmonary flow (Table 243). Disorders Due to Anatomic Anomalies (2. Furosemide can be administered for diuresis at an initial dose of I mg/kg intravenously. Cyanotic Heart Disease The common denominator with these lesions is admixing ofdeoxygenated venous blood with oxygenated arterial blood resulting in cyanosis. D ec reas E mergen cy D ep artm e nt I nterv entio n on ary F low Tetralogy ofFallot Supplemental oxygen should be administered to the cyanotic infant with CHD. and 75o/o to 85o/o in patients with normal visceral situs and dextrocardia. The patient should be placed on a cardiac monitor and intravenous access obtained. such as from increased pulmonary resistance or decreased systemic resistance. This is due to anomalous drainage of the left pulmonary veins into a persistent left superior vena cava (vertical vein) together with the irurominate vein and right superior vena cava. The T wave in Vr should be inverted after the first week of life. Cyanotic CHD Decreased pulmonary flow Tetralogy of Fallot Pulmonic stenosis Pulmonic atresia Tricuspid atresia Ebstein's anomaly I ncreased pulmonary flow Transposition of the great arteries Total anomalous pulmonary venous return Truncus arteriosis Hypoplastic left heart syndrome .1 mcglkglmin. Cardiac catheterization is generally used for balloon atrial septostomy. and most patients can undergo initial operative intervention based on echocardiographic results. initially.2) Congenital heart disease is commonly divided into cyanotic and acyanotic lesions. The ECG in the normal infant has right axis deviation and a dominant R wave in the right chest leads. Prostaglandin Er (alprostadil) treatment of the cyanotic infant with CHD causes dilatation of the ductus arteriosis and provides adequate pulmonary blood flow until surgical intervention occurs. Cardiology consultation should be obtained and the patient admitted to the pediatric intensive care unit./or corrective surgery provides definitive management of CHD anomalies. creating a right to left shunt. Digitalization may be required with half of the digitalizing dose given Constituting 10Yo of all CHD. Prostaglandin Er will maintain patency of the ductus arteriosis.egg on side" appearance to the cardiac silhouette. valvuloplasty. and j itteriness. urinary tract. For the infant with cyanotic CHD. The incidence of CHD is almost 100% in the presence of visceral situs inversus and dextrocardia. A pressure gradient exists between the pulmonary circulation and the systemic circulation. Palliative and.134 t EtrnRcrNcy MnorcrNn: THE Conn Cunrucur-ul. and the right heart abnormally convex in the frontal view. Total anomalous pulmonary venous return without obstruction presents with a "snowman" or "figure of eight" cardiac silhouette. Thus.

Antimicrobial prophylaxis for endocarditis is required for all patients. and radiographs show decreased pulmonary flow and a normal to enlarged cardiac silhouette. and the ECG reveals right axis deviation and right ventricular hypertrophy. Echocardiography confirms the diagnosis. Cyanosis occurs shortly after birth.2 mg/kg/dose) can be administered to decrease pulmonary blood flow and relieve anxiety. and agitation initiated by crying or straining. and caval-pulmonary isolation procedure when the patient is between 1. The ECG in each will show right ventricular hypertrophy. A harsh systolic ejection munnur is heard over the pulmonic area along with a single second heart sound. The tricuspid regurgitation produces a holosystolic murmur over the anterior left chest and a gallop is common. Left axis deviation and left ventricular hypertrophy are seen on the ECG. Bolus infusion of intravenous fluids or administration of phenylephrine can raise systemic pressures and decrease right-to-left shunting in refractory 135 Pulmonary Atresia Volume load stenosis). The degree of cyanosis and type of clinical dysfunction depends on the severity ofthe right ventricular outflow tract obstruction. Symptoms depend on the degree of stenosis. Severe cases will show right axis deviation on the ECG. a right bundle branch pattern. At least half of the patients will have a harsh holosystolic murmur along the left sternal border. BlalockTaussig). The Blalock-Taussig shunt is most commonly used and involves anastomosing the right subclavian artery with the ipsilateral pulmonary artery.. morphine sulfate (0. Definitive surgical management Definitive surgical management is to correct the ventricular septal defect and relieve right ventricular outflow obstruction. Cyanosis usually presents within the first few weeks of life but patients with a large ventricular septal defect may present with symptoms of congestive cardiac failure. Patients with a ventricular septal defect are described as having an extreme form of tetralogy of Fallot with the entire right aPressure may be normal.Cenuovescur-AR DISoRDERS TABLE 2-44. decreased right atrial emptying. Radiographs reveal a normal heart size with decreased pulmonary flow. overriding / cases. Chest x-rays reveal a "bootshaped" cardiac silhouette. the second heart sound will be single. symptoms are mild and fatigue is the only complaint. and hypertrophy ofthe right ventricle.. Milder cases only require medical management with valvuloplasty or surgical repair for more severe cases. ventricular output ejected into the aorta. Prostaglandin E1 (alprostadil) infusion is required for the severely cyanotic infant. Continuous murmurs of a patent ductus arteriosis or bronchial collateral flow are heard with a single loud second heart sound. followed by superior vena cava to pulmonary artery anastomosis (bidirectional Glenn shunt) and a Pulmonic Stenosis Epslein's Anomaly Pulmonic vahular stenosis is the most common form of right ventricular obstruction. ventricular septal defect.g.1 mg/kg) intravenously can be used if other measures fail. resulting in tricuspid regurgitation. Large P waves. of an abnormal tricuspid . This rare condition consists of downward displacement valve. Treatment of hypercyanotic spells involves placing the patient in the knee-to-chest position in a calming environment. Radiographs may be normal or show right atrial or ventricular enlargement with decreased pulmonary vasculature. begins with an aorto-pulmonary shunt (e. ventricular septal defect). dyspnea. tetrad of right ventricular outflow obstruction (pulmonic of the aorta. Acyanotic CHD Pulmonary valve atresia may occur with or without an intact ventricular septum. Presentation in infancy implies severe disease usually associated with pulmonic stenosis. In many patients. Propranolol (0. a poorly functioning small right ventricle. Prostaglandin E1 (alprostadil) infusion is required until definitive shunt placement. The entire systemic venous return enters the left heart via a patient foramen ovale or associated atnal septal defect.5 and 3 years of age. and right-to-left shunting between the atria. Patients may exhibit hypercyanotic or "tet" spells characteized by abrupt cyanosis. The second heart sound is single and loud and often there is no murmur. Cases with an intact septum account for 25o/o of newborn cyanotic heart disease and Atrial septal defect Ventricular septal defect Atrioventricular septal defect Patent ductus arteriosis Pressure load Coarctation of the aorta Aortic stenosis Hypertrophic heart diseasea Mitral valve prolapsea severe symptoms occur with closure of the ductus arteriosis shortly after birth. Tricuspid Atresia This lesion may be associated with other anomalies (e.g. but cyanosis occurs when obstruction is severe and right to left shunting occurs through a patient foramen ovale or ventricular septal defect. Dysrhythmias such as ventricular extrasystoles or supraventricular tachycardia are frequent. If needed.

A right aortic arch is present in almost half of the patients. Right atrial blood passes either to the right ventricle or via a patent foramen ovale or atrial septal defect to the left atrium. mitral and aorlic valves) and of the ascending aorta. diuretics. Hypoplastic Left lIeart Syndrome Usually diagnosed within the first day of life. if necessary. or combined ventricular hypertrophy. Over the first month of life. and possibly mechanical ventilation with positive end-expiratory pressure prior to definitive surgical repair. left. and poor growth. a single loud second heart sound. The foramen ovale and ductus arteriosis allow mixture of oxygenated and deoxygenated blood. It is more common in infants of diabetic mothers and in males (3:l). pulmonary hypertension is absent and cyanosis is mild to nonexistent. Patients presenting in pulmonary edema require diuretics. most often seen with an infracardiac connection. The site of this connection. and a holosystolic murmur from the ventricular septal defect. Radiographs show an "egg-onside" cardiac silhouette with a narrow mediastinum and increased pulmonary flow Patients require emergent prostaglandin E1 (alprostadil) infusion followed by balloon atrial septostomy (Rashkind procedure). a "snowman" appearance is seen on chest x-ray due to the supracardiac shadow. In the patient with pulmonary venous flow to the left innominate vein and a persistent left superior vena cava. A "scimitar syndrome" has been described in which the connection between the right pulmonary veins and inferior vena cava produce a crescent-shaped vertical shadow in the right lower lung fields on lateral chest radiographs. and about 50% will also have a ventricular septal defect and present with congestive cardiac failure. The patient in congestive heart failure should be managed with oxygen. Totsl Anomalo u s Pulmonary Venous Return In this rare lesion. Those with mild to moderate disease may need tricuspid valve repair or replacement as young adults. and coronary circulations in this anomaly. The degree of cyanosis depends on the amount of pulmonary blood flow.and tachydysrhythmias along with up to a 9o/o incidence of sudden death as adolescents or young adults. fatigue. supracardiac. along with amount of pulmonary venous obstruction. this syndrome features underdevelopment of the left side of the heart (left ventricle. ductal closure produces hypoperfusion with weak . which constitutes less than l% of CHD. and. Patients with an intact ventricular septum will have an arterial switch (Jatene) procedure as a neonate while those with a 7oh ventricular septal defect can undergo this procedure within the first 2 to 4 months of life. and digoxin. while control of supraventricular dysrhythmias is important in the older patient. the pulmonary vasculature resistance drops and the infant develops congestive heart failure with tachypnea. pulmonary. With the aorta arising from the right ventricle and the pulmonary artery from the left ventricle. early diastolic decrescendo murmur in the upper right and mid-left sternal border. Radiographs reveal enlargement of the cardiac silhouette and pulmonary vasculature. results in neonatal cyanosis and pulmonary edema and requires emergent surgical repair. Severe obstruction to pulmonary venous return.136 / EnmncrNcy MrnrcrNr: Tun Conn CunrucuLUM a prolonged P-R interval are seen on ECG. Patients have bounding pulses. spiked P waves. Since these patients are "ductus dependent" for systemic circu- lation. Three anatomic classifications exist based on the location of the connection between the pulmonary venous return and the systemic venous return: infracardiac. repair ofthe aortic arch. two parallel circuits are formed. digitalis. and cardiac. In patients without pulmonary venous obstruction. The ECG shows right ventricular hypertrophy with tall. both systemic and pulmonary venous blood flows to the right atrium. Truncal valve insufficiency produces a high-pitched. there is no direct pulmonary venous connection with the left atrium. Increased Pulmonary Flow Transposition of the Great Arteries Transposition ofthe great arteries accounts for 5o/o to of all CHD but is the most common cardiac lesion in cyanotic neonates. oxygenation. Increased flow through the mitral valve can produce an apical diastolic rumbling murmur. Newborns with cyanosis require prostaglandin infusion until surgery. and the right ventricle serves to main- tain both pulmonary and systemic circulations. hence. Truncus Arteriosis A single arterial trunk (truncus arteriosis) originates from the heart to supply the systemic. Patients also have a ventricular septal defect resulting in admixture of blood. Definitive treatment involves surgical repair of the ventricular septal defect and conduit placement between the pulmonary arteries and right ventricle (Rastelli procedure). Infants with a large left-to-right shunt and mild to mod- erate obstruction to pulmonary venous return will develop pulmonary artery hypertension and mild cyanosis. The ECG may show right. Intraatrial baffle procedures (Mustard or Senning) have been done in the past but patients commonly have brady. Pulmonary venous hypoplasia blood passes to the right atrium via the foramen ovale or atrial septal defect. Radiographs show decreased pulmonary flow. and right atrial and ven- tricular hypertrophy produce an enlarged cardiac silhouette. results in three clinical patterns.

Radiographs reveal a prominent left atrium. Lesions producing a volume load are more com- mon. Most with atrial septal defects are patients should be referred to the cardiologist for definitive evaluation. ventricular septal defect is the most common cardiac malformation. and those posterior and inferior to the fossa ovalis. and can confirm the presence of congestive heart failure. Patients rapidly increasing shunt flow. it is not considered a true atrial septal defect. and pulmonary artery. Surgical options include palliation (Norwood Radiographs reveal increased pulmonary vascularity and and Fontan procedures) and heart transplantation. feeding fatigue. Although usually of no hemodynamic significance. Up to 50% have spontaneous closure of the defect before 4 years of age. From 5o/o to 33oh of adults have a patent foramen ovale (valvular competent patent foramen ovale). Ventricular S eptal D efect Accounting for 25Yo of CHD. with left-to-right shunt lesions predominating.|. Right ventricular hypertrophy is seen medium systolic ejection munnur at the left middle to upper sternal border. Increased flow from the right ventricle to the pulmonary artery produces a 53. Lesions producing a pressure load are a result ofobstruction to ventricular outflow or narrowing of one of the great vessels. Decreasing pulmonary vascular resistance in the first few weeks after birth results in increased left-to-right shunting in patients with large ventricular septal defects. those at the upper atrial septum (sinus venosus). The ostium primum defect is in the lower portion of the atrial septum and usually is accompanied by a defect in the mitral valve. With increasing age. fully oxygenated blood returns to the lungs.Cannrov. A thdll may be present. Biventricular hypertrophy is seen on ECG.scur-AR DISoRDERS / L37 develop cardiomegaly and increased pulmonary vascularity on chest x-ray. rales. recurrent pulmonary infections. Asymptomatic asymptomatic through childhood. Atri oventric u I ar S ept al D efe ct This group includes the ostium primum defect and the endocardial cushion defect. Volume Loud With all these lesions. the ECG and chest x-ray are normal. When the right-to-left shunt ratio is greater than2'. Surgical repair early in childhood is indi- cated for symptomatic patients and those with shunt ratios of greater than 2:1. Increased flow across the mitral valve produces a diastolic rumble. Isolated atrial septal defects include those at the fossa ovalis (also known as ostium secondum and is most common). Defects may be found in various anatomic locations. Patients in congestive failure also have an Isolated Atrial Septal Defects patients be treated with diuretics and digoxin. on ECG. left ventricle. conditions resulting in high right atrial pressures can produce righrto-left shunting through the patent foramen ovale. and congestive heart failure in early infancy. Shunt dynamics are determined by resistance and relative pressures of the pulmonary and systemic circulations as well as the size of the defect. Atrial Septal Defects Pqtent Forqmen Ovale The foramen ovale normally permits right-to-left flow in utero. When the systemic and pulmonary vascular resistance are almost equal. These patients then present with pulmonary edema at 6 to 8 weeks of age. Since there is no deficiency ofseptal tissue. Patients with large defects have poor growth. resulting in development of congestive heart failure and a predisposition to atrial dysrhythmias. Surgical repair is indicated for symptomatic infants. The precordium is hyperdy- namic and the holosystolic murmur is less harsh. a communication exists between the systemic and pulmonary circulation.A. Large uncorrected ventricular septal defects result in increasing pulmonary vascular resistance. A characteristic feature is a widely split and fixed second heart sound. and in most infants closes during the first year of life. the left-to-right shunt may increase. increasing right atrial and right ventricular size with or absent peripheral pulses and shock. The ascending aorta may be inconspicuous resulting in a triangular cardiac silhouette. Since the shunt is left to right. the shunt becomes bidirectional and cyanosis develops (Eisenmonger complex). Patients with small defects are asymptomatic but have a loud harsh holosystolic murmur at the lower left sternal border. high flow across the tricuspid valve produces a mid-diastolic munnur. Right ventricular hypertrophy and an rsR' in the right precordial leads are seen on ECG. Patients presenting with congestive heart failure should Acyanotic CHD Acyanotic heart lesions can be subdivided into those that produce a volume load or a pressure load on the heart. A left-toright shunt occurs across the atrial defect and mitral . All require antimicrobial prophylaxis for endocarditis. but hemodynamics depend on the size of the shunt and the pulmonary vascular resistance. and hepatomegaly.

Surgical closure ofthe patient ductus is a low risk and preferable treatment patients.01 to 0. Cardiac auscultation reveals a short systolic mid-left sternal murrnur transmitted to the left intrascapular area.r insufficiency is present. Auscultation reveals a fixed. Indentation of the aorta at the narrowing. Femoral pulses are delayed compared to radial pulses. This flow is detrimental to the normal infant but may be life sustaining in those with CHD associated with decreased pulmonary flow. and lower extremity pulses are diminished or absent. Left ventricular or biventricular hypertrophy is evident on ECG in the presence ofa large patent ductus. Those with large defects exhibit failure to thrive and may present with congestive heart failure. The classic finding on physical examination is disparity in pulses and blood pressures of the arms and legs. and prostaglandin Er (alprostadil) infusion. In patients that depend on a patent ductus. a rumbling mid-diastolic murmur at the apex. Definitive surgical therapy should be performed and transient hypertension is seen in the postoperative period. Brachial blood pressure is above the 95th percentile for age and is higher than blood pressure noted on the legs (a reversal of normal findings). and often first-degree AV block. high pressure aortic blood flows to the pulmonary system as pulmonary vascular resistance falls. Examination reveals bounding arterial pulses. Ninetyeight percent occurjust distal to origin ofthe left subclavian artery atthe area ofthe ductus arteriosis (postductal). also known as the atrioventricular septal defect (AVSD). and leukocytosis characteize the slmdrome. and normal functional closure occurs shortly after birth. such as those with pulmonic stenosis. logic closure. Coarctation is the most common CHD associ- valves. along with preand poststenotic dilatation. widely split second heart sound. Treatment includes bowel decompression and antihypertensive agents. Radiographs reveal pulmonary vascular congestion and an enlarged cardiac silhouette. The patient should be stabilized for surgical repair with furosemide. Patients with a small patent ductus are asymptomatic but may develop heart failure later in life.f 38 / EnnRcrNcn MsorcrNr: THn Conn Cunrucururr. Symptoms usually develop early in infancy with failure-to-thrive. . Left-to-right shunting is both transarterial and transventricular inAVSD. and a pulmonary systolic ejection murmur. A prominent pulmonary artery with increased pulmonary vascular markings are seen radiographically. produces a "figure of three" sign. or hypoplastic left heart syndrome. fever. recurrent pulmonary infections. The patients have a hyperdynamic precordium and palpable thrill. Surgical repair is indicated for all defects. Patients with postductal coarctation may have only mild symptoms. Infectious endarteritis is a risk at any age no matter what the size of the ductus. right ventricular conduction delay. The ECG shows biatrial and biventricular hypertrophy. hyper- tension. A bicuspid aortic valve is present in over 70Yo of patients. Radiographs show rib notching between the fourth and eighth ribs in children over 5 years of age. When the narrowing occurs proximal to the ductus arteriosis (preductal). such as lower extremity fatigue. or subaortic stenosis. Mitral insufficiency produces an apical diastolic rumble. Abdominal pain. postoperative mesenteric arteritis (postcoarctectomy syndrome) occurs. Hypertension occurs in the vessels proximal to the coarctation. a split 52. prostaglandin (alprostadil) is administered at 0. differential cyanosis occurs as deoxygenated right ventricular blood flows across the ductus to perfuse the lower half of the body. Preductal coarctation is frequently associated with other cardiac defects and produces heart failure early in infancy. These patients exhibit failure to thrive and may have a variety of auscultory findings depending on the accompanying heart defects. a harsh holosystolic murnur at the lower left sternal border. digitalis. "machinery" murmur. The patient with a complete AVSD has increased pulmonary vascular markings with large pulmonary arteries and enlarged cardiac silhouette on chest x-ray. Patent Ductus Arteriosis The ductus arteriosis connects the left pulmonary artery to the aorta. consists of contiguous Coarctation of the Aorta atrial and septal defects and markedly abnormal AV Constituting 5o/o to 8o/o of CHD. may permit pharmaco- in all ated with Turner's syndrome. A bicuspid aortic valve results in a systolic ejection click or suprasternal notch thrill. MRI is the diagnostic modality of choice. Most patients are asymptomatic but more severe lesions are associated with easy fatigability and recurrent pulmonary infections. and char- acteristic left upper sternal thrill and a continuous. Patients with minimal atrioventricular (AV) valve involvement have minimal symptoms. The ECG can be normal or demonstrate left ventricular hypertrophy. left axis deviation. such as indomethacin. and congestive heart failure.05 E1 mcgk{min. coarctation of the aorta is a constriction of the descending aorta. Pressure Load The endocardial cushion defect. Occasionally. Valvular abnormalities vary. If the ductus remains patent. Down syndrome is associated with the complete form in which there is a sin- gle AV valve. Prostaglandin inhibitors. and a pulmonary systolic ejection murmur. Surgical correction is definitive but may iesult in pacemaker-requiring heart block or other dysrhythmias. tricuspid atresia.

Am Heart J 199 4 . and nearly 3. Cardiac issues in the pediatric emergency room. Nelson s essentials of pediatlics. Philadelphia: Lea & Febiger.37 (1):179-192. et al. Bank ER. Perloff JK The clinical recognition of congenital heart disease.3 1(3):573-582. 1996. 1994. Treatment. 2) Prolapse of the mitral valve is a common condition in which the valve leaflets bellow into the left atrium during systole. eds. Pinsky WW. Radiographs show a prominent ascending aorta. pulses decrease. ReisdorffEJ. Kleigman RM. SELECTED READING Aghababian RY. Physical findings vary with the degree of stenosis and anatomic type of lesion. Gersh Bt McGoon MD. often bifid pulse. or syncope. Pediatric emergency medicine. Occasionally. 1993. Ped ian' C i n North Ant 1 994. Hypoplastic left heart syndrome. 6. Bull C. Radiol Clin North Am 1993. Behrman RD. eds. Radiol Clin North Am 1993. Philadelphia: Saunders. Moss AJ.4 1 (5):99 I -1 0 1 5. Tetralogy of Fallot.6. aortic stenosis is found more often in males (3:l). Ann Thorcc Surg l99l. 1993. Flynn PA. Arvin AM. Presentation in infancy is termed critical aortic stenosis and it is accompanied by congestive heart failure and shock. DiMaio AM. Dysrhythmias may be treated with diisopyramide or amiodarone. A late systolic murmur is heard when there is mitral regurgitation. Engle MA. West J lvIed 1992. the older child has a history of easy fatigability. Norwood WI Jr. One-. I 1992. Roberts MR. Auscultation reveals a midsystolic click that becomes more audible with standing or Valsalva. least 60 mm Hg. Because Over the past 20 years cardiac transplantation has evolved from an experimental procedure to an accepted treatment for end-stage heart failure. Philadelphia: Saunders. McNamara DG. A discrete subvalvular membrane is present in 20%o of patients and results in outflow obstruction. eds.Cerurove. 1994. exertional chest pain. No specific treatment is indicated. Diagnosis is confirmed by echocardiography. angina or weakness. The cardiomyopathy may or may not cause left ventricular outflow obstruc- tion. Patients with echocardiographically confirmed prolapse and an audible murmur of mitral regurgitation require antimicrobial prophylaxis for dental. Singh J. below). Aortic stenosis may also be supravalvular or the obstruction may be due to asymmetric septal hypertrophy (see Hypertrophic Heart Disease. 1) Also known as idiopathic hypertrophic subaortic stenosis (IHSS). Hypoplastic left heart syndrome. five-. Mayo clinic practice of cardiology. Englewood Cliffs. Patients are usually asymptomatic but can have chest pain or palpitations. Agents that increase contractility. 2. 1996. Sudden death has been reported with commonly.68(5):7 07 -7 1 I. Groothius JR. As stenosis progresses. Pediatr CIin North Ant 1990. Cun'ent pediatric diagnosis and treatment. Hay WW. Haworth SG. should be avoided. Approximately 1. Physiology of congenital heart disease. Cardiac evaluation of infants. Wiegenstein JG. Gundry SR.600 transplants are performed each year in the United States. Philadelphia: Hanley & Belfus. and its intensity increases with standing or Valsalva (increased preload) and decreases with squatting (increased afterload). Pediatr Clin NorthAm 1992. Patients who are otherwise asymptomatic and without clinical findings on examination should be considered as having a normal variant of the valve. of cardiovascular disease.7) Complications Mitral Valve Prolapse (2. Clues in diagnosing congenital heart disease. Philadelphia: Saunders. and . or fifth decade of life. Arciniegas E. 70o/o. St. it has been associated with numerous medical conditions. Louis: Mosby. and tenyear survival rates are approximately 90o/o.39(5):955-986. 52(3):688-695. Nadas' pediatric cardiology. Burton DA. Magnetic resonance of congenital cardiac disease: an update. usually with betablockers.39(5):987 1006.37(1): 137 150. NJ: Prentice Hall. eds. More is asymptomatic until the thir4 fourth. Pediatr Clin North Am 1992. gastroin- testinal.S.R DTsoRDERS Aortic Stenosis Accounting for 5o/o of CHD. Radiographs and ECGs are normal.. CARDIAC TRANSPLANTATION (2. is aimed at decreasing the heart rate and increasing preload.31(3):553-571. Gillum RF. The infant with cyanosis in the emergency room. Hathaway WE. such as digitalis or isoproterenol. Examination reveals a brisk. Flyer DC. Stenosis of the aortic valve occurs in75%o of cases and a bicuspid valve is the most common defect. | 27 (4) :9 19-927 - Giuliani ER.scur-A.000 worldwide. Clinical symptoms depend on the degree of outflow obstruction. 156(4):392-398. Pediatr Clin North Am 1990. Ehlers KH. this defect also includes those patients with asymmetric septal hypertrophy. epidemiology of congenital heart disease in the U. Emergency management Boston: Butterworth-Heinemann. ed. Patients may be asymptomatic or have exertional dyspnea. Crowley Jl Oh KS. Hypertrophic Heart Disease / I39 (2. eds. Balloon valvuloplasty is standard treatment for symptomatic patients or those with a resting pressure gradient of at prolapse of the mitral valve is so common. Telltale signs of congenital heart disease. the patient aortlc stenosrs. and genitourinary surgical procedures. Arch Dis C hi ld t993 . Radiographs and ECGs are usually normal. Ledesma-Medina J. Cabalka AK.2. The ECG is normal but may show left ventricular hyper- trophy with long-standing severe stenosis. Parsley JW. Garson A. and the aortic systolic murmur radiating to the neck becomes louder and harsher. Newman B. 1990. a suprasternal thrill appears. The science and practice of pediatric cardiology. ed. The first year of life. Bricker JT. Bailey LL. A crescendo-decrescendo systolic murmur is present.

or under study. Rejection may occur at any time. Occasionally patients may present with complaints of fatigue.140 / 50o%. though. The most important risk factors for rejection include female recipient (especially multiparous). The second period is the maintenance phase. during which immunosuppressive medications are given at lower doses. emergency physicians must become increasingly skilled in the evaluation of the cardiac transplant patient in the ED. verapamil. In general cardiac function of the transplanted heart is excellent with a nearly normal left ventricular ej ection fraction. ketoconazole. but not so much as to invite infection. Physiologically the transplanted heart functions differently from the normal heart in several ways. in general. especially of atrial origin.g. Successful long-term immunosuppressive therapy requires depressing the patient's immune response enough to prevent rejection. and for congenital heart defects in pediatric patients. Drugs that increase cyclosporine levels include diltiazem. Arrhythmias have been shown to be associated with rejection. the pro- cedure has been performed in patients with refractory angina. and survival rates improve. Echocardiography may prove useful in adult patients with rejection. Other immunosuppressive medications used. carbamazepine. The most common regimen currently employed for maintenance consists of triple drug therapy: cyclosporine. benign cardiac tumors. and complications associated with the use of immunosuppressive medications. dias- . phenytoin. or increased nephrotoxicity. The most common reason for cardiac transplantation is end-stage heart failure. malignancy. The majority of patients with acute rejection are asymptomatic. Cardiovascular drugs after cardiac transplantation Drug Effect in recipient Digitalis Normal increase in contractility. fluconazole. Similarly. bromocriptine. More recently. and to perform warm-up exercises for 5 to 10 minutes prior to strenuous physical activity. The resting heart rate is usually higher (e. include antithymocyte globulin. FK 506. Advances in immunosuppressive therapy account for much of the improved survival rate in cardiac transplant TABLE 2-45. Most immunosuppressive protocols are divided into two periods. Similarly. OKT3. Emergency physicians should alter the doses or add or withdraw immunosup- pressive medications only after discussion with the patient's transplant physician. and therefore lacks efferent and afferent fibers. there is poor correlation between patient symptoms and rejection. The leading causes of morbidity and death following cardiac transplantation are rejection and infection. rapamycin. and mizoribine. metoclopramide. As the number of transplant operations performed each yeat increases. however. Phenobarbital. Err. 90 to 100 beats per minute) due to this lack of parasympathetic control on the sinoatrial node. and erythromycin. therefore. or palpitations. symptomatic cardiac arrhythmias. coronary occlusive disease in previously transplanted patients. Less than l}Yo of patients with rejection present with hemodynamic compromise.. human leukocyte antigen (HLA) mismatch. resulting in increased or decreased levels. methylprednisone. it is relatively uncommon after I year without significant alterations in immunosuppression. azathiopine. transplant patients are instructed to shift gradually from the supine to a standing position. The first period is the induction phase and involves the administration of high doses of immunosuppressive drugs for the first few weeks following surgery to prevent rejection. and female and younger donor hearts. Acute cell-mediated rejection is responsible for the vast majority of such episodes. RS-61443. minimal AV nodal effect None lncreased contractility and chronotropy I ncreased contractility and chronotropy Normal increase in inotrophy and chronotropy No vagalytic effect NormalAV block No reflex tachycardia No reflex tachycardia lncreased antagonist effect during exercise Atropine Epinephrine Norepinephrine lsoproterenol Quinidine Verapamil Nifedipine Hydralazine Beta-blockers Mechanism Denervation Denervation Denervation Hypersensitivity Denervation Hypersensitivity No neuronal uptake Denervation Direct effect Denervation Denervation Denervation patients. Other serious complications include allograft coronary artery disease. and lowdose prednisone. there are a number of drugs that interact with cyclosporine. cardiac transplant patients depend on circulating cate- cholamines to increase heart rate and contractility in order to increase cardiac output in response to stress or exercise.mncnNcy MnnrcrNe: THr Conr CunnrculuM respectively. and rifampin cause a decrease in cyclosporine levels. malaise. but 90%o occur within the first 6 months. The most significant difference is that the transplanted heart remains denervated. The gold standard for the diagnosis of acute rejection in adults is endomyocardial biopsy. See Table 245 for the effect of commonly used cardiac drugs in transplant patients. Cardiovascular drugs should be used with caution in these patients since these medications may have an altered effect due to denervation. Rejection Allograft rejection remains one of the leading causes of morbidify and mortality in transplant recipients.

also known as graft atherosclerosis. alone or in combination. the gastrointestinal tract.. Unlike normal atherosclerosis. The majority of life-threatening infections occur in the first 3 months following surgery (e.ns tolic dysfunction appears to be an early and sensitive finding. Candida. urine. All patients require a chest x-ray. Complications such as thromboembolism and infection limit their use as permanent replacements. TABLE early or late. Currently their only role is to serve as a short-time bridge to cardiac transplantation. Other treatment measures include the use of cyclosporine and FK 506. In this situation. and Coccidioides Sternal-wound infections and mediastinitis Staphylococci Enteric gram-negative bacilli Mycoplasma hominis Mycobacteria Candida species CNS infections T. early).lococcas species and gramnegative organisms. continuous cardiac monitoring. The diagnosis of rejection should be confirmed by biopsy (or echocardiography in the case of pediatric patients) prior to initiating treatment. and occur in approximately 20Yo of patients per year of follow-up. Echocardiography is already the primary tool to diagnose rejection in the neonate and pediatric cardiac transplant patient due to its less invasive nature. and usually involve Staphl. Allograft Coronary Artery Disease Allograft coronary artery disease. followed by blood. The lung remains the most common site of infection in cardiac transplant patients. or chronic rejection.g. Fever may not always be present in these patients. gondii JC virus (progressive multifocal encephalopathy) Skin Varicella-zoster virus (reactivated) patients after 1 year posttransplantation. usually methylprednisolone I g IV per day for 3 days. is the leading cause of death in these L47 Early and late infectious complications of heart transplantation Early (<3 months after transplantation) Pneumonia Nosocomial bacteria Cytomegalovirus (CMV) Legionella species Aspergillus species Streptococcus pneumoniae Toxoplasma gondii Rare pathoge ns: Mycobacte ri u m tube rcu loslq herpes simplex virus (HSV). often catheter-related. Because the heart is denervated cardiac transplant patients do not experience angina.. / Phycomycetes (rhinocerebral phycompycosis) ucocutaneous infections HSV Candida species Abdominal infections CMV and HSV (esophagitis and gastroenteritis) Cholecystitis Urinary tract infections Catheter-associated bacterem ia Late Pneumonia Pneumocystis carinii Nocardia asteroides CMV Community-acqui red bacteria CNS infections Listeria monocylogenes (meningoencephalitis) Cryptococcus neoformans (meningitis) N. All cardiac transplant patients with signs or symptoms of infection require a thorough evaluation. Bloo4 urine. they may present with new-onset or worsening shortness of breath. Graft failure. chest fullness. transplant coronary artery disease. the specific drug regimen to be used is best determined in consultation with the patient's physician. Risk factors for allograft coronary artery disease include hyperlipidemia. and arrangement for definitive diagnosis. Standard therapy for acute rejection involves high-dose corticosteroids. Prophylactic antibiotics should be initiated in the ED. Rather. and is a diffrrse process that effects both the proximal and distal coronary vessels. Late infections (>3 months posttransplant) are less common.g. and sputum should be sent for analysis and culture. vasopressor agents and empiric corticosteroid therapy may be initiated following discussion with the transplant physician. this disease is concentric and tubular. It is detectable angiographically in 30Vo to 50% of recipients by 5 years after surgery. obesiry donor age. fever does not always indicate infection (e. highly specialized centers. AMI. when immunosuppression is maximal.CenotovRsculen Dlsonor. gondii Aspergillus or Candida species (brain abscess) Infection The use of immunosuppressive medications to prevent allograft rejection results in an increased risk ofinfection. . a sign of rejection). The total artificial heart has been removed from clinical use except in a few. asteroides (brain abscess) M T. and sudden death. or signs and symptoms of congestive heart failure. During this period most infections are nosocomial. are the most common presenting symptoms of allograft coronary artery disease. Infectious complications are usually categorized as either 246. Histoplasma. See Table 246 for a list of early and late infectious complications. and donor ischemic trme. similarly. All patients suspected of acute rejection require admission. the only exception is the hemodynamically unstable patient. and the sternal wound.

In: Hosenpud JD. Blood pressure may be transiently elevated for a number of reasons in the ED. Physiology and hemodynamic assessment of the transplanted heart. Keeping the arm lowered at the patient's side or having the patient exert to hold the arm straight out may increase the pressure by as much as 10%. Cardiac transplantation. prog Cardiov as c Dis 1 99 1 . Ifthe cardiac rhythm is irregular. diclofenac.50:200-21 l. The frequency depends primarily on the specific immunosuppressive drugs utilized. HYPERTENSTON (2. After I year renal function tends to remain stable. Approximately 60 million people in the United States have been found to have a blood pressure greater than 140/90 or have been told by a physician that they have hypertension. An ECG should be performed and blood drawn for cardiac enzymes. Nephrotoxicity may present as transient acute renal failure in the first few months following transplantation. Cutaneous malignancies (usually squamous cell) are the most common tumors associated with the use of azathioprine. Cardiac transplantation: a review. Demographic differences apply to both primary and complicated hypertension. 1 g: 141-148.142 / ElanRcrNcy Mnolcnr: Tun Coru Cunruculurr. occasionally Korotkoff's sounds do not become inaudible with release of cuff pressure. before a definitive diagnosis is made. eds. The patient should be relaxed while the pressure is checked.8) Malignancy Hypertension is one of the most common illnesses in The development of malignant neoplasms is a major side effect of immunosuppressive therapy. The only definitive method to make the diagnosis is coronary angiography. Infections in heart transplant recipients. Oaks TE. aminoglycosides. the average ofseveral readings is considered the actual pressure. including cimetidine. Morton MJ. leading to confusion in diastolic reading. referred to as posttransplant lymphoproliferative disease. Calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors are the drugs most frequently used to treat this complication. PTCA and CABG are not usually effective in the treatment of allograft coronary artery disease. Hypertension occurs in 50% to 100% of cardiac transplant patients on cyclosporine. Echocardiography may reveal segmental wall motion abnormalities in the presence of ischemia. The higher recording of either arm should be considered the more accurate reading. a frequent condition encountered in the ED. The current estimate of the risk of malignancy after cardiac transplantation is l% to 2o/o per year. Starr A. 69-l 89. The first muf- . New York: Springer-Verlag. 1991. and continuous cardiac monitoring and IV access should be established. are hypertension and nephrotoxic- ity. Complications of Immunosuppressive Medications A number of side effects are associated with the use of immunosuppressive medications. The two most common. Men and blacks have the highest prevalence of hypertension. Br J Biomed Sci 1 1993. blood pressure will fall to near normal if rechecked after pain and anxiety are controlled. but severe and complicated disease still occurs. Because of the disease's diffuse nature. Miller LrWl Long-term complications of cardiac transplantation. and important. The emergency physician must be aware of a number of medications that exhibit a nephrotoxic synergistic effect with cyclosporine. It is. In most cases. CIin Infect Dis 1 994. SELECTED READING Hosenpud JD. Nephrotoxicity is another common side effect of chronic cyclosporine use. with several readings taken over time. the world. Petri WA. In contrast the most common tumor linked to cyclosporine therapy is a unique form of lymphoma. especially in underserved or noncompliant populations. The clinical presentation of posttransplant lymphoproliferative disease ranges from a mild lymphadenopathy and fever to widely disseminated disease. Norman DJ. and trimethoprim with sulfamethoxasole. Severe disease is generally more common in the middleaged with a peak incidence at 40 to 50 years. Cobanoglu A. While the systolic pressure is usu- ally easily determined. The equipment and examiner hands should be warm to avoid spurious elevations. Retransplantation is the only option for the majority of such patients. Measurement of the Blood Pressure The blood pressure should be checked in a standardized manner. the emergency physician should be thoroughly familiar with all aspects of this condition. therefore. It tends to develop within 4 to 6 weeks after surgery and usually requires multiple drug therapy to control. ranitidine. Improvements in early recognition and treatment of hypertensive patients over the last two decades have lowered the incidence of complications. The arm should be at the level ofthe heart and held by the examiner.r The patient should be placed on supplemental oxygen. The incidence of this tumor peaks 3 to 6 months after transplantation.33 :229182. The majority of the decline in renal function occurs within the first 6 months following surgery. Since rapid identification and treatment of hypertension-associated illness may make a critical difference in patient outcome. Wallwork J.

hypoperfusion. Cerebral hypoperfusion may occur at mean arterial pressures as high as 110 in those individuals with chronic systemic hypertension whose vascular beds no longer function with normal autoregula- tion. Normal blood flow is maintained only in a much narrower range of mean arterial pressure (MAP) compared with those without vasculopathy. and hormonal influences. and Treatment of High Blood Pressure (JNC-V) according to the risk of developing cardiovascular and cerebrovascular complications (Table 247). However. kidneys. There is no absolute pressure at which injury occurs.CennrovRscur-AR DTsoRDERS fling of Korotkoff's sounds is then considered to be the diastolic pressure. These patients are appropriately treated with intravenous medications and admitted to intensive care settings. vascular resistance. and pituitary release of argenlne vasopressln. and the inotropic state of the myocardium. The latter result from the actions of the reninangiotensin-aldosterone system. present in most organs. Fibrinoid material leaks into the vascular wall and eventually narrows the lumen with subsequent tissue ischemia. Classification of blood pressure in adults aged 18 and older" Category Systolic Diastolic (mm Hg) (mm Hg) <1 30 Normal 1 30-1 39 High normal Hypertension 1 40-1 59 Stage 1 (mild) 1 60-1 79 Stage 2 (moderate) 1 80-209 Stage 3 (severe) >210 Stage 4 (very severe) aPatients not acutely ill or taking antihypertensive tion. These include fluid shifts affecting intravascular volume. Individuals with long-standing hypertension may not experience vascular damage even with very high pressures (>130 diastolic) for short periods of time. The diagnosis of hypertension requires a reading greater than 140190 on two occasions at separate sessions. sympathetic tone. To protect critical vascular beds. without evidence of end-organ damage. The variable response of the vasculature to changes in blood pressure permits constant blood flow despite wide fluctuations in mean arterial pressure from 60 to 150 mm Hg. Hypertensive crisis is defined as severe hypertension (usually greater than 120 diastolic). There are multiple hemostatic control mechanisms to prevent injury to the vascular endothelium by higher than normal pressures. 1 993. renal. These patients can have the hypertension controlled more gradually with oral medications over 24 to 48 hours. With increasing pressures. A hypertensive emergency exists when there is severe hypertension associated with acute end-organ damage to the cardiovascular system. The physiology of autoregulation accounts . and patients who discontinue their normal regimen of antihypertensive medication. The diastolic pressure occurs when there is runoff of blood from TABLE 2-47. Definitions Hypertension is classified by the Fifth Report of the Joint National Committee on Detection. of most concern in the central nervous system. Diastolic pressures as low as 100 mm Hg have been known to precipitate complications in these circumstances. In hypertensive patients. Hemodynamics and Pathophysiology Blood pressure reflects a complex relationship between cardiac output and systemic vascular resistance. and cardiac complications are children with acute glomerulonephritis. Many interrelationships determine the ultimate tissue damage that occurs to vascular beds as a result ofhypertension. With chronic vascular disease or hypertension. The circulation adjusts to forces that ultimately affect the pressure. is most critically functional in the central nervous system. A hypertensive urgency exists when there is severe hlpertension. occurs when pressures fall outside these ranges. Evaluation. afterload. Patients at risk for neurologic. the arterioles respond to changes in blood pressure so that changes in flow are minimized. Evaluation. adrenal release of epinephrine and norepinephrine. <85 85-89 90-99 1 00-1 09 110-119 >120 medica- Modilied from the Fifth Report of the Joint National Committee on Detection. an autoregulatory process is activated in which tissue perfu- sion is maintained by arteriolar vasoconstriction. the normal autoregulatory responses are impaired. The clinical manifestations of hypoperfusion or hyperperfusion can occur with more modest fluctuations in pressure. this system of autoregulation fails with resulting vascular injury. the limits are reset at a higher level. With mild to moderate increases. Autoregulation. young women with preeclampsia. or hematologic system. much lower pressures may precipitate complications. Cardiac output is defined as heart rate times stroke volume-itself dependent on preload. if the pressure rise is gradual. However. Systemic vascular resistance is determined by neurohumoral control mech- anisms and renal vascular resistance. central nervous system. Peak pressure occurs during the systolic part ofthe cardiac cycle during which the pulsation of flow from the ventricle to the aorta exerts its maximal effect on the arterial wall. in a previously normotensive individual. and Treatment of High Blood Pressure (JNC-V). / 143 the arteries to lower pressure areas in the circulation while the heart is in its refilling phase.

Auscultation of the upper abdomen and flanks may reveal the bruits of renal artery stenosis. and pulmonary systems. Therefore. Risk factors for cardiovascular disease are important in deciding the need for intervention. Hyp ert ens iv e Enc ep hal op athy This condition results from the failure of protective central nervous system autoregulatory mechanisms. The desired degree and speed ofblood pressure change depends on a careful analysis of the risks of hypoperfusion and the potential dangers of persistently elevated pressures. The collapse of normal compensatory systems leads to ischemia and encephalopathy. and mural thrombi of the brain. Signs ofright or left ventricular failure should be sought. focal neurologic deficits. Damage to the vessel intima leads to fibrinoid necrosis. chronic hypertension. and past history of hypertensive emergency or urgency are elicited. stroke. As a general guideline. renal function if tests. .8.6) Conditions Requiring Immediale Lowering of Blood Pressure (Ilypertensive E mergencies) The presence of end-organ damage with elevated blood pressure is a hypertensive emergency. Examination Markedly elevated readings should be checked with attention to proper technique. sudden elevations in blood pressure in previously normotensive patients). and altered mentation indicate central nervous system dysfunction. Symptoms that may indicate a true emergency should specifically be sought (Table 248). searching for signs of end-organ damage should be performed. compliance with treatment. An ECG should be obtained to determine the presence of myocardial strain TABLE 248. Less than lYo of all hypertensive patients ever experience a hypertensive crisis.1) (See 12. A CT scan of the head is indicated if signs of CNS dysfunction are present. Since carbon dioxide regulates cerebral blood flow. In some cases immediate reduction is neces- TABLE 2-49. Advanced age. Loss of vessel integrity may be demonstrated by fundoscopy. Given the large number of patients with hypertension. Drugs to exacerbate hypertension MAO inhibitors Sympathomimetics Cocaine Anti histami nes/decon gestants Anticholinergics Tricyclic antidepressants Oral contraceptives Nonsteroid antiinflammatory drugs Ergotamines Steriods sary. Concurrent chronic illness may be a predisposition for hypertension. however. There are. circumstances where end-organ damage can occur with mild to moderate elevations (children. Current or recent use of medications known to cause hypertension is sought as well as discontinuance of antihypertensive drugs (Table 249). or ischemia. The presence of a sympathomimetic toxidrome may indicate medication as the cause of the hypertension. renal. these individuals represent a significant segment of the population. and cerebral vascular disease predispose to this condition. Diastolic pressures in these cases generally exceed 120 mm Hg. Toxic screens may confirm drugs as the cause of the hypertension and may be helpful in those cases suspicious for this etiology. An examination of the CNS. A chest x-ray to evaluate the mediastinum. loss of flow. Acute Hypertensive Crisis (2. History The duration of hypertension. hypercapnea exacerbates the clinical syndrome. cardiovascular. A history of seizures. and urinalysis should be performed on all patients hypertensive emergency is suspected. pregnant women.3. History in the hypertensive patient Duration of hypertension Medications and compliance Symptoms of cardiac ischemia or failure Symptoms of CNS dysfunction Recreational drug use Postmortem examinations reveal petechial hemorrhages. leading to cerebral edema. and retinal hemorrhages and exudates can occur. heart size. edema. the lower limit of cerebral autoregulation is about 25o/obelow MAP. microinfarcts. it is usually safe to lower the pressure to this degree. or signs of cardiac failure should be performed. Laboratory Testing A complete blood count. Segmental spasm of arterioles. The goal is to reduce blood pressure within I hour. but not more. The brain is flooded with transudate. in patients requiring rapid pressure reduction. Ifstill elevated. differences in upper extremity pressures should be sought. Proteinuria and hematuria may indicate renal damage.744 t EurRcnNcv MBucrNn: THn Conr CuRrucurunr for the nonlinear relationship between blood pressure and clinical symptomatology. electrolytes.

visual disturbance. controver- sial. some recommend treatment of hypertension associated with intracerebral bleeding when systolic pressures exceed 170 in the absence of hydrocephalus or vasospasm. Nausea. Ehlers-Danlos syndrome. The addition of nimodipine may protect against vasospasm and ischemia. and myocardial infarction. While it is true that hypertension is associated with an increased early mortaliry there is no evidence at the present time that immediate blood pressure reduction improves neurologic outcome or mortality. nystagmus. The MAP should be lowered by no more than 20o/o. and coma may occur. and the approach to these patients is controversial. paraplegia. and pregnancy are other causative factors. may be the presenting complaint. Treatment of hypertension in the poststroke period is. Blood pressure should be reduced gingerly (approximately 20o/o of MAP) and if there is worsening of neurologic deficit. aphasia. The absolute level of blood pressure alone does not distinguish pathologic processes involved. 25% of victims die within the first 24 hours and 90%o die within a year of presentation. A sudden tear of aortic intima with extravasation of blood into the media of the aorta occurs. Sodium nitro- sion. The treatment goal of hypertensive encephalopathy is to decrease the pressure. About 2. This may be a response to increased intracranial pressure. Ultimately. While controversial. unless volume overload is specifically determined to be present. however. intracerebral hemorrhage. Precipitous reduction below the limits of autoregulation may provoke worsening ischemia. Ischemic stroke produces a zone of severe tissue hypoperfusion immediately surrounding the blocked vessel. The patient should be followed closely and the pressure permitted to return to elevated levels if there is deterioration in the clinical status following antihypertensive therapy. prior to instituting treatment. seizures. or embolism) must be considered and evaluated by CT or MRI. Interruption of flow to a branch of the aorta may lead to acute stroke. High cerebral perfusion pressures are necessary for blood flow into the ischemic zones. Longterm control of hypertension reduces the incidence and severity of cerebral vascular disease. occasionally projectile. Nitroprusside is the drug of choice for hypertensive encephalopathy. High blood pressure may be necessary to maintain brain viability and avoid ischemia and vasospasm. luetic aortitis.000 new cases ofaortic dissection occur annually in the United States. blindness. Anatomic and hemodynamic factors subject the proximal aorta to maximal flexion and shearing stress.Cerurovescur-AR DTsoRDERS / 145 Hypertensive encephalopathy usually begins insidiously and progresses over several days. Hypertensive encephalopathy is a diagnosis of exclusion. vomit- Very high blood pressure (>120 diastolic) can be lowered by judicious use of agents that optimally have very ing. The ideal drug for this condition maintains cerebral blood flow. The goal is to reduce the pressure modestly to the 140 to 160 systolic range with intra- venous controllable agents. has rapid onset of action and short half-life. admission to intensive care and insertion of arterial catheters for continuous blood pressure readings should occur. transient hemiparesis. Alternatives are labetalol or nicardipine administered intravenously. Most patients with hypertensive crises are volume depleted and do not require diuretics. but Marfan syndrome. It has the hemodynamic responses of other calcium channel blockers and may ameliorate the hypertension associated with this disease. Stroke Acute Aortic Dissection Hypertension is the major risk factor for stroke. cerebrovascular thrombosis. Diuretic therapy can then be administered. Subarachnoid and Intracraniul B leed Bleeding in and around the brain is often associated with hypertension. and does not adversely affect the heart or other organs. Stroke syndromes (subarachnoid hemorrhage. there is little evidence that acute treatment affects the outcome. Children may present with abdominal symptoms. The drug can be started in the ED with automated blood pressure recording every few minutes. . A25o/o reduction in the mean arterial pressure is generally tolerated without untoward effects. prusside or labetalol are the most appropriate. With each systole. Reflex volume retention may occur after sev- eral days of nondiuretic antihypertensive therapy. medication should be immediately discontinued. Deficits related to loss of proximal aortic integrity may cause acute myocardial infarction. stroke. confu- few CNS effects and are short acting. Blood pressure is frequently elevated in acute stroke. blood dissects for varying distances in either direction. While hypertensive patients have a higher mortality than normotensives. Vomiting. Tissues distant from the central area are subjected to relative ischemia with potential viability. aortic valve incompetence and hemopericardium. The pressure normally declines without specific therapy over several days after a stroke. the result ofirritant effects ofblood in the CNS. The drugs must be administered intravenously and require an intensive care setting with arterial blood pressure monitoring. or the result of chronic hypertension. coarctation. allowing inherent autoregulatory mechanisms to function. bicuspid aortic valve. Hypertension is responsible for more than 50% of the cases.

or aortography. Episodes may be triggered by stimulation of nervous pathways below the cord lesion. nausea. There may be a significant difference in blood pressure between the upper extremities. or acute neurologic deficits occur. sodium nitroprusside. or phentolamine can be used in much the same way one would approach any patient with sympathomimetic cholamines. Additionally. abdominal pain. indicating partial compression of a subclavian artery. Blood pressure should be lowered immediately to limit the extent of dissection. increased oxygen demands. and diaphoresis.u*) should be minimized by the administration of beta-blocking agents such as propranolol. vomiting. the shearing stress (dP/dT. or nitroprusside. Preservation of myocardial tissue by enhancing coronary perfusion is also critical. or signs of sympathomimetic overactivity are usually present. Systolic blood pressure should be to less than ll0 mm Hg with nitroprusside. These patients may experience sudden severe hypertension with headache. If dissection is suspected. Beta-blockers given without concomitant alpha-blockade may significantly worsen the hypertension. A history of medication use and interaction. and chest pain. PCP. Patient education is of utmost importance in preventrng recurrences. Nitroprusside is useful in refractory cases. Decreasing heart rate. extremity pain. or esmolol. Drugs inducing tachycardia should be avoided. but the current favorite is cocaine. myocardial infarction. The clinical manifestations simulate those of pheochromocytoma. and severe hypertension when they ingest medications or foods with tyramine or sympathomimetic properties Syndromes of Catecholamine Excess (Table 2-50). Treatment is usually successful with phento- There are a number of secondary causes ofhypertension related to the presence of elevated circulating cate- lamine. or extremity ischemia. Either phentolamine or labetalol can be used for the treatment of hypertension in these patients. nausea. Therapeutic interventions should reduce cardiac work and oxygen demand. labetalol. and wall tension may ameliorate the condition. Pheochromocytoma Pheochromocytoma is a rare cause of hypertension. labetalol. Patients with this disorder can be treated with an alphablocker (phentolamine) or labetalol. diaphoresis. Me di c ation W thdrawal Syndro m e s The sudden cessation ofcentrally acting antihyperten- sive medications is a common cause of acute severe hypertension. which produces a wide range of symptoms. and diet pills may lead to this syndrome. abdominal pain. afterload.746 / EunncnNcy MrorcrNn: paraplegia (involvement of Tur Conr CunnrculuM anterior spinal vessels). MRI. Drugs such as amphetamines. and depressed ejection fractions occur with hypertension. This condition should be suspected in patients for whom no other explanation is apparent. Hypertension Associated with Spinal Cord Syndromes Patients with a variety of serious spinal cord diseases may experience a syndrome of sympathetic overactivify characlerized by headache. Drug Interactions Patients on MAO inhibitors may experience sudden overactrvlty. it is classically suspected on the basis of paroxysms of headache. diagnosis should be made rapidly with contrast enhanced Cl transesophageal echo (TEE). The pain may be present in the anterior chest or in the interscapular area and is controlled with difficulty. If that is not possible or effective. reflex bradycardia. Aortic dissection presents with severe pain that is usually maximal at onset. simply restarting the original medication usually brings about a smooth reduction in blood pressure. The initial approach is to remove any stimuli that might be causing the reflex autonomic activity. Hemodynamic demands resulting from severe hypertension can lead to unstable angina. Recreational Drugs Street drugs with sympathomimetic properties can precipitate severe hypertension. labetalol. LSD. anxiety. Clonidine and beta-blockers are the drugs most commonly implicated. diaphoresis. While it may present with sustained hypertension. and high blood pressure. back pain. focused history and examination. or pulmonary edema. they are important to recognize since their treatment is significantly different from other secondary etiologies. severe hypertension. Dissection of proximal and complicated distal dissections require surgical repair while the uncomplicated distal tear can be reduced treated medically. preload. While these are uncommon. It is often described as tearing or ripping. phenyl- propanolamine. Most may be suspected or recognized by a careful. Nitroglycerin and loop diuretics are the first-line drugs. palpitations. Myocurdial Ischemiu andAcute Pulmonary Edema Coronary artery disease. Depending on the degree of distal aortic involvement. If the patient is asymptomatic and does not meet criteria for a hypertensive emergency. intestinal infarction. .

exudates. convulsions. and blindness may also occur. These individuals are predisposed to abruptio placentae. any patient with blood pressures greater than 140/90 or who experiences a rise in the blood pressure as stated above are preeclamptic. Almost any renal pathologic process can cause the syndrome. High blood pressure. MAO inhibitor interactions Trycyclic antidepressants Sympathomimetics Caffeine Dextromethorphan Meperidine Antihistamines Foods containing tyramine Cheese Wine Beer Chocolate Pickled herring Yeast Chicken liver Broad bean pods Sauerkraut Yogurt Salami / 747 been used with success. Conditions Requiring Lowering of Blood Pressure over 24 Hours Preeclampsia and Eclampsia Normal pregnancy is characterized by a gradual fall of the blood pressure to a nadir that occurs at about 20 weeks' gestation. depressed mentation. Other findings in the preeclamptic patient include proteinuria (+l or greater on dipstick) and edema. If left untreated. Malignant Hyp ertension When severe hypertension results in the failure of autoregulation. ultimately. these patients should ideally be monitored in a setting capable of carefully attending to both mother and fetus. Note that this is lower than the definition of hypertension in nonpregnant adults. Preeclamptic patients require medications to prevent seizures. occurring in 8oh to l0% of all pregnancies. Retinal hemorrhages. The blood pressure criteria therefore are most important. Blurred vision. Nitroprusside may cause fetal cyanide poisoning and ACE inhibitors are not considered safe in pregnancy. which is at its worst in the morning and is usually occipital or frontal. Loss of arteriolar and capillary wall integrity leads to exudation of plasma constituents and obliteration of the vessel lumen. a level at which placental hypoperfusion is unlikely to occur. focal neurologic deficits. Labetalol and calcium channel blockers are also effective agents. the upper limits of diastolic pressures are 75 mm Hg in the second and 85 mm Hg in the third trimester. Drug treatment should be started with a goal of reducing the diastolic to 90 to 100 mm Hg. proteinuria. although dilantin may also be used. coma may ensue. Thereafter. Confusion. leading to worsening hypertenslon. Patients with malignant hypertension present most commonly with headache (85o/o). Nitroprusside is effective but cyanide toxicity is more likely in the cause or result setting of renal dysfunction. fetal demise as well as serious maternal illness may occur. loss of acuity.Cenorovescur-{R DTsoRDERS TABLE 2-5O. although others have Renal Insfficiency Acute deterioration in renal function may be either a of severe hypertension. Pure beta-blockers may decrease renal plasma flow and should be avoided. and acute liver and renal failure. It is important to note that some medications commonly used in nonpregnant patients with hypertensive emergencies are contraindicated during pregnancy. and all three classic abnormalities may not be present at the time of diagnosis in all patients. widespread fibrinoid necrosis results. and. intracranial hemorrhage. Because of the high incidence of maternal-fetal complications during the treatment of hypertension in pregnancy. An increase of greater than either 30 mm Hg in the systolic or 15 mm Hg in the diastolic pressure over baseline values defines hypertension during pregnancy. Changes in other vascular beds lead to hematuria. vascular changes ensue. Prophylactic medications should be used in those with diastolic pressures greater than 100 or with other signs of advanced disease. excessive sleepiness. The fundoscopic changes are usually present bilaterally. and papilledema are the primary clinical manifestations. A pregnant patient not previously known to be hypertensive with a blood pressure greater than 105 diastolic should be considered to have a hypertensive emergency. ultimately. Mortality rates approaching 90% within 1 year . These cri- teria may not occur simultaneously. the pressure gradually rises to normal levels at term. As a result of complex neurohumoral changes during normal pregnancy. Therapy should be directed at reducing systemic vascular resistance without compromising renal blood flow. and. may lead to potentially serious complications. there is activation of hormonal mechanisms. renal failure. The prognosis is unrelated to the type ofretinal change present. Ultimately. After 20 weeks' gestation. As renal function deteriorates. Magnesium is the preferred drug for this purpose. disseminated intravascular coagulation. Magnesium and hydralazine are the most commonly used medications for this indication. Untreated malignant hypertension has a dismal prog- nosis.

reduces angina and ventricular response in atrial fibrillation. Once there is improvement of the blood pressure in the ED. # cardizem CD:180-240 mg/day Actions similar to verapamil. and gynecomastia. and initial hypotension.148 / EnrncrNcv MnorcrNo: Tnn Conn Cunnrculurvl have been reported. # 10-40 mg/day Mechanism of action similar to other ACE inhibitors. avoid in diabetics . drug of choice hypertension with high renin levels. Uremia. # oral or sublingual:10-20 mg Sustained release preparation available Blocks calcium entry and dilates arterioles with afterload reduction. and COPD Calcium antagonists Nifedipine. sodium. may cause neutropenia. inhibiting chloride reabsorption in ascending loop. 1 2. CHF. CHF. hypotension. This approach may be used even in patients with papilledema. The degree of renal involvement is a good prognostic indicator. full effect may not be manifest for a week. diabetic nephrophathy. hyperglycemia. dosage should be reduced in renal failure. the stable. drug of choice in hypertensive emergency. sparing potassium. increases effects of ototoxic and nephrotoxic drugs Hydroch loroth iazide. prolonged action in renal disease Lisinopril. low GFR states. reduces angina. and myocardial infarction account for most deaths. pulmonary edema. contraindicated in CHF. and to mobilize large volumes. relatively contraindicated in diabetes. also suppresses aldosterone. oliguria. The clinical slmdromes often coexist to varying degrees. When the evidence of end-organ damage is limited to fundoscopic changes. diminishes heart rate and output and renin levels. TABLE 2-51. hyperuricemia. interacts with beta-blockers and digitalis with worsening bradycardia and AV blocks. and p2-antagonist. maximal effect in 1 week. and increase calcium. used with thiazide diuretics in cirrhosis and nephrotic syndrome. heart block. drug of choice for PSVT. compliant patient can be discharged on oral medications as long as follow-up in the next 24 hours can be assured. hirsutism. asthma. Although hypertension affects every organ system. hyponatremia. relatively contraindicated in diabetes. # 80-120 mgitid Sustained release preparations available Blocks calcium entry and dilates arterioles with afterload reduction. thus reducing angiotensin ll synthesis. The goal is to get the blood pressure into a more acceptable range (160 to 180/100 to 10) over 24 hours. 50-1 00 mg/day Aldosterone antagonist causing sodium excretion. may cause severe electrolyte depletion-potassium. may cause hypotension. fatigue. CHF. recommended agent for initiation of oral therapy for mild uncomplicated hypertension. This can often safely be accomplished with oral medications. 10-80 mg/day Loop diuretic. once a day dosing adds to convenience and compliance Diuretics Furosemide. hypercalcemia. and COPD Labetalol. Treatment of hypertension not requiring hospitalization Adrenergic antagonists Atenolol. asthma. high potassium losses. asthma. and COPD Metoprolol. decreases placental flowcontraindicated in pregnancy Spironolactone. causes hypokalemia. contraindicated in Wolff-ParkinsonWhite syndrome Diltiazem. avoid in aortic stenosis Verapamil. uric acid. and liver injury Angiotensin-converting enzyme antagonists Captopril. heart block. the blood pressure can be lowered more gradually than is necessary in true emergencies. heart block.5-50 m giday Thiazide diuretic. signs and symptoms of failure of one organ system may predominate. severe angioedema. # 100-400 mg/bid or-Fr-. well absorbed with high pass metabolism through liver dosage adjustment in liver or kidney disease not required. congestive heart fail- ure. stroke. AV conduction problems. and CHF. shorter half-life than labetalol and crosses blood-brain barrier. # 25-50 mg/bid or tid Suppresses ACE in lung. impotence. # 50-450 mg/day Preferential pr-antagonist. # 25-100 mg/day Preferential p-antagonist. inhibits reabsorption of sodium and chloride in ascending loop and proximal distal tubule. and blood sugar levels. may cause severe hypotension and precipitate myocardial and stroke. may cause hyperkalemia and endocrine problems like acne. ideal starting agent for mild hypertension. relative contraindications are diabetes.

and COPD 1-2 min 10-30 min Br-antagonist. cr2-antagonist. reduces blood pressure without reflex tachycardia (Br-antagonism). Fr-. The major effort in the ED is to rule out end-organ injury. may result in severe hypotension if relative hypovolemia exists Magnesium sulfate Bolus:4-O g of 10% soln. and hypertension due to cocaine Phentolamine Bolus:5-15 mg lV push 1-2 min 30-90 min or-. Raynaud's disease.5-2. MAO crisis). contraindicated in heart block. Ifno evidence of end-organ damage is found. The elderly. and patients with cardiac disease or volume depletion. should be started on lower than usual doses to prevent side effects oforthostasis and tissue hypoperfusion. causes tachycardia.0 pg/mg/min <1 min 2-5 min Direct vasodilator. cough. contraindicated in pregnancy.0 mg q6hr 10-15 min 4-6 hr ACE inhibitor. needs arterial line.Cennrovescut-AR DTsoRDERS Severe Hypertension in the Asymptomatic Patient Some patients have markedly elevated blood pressure with no evidence of end-organ damage. highiirst pass liver metabolism. hypotension.25-1 0. intravenous drugs with short half-lives and predictable responses should be used.25-5. severe orthostasis. may cause cyanide toxicity 'l min Nitroglycerin lnfusion:5-100 pg/min 2-1 0 min Direct vasodilator. although treatment can be initiated in ED. angioedema. marrow depression. A significant number of patients experience a reduction in blood pressure with simple. renal func- tion tests. Bz-antagonist. drug of choice for aortic dissection. Drugs recommended in the treatment of hypertensive emergencies Drug Dose arld route Nitroprusside lnf Esmolol lnfusion:200-500 pg/kg/min x 4 min.0 mg/min 2-10 min 2-G hr Bolus:20-80 mg/10-15 min to maximum of 300 mg crr-. decreases myocardial work. ? ellicacy in patients on p-antagonists. and hypotension Enalaprilat Bolus:1.5 mg every 5 min to 15 mg/hr max Calcium antagonist. titratable. the therapeutic response is TABLE 2-52. may precipitate angina and tachycardia and elevate ICP and dP/dT Nicardipine These drugs are administered intravenously and require monitoring with arterial cannulation in intensive care. then 50-300 pg/kg/min Onset Duration usion: 0. increasing by 5-10 min 1-4hr 2. relatively contraindicated in diabetes. Furthermore. hypotension. diabetes. CHF. causes headache Labetalol lnfusion: 0. well absorbed. titratable. may precipitate respiratory depression. heart block. The approach to these patients in the ED is controversial. nonpharmacologic measures such as / 149 patients. Optimally the patient should be started on normal maintenance antihypertensive therapy and follow-up arranged in accordance with the recommendations of the JNC-V (Table 2-52). asthma. Reducing blood pressure to normal levels rapidly has not been shown to decrease complications in these Medications Used in the Treutment of Hypertensive Emergency There are now a wide variety of agents available for the treatment of all stages and degrees hypertension. While several oral preparations are available that can lower blood pressure rapidly. and a chest x-ray. stroke) may occur with overly aggressive therapy. drug of choice for all conditions except eclampsia. severe complications (myocardial infarction. Treatment can be initiated from any of the major classes of antihypertensive medications available (Table 2-51). tritratable and short acting. . 2-5 min 5-1 0 min lnfusion:1 g/hr Drug of choice for eclampsia. bronchospasm. arrhythmogenic. increases ICP. contraindicated in CHF and aortic stenosis. rapid fall in blood pressure in hyperreninemia. A careful history and physical examination are augmented by ancillary tests such as an ECG. When serious elevations ofblood pressure occur in association with end-organ damage or one of the several conditions mandating immediate control. urinalysis. sexual dysfunction lnfusion: 5 mg/hr. renal failure Hydralazine 10-20 mg lV or lM 10-15 min 1-6 hr Preeclampsia only indication. dose reduction unnecessary in hepatic/renal failure. headache. rest and control ofpain and anxiety. drug of choice for coronary ischemia and pulmonary edema. drug of choice for catecholamine crises (pheochromocytoma. the patient can be started on oral antihypertensive therapy and follow-up arranged.

nausea. Treatment is now widely available and effective in ameliorating some of the serious effects of chronic hypertension. antihypertensive drug withdrawal). including hypertension. At nonurgent levels. It is useful in the treatment of aortic dissection and hypertension due to high catecholamine levels (pheochromocytoma. Prolonged administration of SNP. Fr-. Other side effects are tachycardia.and venodilating properties that generally lower blood pressure while reducing ischemia. Hypertension is one of the most common diseases in adults throughout the world. in high doses increases risk of toxiciry and levels of cyanide and thiocyanate should be monitored. Relative hypertension is therefore common in this group. It may precipitate severe hypotension. diarrhea. has no appreciable effect ofcardiac output or rate. the same principles of care should apply to this patient population as it does to those in the ED except that much fewer diagnostic and therapeutic alternatives are available. SNP decreases vascular resistance and pulmonary wedge pressure. so close monitoring of the patient is essential. It is often impossible to identif' the lesion causing neurologic symptoms without CT or MRI. and is the drug of choice for hypercatecholamine states. Patients with cerebral ischemia comprise a diverse group whose treatment is controversial in any setting. Sodium Nitroprusside Prehospital Care of the Patient with Severe Hypertension Sodium nitroprusside (SNP) is a potent direct-acting vasodilator.1-receptors.8. and serious hypotension and critical organ hypoperfusion may occur (Table 2-52). The patient who is hypertensive but asymptomatic can be transported without specific treatment of the hypertension per se. Patients with potential cardiac ischemia should be assessed for reversible pathophysiologic responses. and should be administered liberally. There are four stages of illness: mil4 moderate. Recommendations for treatment are based on the stage of disease and associated conditions. vomiting. Chronic Hypertension (2. two readings. The committee defined categories of illness based on the level of elevation of blood pressure and underlying cardiovascular risks (Table 247). and very severe. It is relatively contraindicated in patients with reactive airway disease. MAO inhibitor reactions. Evaluation. and blood pressure response can be closely titrated. delirium. Common side effects are hypotension. Control ofblood pressure . Most prehospital ALS units have sublingual nitroglycerin available. and overdose of epinephrine preparations. and Treatment of Hypertension (JNC-V) recently analyzed the literature regarding hypertension and its treatment. It is also the drug of choice for crises due to pheochromocytoma. diabetes. and tinnitus. It is therefore important for all health care providers to identifu patients at risk. and headache.2) Labetalol Labetalol is an ot-. and Bz-antagonist. DeJinitions The Joint National Committee on The Detection. convulsions. It can be administered as a bolus or as an infusion and may cause profound hypotension in volume-depleted patients. muscle spasms. In general. severe. Phentolamine Phentolamine is a pure c-antagonist. taken at separate visits. Prehospital patients are often anxious and in pain. Intravascular volume should be maintained. and increases cerebral and renal blood flow Nitroprusside is metabolized to cyanide and then to thiocyanate in the liver. which makes it an ideal drug for acute hypertensive emergencies. nausea. are required for definitive diagnosis. with most affinity for cr.f 50 / EurncrNcv MrorcrNr: THn Conn CunrucuLUM not controlled. Thiocyanate is excreted in urine. In the fiel4 it is best to avoid aggressive lowering of the blood pressure as such treatment could adversely impact cerebral perfusion. vomiting. This drug has vaso. apprehension. Its effects are manifest within a minute of commencement of infusion. which can influence the ischemia. or atrioventricular block. Treatment should by augmented with antihypertensive agents from other classes of drugs (SNP reacts adversely with cloni- dine and methyldopa). cocaine and amphetamine intoxication. reducing preload by venodilatation of capacitance vessels and afterload by general arteriolar dilatation. CHE. It reduces not only blood pressure but also the shearing forces on the proximal aorta. It can be administered as a continuous infusion or in intravenous boluses or orally. clonidine withdrawal. Reassurance and pain reliefoften ameliorate exaggerated responses from those conditions. generally beyond 72 hours. Liver disease will therefore result in cyanide toxicity while those with impaired kidney function may demon- strate significant thiocyanate levels and toxicity. Many studies over an extended period of time have conclusively demonstrated the importance of even mild blood pressure elevation as a risk factor for vascular disease.

physical examination. medications (sympathomimetics. then the patient should be treated for anxiety and pain and be permitted to rest if possible. Many disparate factors are associated with essential hypertension-race. or transient conditions such as anxiety or pain. and routine labs (BLIN. Consideration should be given to the possibility of pheochromocytoma. and medication withdrawal in those individuals with a history or physical examination suspicious for these conditions. . Mild hypovolemia may ensue with compensatory tachycardia. followup should be arranged according to the recommendations of the JNC-V (Table 2-53). Oral medications suggested for the treatment of these individuals are found in Table 2-51. modification of other risk factors should accompany the efforts made to reduce blood pressure. A third group of patients may be hypertensive based on renovascular mechanisms.2. Therefore. Blood pressure elevation.1) Most patients with hypertension do not suffer from secondary causes. patient educa- tion. metabolic. monitoring. is called essential. These patients should be encouraged to discontinue any medications or drugs that might contribute to the hypertension. If still elevated. One should be suspicious of secondary causes in patients who are young at onset. it may cause serious vascular disease if left untreated over time. not related to discoverable renal. JNC-V recommendations for approach to patients with hypertension on initial screening Systolic Diastolic 30 130-'139 1 40-1 59 1 60-1 79 85-89 90-99 <1 1 80-209 >210 <85 1 00-1 09 110-119 >120 Recommendations Recheck Recheck Recheck Evaluate Evaluate Evaluate in 2 years in 1 year in 2 months or refer within 1 month or refer within 1 week or refer immediately Modified from the Filth Report of the Joint National Committee on Detection. creatinine. abdominal and flank bruits also indicate secondary causes. Even though the illness is unrelated to these pathologic processes.8. adrenal. when appropriate. diet. and treatment of hyperten- sion is now the most common reason for a visit to a physician in the United States. These patients are sensitive to drugs that blunt adrenergic response. They should be carefully educated about the need for follow-up evaluation for secondary causes of their illness. renal failure or renal vascular disease. Since a large percentage of the adult population has unrecognized hypertension. Some patients have heightened arteriolar tone. caffeine. and CXR) prior to the initiation of treatment in the ED. Essential (2. TABLE 2-53. vascular disease. or hormonal basis.2) For a small percentage of patients. If the patient is asymptomatic and the reading is not so high as to require a search for end-organ damage (2101120 or greater). Elevated blood pressure in those individuals not known previously to be hypertensive should be rechecked in the ED before discharge.2. initiation of treatment for this condition. and that followup should be secured. adrenal adenoma. the ED is an important locus for detection. hypertension has an underlying renal. High levels of angiotensin II result in hypertension. sex. coarctation of the aorta. cardiac. The same principles apply to patients who are known to be hypertensive as to those who are unaware of the problem. hormonal. The patient should have a brief history.In those with very high pressures. U/A. or who have severe or refractory disease. and Treatment of High Blood Pressure (JNC-V).Ce-norovescut-{R DTsoRDERS does not totally eliminate cardiovascular and cerebrovas- / l5l Screening for Hypertension in the ED cular risk. The Hypertensive Patient Who Presents for Evaluation of an Unrelated Condition Many patients are found to have elevated blood pressures in ED triage. Some readings will be higher in the ED setting and may not accurately reflect true ambulatory levels. and the presence of The evaluation. volume overload.8. 1 993. Sudden deterioration in patients whose pressure has been previously well controlled. such as surgery or specific medications. obesity. Multiple factors cause the kidney to produce higher quantities of renin. Evaluation. Calcium channel antagonists are particularly useful in these patients. There are a number of pathophysiologic subsets. amphetamines). this subset of patients responds best to ACE antagonrsts. but unassociated with a condition requiring immediate treatment. and. Secondary (2. In some patients there is a high degree of resting sympathetic tone resulting in a hyperdynamic circulation with tachycardia and increased cardiac output. Identification is important since it may allow for tailored therapy. cocaine. Patients should be encouraged to continue their antihypertensive medications and to take them regularly. it may be appropriate to begin antihypertensive medication. ECG. lytes. A call to the primary care physician who will ultimately care for the patient may be appropriate so that preferences and formulary requirements for long-term medication can be discussed. age. and tobacco use.

Ann Intern Med 1995. or calcium channel blockers can cause severe hypertension.12:l:73-89. Am J Cardiol 1993. Large tumor emboli may become lodged at the aortic bifurcation. hyponatremia. Gifford RW Jr. While most adolescents are asymptomatic. children are much more likely to have a secondary cause. Drugs 1994. MA:BDR-UpToDate. dysrhythmias. Except in adolescents. >122/130 10-12 years 13-15 years SELECTED READING iall. Kaplan NM.122(12):937 -939. Probst BD. A practice guideline revisited: screening for hypertension. Arch Intern Med 1993. Lancet 1994. kidneys. growth failure. the same medications can be used to treat hypertensive emergencies in children as are used in adults. clinical aspects. Oparil S. usually originating from the area of the fossa ovalis. They are made up of a mucopolysaccharide myxoid matrix with endothelial mesenchymal cells. and extremities. Rapid rise in blood pressure as seen in acute glomerulonephritis may lead to initial manifestations. abnormalities with An idea whose time has come-and gone [editor- Fagan TC. Four-fifths of these tumors are benign. cardiac ischemia. and Treatment of High Blood Pressure. fever. children may present with nonspecific symptoms such as poor feeding. metabolic alkalosis) and volume depletion. which occurs'in 30oh to 60Yo of patients. and an elevated IgG. leukocytosis. Acute hypertension after stroke. Nitroprusside. Houston MC. The Fifth Report of the Joint National Committee (JNCY). angioedema. Management of hypertensive emergencies. or myocardial infarction. Laboratory findings may show a vaiety of abnormalities including anemia (generally hemolyic). comprising only 0. Acute reduction of blood pressure in asymptomatic patients severe hypertension. Alpha-blockers and ACE inhibitors can lead to hypotension. Prog Cardiovasc Dis 1989. Rose BD. Myxomas. phentolamine.001% to 0. ACE inhibitors are associated with renal failure. polypoi( and friable. Patients on these medications who develop symptoms should be assessed for these side effects and then treated based on the symptomatology and laboratory found. clubbing of the fingers. arthralgias. They may lead to a variety of serious side effects that may precipitate ED visits. thrombocytopenia. labetalol. These emboli most commonly flow to the brain (50% of cases when embolization occurs). JAMA 1991.9) Benign Tumors Myxomas Primary tumors of the heart are rare. Significantly elevated blood pressure should be identified in children and correlated with the 90th percentile levels for each age group (Table 2-54). and behavioral abnormalities. especially with concomitant diuretic use. The scientific basis for treatment decisions Nern'ology 1993 :43:461467 . rashes.266:6. Classification of hypertension at the 90th percentile for children by age (significant/severe hypertension) Age Calhoun DA. embolization from a left atrial myxoma should be con- . and treatment ofhypertensive crises. Pathophysiology. About 20oh are found in the right atrium and the remainder in the right or left ventricle. Clinically. Pharmacological management of hypertension in paediatric patients.149:2169-2170. In patients who have normal sinus rhythm. Kaplan NM. Treatment of hypertensive crisis. Arch Intern Med 1989.72:3H-9H. weight loss.153:152t 183. Patients can have profound symptomatology from these side effects. and hypotension. Beta-blockers and calcium channel blockers can cause hypotension or bradydysrhythmias. are generally found in 30to 60-year-olds and are primarily atrial in location. computer laser optical disk.32:2:99-148. 1995. and Raynaud's phenomenon. and nicardipine are the nausea and vomiting as firstline intravenous medications recommended. Powers WJ. Clinical manifestations in 90% of cases of myxomas generally include systemic illness including fatigue.48(6). 344( l2):1335-l 338. Wellesley. Evaluation. three-fourths are in the left atrium. PRIMARY TUMORS OF THE HEART (2. Controversies in the diagnosis and treatment of hypertension: a personal review of JNC Y. Ventricular myxomas are more common in children than adults. Management of hypertensive crises. Hypertension in Children The incidence ifhypertension in children ranges from lohto l0% depending on the population studied. clonidine. Complications of Antihypertensive Therapy Antihypertensives are among the most widely prescribed medications in the world. The other major clinical manifestations result from tumor embolization. Diuretics can cause electrolyte disturbances (hypokalemia. In general. Hypertensive disorders of pregnancy. UpToDate in Medicine. Joint National Committee on Detection. Weber MA. Littenberg B. Pathologic examination of myxomas show them to be gelatinous masses that are pedunculated.152 / ElmncrNcy MsnrcrNn: Tun Coru CunrucuLUM IABLE 2-54. N Engl J Med Systolic bp 0-7 days >96/1 06 8-30 days >1041110 >1121118 >1161124 <2 years 3-5 years 6-9 years Diastolic bp 16-18 years >74182 >1261134 >76/84 >78/86 >82/90 >136/144 >142/150 >86192 >92198 Modified from Miller K. Hypertension. the most common of these tumors. 1990. Sudden withdrawal of beta-blockers.5oh of routine postmortem examinations. 3. an elevated sedimentation rate. Emerg Med Clin North Am 1994. Vol.323:17. where essential hypertension prevails.

These tumors are frequently associated with constitutional symptoms and symptoms of low cardiac output. There may be a danger in using arteriography for diagnosis since the catheter may dislodge parts of the myxoma. The chest radiographs may show left atrial enlargement and findings of pulmonary venous congestion. Thirty percent of these are associated with tuberous sclerosis and. clubbing. There may also be what sounds like an early third heart sound. but isolated rheumatic tricuspid valve disease is rare. Other Benign Tumors Other benign cardiac tumors are very rare. and chest pain. the two-dimensional echocardiograph helps to distinguish a left atrial myxoma from an intraatnal thrombus (which is more common). Left ventricular myxomas make up about 5oh of myxomas and are associated with syncope and chest pain. fatigue. which shows all four chambers. these symptoms may be episodic and may change with body position. The clinical manifestations of these tumors includes jugular venous engorgement with prominent "a" waves.90o/o are multiple. Affected individuals are . This produces symptoms of pulmonary venous hypertension and righr sided heart failure that may include dyspnea on exertion. In addition to these auscultatory findings. palpitations. These include rhabdomyomas and fibromas. but a myocardial infarction may be the first evidence of a left atrial myxoma. The rarest of these tumors include mesotheliomas. Left atrial myxomas may also have symptoms associated with their intercavitary location and the mobility of the tumor. Right-sided heart failure may occur when the tumor has been present for some time. If there is a transient. Retinal artery embolization may occasionally occur and generally is associated with ipsilateral middle cerebral artery embolization and neurologic abnormalities. and congenital benign thyroid rests. there may intermittently be the sounds of mitral stenosis (unlike that of rheumatic mitral stenosis. Commonly. infective endocarditis and vasculitis. The electrocardiograms in cases of left atrial myxoma generally reveal normal sinus rhythm with or without signs of left atrial hypertrophy. Echocardiography is diagnostic. There may be evidence of aortic stenosis due to outflow tract obstruction. The associated findings are peripheral edema. peripheral edema. A calcified right atrial myxoma may directly damage the tricuspid valve producing signs and symptoms of severe tricuspid regurgitation. but there may also be atrial fibrillation. Symptoms may be constitutional or may involve syncope. and there is usually evidence of mitral valve or aortic valve involvement. or right axis deviation. The physical examination of patients with left atrial myxomas may reveal a loud first heart sound that is frequently split. These retinal artery emboli may cause transient or permanent loss of vision. almost always occurring in children. paroxysmal nocturnal dyspnea. The differential diagnosis of right atrial myxomas includes rheumatic tricuspid valve disease. These tumors are found on the valves and the associated symptoms depend on which valve is involved. Coronary artery emboli are rare.Cerol. lipomas. syncope may occur. When pulmonary emboli occur. In addition. dyspnea on exertion. which generally is constant). Atrial fibrillation is more common with rheumatic tricuspid valve disease. complete obstruction. Fibromas may occur at any age and tend to be solitary. This sound comes between the normal locations ofthe second and third heart sounds and represents the "tumor plop" as the tumor shifts. These tumors are associated with dysrhythmias and sudden death. Right ventricular myxomas are rare and may produce evidence of either pulmonary valve or tricuspid valve obstruction. Right atrial myxomas make up about 20%o of cardiac myxomas. generally hemangiosarcomas. and cyanosis. Since myxomas may be multiple and may involve more than one chamber. the four-chamber echocardiograph is preferred to the M-mode echocardiograph. papillary fibroelastomas. dyspnea / I53 on exertion. Embolization from right atrial myxomas is less common than from left atrial myxomas. and ascites. Treatment is surgical. Malignan-r{umors Almost all malignant cardiac tumors are sarcomas. which may temporarily create blockage of the mitral valve or pulmonary vein orifices. cough. right atrial hypertrophy. As with myxomas of the left atrium.ovesculAR DTsoRDERS sidered ifbacterial endocarditis has been ruled out. CT of the heart and MRIs have been also been used for diagnosing myxomas. or symptoms compatible with pulmonary embolization. The differential diagnosis of a left atrial myxoma includes mitral valvular disease and" when there is a predominance of systemic symptoms. Importantly. right bundle branch block. which may embolize. Symptoms in patients with this condition may include fatigue. The electrocardiographic findings of right atrial myxomas generally reveals normal sinus rhythm. orthopnea. they are associated with tricuspid valve obstruction. hemangiomas. Rhabdomyomas are rarely seen in adults. hepatomegaly. The treatment for myxomas (no matter from which chamber they may arise) is surgery. hemoptysis. they may be small and there may be relatively few symptoms. which generally is curative. right atrial myxomas are diagnosed using two-dimensional echocardiography. low voltage. pulmonary edema. while normal sinus rhythm is more common with a right atrial myxoma. The diagnostic test of choice is the two-dimensional echocardiograph.

1) Early (Endocarditis Secondary to Sepsis) (2.1. Silverman NA. and fibrous histiocytomas. teratomas. Primary tumors and cysts of the heart and pericardium. Traditionally. Mayo Clin Ptoc'1980. Myocardial infarction without atherosclero sis. Atlas of tumor pathology. Peters MN. particularly in females.23 1 :95 1-9 59. ed. it can be caused by fun- gal. Left atrial myxoma: report ofa case involving hemodynamic. Three-fourths of patients have distant metastases at the time of diagnosis of a cardiac sarcoma. et a[. or thrombotic factors. 1. and myocardial infarction: neurologic and echocardiographic diagnosis: surgical treatment. Am Heart J 1976.10. Eur Heart J 1980. Smith DC. Bonte J. et al. Diagnostic feature of right ventricular myxoma. Cheitlin MD.2007 J009. Most commonly bacterial. Hall Rl Cooley DA. Washington. tachycardia. McAllister HA. collagen-vascular. In: Harvey WP. ed. Lipkin DP. GoldschlagerA. Al-Kutoubi MA. Pericardial Primary pericardial tumors include pericardial cysts. infective endocarditis has been categoized as acute or subacute and right. Treatment is surgical and they are rarely found to be malignant. Hall RJ. Snyder NS.8 I :520-523 MYOCARDIAL MANIFESTATIONS OF SYSTEMTC DISEASES (2. Frazier OH. Other malignant cardiac tumors include rhab- domyosarcomas. fascicle I 5. Pericardial cysts: a radiographic-pathologic correlation and review.. dyspnea.84:230. Acute. Left atrial myxoma diagnosed by computerized tomography. Echocardiographic diagnosis ofleft atrial myxoma. Am J Med 1869:50:113. Peri-cardial mesothelioma.994.30:82. Krzyaniak R. JAMA 197 4. Cooley DA. Infections can attack the heart directly or secondarily damage the cardiovascular system through the immune response to the infection. The clinical syndrome of atrial myxomas. Acta Neurol Belg l98l:' 81:215. Alexander RW eds The heart. Danielson GK. Grehl TM. J Thoracic Cardiovasc Surg 1980. including the heart and blood vessels.10. McGoon DC. Infections (2. Mercier LA. Giuliani ER. Left ventricular myxoma: echocardiographic diagnosis and review of the literature.91:240. An J Med 1977:'63:816. et al.125: 15-20. prolapsed mitral valves. Following biopsy for confirmation. Farooki ZQ. Toxins can have a variety of cardiovascular consequences.1:453. Symptoms vary with the part of the heart involved. Fenoglio JJ.g. Right-sided endocarditis involves the tricuspid or pulmonic valves and is . Schlattenberg T. GoldschlagerN. McAllister HA. Lau FY. Right atrial myxoma with right-to-left shunt and polycythemia presenting as congenital heart disease. valves previously damaged by diseases including rheumatic valvular disease and previous endocarditis) and intravenous drug abusers. If the tumor grows primarily in the chambers. Feigin DS. prosthetic valves. second series. New York: McGraw-Hill.10) A number of systemic diseases can adversely affect the cardiovascular system. de Castro CM.48:256 Williams DB. Mesotheliomas are malignant and yield a poor prognosis. Neoplastic heart disease.or left-sided. DC: Armed Forces Institute of Pathology. The presumptive diagnosis is made with echocardiography. et al. Current problems in cardioLogy.55:80. Baldwin Bl Symbos PN. 191 : 127. Hurley EH. McAllister H. Rodiology 1977 . A discussion of systemic illnesses that can damage the heart and vessels could fill a volume. 1979. Right atrial myxoma: unusual presentation with cyanosis and clubbing. Meller I Teichholz LE. McAllister HA Jr. right hemiparesis. treatment is palliative. These sarcomas infiltrate the heart and pericardium and metastasize. Subacute syndromes tend to be more indolent and infrequently metastasize to other locations. Harvey WP. rickettsial. Teratomas occur in infants and children.591. Clinical aspects of cardiac tumors.230:695. congenital heart disorders. Ann Surg 1980. Br J Radiol 1982. fulminant syndromes tend to be caused by more virulent organisms that are prone to metastasize to other foci. Am J Med 1970. fibrosarcomas. and mesotheliomas. In: Schlant RC. Chicago: Year Book Medical. et al. Videan P. Tumors of the cardiovascular system In: McAllister HA. McAllister HA Jr. Metabolic derangements affect tissues throughout the body. Primary cardiac tumors in children. liposarcomas.1) Infective endocarditis can present in a plethora of ways. and the consequences can be devastating. JA MA 197 5 . Am J Sttrg1'979 138:68-76. Chest I 982. Primarily myocardial tumors produce congestive heart failure. Sutton D. O'Neil MB. Madewell JR. Atrial myxomas: a review of clinical experience in 40 patients. Franken P. surgical histologic and histochemical characteristics. Pericardial cysts are the most frequent benign tumor of the pericardium. et al. Yitling FP. Am J Cardiol 1968. Left atrial myxoma with left retinal emboli.21:328.754 / ElrencrNcy MporcrNn: TnE Conr CunnrculuM usually male adults from the ages of 30 to 60. Pouget B. Cardiac myxomas: a clinical diagnostic challenge. Frenay JJ.55:371. et al. These cysts are usually an unexpected finding on routine chest radiographs even though they may cause chest pain. SELECTED READING Arciniegas E. Primary cardiac tumors. Schlant RC. The mesotheliomas may present with signs of constriction of the pericardium and vena caval obstruction. Popper R. and this discussion will be limited to the more common disorders with emphasis on those that can have an emergency presentatlon. 1978. and a cough. Am J Cardiol 1972.79:. Hertzler GL. Sutton MGS. et al. arteries and veins (8th ed). Talley RC. If the pericardium is involved pericardial effusion and associated symptoms develop. Roudaul R. Cardiac fibroma: longterm survival after excision. It primarily afflicts anatomically defective structures (e. et al. Pichard AD. J Thorac Cardiovasc Surg 1982. primary malignant lymphomas.43:62O. Malo Clin Proc 1968. Fenoglio JJ. et al. hnmunologically mediated diseases can damage the heart and vessels. The most common location on a chest radiograph is the right costophrenic angle. sterile. et al. Hakimi M. Glasser SB Bedynek JL. symptoms of obstruction predominate. Hall RJ. Right atrial myxoma in an asymptomatic child: echocardiographic diagnosis.

the classic findings may include any or all of the following: splenomegaly. It is not uncommon to require that several sets of blood cultures be obtained before the culprit organism is identi- / I55 Cardiovascular syphilis occurs in the tertiary stage of the disease after a 15. 1. Myocarditis can complicate diphtheria. arthritis. In tuberculosis. During the convalescent phase cardiac manifestations may appear and even be fatal. fever. and aortic regurgitation are the most common manifestations. mately 10% of patients during stage 2. arthralgias and arthritis. fatigue. mitral valve incompetence. I 0. streptococci. On physical examination. cardiac. Constrictive pericarditis can develop and is prevented by corticosteroids. Men in their late 40s are most commonly affected. chorea. 2) Acute rheumatic fever.Cenorovescur-{R DTsoRDERS IV drug abusers. fied. Late (Rheumatic Fever Secondary to Group A Streptococcal Infection) (2. feri. the organisms responsible for late prosthetic valve endocarditis are staphylococci and streptococci. Kawasaki disease. three sets ofcultures are obtained at least 2 hours apart. and sudden death. and pericardium is seen. and racic echocardiography. is thought to be an infectious disease. rash. night sweats. erythema migrans. fever. the mucocutaneous lymph node syndrome. more colnmonly seen with Other ways of classiffing infective endocarditis are native valve endocarditis. although temporary pacemaker insertion may be needed in some patients. Staphylococci and streptococci are the common infective agents in native valve endocarditis. Onset is variable and can range from effrr- sion without manifestations of infection to fever with chest pain. The 2o/o mortality results primarily from cardiac involvement. there is neurologic. When infective endocarditis is seen in IV drug abusers. strawberry tongue. with aneurysms. Roth's spots. but when it occurs congestive heart failure and death may ensue. Osler's nodes. coronary artery disease secondary to stenosis of the coronary ostium. while aortic and mitral stenosis are characteristically long-term sequelae. while the patient is not experiencing rigors. Fungi. Complaints can be as general as increased fatigability. Acutely. myocarditis. lymphadenopathy. or chills. which occurs months to years after the initial infection. although21%o of the cases are women. myocardial infarction (MI). it is usually due to staphylococci. Left main coro- nary disease due to ostial stenosis requires bypass surgery. Frank carditis is uncommon. hepatosplenomegaly. Cardiac disturbances follow peripheral nerve conduction abnormalities and are caused by the action of a toxin released by Corynebacterium diphtheriae infecting the nasal or pha- . Generally. If symptoms are severe and the patient is presenting with signs of sepsis or is demonstrating signs of seeding to metastatic foci. Heart block. and anorexia to severe rigors and an acute onset ofheart failure. also known as Lyme borreliosis. staphylococci. dry and cracking lips. heart murmurs. therapy should be initiated and directed toward the most likely causative organism based on the above discusslon.to 30-year latency period. with disturbances of the cardiac conduction system. Lyme's disease. over weeks to months. Imaging of the heart by standard transtho- Fever. Some authorities recommend early pericardiectomy before constrictive pericarditis develops because surgical treatment of constrictive pericarditis is technically difficult. Management of infective endocarditis is based on the organism obtained from blood culture. and carditis. and gram-negative bacilli are the most common culprits seen in early (<2 months postsurgery) prosthetic valve endocarditis. arrhythmias. Transient myocarditis with intermittent heart block of varying degree is seen in approxi- the vegetative process. A lymphocytic cellular infiltration of the myocardium. or transesophageal echocardiography may allow visualization of joint involvement. pleural rub. MRI. there can be aortic and mitral regurgitation. Stage 2 consists of desquamation of hands and feet. and dissection has not been reported. Cardiac manifestations are usually self-limite4 even without treatment. and headache are common in this early phase of Lyme borreliosis. or pericardial rub. Aortic aneurysm. Confirmation of the diagnosis is made by the retrieval ofthe causative organism from blood cultures. and lymphadenopathy. is a systemic infection with the spirochete Borrelia burgdor- Approximately 50% of patients present with an expanding erythematous lesion. ultrafast CT. erosion of a caseous node adjacent to the pericardium into the pericardial sac leads to tubercu- lous pericarditis and is reported to occur during chemotherapy. early or late prosthetic valve endocarditis. The ascending aorta (60%) and transverse arch(25%) are most commonly involved. Diagnosis is suspected based on avaiety of presenting symptoms. and cardiomegaly may occur during acute rheumatic fever. although chronic dilated cardiomyopathy has been seen dunng this period. During stage 2. Left-sided endocarditis involves the aortic and mitral valves. Compression of neighboring structures can lead to symptoms. Janeway lesions. is a clinical syndrome of fever. new heart murmurs. which is caused by a systemic immunologic reaction to group A Streptococcus pyogenes pharyngitis. red swollen soles and palms. or endocarditis ofIV drug abuse. Neurologic manifestations dominate stage 3. rash. endocardium. pericardial effirsions. During the first phase there is fever. splinter hemorrhages. conjunctival congestion. malaise. Most commonly syphilitic aneurysms manifest as chest pain. or gram-negative bacilli. Beyond 2 months after prosthetic valve surgery. and carditis.

Both the cardiac conducting system and autonomic innervation can sustain damage. which is caused by T. Every patient with new-onset superventricular tachycardia should be assessed for hyperthyroidism. shock and vascular collapse are the major manifestations. or brain. degeneration. results in a breakdown of cellular immunity leading to opportunistic infections with numerous agents. Low voltage P waves and QRS complexes. or iatrogenic administration of corticosteroids. The mortality of diphtheria with ST:T wave abnormalities is 28o/o versus 60/o to l0% with no ST:T wave abnormalities. . No pathogen was identified in 82% of the cases with myocarditis. with atrial fibrillation a common presentation. nonspecific T wave changes. self-limited infection. Cushing's syndrome. The disease has a predilection for the right ventricle. with hypotension. by the human immunodeficiency virus (HIV). gambiense and T. and signs of right-sided heart failure are present commonly. Myocarditis can also complicate severe cases of typhoid fever. muffled heart sounds. Endocrine and Metabolic Diseases (2. can affect the heart in both the acute and chronic phases of the disease. T gondii is a ubiquitous parasite that causes disease in both immunocompetent and immunocompromised individuals. and atrial fibrillation. with arrhythmias and congestive heart failure. In a study of patients over 40 years of age with Cushing's syndrome. Heart failure is rare but can occur and is associated with cardiomyopathy or pericardial effirsions. Hypertension responds to the usual treatment regimens. which arises from hypersecretion of growth hormone by pituitary tumors. Adrenal crisis occurs in periods of stress such as surgery trauma. Cryptococcal myocarditis can also occur in AIDS patients. which was asymptomatic. and T:wave inversions or flattening may be seen on the ECG. Trypanosoma cruzi. cruzi and is endemic from Mexico to northern Argentina and Chile. Hyperthyroidism can present as cardiac disease. Patients with AIDS are at high risk to develop caused toxoplasmosis and can have severe disseminated disease involving the heart.r ryngeal mucosa. In one autopsy study 52Yo of AIDS patients had mild focal myocarditis. T. Hyperaldosteronism presents with hypertension and hypokalemia. though rarely disseminated disease is seen in the absence of immune deficiency. and a jugular venous hum as well as a dynamic apical pulse can sometimes be detected. and tachycardia. A pancarditis characterized by mononuclear cell infiltrations frequently occurs in the acute phase of infection. Bradycardia is a hallmark of hypothyroidism. when it occurs. If present. Fibrosis and destruction of myocytes develops.10. Bounding pulses are the rule. and can affect the heart. as well as Trichonelli spiralis and Tbxoplasma gondii are known to affect the heart. Chagas's disease.2) (See 13. Cardiovascular collapse can occur. Echocardiographic evaluations syndrome. Congestive heart failure.3) Derangements of the endocrine system can adversely affect the cardiovascular system. over 90oh have systolic blood pressures less than 110 mm Hg.156 / EMnRcsNCy MrorcrNn: Tur Coru CuRnrculul. may be related to hypertension rather than a direct effect of growth hormone. and must be instituted carefully with concomitant medical therapy for in hypothyroidism have found slowed myocardial relaxation. Parasites can invade the myocardium and cause myocarditis. Dizziness on standing and syncope can occur. The acquired immunodeficiency syndrome (AIDS). In autopsy cases myocardial fibers can be swollen and vacuolated. The most common cause of death in acute Chagas's disease is congestive heart failure secondary to severe myocarditis. Prognosis is poor after the development of heart failure. Hyperthyroidism leads to increased inotropy and chronotropy and decreased peripheral vascular resistance. gambiense. African trypanosomiasis is caused by the parasites T. 95Yo had hypertension and almost 50% had congestive heart failure. Disturbances of rhythm can occur. or infection. paroxysmal atrial tachycardia. Mortality can result from cardiovascular disease. with sinus tachycardia. which is chronic pnmary adrenocortical insufficiency. Arrhythmias. Hypotension is the major cardiovascular manifestation of adrenocortical insufficiency. or larynx. Heart failure is more common in older patients but can be seen in younger patients. In patients with Addison's disease. or adrenal crisis. Cardiomegaly is seen at autopsy but does not lead to overt cardiac disease. and in undiagnosed or inadequately heated patients with adrenal insufficiency. Thyroid replacement therapy can exacerbate angina pectoris in patients with coronary artery disease who develop hypothyroidism. Hypertension with congestive heart failure can result from elevated serum levels ofadrenal cortical hormones. are the causative agent of sleeping sickness. Cardiac involvement manifests as myocarditis. whether from Cushing's disease. lung. and pericardial effirsions. In acute adrenocortical insufficiency. Hypertension and atherosclerosis were the cause of death in 40% of patients dying from Cushing's angina. and conduction disturbances are the electrocardiographic manifestations. Cardiomegaly and hypertension are seen in acromegaly. rhodesiense. and falty infiltration are seen ln autopsy speclmens. symptoms are those of hypokalemia and relate to the degree ofpotassium depletion. Immunocompetent patients usually have a benign. Nonspecific ST segment and T wave changes can be seen. Long-term corticosteroid therapy may increase a patient's risk ofatherosclerosis. low voltage. septal cardiomyopathy. Chronic disease presents as cardiac disease years after the initial infection. and T rhodesiense. Myocardial necrosis. These parasites are transmitted through bites of the tsetse fly.

and cardiac involve- . 157 Rheumatologic (2. On rewarming they become erythematous. It is thought that effects of thiamine deficiency on sympathetic nuclei causes the loss of sympathetic tone. Pericardial effirsions can be massive and require emergency pericardiocentesis. and reversal of electrocardiographic abnormalities has been reported. and stress testing. pericardial effusions (19%). Necrosis and fibrosis is seen on pathologic examination. low voltages on the electrocardiogram. leads to dys- pnea on exertion. Scurvy. Tlwave changes. and cases of sudden death among these children may be due to abnormalities of conduction. pulmonary hypertension (16%). Lupus patients presenting with acute chest pain or other cardiovascular complaints need a thorough evaluation for pericardial and pleural effirsions. and myocardial infarction. There were valvular heart lesions (27%). Since this deficiency is often associated with beriberi. Doppler cardiography.3) disease and increased mortality from myocardial infarction (MI) and sudden death. In a recent evaluation of patients with SLE with echocardiography. tachycardia. most commonly to a drug. and Orientals who eat a diet high in polished rice. Severe clinical pericarditis with effusions and tamponade occurs rarely. A patient with diabetes mellitus with acute gastrointestinal complaints or severe nonspecific symptoms / Allergic myocarditis is an acute cardiomyopathy caused by a hypersensitivity reaction. has been associated with sudden death. Beriberi is due to thiamine deficiency and causes highoutput cardiac failure due to reduced peripheral vascular resistance from arteriolar vasodilation. MIs without chest pain. though it is seen in alcoholics. valvular heart disease. the vitamin C-deficiency disease. Pericarditis. palpitations. though autopsy studies show cardiac involvement. Vahular heart disease with leaflet scarring. The cardiac abnormalities seen in hypervitaminosis D are those of hypercalcemia. Abnormal T waves and ST segments resolve with niacin replacement.rsions. Systemic sclerosis (scleroderma) is associated with cardiac fibrosis in greater than 50o/o of autopsy specimens. Clinical cardiac disease is less common in patients with rheumatoid arthritis. Pathologic abnormalities are limited to the myocardium. and conduction abnormalities are most often seen. Penicillin. a third heart sound. Enriched bread has all but eliminated beriberi in Western countries. it is difficult to separate the cardiac abnormalities between the two conditions. pleural effi. Raynaud's phenomenon is often a presenting manifestation of collagen vascular diseases that heralds systemic disease by years. The collagen vascular diseases have a number of cardiovascular manifestations. individuals who eat unusual diets. Physical findings are those of biventricular failure with peripheral edema (wet beriberi). It is often said that individuals with diabetes are prone to have silent MIs. Selenium supplementation is reported to prevent this disease. A cardiomyopathy with fatty degeneration of the myocardium has been described. In some cases a mixed sensory and motor peripheral neuropathy dominates the clinical picture (dry beriberi). The protein deficiency disease kwashiorkor is associated with bradycardia. Emergency intravenous vitamin C has been advocated as a treatment for the heart disease associated with scurvy. and chordae tendineae rupture leads to aortic and mitral regurgitation sometimes requiring valve replacement. Drug-induced acute pericarditis has been associated with hydralazine and procainamide. Treatment with corticosteroids has been found to potentiate coronary atherosclerosis in lupus patients. the deficiency disease ofniacin. and involvement of long segments of smaller arteries is characteristic and difficult to treat. that is. thickening of chordae tendineae. Cardiac enlargement. The hands turn white and then cyanotic. ventricular failure. and edema. and systemic sclerosis. including women less than 40 years of age). Clinical valvular heart disease and conduction defects are uncommon but can be seen in rheumatoid arthritis. Myocardial infarction in young women is thought to be secondary to vasculitis. and pharmacologic prophylaxis with various arterial dilators has had mixed sucCCSS. and myocardial infarction (7o/o. sparing the endocardium and pericardium. vasculitis.R DTsoRDERS Diabetes mellitus leads to early onset of coronary artery should be monitored closely and have an electrocardiographic evaluation. A cardiomyopathy of children in a region of China with selenium poor soil has been described. and is a reversible ischemia of the hands and sometimes feet that is triggered by cold exposure and other factors.10. The characteristic pathologic of allergic myocarditis is cellular infiltrates of eosinophils and large mononuclear cells. Raynaud's phenomenon is a vascular syndrome seen in rheumatoid arthritis. Wasting of the fibers of the cardiac conducting system has been described in children dying of kwashiorkor. with deposition of calcium in necrotic myocardial cells. sulfonamides. and tetracycline have been causative. with histologic changes of muscle fiber vacuolation and intracellular edema. and ulcers and gangrene ofthe feet. methyldopa.75%o had cardiac disease. Clinical complications are intermittent claudication. systemic lupus erythematosis (SLE). and a prolonged QT interval.Cerolovescur/. though autopsy studies show involvement of the pericardium in 40% of patients. and a widened pulse pressure are character- istic physical findings. Exposure to allogeneic serum can also lead to allergic myocarditis. Peripheral vascular disease secondary to atherosclerosis also occurs at an earlier age and with increased frequency in diabetes. Pellagra. Primary Raynaud's phenomenon can occur.

It is thought to be a regulation disorder of eosinophils related to the chronic leukemias. granulomatous disorder. impaired diastolic filling. The hypereosinophilia syndrome is a condition of high levels of circulating eosinophils with no apparent cause. systolic dysfunction. Cardiovascular diseases account for 30% to 50% of deaths in patients with ESRD. therefore. hyperkalemia. A wide variety of conduction disturbances are seen including first-. in the absence of other known causes of these defects. ESRD contributes to cardiovascular disease in a num- ber of ways. hypertension. particularly in young men. supraventricular tachycardia. bundle branch block. aortic incompetence or conduction disturbances may be the presenting feature of ankylosing spondylitis. fluid retention. Hypertension in ESRD patients may be caused by the use of erythropoietin (when used to correct the anemia associated with ESRD. It is characteizedby the presence ofnoncaseating granulomas found in multiple body tissues. Hypertension and lipid abnormalities are frequently seen in these patients. and pericarditis 3%. ventricular arrhythmias. infections. and left atrium. and altered neural control. The heart and nervous system are particularly r. Clinical heart failure due to fibrosis of the myocardium occurs in less than 10% of patrents. car- duction abnormalities including complete heart block (the most frequent. arrhythymias. second-. This involvement is frequently limited to a small portion of the myocardium and is often clinically silent with only 40%o to 50% of patients with cardiac sarcoidosis at autopsy having been diagnosed with sarcoidosis during their lifetime. and thiamine deficiency. infiltration of tissues with amyloid protein occurs. . ventricular septum. The role of uremia itself has been questioned to contribute to increased incidence of atherosclerosis. Factors that contribute to an alteration in the loading conditions on the heart include anemia and arteriovenous fistulas (used for easier access in hemodialysis patients). elevated plasma renin activity. bundle branch block (with right bundle branch block more common than left bundle branch block). volume overload. documented in 23%o to 30% of patients with myocardial sarcoidosis). MIs about l0%o. which leads to changes in the neural control of circulation. believed secondary to deficiencies in lipoprotein lipase and hepatic triglyceride lipase. left ventricular hypertrophy. Diastolic filling may be altered by pericardial disease. as a result of their decreased synthesis. commonly seen in chronic renal failure). right atrium. Aortitis in ankylosing spondylitis is characterized by adventitial scarring and intimal proliferation causing thickening of the proximal aortic wall behind and above the sinuses of Valsalva. Myocardial involvement has been found to occur in 20Yo to 27o/o of patients with the diagnosis of sarcoidosis. first-degree atrioventricular block. Congestive heart failure. and sudden cardiac death. hypocalcemia. and valvular heart disease. and Wolff-Parkinson-White syndrome. Often. papillary muscles. the diagnosis of ankylosing spondylitis should be entertained. are the left ventricular free wall. and con- Renal (2. In amyloidosis. ventricular aneurysms. The average sur- vival after the onset of cardiac symptoms has been reported to be I to 2 years.4) Cardiovasular complications are the leading cause of death in patients suffering from end-stage renal disease (ESRD).f 58 / ErrrencrNcyMnolclNt: Tnr Conr CunrucuLUM ment is a poor prognostic sign. The most commonly encountered lesions are aortic incompetence and conduction defects. with heart failure causing approximately 15% of these deaths. and conduction abnormalities including heart block are possible consequences. and cardiac manifestations include endomyocardial fibrosis. right ventricle. and third-degree atrioventricular block. metabolic acidosis. Sarcoidosis is a multisystem. The cause of heart failure in renal failure patients is multifactorial. These causes can be subdivided into loading conditions. Amyloidosis may be a primary disorder or secondary to multiple myeloma. heredity. as well as decreased amounts of high density lipoproteins. Patients with ESRD also frequently suffer from autonomic neuropathy. Clinical manifestations include congestive heart failure. myocardial fibrosis. Impairment in systolic dysfunction is seen with MIs. and myocardial fibrosis. pericardial tamponade from pericardial involvement. fascicular block. The aortitis may extend to below the aortic root to the base of the mitral valve and into the ventricular septum causing a subaortic fibrous ridge. Tissue damage results from major basic protein and other eosinophil products designed to destroy parasites. The prevalence with which aortic incompetence and atrioventricular blocks are seen increases with both age and duration of the disease. and valvular disease (such as the calcium deposition seen on valves due to secondary hyperparathyroidism. Aortic valve disease is seen inlohto 10% of patients with ankylosing spondylitis.10. There can be cardiomegaly with diffirse deposition of amyloid in the myocardium. diomyopathy. Treatment should be specific for the clinical manifestation and should include steroids unless a definite contraindication exists. Patients with ESRD are prone to elevated very low density lipoproteins.ulnerable to damage. erythropoietin can lead to the increase in peripheral vascular resistance and increase in blood viscosity). uremic toxicity. or sympathetically mediated vasoconstriction. val"ular disease. The different cardiac structures involved" in decreasing order offrequency. Heart disease is a frequent complication of ankylosing spondylitis. which cause a high cardiac output state. or chronic inflammatory diseases such as rheumatoid arthritis.

Other symptoms of these interactions include fever. Sodium bicarbonate infusion can reverse both QRS widening and hypotension and is felt to be protective against lethal arrhythmias. Some studies have indicated cardiac arrest to be the cause of death in approximately 9%o of ESRD patients. The introduction of Digibind the Fab fragment of a digoxin-specific sheep monoclonal antibody.10. After ingestion. Cocaine is a potent inducer of vasospasm. These substances inhibit the enzyme monoamine oxidase and lead to elevated brain levels of norepinephrine. A dose of 0. electolytes. Rupture of protocol with intubation. Toxic Exposures (2. Paroxysmal tachycardia with block and bidirectional ventricular tachycardia are uncommon except in the setting of digoxin toxicity. In an acute overdose. A phase of catecholamine depletion then occurs. The antimalarial chloroquine in overdose has a direct toxic effect on the myocardium. serum potassium is of great prognostic significance. Procainamide. Bradycardia. Monoamine oxidase inhibitors (MAOI) are used as antidepressants. a 1. patients with a pericarditis will complain of chest pain. which may be located anywhere on the precordium. death can result. and subarachnoid hemorrhage. but a prehospital been reported in many organs. serotonin. with cardiovascular collapse that is poorly responsive to therapy. Cardiac arrhythmias are often seen in the ESRD patient. so digoxin toxicity leads to a combination of tachydysrhythmias and heart block. Widening of the QRS complex is associated with arrhythmias and seizures. have a pleuritic component to it.5) A number of systemic poisonings adversely affect the cardiovascular system. and the ascending aorta has been reported. Intractable cardiogenic shock occurs within the firstT2 hours after ingestion and carries a poor prognosis.0 nEQL. MIs. CHF. there is a progression from an asymptomatic phase (0 to 12 hours) to a phase of central catecholamine excess. which in overdose produces cardiogenic shock. Echocardiography has demonstrated pericardial effrrsions in 32o/o to 560/o of patients starting dialysis who are asymptomatic. left ventricular hypertrophy. or in ESRD patients presenting with hypotension despite signs of fluid overload may be due to a significant pericardial effusion. pericardial disease. The mechanism for this form of pericarditis is much less clear. Late pericarditis tends not to respond to dialysis and is more severe with an increased likelihood of complications. and alteration in drug metabolism (e. Ventricular fibrillation has been seen to be the terminal rhythm in 25% of deaths that occur at dialysis centers. A friction rub may be observed in up to 95% of these patients with it having an evanescent quality that changes moment to moment. Uremic pericarditis has been classified by some authorities as early pericarditis as it tends to occur in patients before they begin chronic dialysis treatment. diaphoresis. and pneumonitis). diazepam has improved resuscitation outcome. A late or dialysis-associated pericarditis is also seen. Digoxin increases automaticity of myocardial cells while decreasing conduction. sympathetic amines. hemorrhagic pleural effusions. coronary aftety disease. In overdose. and dopamine. premature ventricular contractions. Myocardial infarctions and strokes occur in association with cocaine use in young healthy people without atherosclerosis.8 mglkg is invariably fatal. and beta-blockers can cause severe hypertension and tachycardia. Prognosis has traditionally been poor. including tyramines found in foods. the absence of a friction rub does not rule out pericarditis. antihypertensives. followed by a phase ofmultisystem failure. with cardiac arrest occurring within I to 3 hours after ingestion. Poisonings can occur from intentional overdose ofthe purified medication or accidental ingestion of the plants from which it is obtained. Colchicine is a plant alkaloid used in the treatment of gout. and be aggravated by lying supine and relieved by sitting forward. Cocaine causes tachycardia and hypertension and is associated with cardiac arrhythmias. Death is rapid. and all degrees ofheart block are seen with digoxin toxicity. and disopyramide are not recommended in treating the arrhythmias associated with tricyclic overdose. with neuromuscular excitation and sympathetic hyperactivity. Hypotension during dialysis not attributable to changes in intravascular volume. Uremic pericarditis is believed to be caused by the accumulation of uremic toxins. therefore. . The cause of these arrhythmias is associated with the constant disequalibrium of fluid. with mortality correlating with potassium levels greater than 5. This form of pericarditis usually responds positively to dialysis in the vast majority of patients. angina pectoris. and acute MI.CenuovRscut-qR DrsoRDERs Uremic pericarditis is frequently encountered in both acute and chronic renal failure patients. and acid-base status. but in severe overdoses bradycardia and hypotension can develop. which leads to an inflammatory serositis involving the pericardium. Pericarditis develops in approximately l5o/o of ESRD patients and has an average mortality of l3%o when it occurs.g. Sudden death occurs with cocaine use. quinidine. and infarctions have / I59 Tricyclic antidepressant overdoses generally present with a sinus tachycardia. digitalis).. Drug interactions with a number of substances.to 6-hour gastrointestinal phase occurs. autumn crocus (Colchicum autumnale) and glory lily (Gloriosa superba). Serum digoxin levels correlate with toxicity. Tachycardia and hypertension are the most common cardiovascular manifestations during this period. Most commonly. including pericardial tamponade. but it may also involve the pleura (causing fibrinous pleuritis. high-dose epinephrine. has revolutionized the treatment of digoxin poisoning. pleural friction rubs.

ed. Sarcoidosis of the heart. Also. Chakko S. the American Heart Association. recent head trauma. within 4 hours) and the delivery of the thrombolytic agent resulted in the greatest benefit. and other organizations. therefore. TREATMENT MODALTTTES (2. The National Heart. this risk is countered by the net reduction in mortality when thrombolytics are used. Fluids. Braunwald E. The heart in ankylosing spondylitis Ann Rhetrm Meggs WJ. In: Braunwald E. p-agonists should be avoided as worsening of vasodilatation may result. Reperfusion using thrombolytic therapy is aimed at cle.000 deaths annually. Platelet receptors for various proteins lead to further aggregation and adhesion. overdoses In severe poisonings. with the complication of negative ionotropy.11. trauma or surgery within previous 2 . the exclusion criteria for thrombolytic therapy are of equal importance.293-305 O'Neill TIW. Clin Cardiol 1993.5 I (6) :7 05-706. End-stage renal disease. The past decade has shown arapid evolution in the approach and treatment of the patient presenting with AMI. and Blood Institute's National Heart Attack Alert Program. making the diagnosis to drug time 60 minutes or less. 1992. certain contraindications to using thrombolytics must be considered. 1994. and vigorous fluid resuscitation is necessary. The longer that a coronary artery is occluded by thrombus. In addition to the eligibility criteria. however. SELECTED READING Diggs P.1 856-1871. If pressors are needed.000 to 700. platelet receptor gly- glucagon. known spinal cord or cerebral arteriovenous malformation or tumor. The greatest risk of using thrombolytics is hemorrhage.1 1) Thrombolytic Therapy (2. Lung. To be clinically eligible. Heart disease: a textbook of cardiovascular medicine Philadelphia: Saunders. potentiating the conversion of prothrombin to thrombin. The ultimate goal remains to give thrombolytic therapy as soon as possible.1) Acute myocardial infarction (AMI) continues to be the leading cause of death in the United States with an estimated 500. Energency managemenl of cardiovascular disease. in turn forming a stable fibrin matrix. Cardiology and co-existing drsease New York: Churchill-Living- stone. numerous studies have indicated that the least amount of time between the diagnosis of AMI (preferably. 1994. ed. All of this ultimately leads to an occlusive coronary thrombus and AMI. Platelets further potentiate clot formation through several mechanisms. The emergency physician is on the front-line of this treatment." The decision to use thrombolytic therapy and which thrombolytic to use must be made in the shortest amount of time possible. there does remain a reduction in mortality even if thrombolytics are not used until 12 hour