UCSF+SFGH

Resident Guide to
Emergency Medicine

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This handbook was developed by the emergency residents at the University of
California San Francisco, with assistance from the faculty at the University of
California San Francisco, San Francisco General Hospital, and Kaiser San
Francisco. Thank you to all the residents and attendings for your contributions,
and thank you to Zlatan Coralic for providing valuable input regarding
medications and their dosing!

Most medication dosages are for adult patients with normal renal function
unless otherwise specified. In patients with renal or hepatic dysfunction,
pharmacy should be consulted and dosages should be adjusted, or an
alternative medication should be used.

Chief Editors:
Hangyul M. Chung-Esaki
M. Kennedy Hall

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 Table of Contents

General Info Page

Contacts 4-6
Resident resources 7-13

Quick reference
Resuscitation 14-38
High risk chief complaints 39-62

Main topics
Cardiovascular Emergencies 63-78
Dermatology 79-89
Endocrine/Metabolic Emergencies 90-108
Environmental Emergencies 109-125
Gastrointestinal Emergencies 126-135
Gynecology/Sexually Transmitted Infections 136-147
Ear/Nose/Throat and Dental Emergencies 148-159
Hematology/Oncology 160-165
Infectious Diseases 166-185
Neurology 186-200
Obstetrics 201-208
Ophthalmology 209-223
Orthopedics 224-228
Pediatrics 229-249
Psychiatry 250-253
Pulmonary 254-260
Radiology 261-271
Renal/Urology/Acid-Base 272-281
Toxicology 282-300
Trauma 301-321

Practical skills
Procedures 322-333
Ultrasound 334-342
Resident as Teacher 343-344

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 Residency Contacts

Residency Contact Info

1. UCSF/Moffitt
505 Parnassus Ave, Rm M24, Box 0203
San Francisco, CA 94143-0203
T) 415-353-1529 F) 415-353-8499

2. SFGH
1001 Potrero Ave, Suite 1E21, Box 1377
San Francisco, CA 94110
F) 415-206-5818

Name E-mail Phone

Chen, Esther esther.chen@emergency.ucsf.edu 415-206-4354
Fee, Chris christopher.fee@ucsf.edu 415-353-8388
Lieu, Sandra sandra.lieu@ucsf.edu 415-206-5752
Phongsasavithes,
eve.phong@ucsf.edu 415-353-1529
Eve
Promes, Susan susan.promes@ucsf.edu 415-353-1529
Robinette, Taylor taylor.robinette@ucsf.edu 415-353-1595

3. Main ED contact info

 Moffitt-Long Hospital 415-353-1681
 San Francisco General Hospital 415-206-8111
 Children’s Hospital Oakland 510-428-3240
 San Francisco Kaiser 415-833-4265

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 Phone Numbers
1. UCSF
*ER *Wards
Main 353-1238 6 Long 3-1921
(fax 3-1796/1792) 6 PICU South 3-1352
Fast track 3-1550 6 North 3-1005
Registration 3-1724/1037 7 Long 3-1631
Supply room 5150* 7 PICU East 3-1955
Nutrition room 5051* 7 North 3-9140
*Labs 8 Long 3-1331
Main 3-1961/1667 8 North 3-1419
(fax 3-1346) 8 South 3-1475
ABG 3-1755 8 East ICU 3-8534
Blood bank 3-1313 9 ICU 3-1621
(fax 3-1316) 9 Long 3-1214
Chemistry 3-1501 10 CCU 3-1007
Cytology 3-1516 10 Long 3-1601
Heme/CSF/UA 3-1747 10 South 3-1737
Immunology 3-1712/6-3883 11 NICU 3-1873
Microbiology 3-1268 12 Long 3-1387
Pathology 3-1613 12 Moffit 3-1361
*Radiology (reading rooms) 14 Long 3-1321
Chest 3-9527 14 Moffit 3-1368
Body (GI) 3-1354 15 Long (L&D) 3-1787
Bone 3-2096 *Other
Neuro 3-1079 Disaster line 5-STAT
NucMed 3-1692 800-873-8232
Pediatric 3-1685/1384 Echo 3-1262
Ultrasound 3-1353 Occ. Health 5-7580
Vasc US 3-1286 Env Services 3-1283
IR Neuro 3-1308 ICU triage 3-9209
IR Body 3-1300 Infxn control 3-4343
On-call Res 3-9027 Interpreter 3-2690
*Pharmacy IT support 4-4100/3-9000
24 hr 3-1028 Med Records 3-2656
ID fellow 443-9503 Needlestick 719-3898
*Urgent OR 3-1545
CODE BLUE 6-1234 Poison Ctr 800-8-POISON
Peds CODE 443-1998 Res. Office 3-1529
Peds resident 443-KIDS RT 3-1350
CODE RED 9-911 Risk Mgmt 3-1842
Stroke code 443-COMA Security 9-911/6-1414

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2. SFGH
Zone 1 6-8194/6-8111 Discharge 6-8178
Zone 1 (fax) 6-4719 *Clinics
Zone 1 (page) 14 3M (Ortho) 6-8265/6-8266
Zone 2 6-5640 4M (surg) 6-5476/6-3228
Zone 1 (red) 6-8373 5M (gyn) 6-3409
Zone 3 6-8059 6M (pedsUC) 6-8838/6-6933
Zone 4 6-8979 Adult UC 6-5830
Zone 3 (page) 16 Dental 6-8104
CODE BLUE 6-1122 Wound clinic 6-8287/6-3719
Registration 6-5258
SW 6-8080 *Wards
Triage 6-8255/6-8057 4E 6-8201
5E 6-8311
*Labs 5R 6-8155
Main 6-8590 L&D (6C) 6-8725
Blood Bank 6-8584/6-6228 Nursery (6H) 6-8363
Chemistry 6-8590 Peds (6A) 6-8181/6-8182
Cytology 6-8222
HIV 6-3578 *Other
Heme 6-8582 Anesthesia 6-1180*341/351
Immunology 6-8593 BABYpgr 719-BABY
Microbiology 6-8576 CPD 6-8005
Serology 6-3578 CPS 558-2650
Echo 6-8315
*Radiology (Res=read rm) Interpreter 6-5133 (8a-5p)
CT scan 6-8069 Spanish (5p-12a) 1877-4163
CT/pm Res 6-5826/6-5898 Other (5p-12a) 1877-4165
Fluoro 6-8070 Infx Control 6-5466/443-1566
IR 6-8036 IT 6-5126/6-5035/6-8602
MRI 6-5949 Med Records 6-4427/6-8640
Nuc Med 6-8580 Needlestick 469-4411
MRI/Neuro Res 6-5798 OR 6-8134
US 6-4147/6-8752 PedsER pgr 1877-1689
US Res 6-8752 Poison control 6-8058
XR 6-8020 Police 6-8063
XR Res 6-8030/6-8445 PsychES 6-8125
*Pharmacy Resident Coord 6-5752
Main 6-8460 Risk mgmt 6-6600
Outpt 6-8107/6-8108 RT 6-8012

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 Resident Resources
By Kendall Allred, Benjamin Hippen Res Ed. Hangyul Chung-Esaki

Online resources
1. Residency website: www.emresidency.ucsf.edu

2. Moodle: www.emresidency.ucsf.edu/moodle

3. Housestaff booklet:
http://www.medschool.ucsf.edu/gme/pdf/Housestaff_Info_Booklet_2010_2011_0
20111.pdf

4. Resident and fellow affairs committee:

http://www.medschool.ucsf.edu/gme/residents/RFA/RFA.html

Occupational injuries
1. When should I go to UCSF Occupational health?
 Flu vaccinations
 PPDs/chest x-rays
 Injuries sustained while working
 Services provided at no charge to employee, but only for work-related injuries

2. What should I do about work related injuries?

 Unless emergent, work-related injury should be reported to Occupational
Health, who will arrange for an examination. They have their own staff
physicians and will provide referrals as necessary
 All work-related injuries are covered under workman’s compensation
insurance. Employees should not visit their personal physicians for work-related
injuries, but go first to Occupational Health

3. Where is Occupational health?

 Main location: 2330 Post St., Suite 460 on Mt. Zion campus
 Satellite: 350 Parnassus Ave, Suite 206
 Website: http://www.occupationalhealthprogram.ucsf.edu

4. Needle stick/fluid exposures

 Report immediately to the Needlestick Hotline at 415-353-7842 (STIC)
 http://www.medschool.ucsf.edu/gme/residents/RFA/BBP_Exposure_Policy_43
010.pdf

Base hospital physician guide

1. Base Hospital Physician (BHP) requirements
 California license
 Board eligibility or board certification in emergency medicine (or certified in
Surgery, Fam Practice, or IM with 3 years of full time ED experience), PGY3-4
EM residents

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  Current American Board of EM certification OR provider status on ACLS,
ATLS, PALS
 completion of Base Hospital Physician course
 Field care Observation (8 hours/year)
 Participate and teach 2 hours paramedic education/year

2. Issues
 AMA: Competent pts with no SI/HI may refuse medical care if they fully
understand risks
o Can’t AMA if: incompetent, minors, AMS, attempted SI/HI, 5150, severe
injury which “competent” pt would seek further care
o Document A&Ox4, GCS 15, competent, not intoxicated, reasonable vital
signs
 Destination
o Usually honor pt’s wishes unless there’s a medical issue – see bulletin board
in radio room for specialty receiving facilities
o Peds (<14) with cardiopulmonary arrest, post arrest, airway obstruction/
respiratory insufficiency  nearest ED
o Peds (<14) with hypotension, status epilepticus, deteriorating MS  nearest
pediatric critical care center e.g. CPMC, UCSF
o 5150 and in police custody need to tranport to SFGH (only locked
emergency psych facility); if on divert, need to clear at another facility and
transfer to PES. others can be transported to EDs of choice.
o Trauma: If pts meet pre-hospital trauma criteria (see base radio room),
transport to SFGH
o Burns: St. Francis unless there’s a concomittant trauma SFGH
o Re-implantation: UCSF, RK Davies, SFGH
o Critical OB: Kaiser, SFGH, CPMC (California), St. Luke’s, UCSF
o Stroke: Kaiser, SFGH, CPMC (Pacific and Davies), St. Mary’s, UCSF
o Sobering center: intoxicated, not on 5150, meeting criteria
 Divert: Available on EM Resource Computer System
 Cardiac arrest
o DNR if:
 Evidence of advanced stages of death
 Valid DNR order (prehospital form, DNR from DPOA, or at licensed health
care facility)
 Unwitnessed cardiac arrest >15 min, pulseless and apneic, confirmed
asystole in 2 leads, no hypothermia or overdose
 Witnessed or unwitnessed blunt/penetrating traumatic arrest with no CPR in
progress, confirmed asystole or PEA <40 bpm, no e/o hypothermia/overdose
o Do not transport if:
 Cardiac arrest w/o hypothermia/overdose
 Adequate airway mgmt and ventilation
 Adequate ACLS (>25 min)
 No ROSC (pulse >60 for at least 5 min)
 No refractory Vtach or Vfib
 Scene safe and appropriate for paramedics to stop ACLS

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  Physician on scene: May offer assistance but let paramedics remain under
base hospital consultation vs. take total responsibility (must give orders and
accompany pt to receiving facility – may be made solely by the Base physician)
 Bridge policy
o Northbound on GG: transport to Marin GH
o Eastbound on Bay bridge transport to Summit or Highland
o Southbound on GG and westbound Bay bridge: facility in SF
o If traffic issues – may consult with CHP, transport to facility in SF
 Out of county: SFFD can’t transfer out of county except for Seton and Kaiser
South SF
 Receiving hospitals: May receive any acute pt and provide ACLS
o VA hospital: Any veteran with stable medical condition
o Chinese hospital: Only stable patients
 Emergency trauma center bypass: If SFGH has a problem declared by
Trauma center director/designee, BHP should assist in determining which pts
may be safely cared for at SFGH vs. closest hospital
 MCI: BHP guides mgmt of MCI, may assist field personnel

Charting Guidelines in the ED

1. Three main points for resident charting
 A major pitfall is inconsistency between HPI, ROS, PE, etc. For example,
patient’s chief complaint is chest pain but the templated or macro-based ROS
states that the patient denies chest pain
 If there is a non-erroneous inconsistency, there must be a note explaining this.
For example, chief complaint was chest pain, patient was chest-pain free in ED
during ROS, so the chart should document “chest pain resolved by arrival in
ED”
 Level of charting is not just about number of elements documented; there
must be medical decision making (MDM) to support the level of charting. When
documenting MDM, the phrase to consider is “justification of medical necessity.”
For example, patient with chest pain has all elements of HPI, ROS, PFSH, and
PE documented for Level 5 chart, and an EKG was ordered, but if the MDM
does not discuss need to r/o ACS, DDx, and EKG results, the MDM does not
support coding the chart as Level 5

2. Documentation requirements for Level 4 and Level 5 (99284, 99285)

charts
 Level 4 documentation requirements (most patients in the ED)
o 4 HPI, 2 ROS, 1 PMH/FH/SH, 5 PE elements OR
o Caveat: “Patient unable to provide history and ROS because ___________”
plus 5 PE elements
 Level 5 documentation requirements (admitted patients)
o 4 HPI, 10 ROS, 2 PFSH, 8 PE elements OR
o “Patient in critical condition” AND diagnosis that supports immediate threat to
life or bodily function (E.g. STEMI, CVA, shock, PNA w/ hypoxia, respiratory
failure)

3. Critical care notes

 Document duration (at least 30 minutes), review of diagnostic testing,
monitoring of vital signs, titration of medications, and plan. Also document
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 discussion with consultants, admitting team, and family
 The diagnosis must support the justification of critical care, including AMS,
shock, head trauma, blunt chest or abdominal trauma, or other condition with “a
high probability of imminent or life threatening deterioration in the patient’s
condition.”

4. Procedure notes
 All procedures must be documented, including degree of attending physician
oversight

Communicating with consultants

1. Medicine: For admission
 Should be brief, approx 2 minutes ONLY
o UCSF: Tell medicine why can't go to Mt. Zion (see CI criteria below)
 Require tele, continuous pulse ox, step down, or ICU
 New need for BiPAP or CPAP
 <40 kg weight (for ACLS weight based dosing)
 >158 kg (350 lb) with mobility problems requiring lift team support
 No known diagnosis requiring extensive work up (consults)
 On HD or likely to require HD
 <24 hours from surgery
 Needing consult not available at Mt. Zion (Neurology, neurosurgery,
vascular surgery, hematology/oncology)
 Need procedure not available at Mt. Zion (ERCP, bronchoscopy)
 GI bleed
 Need for chemotherapy
 Pregnant requiring fetal monitoring
o SFGH: Tell medicine that they aren't Family Medicine patient
 Things to cover
o Patient name and MRN
o Working Dx at time of Consult
o Brief history/HPI (1-3 sentences)
o Relevant PMH
o VS and major PE findings
o Pertinent labs/studies (include pertinent pending studies)
o Significant ED course

2. Cards: Last echo, last EKG, last cath report. You can also call them for "early
follow up"
 SFGH: Call cards to set up outpatient stress tests

3. Neurosurgery: They like images; if you don’t have images, better to also ask
"question about which imaging"

4. Ortho
 Consult: Have films, e.g. if shoulder good axillary. Consider ESR/CRP for
infectious complaint
 Followup: Get their insurance (this helps them refer to UCSF/SFGH/St. Lukes),
phone number

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5. Peds: Vaccination status, PMH, PMD information

6. OB: Age GsPs, how many weeks they are (by dates/US), their beta quant (or
pending), what the pelvic exam is like

7. Optho: Visual acuity, EOMs, pupils (incl. APD), IOP, slit lamp if you did one

8. Gen Surg: White count, abnormal VS, belly exam, imaging

9. Derm: Consider taking photo with your mobile device and emailing it to them
(get patient consent!)

10. Radiology: Justify why are you want to bring in a tech in middle of night
 MRI: Cauda equina syndrome, posterior circulation stroke with deficit within
widow, epidural abscess (also call neurosurgery)
 U/S: ectopic, testicular torsion

11. Neuro (stroke): Time last normal, symptoms and deficits

Coordinating Follow-up on Discharge

1. UCSF
 In general, you can use the discharge coordinator. In Filemaker, click with
"Discharge Coordinator" button, fill out the fields and print. [*Note, this will
change soon with epic]
 Other patients will need follow-up arranged by certain consultants. Use the
attending/other residents to guide you in this process. Most of the time, they
don't need to see the patient but just need basic info. Make sure to document
who you talked to the plan you discussed
 You can email primary care doctors or call them if you need on a case-by-
case basis

2. SFGH
 There is no discharge coordinator at SFGH. Most surgical services you
consult will give you time and dates for their follow-up appointments. ISIS clinic
has drop in hours (see posted schedule in Zone 1). Wound clinic appointments
are made by clerk (hand written orders must be filled out by you, run by RNs)
 Cardiology, family medicine, neurology can help facilitate follow-up in patients
followed by their services
 You can email primary care doctors or call them if you need on a case-by-
case basis

Death in the Emergency Department

1. Family meeting strategy (GRIEV_ING)
 Say I'm sorry for your loss
 Gather: Get them to patient care room, wait for people to arrive, tissues
 Resources: Chaplain, family member, etc (this way the chaplain will stay in
the room, you can leave in 5-10 min)

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  Identify: "I am the DOCTOR caring for PATIENT NAME, what do you know
happened? Fire a warning shot for the bad news (critical condition, never woke
up). Fill in the gap of time before
 Educate: Avoid jargon. Go slow, make sure they understand, do you
understand where everyone is right now.
 Verify: You HAVE to use the word Dead or Died- avoid euphemisms like
passed away
 _(pause): It’s OK for silence, it’s OK to touch family, allow emotional moment
 Inquire: Do you have any questions?
 Nuts and bolts: Inquire about organ donation, funeral services, personal
belongings, offer the family opportunity to view the body- dont sign
the death certificate
 Give: Give them your card and contact information, offer to answer any
questions that arise later

2. UCSF death packet (done by resident)

 Call Medical Examiner
o Gather all this info BEFORE calling them
 PMD name
 Patient's last visit
 Address
 Sig other/next of kin
 DOB
 Call Donor network
 Forms
o Discharge form
o Death report
o Brochure for family, number for Decedent Affairs
o Autopsy: Identify next of kin, obtain consent
 Tips: Get the phone number of at least one member of the family,
anybody. Try to call the PCP
 Questions? Call the patient relations phone number at Moffit: (415) 353.1936

3. SFGH
 Usually attending fills out the Postmortem Form
o Section 1: Done by MD
o Section 2 & 3: Done by charge nurse
 Obtain primary care doctor and phone number, contact for next of kin

24 hour pharmacies
*subject to change
1. San Francisco
 Walgreens 498 Castro St San Francisco, CA 94114 – (415) 861-3136
 Walgreens 3201 Divisadero San Francisco, CA 94123 – (415) 931-6417

2. South city

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  Walgreens 2238 Westborough Blvd S San Francisco, CA 94080 – (650) 873-
0551

3. Other
 Walgreens – at 216 Westlake Center Daly City, CA 94015 – (650) 756-4535
 Rite Aid – at 666 Concar Drive San Mateo, CA 94402 – (650) 573-8551
 Walgreens – at 2300 Otis Dr Alameda, CA 94501 – (510) 523-7043
 Walgreens – at 45 S El Camino Real Millbrae, CA 94030 – (650) 697-3970
 Walgreens – at 1420 Howard Ave Burlingame, CA 94010 – (650) 342-2977
 Walgreens – at 830 3rd Street San Rafael, CA 94901 – (415) 455-9919
 Walgreens – at 1414 El Camino Real San Carlos, CA 94070 – (650) 637-
9777

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 Resuscitation Algorithms

ACLS Algorithms

Always consider H’s and T’s

Hypovolemia Toxins (OD, ingestion)
Hypoxia Tamponade, cardiac
Hydrogen ion/Acidosis Tension PTX
Hyper/Hypo K Thrombosis, coronary
Hypothermia Thrombosis, pulmonary
Hypoglycemia Trauma

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 ACLS Meds
Drug Dosage

Adenosine SVT
6 mg IV rapid push --> 12 mg --> 12 mg (1-2 min between doses)

Amiodarone SVT, VT (with pulses)

150 mg IV over 10 min, repeat q10min, max 2.2g/24hours
or 360 mg IV over 6 hours (1 mg/min) then 540 mg IV over 18
hours (0.5 mg/min)
Pulseless Arrest (VF/pulseless VT)
300 mg IV/IO once, then 150 mg IV/IO once

Amrinone CHF refractory to diuretics, inotropes, vasodilators

0.75 mg/kg IV over 10-15 min then 5-15 mcg/kg/min

Atropine Symptomatic bradycardia

0.5 mg IV, may repeat to max 3 mg
Asystole/PEA
1 mg IV/IO, may repeat q3-5min, max 3 mg (0.04 mg/kg)
*Tracheal: 2-3 mg diluted in 10 mL NS

β-blockers Suspected MI, rate control, hypertension

Metoprolol 5 mg slow IV q5 min (total 15 mg); 50 mg PO BID to start
Atenolol 5 mg IV over 5 min q10 min x2, if tolerate, 50 daily to start
Propranolol 0.03 mg/kg slow IV q2-3 min (max 1 mg/min)
Esmolol 0.5 mg/kg IV over 1 min  0.05-0.3 mg/kg/min (t1/2 2-9 min)
Labetalol 10 mg IVP over 1-2min, repeat or double q10 min (max 150 mg),
or gtt 2-8 mg/min

Calcium Hyperkalemia, hypocalcemia, CaB/BB OD

Chloride 8-16 mg/kg (5-10 mL) IV, repeat prn

Digibind Dig toxicity (arrhythmia, CHF/shock, hyperK, levels >10-15

ng/mL + sx)
Chronic intoxication: 3-5 vials
Acute OD: 1 vial = 40 mg/0.6 mg digoxin (avg 10 vials)

Digoxin Rate control in AF/flutter, refractory PSVT

10-15 mcg/kg (lean BW) load

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Diltiazem AF/flutter, narrow complex refractory PSVT
15-20 mg (0.25 mg/kg) IV over 2 min, repeat 20-25 mg (0.35
mg/kg) q15 min over 2min

Dobutamine CHF/pulm congestion with shock

0.5-20 mcg/kg/min, titrate so HR incr <10% baseline

Dopamine Symptomatic drug (second line), hypotension

Low 1-5 mcg/kg/min (renal perfusion)
Mod 5-10 mcg/kg/min (“cardiac” beta)
High 10-20 mcg/kg/min (“vasopression” alpha)

Epinephrine Cardiac arrest

1 mg (10 mL of 1:10,000) q3-5 min, flush with 20 mL IV NS
*Tracheal: 2-2.5xIV dose diluted in 10 mL NS
Severe bradycardia/hypotension
1-10 mcg/min (1mL of 1:10,000 in 100 mL NS =1 mcg/mL)
Anaphylaxis, severe allergic reactions
0.3 mg IM (0.3 mL of 1:1000) repeat q10-15 min prn or
1mL of 1:10,000 (100 mcg) slow IV then 0.02 mcg/kg/min gtt (5-
15 mcg/min)

Flumazenil Benzodiazepine OD (do not use if seizure/withdrawal!)

0.2 mg IV over 15 sec --> 0.3 mg IV over 30 sec --> 0.5 mg IV
over 30 sec, repeat q1 min until response or max 3 mg

Glucagon Adjuvant for CaB/BB toxicity

1-5 mg over 2-5 min

GpIIb/IIIa NSTEMI/UA
A1bciximab ACS with planned PCI: 0.25 mg/kg IV bolus (within 10-60 min
(reopro) before) then 0.125 mcg/kg/min
Eptifibitide ACS: 180 mcg/kg IV bolus then 2 mcg/kg/min
(Integrilin) PCI: 135 mcg/kg IV then 0.5 mcg/kg/min, repeat bolus in 10 min
Tirofiban ACS/PCI: 0.4 mcg/kg/min for 30 min then 0.1 mcg/kg/min
(Aggrastat)

Heparin AMI
60 IU/kg bolus (max 4000) then 12 IU/kg/hr (1000/hr max)
adjust to aPTT - goal 1.5-2x control (50-70s) x48 hours or until
angio
*check aPTT at 6, 12, 18, 24 hours

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Ibutilide SVT (AF/flutter)
0.01 mg/kg (or 1 mg IV if >60 kg) over 10 min, may repeat in 10
min

Isoproterenol Symp bradycardia (temp), refractory torsades, BB tox

2-10 mcg/min, titrate to HR

Lidocaine Cardiac Arrest

1-1.5 mg/kg IV then 0.5-0.75 mg/kg, repeat 5-10 min (max 3
mg/kg)
*Tracheal: 2-4 mg/kg

Magnesium Torsades
Sulfate 1-2 G (in 50-100 mL D5W) load over 5-60 min IV then 0.5-1 G/h
Cardiac Arrest
1-2 G diluted in 10 mL D5W IVP

Mannitol Increased ICP

0.5-1 G/kg over 5-10 min, then 0.25-2G/kg q4-6h prn
*monitor Na, Osm

Naloxone Opiate intoxication

0.4-2 mg q2 min, up to 10 mg (titrate)

Nitroglycerin Angina, AMI, CHF, hypertensive urgency

SL 0.3-0.4 mg q5 min x3
IV bolus: 12.5 to 25 mcg
IV gtt: 10-20 mcg/min, titrate up to effect

Nitroprusside Hypertensive crisis, reduce afterload

0.1 mcg/kg/min, titrate q3-5 min

Norepinephrine Hypotension
0.5-1 mcg/min, titrate up to 30 mcg/min

Procainamide Recurrent VF/VT

20 mg/min IV (max 17 mg/kg), gtt 1-4 mg/min

Sodium Hyperkalemia, acidosis, Tox (TCA, cocaine, benadryl)

Bicarbonate 1 meq/kg IV bolus, repeat q10 min

Vasopressin Cardiac Arrest

40 U IVP x1

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 Guide To “Amps”
Amp = ampoule = container drug is stored in. Usually they are standardized but
there are different size amps in different hospitals. JHACO and the other folks
frown on orders that are written as "amps" as the actual volume of an amp is not
standardized, and if you write amp, you will be asked to clarify – the pharmacist’s
least favorite thing to ask you to do.

Correct ways to write orders for meds in “amps”

 1 amp Ca gluconate = Ca gluconate 1 gram IV x 1

 1 amp Ca chloride = Ca chloride 1 gram IV x 1
 1 amp Epinephrine = 1:10,000 Epinephrine 1 mg IV x 1
 1 amp D50 = D50 25 grams IV x 1
 1 amp D25 (peds) = D25 10 grams IV x 1 (should be wt based for peds)
*Neonates and small infants usually need D10
 1 amp Bicarb = Sodium bicarb 50 mEq IV x 1
 1 amp of Bicarb (peds) = Sodium bicarb 4.2% 10 mEq IV x1 (should be wt
based for peds)
 1 amp Atropine = Atropine 1mg IV x 1
 1 amp of cardiac Lidocaine = Lidocaine 2% 100 mg IV x 1 (same one used to
anesthetize the IO (1-2ml), or for ICP RSI pre-med)

20
 Pediatric Quick References
2nd to 98th %ile (Modified from Eddie Book)
Age Wt (kg) HR RR SBP DBP ETT* Blade
1mo 4 110-180 30-60 70-100 30-65 3.5 Miller 0
3mo 5-6 120-140 30-50 60-100 30-65 3.5-4 Miller 0-1
6mo 7 90-170 25-40 75-110 40-65 4 Miller 0-1
9mo 8-9 120-140 23-33 70-120 40-65 4-4.5 Miller 0-1
1-2yo 12 80-150 20-30 80-110 40-65 4.5 Miller 1-2
3-4yo 16 70-140 20-30 80-115 45-70 5 Miller 2
5-6yo 20 65-135 18-25 85-120 45-75 5 Miller/Mac 2
7-8yo 26 60-135 18-25 85-125 50-80 5-6 Miller/Mac 2
9-12yo 30 60-130 15-20 90-130 50-85 6-7 Miller/Mac 2-3
>12 yo 50 60-120 15-20 90-140 50-85 7.5 Miller/Mac 2-3
*0.5 smaller for cuffed tube

Pediatric Modified GCS

Child Infant Score

Spontaneous Spontaneous 4
To speech To speech 3
Eyes
To pain only To pain only 2
No response No response 1

Oriented, appropriate Coos and babbles 5

Confused Irritable cries 4
Verbal Inappropriate words Cries to pain 3
Incomprehensible words Moans to pain 2
No response No response 1

Obeys commands Spontaneous, purposeful 6

Localizes pain Withdraws to touch 5
Withdraws to pain Withdraws to pain 4
Motor
Flexion to pain Abnormal flexion to pain 3
Extension to pain Abnormal Extension to pain 2
No response No Response 1

21
PALS Algorithms

*consult peds

22
23
24
APGAR 0 1 2
Activity (tone) Ø Arms/legs Active movement
flexed
Pulse Ø <100 ≥100
Grimace (reflex irritability) Ø Grimace Sneeze/cough/pull
away
Appearance (skin) Central Acrocyanosis Nl
cyanosis
Respiration Ø Slow, irregular Nl, crying
*Check at 1,5,±10min. Normal: 7-10, full neonatal resus if ≤3

25
 PALS meds
Drug Indications/Dosage

Adenosine SVT
0.1 mg/kg IV/IO rapid push (max 6 mg)
2nd dose 0.2 mg/kg IV/IO rapid push (max 12 mg)

Albumin Shock, Trauma, Burn

0.5 to 1 g/kg (10 to 20 mL/kg of 5% soln) IV/IO rapid infusion

Albuterol Asthma, Anaphylaxis (bronchospasm), Hyperkalemia

MDI: 4-8 puffs INH q20min prn with spacer or via ETT
Nebs: 2.5 mg/dose (<20 kg) or 5 mg/dose (>20 kg) INH q20
min prn
Cont neb: Start at 5 mg/hr INH (increase prn to max 20 mg/h)

Alprostadil Ductal-dependent Congenital Heart Disease

(PGE1) 0.05 to 0.1 mcg/kg/min IV/IO infusion then 0.01 to 0.05
mcg/kg/min IV/IO

Amiodarone SVT, VT (with pulses)

5 mg/kg IV/IO load over 20 to 60 min (max 300 mg), repeat to
max 15 mg/kg/day or 2.2 g
Pulseless Arrest (VF/pulseless VT)
5 mg/kg IV/IO bolus (max 300 mg), repeat to daily max 15
mg/kg or 2.2 g

Atropine Bradycardia (symptomatic)

0.02 mg/kg IV/IO (min 0.1 mg, max 0.5 mg child, max teen 1
mg), may repeat x1
0.04 to 0.06 mg/kg ETT
Toxins/Overdose (organophosphate, carbamate)
0.02 to 0.05 mg/kg (<12 years) OR 0.05 mg/kg (>12 yrs)
IV/IO, repeat q20-30 min until atropine effect (dry mouth,
tachycardia, mydriasis) or symptom reversal

Calcium Chloride Hypocalcemia, Hyperkalemia, Hypermagnesemia, Ca

10% Blocker overdose
20 mg/kg (0.2mL/kg) IV/IO slow push during rrest, repeat if
severe hypotension

26
Dexamethasone Croup/Asthma
0.6 mg/kg PO/IM/IV (max 16 mg)
(for asthma, child should return for 2nd dose in 24-36 hours)

Dextrose Hypoglycemia
0.5 to 1 g/kg IV/IO (D25W 2-4mL/kg; D10W 5 to 10 mL/kg)

Diphenhydramine Anaphylactic Shock

1 to 2 mg/kg IV/IO/IM q4 to 6 hrs (max 50 mg)

Dobutamine Congestive Heart Failure, Cardiogenic Shock

2 to 20 mcg/kg/min IV/IO infusion; titrate

Dopamine Cardiogenic Shock, Distrubutive Shock

2 to 20 mcg/kg/min IV/IO infusion; titrate

Epinephrine Pulseless Arrest, Bradycardia (symptomatic)

0.01 mg/kg (0.1 mL/kg) 1:10,000 IV/IO q3-5 min (max 1 mg)
0.1 mg/kg (0.1 mL/kg) 1:1000 ET q3-5 min
Hypotensive Shock
0.1 to 1 mcg/kg/min IV/IO infusion
Anaphylaxis
0.01 mg/kg (0.01 mL/kg) 1:1000 IM thigh q15 min prn (max
0.5 mg)
Auto-injector 0.3 mg (≥30 kg) IM or JR injector 0.15 mg (10-
30kg) IM
0.01 mg/kg (0.1 mL/kg) 1:10000 IV/IO q3-5 min (max 1mg) if
hypotn
0.1 to 1 mcg/kg/min IV/IO infusion if hypotn despite fluids and
IM dose
Asthma
0.01 mg/kg (0.01 mL/kg) 1:1000 SQ q15 min (max 0.5 mg;
0.5 mL)
Croup
0.25-0.5 mL racemic soln (2.25%) in 3mL NS INH or 3mL
1:1000 INH
Toxins/Overdose (BB, CaB)
0.01 mg/kg (0.1 mL/kg) 1:10000 IV/IO (max 1 mg), consider
higher doses up to 0.1 mg/kg 1:1000 IV/IO
0.1-1 mcg/kg/min IV/IO infusion

Fentanyl Sedation, pain control

1 mcg/kg IV, 1.5-2 mcg/kg IN (half dose in each nostril)

27
Furosemide Pulmonary Edema, Fluid Overload
1 mg/kg IV/IM (max 20 mg unless chronically on diuretic)

Hydrocortisone Adrenal Insufficiency

2 mg/kg IV bolus (max 100 mg)

Inamrinone Myocardial Dysfunction and Increased SVR/PVR

Load: 0.75-1 mg/kg IV/IO slow bolus over 5 min, (may repeat
x2 to max 3 mg/kg) then 5-10 mcg/kg/min IV/IO

Ipratropium Asthma
bromide 250-500 mcg INH q20 min prn x3 doses (with albuterol)
Do not use if known peanut/soy allergy

Lidocaine VF/Pulseless VT, Wide-Complex Tachycardia (with

pulses)
1 mg/kg IV/IO bolus then 20-50 mcg/kg/min IV/IO infusion
(repeat bolus if infusion >15 min after initial bolus)
2 to 3 mg/kg ETT

Magnesium Asthma (refractory status), Torsades de pointes,

sulfate Hypomagnesemia
25 to 50 mg/kg IV/IO bolus (pulseless VT)
OR over 10 to 20 min (VT with pulses)
OR over 15-30 min (status asthmaticus), max 2 g

Methyl- Asthma (status), Anaphylactic Shock

prednisolone Load: 2 mg/kg IV/IO/IM (max 80 mg), use acetate salt IM
Maintenance: 0.5 mg/kg IV/IO q6hrs (max 120 mg/d)

Midazolam Sedation
0.05-0.1 mg/kg IV, 0.2-0.5 mg/kg IN

Milrinone Myocardial Dysfunction and Increased SVR/PVR

Load 50-75 mcg/kg IV/IO over 10-60 min then 0.5 to 0.75
mcg/kg/min IV/IO gtt

Naloxone Narcotic reversal

Total: 0.1 mg/kg IV/IO/IM/SQ bolus q2 min prn (max 2 mg)
Partial: 1 to 5 mcg/kg IV/IO/IM/SQ, titrate
Maintain: 0.002 to 0.16 mg/kg/hr IV/IO infusion

28
Nitroglycerin Congestive Heart Failure, Cardiogenic Shock
0.25 to 0.5 mcg/kg/min IV/IO infusion, increase 0.5-1
mcg/kg/min q3-5 min prn to 1-5 mcg/kg/min (max 10
mcg/kg/min)
Teens: 10-20 mcg/min, increase 5-10 mcg/min q5-10 min
prn, max 200 mcg/min

Norepinephrine Hypotensive (distributive) shock

0.1-2mcg/kg/min IV/IO infusion; titrate

Procainamide SVT, Atrial Flutter, VT (with pulses)

15 mg/kg IV/IO load over 30-60 min (do not use with amio)

Sodium Metabolic Acidosis (severe), Hyperkalemia

Bicarbonate 1 mEq/kg IV/IO slow bolus
Sodium Channel Blocker Overdose (TCA)
1-2 mEq/kg IV/Io bolus until pH >7.45 then IV/IO infusion of
150 mEQ NaHCO3/L solution to maintain alkalosis

Sodium Cardiogenic Shock (high SVR), Severe Hypertension

Nitroprusside 1-8 mcg/kg/min (<40 kg) OR 0.1-5 mcg/kg/min (>40 kg) IV/IO
infuse

Terbutaline Asthma (status), Hyperkalemia

0.1-10 mcg/kg/min IV/IO infusion; consider 10 mcg/kg IV/IO
load over 5 min
10 mcg/kg SQ q10-15 min until IV/IO gtt begun (max 0.4 mg)

29
 Adult Convulsive Status Epilepticus
STAGE ACTION
Impending SE, Skip this stage if patient received 2 doses of benzodiazepines
0-10 minutes (e.g. diastat) prior to arrival in ED
Lorazepam 2 mg IV
 Repeat in 5 min for persistent seizure (max total 4 doses,
including pre-hospital doses), may use 4 mg doses if not
responsive
 Alternates: Midazolam 5-15 mg IV x2 or Diazepam 5-10 mg
IV x2
 If no IV access, use Lorazepam 5 mg IM (max 8 mg),
Midazolam 5 mg IM, Diastat rectal gel 20 mg
 Eval: ABCs, labs (glucose, CBC, BMP, Ca, Mg, Phos, LFTs,
AED levels, urine tox, cxs)
 If seizure persists 5 minutes after 2nd dose, proceed to next
stage
Established SE, Fosphenytoin 15-20mg/kg IV run over 10 min (at 150 mg
PE/min) (limited by hypotension) or Phenytoin 1 g or 18-20mg
10-20 minutes /kg IV over 1 hr (50 mg/min, slow to avoid extrav, burning,
hypotension, arrhythmia)
 Need to monitor mental status, cardiac monitoring
 If sz stops but patient doesn’t awaken rapidly at any point,
or if need to intubation with paralysis, obtain EEG ASAP
 If seizure persists after completion of infusion, proceed to
next stage
Refractory SE, 1) Phenobarbital 20mg/kg IV over 10 minutes (50-100
Coma induction mg/min) OR
20-30 minutes 2) Valproate 40 mg/kg IV run over 10 minutes, repeat 20
mg/kg over 5 min
OR may use midazolam/propofol as below
 Intubate with RSI, stat Neuro consult
 If seizure stops, admit to ICU and obtain EEG ASAP
 If seizure persists, proceed to coma induction or use
pentobarb as below
Coma induction *FIRST LINE:
>45 min 1) Midazolam 0.2 mg/kg load then 0.2-0.4 mg/kg bolus q5
min until sz stop (max 2 mg/kg), then start 0.1 mg/kg/h gtt
(0.05-2 mg/kg/h) OR
2) Propofol 1 mg/kg IV load, repeat 1-2 mg/kg bolus q3-5
min until sz stop (max 2 mg/kg), then start 2 mg/kg/h gtt (1-15
mg/kg/h)
*SECOND LINE:
Pentobarbital 5-10mg/kg IV load at 50 mg/hr then 5 mg/kg
boluses until sz stop, then start 1 mg/kg/h gtt (0.5-10 mg/kg/h)

Consider topamax 150-750 mg bid via NGT if all else fails

 Need to obtain EEG ASAP

30
 Definition: Continuous sz >5min or 2 or more discrete sz without complete
inter-sz recovery; others may use 30min threshold
 Do NOT mix phenytoin w/dextrose as it will precipitate! if via IV need cardiac
monitoring)
 Status w/o response to tx
o R/o INH OD: Give pyridoxine/vit B6 5g IV over 5min
o Hypoglycemia: give D50W IV
o Eclampsia: Magnesium sulfate 4-6g IV (or 5g IM each buttock) then 2-3g/hr
if intact patellar reflex
*if loss of patellar reflexes or RR<12 or UOP<100/4 hrs, give Calcium
gluconate 1g IV for Magnesium overdose

31
 Pediatric (1mo - 2 yrs) Convulsive Status Epilepticus
STAGE ACTION
Impending Skip this stage if patient received 2 doses of benzodiazepines
SE, (e.g. diastat) prior to arrival in ED
0-10 minutes Lorazepam 0.1mg/kg IV
 Repeat in 5 min for persistent seizure (max total 2 doses,
including pre-hospital doses)
 If no IV access, use midazolam
 Eval: ABCs, labs (glucose, CBC, BMP, Ca, Mg, Phos, LFTs,
AED levels, urine tox, cxs)
 If seizure persists 5 minutes after 2nd dose, go to next stage
Established Fosphenytoin 30mg/kg IV run over 10 minutes
SE,  CALL PICU AND CHILD NEUROLOGY when loading
fosphenytoin
10-20  If seizure stops but patient doesn’t awaken rapidly at any point,
minutes or if intubation with pharmacologic paralysis is
necessary, obtain EEG ASAP
 If seizure persists after completion of infusion, go to next stage
Refractory Phenobarbital 20mg/kg IV run over 10 minutes
SE,  If seizure stops, admit to PICU and obtain EEG ASAP
20-30  If seizure persists after completion of infusion, repeat 20mg/kg
minutes IV over 10 minutes
 If seizure persists after second loading dose (total 40mg/kg),
proceed to coma induction
Coma Facilitate rapid PICU admission in anticipation of coma induction
induction, Prepare for airway control and invasive BP monitoring
45 minutes Obtain EEG ASAP in anticipation of coma induction
*FIRST LINE:
Midazolam 0.2mg/kg IV bolus (max 10mg) and start infusion
at 0.1mg/kg/hr
 If seizure persists, start pentobarbital and wean midazolam
 Consider pyridoxine trial (100mg IV) prior to starting
pentobarbital
*SECOND LINE (after midazolam fails):
Pentobarbital 10mg/kg IV bolus and start infusion at
1mg/kg/hr
 Repeat pentobarbital 5mg/kg IV bolus every 30 min and
increase infusion by 1mg/kg/hr every hour until seizure cessation
AND burst-suppression on EEG
Coma phase Continue coma medication x 24 hrs after last seizure
Continue all prior anti-epileptic drugs at maintenance dosing
Weaning Midazolam: reduce gtt by 0.05mg/kg/hr q3hrs
phase Pentobarbital: reduce gtt by 1mg/kg/hr q6hrs

32
Repeat Restart previous effective coma medication x 24 hours
coma phase Add topiramate 10mg/kg NG
(recurrent
seizures
during wean)

33
 Pediatric (> 2 yrs) Convulsive Status Epilepticus
STAGE ACTION
Impending Skip this stage if patient received 2 doses of benzodiazepines
SE, (e.g. diastat) prior to arrival in ED
0-10 minutes Lorazepam 0.1mg/kg IV (max 4mg/dose)
 Repeat dose in 5 min for persistent seizure (max total 2
doses, including pre-hosp doses)
 If no IV access, use midazolam
 Eval: ABCs, labs (glucose, CBC, BMP, Ca, Mg, Phos, LFTs,
AED levels, urine tox, cxs)
 If seizure persists 5 minutes after 2nd dose, proceed to next
stage
Established Fosphenytoin 30mg/kg IV run over 10 minutes (max
SE, 150mg/min)
10-20 minutes  CALL PICU AND CHILD NEUROLOGY when loading
fosphenytoin
 If seizure stops but patient doesn’t awaken rapidly at any
point, or if intubation with pharmacologic paralysis is
necessary, obtain EEG ASAP
 If seizure persists after completion of infusion, proceed to next
stage
Refractory Use ONE of the following agents: Valproate is preferred as
SE, first-line, but levetiracetam should be used if valproate is
20-30 minutes contraindicated (known or suspected inborn errors of
metabolism or liver disease)
Valproate 20mg/kg IV over 4 minutes
Levetiracetam 30mg/kg IV (max 3 grams) over 6 minutes
 If seizure stops, admit to PICU and obtain EEG ASAP
 If seizure persists after completion of one of the above meds,
proceed to coma induction
Coma Facilitate rapid PICU admission in anticipation of coma
induction, induction
45 minutes Prepare for airway control and invasive BP monitoring
Obtain EEG ASAP in anticipation of coma induction
FIRST LINE:
Midazolam 0.2mg/kg IV bolus (max 10mg) and start
infusion at 0.1mg/kg/hr
 If seizure persists, start pentobarbital and wean midazolam
SECOND LINE (after midazolam fails):
Pentobarbital 10mg/kg IV bolus and start infusion at
1mg/kg/hr
 Repeat pentobarbital 5mg/kg IV bolus every 30 min and
increase infusion by 1mg/kg/hr every hour until seizure
cessation AND burst-suppression on EEG
Coma phase Continue coma medication x 24 hrs after last seizure
Continue all prior anti-epileptic drugs at maintenance dosing

34
Weaning Midazolam: reduce gtt by 0.05mg/kg/hr q3hrs
phase Pentobarbital: reduce gtt by 1mg/kg/hr q6hrs
Repeat coma Restart previous effective coma medication x 24 hours
phase Add topiramate 10mg/kg NG
(recurrent
seizures
during wean)

35
 Therapeutic hypothermia
1. Indications
 Post-cardiac arrest with return of spontaneous circulation to normal rhythm
o Assess if witnessed, time and duration of arrest, rhythm (VF/VT; may
consider PEA/asystole)
 Inclusion: Known time of arrest (prefer <1h down time), comatose, usually age
≥18, SBP ≥90 mm Hg (spontaneous or with fluids/pressors)
 Exclusion: Status epilepticus or other cause of coma, pregnancy, known
terminal illness/DNR/DNI, known severe coagulopathy

2. Logistics
 Call Neuro 443-2662 @ UCSF, 443-6378 @SFGH
 Exam: Check brain stem reflexes (pupils, corneal, oculocephalic reflex), best
motor response esp prior to intubation/sedation
 Intubate, sedate; place temp sensing foley/ check rectal
o Sedation: Midazolam 2-6 mg/hour and fentanyl 25-75 mg/hr, or propofol 0-
100 mcg/kg/min if HD stable
 Goal temp: 33 °C

3. Protocol
 Start cooling ASAP if appropriate to reach goal temp. do it FAST but avoid
overshoot
o Ice pack to head, neck, groin, axilla, torso, limbs
o Cooling blankets (over and under patient)
o 1L IV bolus of chilled NS (4 °C)
o NGT and bladder lavage with iced saline
o Endovascular cooling: placed by Neuro ICU fellow
o Turn off vent humidifier–use Heat Moisture Exchanger
o Turn off room thermostat/other warming sources
 Maintenance
o Eliminate shivering: Warm hands/feet, meperidine, buspar, Mg gtt; NM
blockade
 Vecuronium 0.1 mg/kg IV, repeat prn or gtt 1 mg/h, titrate 0-5 mg/h to ¼
twitch; if RF, use cisatracurium
o Keep NPO x 48h
o maintain glucose <140 with insulin gtt
o Monitor K, replace to 3.4 only (rebound hyperkalemia with rewarming)
o Replete Mg if needed to normal levels
o Maintain CPP >60, avoid hypotension
o Check ABGs – make sure to rewarm before reading
 Rewarming
o 24 h post cooling, goal 37 °C over 18-24 h  maintain 36.5 – 37 °C in 1
st

24h to avoid rebound hyperthermia

 Complications
o Cardiac arrhythmia (bradycardia, vfib)
o Coagulopathy, plt dysfunction
o UTI/PNA 2/2 poor PMN function
o SIRS 2/2 rapid rewarming
o Metabolic abnormality – hypokalemia, hyperglycemia, pancreatitis, ileus

36
4. Prognosis after hypoxic brain injury
 Defer until 1-3 days post CPR, unclear w/ hypothermia
 Poor prognostic sx: Myoclonus status epilepticus in 1 24 h with 1° cardiac
st

arrest, no pupil reflexes (1-3 days post), no corneal reflexes (3 days post), no
extensor/motor response (3 days post)

37
Sepsis

38
 High Risk Chief Complaints
By Jenny Wilson, Dina Res ed. Jillian Mongelluzzo Faculty ed. David Thompson
Wallin, Joe Freeman

Abdominal pain
1. General approach
 Check on patient before ordering meds/labs
 “Shotgun” approach for the patient with acute abdominal pain
o Cardiac monitor
o EKG
o UPreg (this will dramatically change your Ddx!!! Obtain ASAP)
o IVF (unless elderly or h/o CHF, usually 1 L NS to start)
o Zofran IV (4mg or 8mg)
o IV pain meds (usually morphine or dilaudid)
o Keep pt NPO until you have a likely dx
 Time sensitive diagnoses: AAA (especially rupture), ACS, perforated bowel,
ruptured ectopic pregnancy, ovarian/testicular torsion, and mesenteric
ischemia

2. History
 Mnemonics
o LMNOPQRST(history tool): Location, Medical history, New, Other
symptoms, Provoking/palliatve, Quality, Radiating, Severity, Timing
o OLDCART(pain assessment tool): Onset, Location, Duration,
Characteristics, Aggravating factors, Relieving factors, Treatment
 Location: Ask pt to point with 1 finger at worst pain. Diffuse or localized? Has
location changed (i.e. epigastric to RLQ in appendicitis)?
 Medical history: History of trauma? Pregnant? Smoker or alcohol abuse?
Vascular risk factors (htn, DM, CAD)? PUD? Sick contacts? New diet? Surgical
history?
 New: If the pt has this pain frequently/chronically, what was different today?
 Other symptoms: Nausea/vomiting? If so, how many times has the pt
vomited? Blood in vomit? Diarrhea, melena, or hematochezia? Passing flatus?
Fever/chills? Dysuria? Dizziness/syncope? Vaginal discharge or bleeding?
Recent weight loss? Jaundice?
 Provoking/palliative: Better or worse with food? Helped with meds? Relieved
with BM?
 Quality: Aching? Burning? Throbbing? Stabbing?
 Radiation: Radiate to groin/back/chest/leg?
 Severity: Not only scale 1-10, but also getting worse?
 Timing: How long ago did pain start? Constant or colicky? If colicky, how
long do bouts last?

3. Exam
 General: Mental status, skin color (jaundiced? Mottled?)
 CV: Murmur, tachycardia
 Resp: Keep in mind lower lobar PNA can cause belly pain

39
  Abd: Bowel sounds, murphy’s sign, rebound/guarding, distension,
percussion, Feel for pulsatile mass, listen for bruits. Rectal exam
o Consider bedside US sooner rather than later, to assess for biliary disease,
pregnancy, AAA, hemoperitoneum in trauma
 GU/pelvic: Assess for hernias/testicular TTP, urethral/cervical discharge
(obtain cultures!); females with pain below the umbilicus need pelvic exams-
CMT, adnexal fullness, os open or closed?
o Consider transvaginal US at this point, if concern for pregnancy and no IUP
seen on transabd US
 Extremities: Good distal pulses? Evidence of PVD?

4. Differential diagnosis
Diagnosis Symptoms Signs Actions
Appendicitis Vague Rebound If clear dx clinically, call
periumbilical or Guarding surgery without
epigastric pain CMT, Psoas, imaging. If unclear:
migrating to RLQ Obturator US (kids, pregnant)
N/V/D, anorexia CT A/P
Biliary disease RUQ or epigastric RUQ TTP Ultrasound
pain, may radiate Murphy’s sign LFTs
to R shoulder
Bowel Crampy diffuse Distension Plain films
obstruction pain Abnl bowel CT if unclear
N/V sounds Once diagnosed:
Bloating NGT
h/o previous surg Surgery consult
or bowel
obstruction
Diverticulitis LLQ pain Rebound If clear dx clinically, call
Constipation or Guarding surgery.
diarrhea (change Heme pos stool CT A/P
from nl) Fever US
Rectal bleeding Barium enema
Ectopic Amenorrhea Adnexal UPreg
pregnancy Vaginal bleeding tenderness or Quantitative serum
Dizziness mass beta-hCG
T&S
Transvaginal US
Call OB-Gyn ASAP
Gastroenteritis Poorly localized No peritoneal No need for CT!
pain signs!
N/V AND! D Can have fever

40
Intussusception Episodic colicky Palpable abd Plain films
pain mass Barium/air contrast
N/V Blood in stool enema
Bloody stool or currant jelly
stool
Dehydration or
lethargy
between
episodes
Mesenteric Gradual to acute Pain out of Lactate
ischemia onset proportion to Plain films
Poorly localized, exam CT
unrelenting, Watch out for MRA
severe pain hypovolemia Angiography
N/V/D and sepsis
Worse c meals
Ovarian torsion Abrupt onset Unilateral TTP Transvaginal US with
Severe unilateral Adnexal pain or Doppler
pain mass UPreg
N/V
Pancreatitis Epigastric or LUQ Distension Lipase
pain Hypovolemia CT A/P with contrast
h/o pancreatitis, 2/2 third Aggressive IVF
alcoholism, biliary spacing NPO
dz (GET
SMASHED
mnemonic)
PID Dull, poorly Adnexal mass Cultures for GC,
localized lower or TTP Chlamydia (can do
abd pain CMT urine PCR at SFGH)
Vaginal d/c Mucopurulent UPreg
Urinary sx cervical or Pelvic US
Dyspareunia vaginal d/c Adjunct HIV, RPR
Fever
Perforated ulcer Sudden severe Diffuse TTP Abd plain films
pain (older pts Peritonitis CT A/P
may have minimal Rigid abd Aggressive IVF
pain) Volume T&S
May radiate to depletion Call surgery ASAP
back SIRS
Ruptured or Severe abd, back, Pulsatile abd Straight to OR if
leaking AAA flank pain mass unstable
Radiation to groin, Diffuse TTP ED US
thigh Abd bruit, CT A/P
Syncope decreased Plain films
distal pulses
Hypotension
Hematuria

41
 Testicular Sudden onset Swollen, tender Involve urology early!
torsion severe pain in firm ED US with Doppler
lower abd, hemiscrotum Formal US
scrotum, inguinal High-riding
area testis with
N/V transverse lie
h/o previous Loss of
episodes resolving cremasteric
spontaneously reflex
Ureteral colic Abrupt onset of Writhing in pain UA
(nephrolithiasis) severe flank pain CVAT CT
Radiates to groin Benign abd IVF
N/V exam
Hematuria
Volvulus Sudden severe Diffuse TTP Pain films
colicky pain Distension Barium enema
Distension Tympany sigmoidoscopy
Recurrent Palpable mass
episodes with cecal
N/V/constipation volvulus
Peritoneal
signs if
infracted
* Adapted from Mahadevan SV and Garmel GM, An Introduction to Clinical
Emergency Medicine, pp. 151-153.

5. Mgmt
 Labs: Consider CBC, BMP, LFTs, lipase, lactate, U/A and UPreg
 CXR (can also eval for free air), KUB (if considering SBO, poorly sensitive)
 Consider further imaging depending on symptoms/exam. Elderly patients with
abdominal pain likely require imaging, but hold off on ordering formal ultrasound
or CT until presented to attending
 Treat pain and nausea!

Altered Mental Status

1. General approach
 MTF = “metabolize to freedom”
 Ranges from acutely life-threatening to just plain drunk
 Incorporate all information available to you (whatever the patient can give,
EMS report, prior visits, nurses’ knowledge of patient)
 View each patient with a fresh lens for this visit. Frequent fliers get sick!
 If VS have any abnormality, even in frequent flyers, you must address it (and
document that you addressed it), even if this is as simple as hanging a liter of
fluid and monitoring for EtOH withdrawal in a tachycardic pt
 Have a very low threshold for testing in an altered patient, and expand your
approach when the patient isn’t clearing as expected

42
2. History
 Often limited, but obtain as much peripheral information (EMS, family, SNF
staff, prior records)
 Dstick in field, therapy given (benzodiazepines, narcan), seizure like activity,
situation (alcohol use, tripped and fell, recent infection)
 Medication list!

3. Physical exam
 Vital signs: Tachycardia? Hypotension? Rectal temperature?
 General: Mental status, GCS, disheveled, EtOH on breath, agitated, etc
 Skin: Remove all clothing and carefully assess for rash, pressure ulcer, etc,
then cover pt and keep him/her warm
 HEENT: Inspect for head/facial trauma. Open mouth if possible. Assess
dentition
 Neck: supple? If possible trauma, consider C-collar
 CV: Tachycardic? Murmur? JVD? Edema?
 Resp: Distress? Crackles? Decreased/absent breath sounds?
 Abd: TTP? Peritoneal signs? Distension?
 Ext: Edema? Evidence of cellulitis or DVT? Pulses
 Neuro: Pupils? Doll’s eye reflex? Moving all extremities? If moving one
extremity less, test if withdraws from pain. Babinski reflex?

4. Differential diagnosis
 AEIOU TIPS
o Alcohol, toxins, drugs
o Endocrine, Electrolytes
o Insulin (diabetes)
o Oxygen, opiates
o Uremia (renal, including HTN)
o Trauma, Temperature
o Infection
o Psychiatric, Porphyria
o Subarachnoid hemorrhage, Space-occupying lesion
5. Mgmt
 Undifferentiated vs. differentiated AMS
o Undifferentiated: Treat as you go, delegate for tasks to occur in parallel
o Differentiated AMS/MTF: Reassess, keep differential broad even in chronic
alcoholics (e.g. infection, SDH and other head bleeds)
 ABCs, IV, cardiac monitor (at least initially), initial vital signs
 EKG especially if history of syncope
 CXR
 Labs: Fingerstick glucose, VBG (immediate results at both facilities), CBC,
complete metabolic panel, LFTs, coags, UA/UCx/UPreg
 Consider other tests: ABG, D-dimer, BNP, Free T4, TSH, UTox, aspirin and
acetaminophen levels, Head CT, C-spine plain films or CT, abdominal plain
films or CT, LP
 Consider empiric abx if high likelihood of infection

43
  Beware of oversedation: Agitation may be due to intracranial bleed!
 Continue to reassess, intervene, and document until the patient is admitted
or discharged
o Set a time to reassess: i.e., q2 hours, document the time and your exam,
as well as any interventions you performed
o Rate of alcohol metabolism = 0.016 BAC/hr. If alcohol, pt should at least
begin to clear by 6 hours; if minimal improvement or worsening after 6 hours
of observation, consider alternative diagnosis
o Monitor for signs of withdrawal: Tachycardia, HTN, tremulousness,
agitation. Keep in mind that liquor stores close at 2 am, so do not discharge a
chronic alcoholic at 2 am—he will be back in the ED at 6 am in florid
withdrawal!

Chest pain
1. General
 5 life-threatening causes of CP that you absolutely cannot miss: ACS, aortic
dissection, pneumothorax, PE, and esophageal rupture
 Always document H&P (and charting) to clearly rule out all 5 of these
diagnoses before discharging patient

2. History
 Onset: Sudden? How long ago?
 Constant or intermittent: “Has there been one moment in the past 6 hours you
were chest pain free, or has it been constant?”
 Chronicity: Similar pain in past? Increasing in frequency and severity?
 Character: Crushing pressure? Tearing to back?
 Associated sx: SOB? Arm/jaw pain? Diaphoresis? Leg swelling?
Nausea/vomiting?
 Risk factors: Crack/meth use? Smoker? Family history? PMH—DM, CAD,
HIV, Lupus, prior pneumothorax or VTE?

3. Exam
 Mental status
 CV: Heart sounds, vessels including neck (JVD), bilateral radial pulses
 Chest wall: TTP? Crepitus? Ecchymoses? Rash?
 Pulm: Crackles? Decreased/absent breath sounds? Resp distress?
 Abd: Mass (e.g. AAA), tenderness, hepatomegaly. Include rectal (GIB may
alter subsequent tx)
 Extremities: Asymmetric edema? Pitting edema? Calf tenderness?

4. Differential diagnosis
 Cardiac: ACS (MI, angina), pericarditis, myocarditis, valvular diseases (AS)
 Respiratory: Pneumonia/other infections, pneumothorax, PE, COPD
exacerbation
 Esophagus: Esophagitis (e.g., candidal), GERD, spasm (nutcracker
esophagus), foreign body, rupture (Boerhaave’s)
 Upper abdomen: Gallbladder disease (cholecystitis or cholelithiasis),
pancreatitis, duodenal or peptic ulcer, hepatic disease
 Aorta: Dissection, aneurysm, aortitis
44
  Chest wall: Costochondritis (Tietze’s disease), contusion, rib fracture, muscle
strain or tear
 Skin: Herpes zoster

5. Mgmt
 IV, O2, cardiac monitor
 EKG: If STEMI, activate STEMI pager
o Soft calls: Fax to fellow
 ASA 325 mg PO or 300 mg PR (unless allergy, suspect head bleed or
dissection)
 CXR: If pt is stable, PA/lat preferred to portable
 Consider bedside DVT and cardiac US if suspect PE
 BP in both arms
 CBC, BMP, troponin, ±coags, (± D-dimer, BNP, other specific tests)
 Additional imaging/studies to consider depending on differential
o CTA PE protocol
o CTA dissection protocol (call radiology to discuss which study to order if PE
and dissection are both high on differential)
o If H&P, CXR suspicious for PNA, order blood cultures, lactate, antibiotics

6. Dispo
 Depends on symptoms, risk factors, work-up. If extremely low risk, close
follow-up arranged, ruled out dangerous causes, and the patient’s symptoms
are fully explained by a benign etiology, may consider d/c home
 Rule-out ACS with risk factors or other patients are admitted to Cardiology,
Medicine, or Family Medicine. Frequently admitted to telemetry (5D tele @
SFGH)
o Recent evidence and AAEM practice guideline suggest patients at low risk
(normal cardiac enzymes, normal or nonischemic EKG, no hypotension, rales
above bases, pain similar to baseline angina) for significant 30-day morbidity
and mortality unlikely to benefit from telemetry monitoring
(www.aaem.org/emtopics/telemtry_bed_usage.pdf)

Fever and Hyperthermia in Adults (T>38 °C)

1. General approach
 Isolation necessary?
 Any obvious cause?
 Any high risk features?
 Does the patient haves sepsis?

2. History
 Time course of fever
 Associated symptoms: Headache, sore throat, ear pain, neck pain, cough, abd
pain, back pain, dysuria, joint pain, rash?
 Sick contacts
 Recent travel
 Risk factors: Recent exposures, indwelling hardware or devices, IVDU,
immunosuppression, sexual history
 Meds?
45
  High-risk features
o Immunosuppression
 Steroids, immunomodulators, or post-transplant
 Neutropenia
 DM
 HIV
o Extremes of age (pediatric fever – see Pediatrics chapter)
o Injection drug use (shooter with a fever): Abscess, cellulitis, wound botulism,
epidural abscess, necrotizing fasciitis, endocarditis
o International travel
3. Exam
 Mental status
 Search for localizing signs e.g. rash, murmur, rhonchi, wound
 High-risk features: Abnormal vital signs despite hydration / antipyretics
 Rectal temp in any sick looking patients, as well as dental/rectal exam for
squirrely patients without an obvious source

4. Differential diagnosis
 Infectious: Viral, bacterial, fungal, rickettsial, mycobacterial, parasitic, etc
o CNS: Encephalitis, meningitis, epidural abscess
o CV: Endocarditis, myocarditis, pericarditis, mediastinitis
o GI: Cholecysitis, cholangitis, hepatitis, gastroenteritis, appenditicits,
diverticulitis, colitis
o GU: UTI/pyelo, PID, orchitis, epidydimitis
o HEENT: Sinusitis, dental, AOM, viral URI, pharyngitis
o Heme/Lymph: Bacteremia, lymphadenitis, malaria, etc
o MSK: Septic arthritis, septic bursitis, osteomyelitis
o Resp: Pna, bronchitis
o Skin: Cellulitis, abscess (including perirectal abscess), fasciitis, etc
 Toxicologic: NMS, serotonin syndrome, sympathomimetics (cocaine, meth,
ecstasy), anticholinergics, malignant hyperthermia, ASA
 Neuro: Cerebral hemorrhage, status epilepticus, hypothalamic dysfunction
 Environmental: heat stroke/ heat exhaustion
 Endocrine: Thyrotoxicosis, Pheochromocytoma
 Rheumatologic
 Neoplasm

5. Mgmt
 Acetaminophen or ibuprofen
 Workup may include
o CXR
o UA and urine culture
o Labs: In those with high-risk features as indicated
 Blood cultures
 Wound cultures
 Joint taps for hot joints
 Chlamydia and gonorrhea testing in PID suspects
46
  Viral DFAs (usually only in admitted patients)
 CT or US of suspect site(s)
 LP if meningitis or SAH is suspected
 Antibiotics AS APPROPRIATE (remember many infections are viral)
o Cultures before antibiotics in all PNA, endocarditis, or septic patients
whenever possible
 Malignant hyperthermia: Dantrolene 1 mg/kg IV until symptoms resolve or
max 10 mg/kg
 Cooling for severe hyperthermia
o Evaporative cooling
o Cooled IV fluids
o Ice packs to groin
o Arctic sun cooling blanket
o Intubate and paralyze if life-threatening (prevent shivering)

6. Dispo
 Low-risk patients with normal work-up or benign cause: D/c home with
supportive care, outpatient follow-up
 Intermediate-risk patients: Antipyretics, fluids, observation in ED, and/or 24
hour recheck
 High-risk patients: Admit
 Sepsis – see Early goal directed therapy algorithm in Resuscitation chapter
o 2+ SIRS criteria + source = Sepsis, need EGDT, likely admission
o Sepsis + organ dysfunction = Severe sepsis, likely need step-down or ICU
o Sepsis + persistent hypotension = Septic shock, need ICU
Headaches in Adults
1. General approach
 History is critical
 Keep your ddx broad (e.g. glaucoma and temporal arteritis)
 Most headaches are benign; key is differentiating who needs CT/LP vs. who
just needs symptom control

2. History
 Onset: Time from onset to reach maximal intensity (Sudden e.g. thunderclap
vs gradual)? Prodrome/aura? Post-traumatic or post-LP?
 Provokes/palliates: Triggers? HA worse with lying down or standing up? With
movement? Associated with photo- or phonophobia?
 Quality: Sharp, dull, associated with aura? History of headaches in the past?
How often? Does this feel similar? In what way does it feel different?
 Region/radiation: Unilateral/bilateral, anterior/posterior
 Severity: “Worse headache of my life”
 Timing: Worse in morning, improves throughout the day, etc.
 Associated symptoms
o Fever
o Neck pain/stiffness
o Vision changes or watery eye
o Nasal congestion
o Photo- or phonophobia
47
 o Aura/focal neuro symptoms e.g. confusion, trouble speaking, trouble w/
walking or balance
o Nausea/vomiting
o Somnolence, AMS, seizure
o Toxic exposures: Multiple family members with HA? HA improved after
leaving home?
o Related to menstrual cycle?
 Red flags
o Sudden onset
o No similar headaches previously
o Concomitant infection
o Altered mental status or seizure
o Focal neurologic deficits
o Headache with exertion
o Age >50
o HIV and immunosuppression
o History of cancer
o Visual disturbances
o Family history or personal history of SAH
o Anticoagulation

3. Exam
 Eyes: Visual acuity, fundoscopic exam, visual fields
 HEENT: Temporal artery tenderness, sinus tenderness, dental/TMJ problems
 Thorough neurological exam: Cranial nerves, motor, sensory, cerebellar, gait.
Look for deficits
 Derm: Associated rash (e.g. petechiae)
 Red flags
o ABNORMAL VITAL SIGNS
o Neurologic abnormalities: Gait, cerebellar testing, strength
o Decreased mental status
o Meningismus
o Fever/Toxic appearance
o Eye findings: Decreased acuity, papilledema, ciliary flush and sluggish
papillary response, elevated intraoccular pressure
o Evidence of trauma

4. Differential diagnosis – see Neurology chapter for specific etiologies

 Blood in the brain: SAH, ICH
 Elevated ICP: Mass, hydro, pseudotumor, infection, sinus thrombosis, NPH
 Meningitis
 Temporal arteritis
 Glaucoma
 Toxic exposure (eg carbon monoxide)
 Post-concussive or TBI-associated
 Hypertensive HA (usually only if diastolic is >120, and dx of exclusion)
 Post-LP headache
 Migraine/tension/cluster HA
 As part of viral syndrome or sinusitis

48
  Associated with dental pain
 Rebound from narcotics/benzos/drugs/EtOH
 Hormonal/pregnancy related

5. Mgmt
 Risk stratification
o Low risk: Typical HAs, no new concerning historical factors, normal neuro
exam. Neuroimaging not routinely indicated
o High risk patient: Red flags on history/exam, focal neuro findings, fever
 Work-up for high risk
o Panoptic, tonopen, and/or optic nerve sheath ultrasound (as indicated)
o Labs: Consider CBC and coags if LP planned or bleeding suspected,
consider utox/alcohol level if there is any AMS, consider ESR/CRP if concern
for temporal arteritis
o Neuroimaging if there is concern for bleed, trauma, mass, increased ICP, or
prior to LP if there are high risk features (see below)
 Non-con head CT: Good screening exam, but can miss subtle findings
 CTA head (SAH protocol) if you have strong suspicion for SAH
 MRI/MRA/MRV (usually ordered only with a neuro consult)
o LP
 For SAH: LP after negative CT. Missed SAH risk up to 5% with neg CT,
depends on time since symptom onset. If <6 hrs, noncom head CT has
100% Sn/NPV (Perry et al, 2011)
 To check opening pressure: Lay pt flat with legs as straight as possible
 CT before LP from Hasbun et al, NEJM 2001
 Papilledema
 >60 yo
 Immunocompromised (at risk for abscess)
 Hx of CNS dz
 Sz w/in 1wk
 Recent head trauma
 Decreased consciousness
 Focal neuro deficits: CN abnormality, Δvisual field, arm/leg drift, aphasia,
inability to answer 2 consecutive questions/commands
 LP contraindications (but do NOT delay abx)
 Infection at site
 Concern for epidural/paraspinal abscess
 Plts<30 or bleeding diathesis (if plt<40 or INR>1.5 consider plt transfusion,
FFP; defer LP to admitting team)
 Mass lesion (brain abscess, tumor, SDH, ICH; herniation is rare unless
significant mass effect)
 CSF analysis: Send cell count w/diff (tube 1), glucose+protein (tube 2),
gram stain+cx (tube 3), cell count w/diff (tube 4); ±HSV PCR, ±CrAg. Collect
and hold excess, esp if considering fungal/cryptococcal cx (up to 10 mL extra
CSF; d/w Neuro)
 LP corrections: For every 600-1000 RBC you can have 1 WBC; ~1mg/dL of
protein per 750 RBCs, CSF glucose ≈ 60% of peripheral glucose level
 Traumatic tap: RBCs should decrease from Tube 1 to 4

49
  Have 2-6 hrs s/p abx to do LP before changes seen in cell count/cx
Condition Color Glucose Protein Cell Diff OP
(mg/dl) (mg/dl) Count
Normal Clear 40-80; <50 <5 WBC 0 <20 cm
Adult 50-75% H2O
of serum
SAH Bloody/ Nml ↑ but <5 WBC Same ↑
xantho <1000 ↑RBC as blood
Bacterial Cloudy/ <40% of 45-500 100- >80 % ↑
Meningitis Purulent serum 100K PMN

Aseptic/ Clear or Nml or ↓ ↑ WBC lymph Nml or

Viral cloudy (>50% (50- 25- (early ↑
Meningitis serum) 220), 2000, mono &
usually usually PMN)
<150 <250
Herpes Bloody/ Nml or ↓ Nml or ↑ 20-500 lymph Nml or
xantho (50-100) WBC, ↑
↑RBC
 Interventions
o ABCs! Intubate for airway protection (i.e. vomiting SAH patient with
declining mental status)
o Pain control and anti-emetics (tailor choices to cause of HA)
 Opiates for immediate relief (can lead to rebound HA)
 NSAIDs for more lasting relief if no bleed (ibuprofen, toradol)
 Compazine 10mg slow IVP works best for migraine, but beware of
akathisia. Consider giving w/ Benadryl. Reglan, zofran less effective
 Triptans, dihydroergotamine (usually 3rd line for migraine in the ED)
o Caffeine or blood patch for post LP HA (call anesthesia)
o Consult appropriate service if there are abnormal findings
6. Dispo
 Admit: All patients with blood in the brain
 Admit: All patients with abnormal LPs (unless you are confident this is viral
meningitis in a reliable patient with good follow-up)
 Observe: Patients in whom you are not sure
 Discharge home with appropriate follow-up: patients who fit the “low risk”
category as described above, who can get relief in the ED and are able to
tolerate POs, etc
Low Back Pain
1. General approach
 “CRAFTI” for 6 dangerous causes: Cauda equina syndrome, Ruptured disk,
AAA, Fx, Tumor, Infection

2. History
 Onset: Acute or chronic? Progressive? Trauma?
 Provokes/palliates: Worse with exertion? Movement? Position?
50
  Region/radiation: Unilateral/bilateral, radiation down leg
 Associated symptoms: Tingling, weakness, fevers, bladder/bowel incontinence
 Red flags
o <18yo: Spondylolysis, spondylolisthesis, discitis, spinal infection, CA,
developmental d/o
o >50yo: CA, fx esp pathologic, AAA
o Trauma (fx)
o Chronic steroid use (fx 2/2 osteoporosis)
o Hx of CA (CA/mets)
o Fever/chills/night sweats (infection, CA); IVDU (infection)
o Immunocompromised/ DM/HIV/transplant (infection)
o Night pain (CA, infection, ankylosing spondylitis)
o Unrelenting pain (CA, infection); pain>6wks (CA, infection)
o Incontinence/saddle anesthesia/bilateral neuro deficit (epidural compression
syndrome)
o Unilateral neuro deficit (herniated disc)

3. Exam
 Vital signs: Temp for infection, BP for AAA
 MSK: Palpate spine, sitting & lying straight leg raise to r/o disk
rupture/herniation (positive if radiates past knee)
 Abdominal exam: Evaluate for pulsatile mass (AAA)
 CVAT: R/o pyelonephritis, ±UA
 Neuro
o Light touch, vibrate (dorsal column - use pager)
o Pinprick/temp (spinothalamic - alcohol swab)
o Walking on toes/heels, reflexes, saddle (buttocks, perineum, prox medial
thighs)
o Reflexes/gait/perianal sensation (cauda equine sydrome)

4. Differential diagnosis
 Consider MSK as well as other organ systems e.g. AAA, GU (pyelo)
 Other: Vertebral osteomyelitis, discitis
 See chart on next page

51
 Diagnosis Symptoms Exam Actions
Cauda  Severe LBP  Patchy LE flaccid
 MRI w/neurosurg
equine shooting down legs weakness and consult; if can’t get
syndrome  Saddle sensory loss MRI (obese,
hyperesthesia/  ↓Rectal tone/nocochlear implant,
Etiology: parasthesia, urinary anal wink, saddleetc) then try CT
Mass or retention (~90% anesthesia, w/myelography
midline disk sens) symmetric LE (requires infusion
herniation  Loss of B/B areflexia & into spinal canal)
(most control/ sexual weakness  Consider
common L4- dysfunction (high  +Straight leg raise
dexamethasone
5) risk if recent trauma  PVR>50-100cc is10mg IV or methyl-
or cancer  concerning prednisolone
consider mets) 30mg/kg IV if
 Can be insidious suspect traumatic
or acute disc herniation
(controversial)
Spinal  Fever + back pain  Fever, local spine  ↑ESR in 95-100%
epidural  High risk: IVDU, tenderness & (90% of immune-
abscess DM, HIV, immune- extremity neuro compromised),
compromised, CA, deficit (based on CBC, bcx
Etiology: CRI, EtOH, recent level→neck, back)  No LP
Staph, strep, surgery/LP,  MRI (or CT
GN bacteria endocarditis myelogram)
 Vancomycin 1 g
IV+ ceftriaxone 2g
IV (or ceftazidime 2
g IV if suspect
pseudomonas)+
metronidazole
500mg IV; ±steroids
 Neurosurg c/s
Spinal  Abrupt severe  ±Weakness/  MRI/CT
epidural radicular back pain sensory loss myelogram
hematoma with prior trauma/  Consult
spinal procedure spine/neurosurgery
Etiology:  ±Loss of bladder/
Trauma,LP; bowel function
coagulopathy

52
 Malignancy/  ↑Risk: >50yo,  Bony midline  XR: Mets often
Bony mets pain>1m, wt loss, tenderness to missed)
h/o CA palpation of spine  CT/MRI/bone scan
Etiology:  Pain worse at  MRI if cord sx
Lung, Breast, night  Immediate
kidney, neurosurg consult
prostate, for new/progressive
myeloma, neuro findings (cord
lymphoma compression)
 Consider
dexamethasone
10mg IV or methyl-
prednisolone
30mg/kg IV
Herniated  30-40yo w/back  +Straight leg raise  Analgesic, muscle
disc/Sciatica pain  95% at L4/5 or relaxants
 Shooting pain L5/S1  Limited bed rest 0-
past knee 2wks then resume
 Worse w/leaning activities
forward/coughing/  Surg consult if
sneezing/straining cord compression or
 Often motor deficit
parasthesias/  No improvement in
numbness/ 3-4 wks: MRI/CT
±weakness myelogram
Vertebral  Acute onset  Tender focal area  T/L/S spine XR
compression  Elderly w/ on spine  NSAIDs & close f/u
fracture osteopenia, with PMD
smoker, steroids
Acute  Sudden twisting  Paravertebral  Supportive,
lumbosacral or fall, new/ muscle spasm & analgesics, back
strain excessive exercise tenderness, no stretching exercises
 Mvmt ↑ pain but neuro deficits
no fever/LE (including straight
tingling/numbness/ leg raise)
weakness

5. Mgmt
 No red flags & sx <1mo: Treat sx X 2wks with analgesics (NSAIDs, opioids) ±
muscle relaxants (e.g. diazepam 5-10 mg PO, carisoprodol, methocarbamol)
o Most get better w/simple analgesic w/in 1-4wks, 90% of LBP gone by 4-6wks
 Positive flag or sx >1mo: CBC, ESR, UA, XR/imaging (see above for specifics)
o ↑Risk of serious pathology if: difficulty sleeping, awakened from sleep/unable
to fall back asleep, pain worse w/walking
o Sudden onset: R/o AAA & renal colic
o <50% of spinal infections have leukocytosis
o LBP in IVDU is infection until proven otherwise (get blood cx, urine cx)
 Rapidly progressive neurological symptoms: Consult neurosurg/spine, get
imaging
53
  Consider repeat visit to ED for pain as red flag (20% of returns w/in 24hrs get
emergency hospitalization)

6. Dispo
 Admit those with high risk conditions: Cauda equine syndrome, spinal epidural
abscess/hematoma, e/o cord compression or motor deficits
 May d/c home if pain controlled, reassuring exam with no red flags, able to
ambulate

Shortness of Breath
1. General approach
 ABCs: Initial management and stabilization supersedes diagnosis! Does this
patient need to be intubated? Are they having failure of oxygenation or
ventilation? Can I reverse it or delay it?
 Despite large differential, there’s a common endpoint: Hypoxia,
hypoventilation, and death
 Pitfalls
o Patients with serious underlying problems may have normal respiratory rate,
pulse ox, and ABG
o ACS and PE can present without chest pain
o Patients can have acute-on-chronic problems, i.e. ptx in an asthmatic, PE in
a pt with COPD, ACS in a CHF pt

2. History
 From pt, family, EMS, records
 Onset? Getting worse? Prior episodes? Chest pain, syncope, or other assoc
sx? URI sx? Fever/cough? Hemoptysis? Orthopnea? PND? Weight gain?
Decreased exercise capacity?
 Recent trauma? Smoke inhalation?
 PMH- smoker? Wt loss? History of asthma, CHF, COPD, CAD, VTE? PE
risk factors?

3. Exam
 ABCs
o Airway: Phonating? History of aspiration of foreign body or secretions?
 Turn on suction, and always have McGill forceps on an airway tray to
remove airway FBs
 Signs of impending airway collapse: Stridor, vomiting, decreased MS
o Breathing: Able to speak full sentences? Resp distress? Accessory muscle
use? Skin color—cyanotic? Showing signs of respiratory fatigue?
 Immediately apply oxygen by NC or nonrebreather face mask in acutely
SOB pt
 Consider needle thoracostomy if concern for tension pneumothorax
o Circulation: hypotension? Skin color? IV access
 Abbreviate physical exam depending on acuity, focusing on cardiac and
pulmonary systems
o Evidence of chest trauma or rib fracture?
o Don’t forget neck veins and lower extremities!!!
o Severe abdominal distension (e.g. ascites) could also cause SOB
54
4. Differential diagnosis
 Common causes of acute SOB: COPD exacerbation, asthma, PNA, ACS,
CHF, pleural effusion, and acidosis (causing tachypnea, not necessarily SOB)
 Life-threatening causes: PE, pneumothorax, and respiratory muscle
weakness (myasthenia gravis, Guillain-Barre, etc)

5. Mgmt
 ABCs, IV, Oxygen, cardiac monitor with continuous pulse ox
 EKG
 Labs: Fingerstick glucose (tachypnea in DKA), VBG (available immediately at
both sites), CBC, BMP, UA/UPreg
o Consider BNP, troponin, BCx
o Consider ABG
 Imaging
o CXR (PA/lat if stable, portable if unstable)
o Bedside US to evaluate for pneumothorax, pleural/pericardial effusion, IVC
enlargement or collapse
o Consider Chest CT, formal echocardiogram depending on scenario
 Nebs
o In wheezy, but stable patient: Albuterol 2.5 mg and atrovent 0.5 mg neb,
may repeat 3x
o In unstable patient: Albuterol 10 mg/hour continuous neb, atrovent 0.5 mg
neb x 3 (some nurses at both sites can set up continuous nebs, but many
times RT will be called)
 Other adjuncts
o Magnesium IV 2 g x 1
o Solumedrol 125 mg IV x 1 or prednisone 60 mg PO x 1
o Epinephrine 0.3 mg IM if anaphylaxis
o Noninvasive ventilation (NIV) e.g. BiPAP/CPAP—can rapidly reverse
SOB patient!
 Evidence strongest in suspected COPD, CHF exerbations
 BiPAP initial settings: 10/5. Max 25-30 cm H2O
 Do NOT use NIV on altered and vomiting pts.
o Empiric abx if PNA, COPD exacerbation are likely
o Lasix if fluid overload is evident on exam

6. Dispo
 Some acute asthma or COPD exacerbations can be “turned around” in the ED
and will not require admission (or will be eligibile for Mt. Zion at UCSF)
o Test ambulatory O2 sat before discharge
 Due to overlap between cardiac and pulmonary SOB, in stable but
undifferentiated patients, obtain all testing before selecting a service for admit
e.g. troponin, BNP

Syncope and Near-syncope

1. General approach – see diagram on next page

55
2. History
 Syncope vs seizure?
o Brief tonic-clonic movement may follow syncopal episode (myoclonus)
o More reliable indicators of seizure: incontinence/oral trauma, tonic-clonic
movement before loss of postural tone, post-ictal state, or history or seizure
 Context in which event occurred
 Associated symptoms (palpitations, cp, sob, headache, etc.)
 Prodrome?
 Black or bloody stools?
 LMP? Pregnancy?
 Any recent illness, med changes, etc?
 Anything that suggests seizure?
 Associated injuries?
 History of syncope?
 Family h/o sudden cardiac death?
 High-risk features
o Syncope accompanied by chest pain or shortness of breath
o Exertional syncope
o History of cardiac disease, especially presence of heart failure
o Older age and associated comorbidities
o Family history of sudden cardiac death
3. Exam
 Mental status
 Cardiac: Murmurs, blood pressures in both arms, orthostatics (if well
appearing)
 Full neurologic exam
 Rectal exam in any patient at risk for GI bleed

56
  Evidence of trauma
 High-risk features
o Hematocrit <30 (if obtained)
o Abnormal vital signs
o Persistently low blood pressure (systolic <90 mmHg)
o Abnormal findings on cardiac, pulmonary, or neurologic examination
o Abnormal ECG
4. Differential diagnosis
 Cardiac
o Arryhthmia: Bradyarrhythmias, tachyarrhythmias, heart block, brugada, long
QT, WPW
o Valvular disease: AS, MS

57
 o Pacemaker malfunction: Battery/generator failure, failure to capture
undersensing, oversensing, etc
o Ischemia
 Outflow obstruction
o PE
o Hypertrophic cardiomyopathy
o Tamponade
o Tension ptx
 Dehydration/hypovolemia
o GI bleed
o Trauma
o Ectopic pregnancy
o Aortic catastrophe / ectopic pregnancy / retroperitoneal hemorrhage
o Nausea/vomiting/diarrhea
o Infection
o Over-diuresis
 Neurocardiogenic
o Vasovagal
o Micturation/defectation/cough-associated
o Situational (i.e. during blood draw)
 Carotid sinus hypersensitivity
 Neurologic: ICH
 Tox
o Drugs of abuse, alcohol, carbon monoxide
o Medication related
 CCBs
 Betablockers
 Diuretics
 Nitrates
 Sedatives
 Meds affecting the QTc
 Metabolic: hypoglycemia, hypoxia, etc.

5. Mgmt
 UPreg in all women of child-bearing age
 Young patients with no high-risk features: EKG, fingerstick, hemaccue
 All others: EKG, CXR, labs including troponin, consider bedside echo

6. Dispo
 Low-risk patients with normal work-up: HOME
 Intermediate-risk patients: Observation in ED or CPOU
 High-risk patients: Admit to cardiology (or appropriate service if a non-cardiac
cause of syncope is apparent)

Vertigo
1. General approach
 Look for deranged vital signs, make sure patient is not in a position to fall

58
  Make sure this is actually vertigo, and not just lightheadedness
o Ask, “do you feel lightheaded, like you are going to faint? Or do you feel like
the room is spinning around? Do you feel like you’re drunk? Are you unsteady
on your feet?”
o Attempt to group the patient into one of three groups: vertigo, near syncope,
or dysequilibrium/ataxia
 In elderly and vasculopathic patients, consider vertigo to be central in origin
until proven otherwise
 Keep your differential broad

2. History
 Onset: sudden? Gradual?
 Provokes/palliates: Positional? Worse with movement? Worse with valsalva or
head-turning?
 Severity: Interfering with ambulation?
 Timing: Intermittent or constant?
 Associated symptoms
o Headache
o Neck pain/stiffness
o Hearing loss, tinnitus, or ear pain
o Recent URI
o Nausea/vomiting
o ANY other neuro symptoms (i.e. diplopia, dysarthria, dysphagia, focal
numbness/tingling/weakness)
 Red flags on history
o Constant, gradually progressive, not affected by movement
o Age over 50 or vascular risk factors
o Recent neck trauma/manipulation
o Any other concomitant neuro symptoms
o Complete unilateral hearing loss
3. Exam
 Red flags on exam
o Any neurologic abnormalities (esp brainstem/cerebellar/gait findings)
o Vertical or BIDIRECTIONAL nystagmus (always central)
4. Differential diagnosis
 Peripheral: BPPV, labrynthitis (aka vestibular neuritis), meniere’s, post-
traumatic (i.e. after a basilar skull fracture), herpes zoster oticus (aka Ramsay
Hunt Syndrome), acoustic neuroma, cerumen impaction, otitis
 Central: Cerebellar or brainstem ischemia/bleed, vertebral artery dissection (in
the setting of any neck trauma/manipulation), migranous vertigo (dx of
exclusion), MS (rarely)

5. Mgmt
 Risk stratification
o Low risk
 Young patients
59
  Sudden onset, severe, intermittent vertigo
 Worse with position/movement
 Horizontal nystagmus (often which fatigues or resoves with ocular fixation)
 Very clear ear symptoms/findings
 No h/o neck trauma/manipulation
 No focal neurologic deficits
 Work-up in high risk
o Adjunctive exam techniques
 Dix-Hallpike maneuver (attempts to reproduce nystagmus/symptoms in
BPPV): Doesn’t usually change management, some neurologists have
abandoned it completely. If positive, consider the Epley (treatment) maneuver
 Head impulse testing: Almost always abnormal in peripheral vertigo, and is
negative in >90% of patients with central problems
 Skew deviation: A sensitive bedside test for detecting early brainstem
process
o Consider neuroimaging
 CT/CTA (stroke protocol) is NOT the test of choice because its evaluation
of the posterior fossa is limited. Noncontrast CTH can rule out acute
hemorrhage or obvious masses, but of limited use in vertigo
 MRI/MRA with diffusion weighted imaging is the test of choice
o Neuro consult: In high risk patients, and most patients getting MRI
o Consider activating acute stroke pager if there are any other focal neuro
deficits on exam or you have high suspicion for an acute central process that is
within the time frame for TPA or IR intervention
 Therapy
o Anti-emetics
o Antihistamines (e.g. meclizine): May not help, but probably won’t hurt
o Benzodiazepines (e.g. diazepam): May mask the symptoms, but can provide
significant relief

6. Dispo
 Admit: All patients with abnormal MRIs, or high risk patients if MRI is
unavailable
 Observe: Patients in whom you are not sure. Don’t discharge patients with
unexplained neurologic deficits. Consider CT, MRI, or neuro consult.
 Discharge home with appropriate follow-up: patients who fit the “low risk”
category as described above, who can get relief in the ED and are able to
tolerate POs, ambulate etc. Rx for symptom relief, but long-term use of
benzos and/or meclizine may interfere with the brain’s ability to compensate

Weakness/Dizzy
1. General approach
 Define/describe the weakness: focal muscle weakness, low energy, or is it
DOE, vertigo, etc?
 Generalized or focal

2. History
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  Onset?
 Get specific - what can’t you do now that you could before?
 Fever? Infectious symptoms?
 Changes in sleep pattern? Diet history?
 Medication changes?
 Depression/psych?
 CHF/COPD symptoms?
 Safety at home?
 Falls?

3. Exam
 Thorough neurological exam
 Cardiac: Murmurs
 Other signs of possible infection, hydration status

4. Differential diagnosis
 Focal: One sided, or only lower/upper extremities, or proximal > distal).
Localize to brain, cord, NMJ, muscles, or systemic
o Emergent causes of unilateral focal weakness: Ischemic CVA, hemorrhagic
CVA, SAH, hemicord problem
o Emergent causes of bilateral focal weakness: Brainstem stroke, spinal cord
compression (i.e cauda equina), myelitis, guillain barre, tick paralysis,
myasthenia gravis, botulism, hypoglycemia/ other electrolyte or endocrine
derangements, hypokalemic periodic paralysis
o Other causes of focal weakness: Post-ictal (Todd’s) paralysis, myositis,
hemiplegic migraine, peripheral neuropathy/plexopathy
 Generalized weakness
o Hematologic: Anemia from GI bleed or malignancy
o Dehydration
o Infection/sepsis: UTI/PNA in older patients, botulism, tick paralysis
o Para-neoplastic syndrome: Lambert-eaton, dermatomyositis
o Meds: Diuretics leading to electrolyte abnormalities or dehydration,
narcotics/sedatives, statins or glucocorticoids leaning to myopathies
o Cardiac: ACS, heart failure, Afib RVR, presyncope
o Autoimmune/inflammatory: Myasthenia, guillain-barre, polymyositis,
polymyalgia rheumatica, other rheum
o Tox: Cyanide, carbon monoxide, organophosphate
o Trauma: Central cord or high Cspine fracture
o Endocrine: Hypothyroidism, adrenal insufficiency, DKA, pregnancy
o Metabolic: HYPOGLYCEMIA, hypokalemia, hyponatremia
o Psych: Depression
o PAIN causing subjective weakness
 Special considerations in ELDERLY patients: Occult infection, metabolic
disorders, stroke, cardiac problems, and medication related problems are the
most common causes of weakness in the elderly. WEAKNESS IS A SERIOUS
COMPLAINT IN THE ELDERLY

5. Mgmt

61
  Activate the acute stroke pager for acute onset of focal weakness
 POC testing: Upreg, udip, EKG, D-stick, hemoglobin, ABG/VBG with lytes and
lactate, guaiac, co-ox
 Labs: cbc, chem 10, UA + others depending on signs and symptoms and age
(CK, trop, BNP, serum ketones, cultures, etc)
 Imaging: CXR, CT head (non-con vs CTA), MRI brain/spine (depending on
presentations)
 Other: LP, tensilon test, or MIF (max inspiratory flow to assess resp status)

6. Dispo
 Admit: All patients with acute abnormal findings on exam or on labs/imaging,
or whenever you have a suspicion for a life-threatening cause of weakness
 Admit: Patients who cannot walk safely, frequent falls, unsafe at home, family
unable to care for patient
 Observe: Patients in whom you are not sure
 Discharge home with appropriate follow-up: Patients with chronic, subjective
weakness who are well-appearing and have a reassuring exam and work-up

Suggested Reading
 Hasbun R, Abrahams J, Jekel J, et al. Computed Tomography of the Head
before Lumbar Puncture in Adults with Suspected Meningitis. N Engl J Med
2001 345:1727-1733
 Mace SE. “Shortness of Breath in Adults.” An Introduction to Clinical
Emergency Medicine: Guide for Practitioners in the Emergency Department.
Eds. Swaminatha Mahadevan and Gus Garmel. Cambridge, UK: Cambridge
University Press, 2008. 485-502
 Mahadevan SV. “Abdominal Pain.” An Introduction to Clinical Emergency
Medicine: Guide for Practitioners in the Emergency Department. Eds.
Swaminatha Mahadevan and Gus Garmel. Cambridge, UK: Cambridge
University Press, 2008. 145-159
 Perry JJ, et al. Sensitivity of computed tomography performed within six hours
of onset of headache for diagnosis of subarachnoid haemorrhage: Prospective
cohort study. BMJ. 2011; 343:d4277
 Simon B and Nobay F. “Altered Mental Status.” An Introduction to Clinical
Emergency Medicine: Guide for Practitioners in the Emergency
Department. Eds. Swaminatha Mahadevan and Gus Garmel. Cambridge,
UK: Cambridge University Press, 2008. 179-191
 Tabas JA and Promes SB. “Chest Pain.” An Introduction to Clinical
Emergency Medicine: Guide for Practitioners in the Emergency Department.
Eds. Swaminatha Mahadevan and Gus Garmel. Cambridge, UK: Cambridge
University Press, 2008. 193-209

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 Cardiovascular Emergencies
By Liz Brown, Nicholas Villalon Res ed. Jennifer Wilson Faculty ed. Jeff Tabas

Chest Pain Basics: see High Risk CC chapter

EKG Basics
1. Normal EKG
EKG element Normal criteria Normal appearance
P wave <100 (2.5 boxes)  I, II;  in aVR
PR interval 120-200
QRS complex <120  I, II, V5, V6; aVR, V1
QTc interval <450 (QT/√R-R)
T wave  I, V6;  aVR; ±  III, V1, V2

2. EKG Changes in Common Medical Disorders

ST elevation or Q wave Location Coronaries
V2-V4 Anterior LAD
V1-V4 Anteroseptal LAD
V1-V6, I, aVL Anterolateral LAD, diag
II, III, aVF Inferior RCA, circ
I, aVL, V5, V6 Lateral Circ, diag
Large R in V1-V3, recip ST  Posterior RCA
V7-V9 Posterolateral RCA

AMI in LBBB (Sgarbossa criteria) Points

ST elevation  1 mm concordant with QRS 5
ST depression  1 mm in V1, V2, or V3 3
ST elevation  5 mm discordant with QRS 2
*3 is 20% sen, 98% spec for AMI

LBBB RBBB
QRS > 120 QRS > 120
Abnormal QRS morph in I, V5, V6 Wide QRS in V1, V2
 Monophasic/slurred/notched R wave  rSR , “rabbit ear”
l

 Absence of septal q wave  qR variant

QS or rS pattern in V1, V2 Deep, wide S wave in V5, V6

Condition Associated EKG findings

CNS Bleed Deep TWI, prominent U waves, prolonged QT
COPD RAD, low voltage, RAH  RBBB
PE Tachy, S1-QIII-TIII, RBBB, RAD, Anterior  T wave
Hyperkalemia Peaked Ts -> wide, flat P2 -> wide QRS -> sine wave

63
Hypokalemia Flat Ts, U waves, U > T waves, ST depression
Calcium Ca -> short QT, Ca -> long QT
Digoxin effect ”Swooping” ST depression, flat/inverted Ts, short QT
Digoxin toxicity PVCs, AV block, Ectopic SVT, V tach
Hypothroidism Brady, low voltage, ST depression, flat/inverted Ts
Hyperthryroidism Sinus tach

3. EKG Findings in AMI

 Early – Hyperacute T waves (not inverted), big R waves
 ST segment elevation that is flat or convex (tombstone)
 Q waves other than aVR and V1
 T wave flattening and inversion

4. Chamber Enlargements
Enlarged Findings
chamber
RAE P wave > 2.5 mm in II or biphasic in V1
LAE Biphasic P in V1 - terminal negative portion >1box wide and deep
RVH RAD, incomplete RBBB, R>S in V1, ST depression V1-V3
LVH R in aVL>11mV, R in V1 or V2 + S in V5 or V6 > 35 mV

ACS
1. Pathophysiology
 Myocardial ischemia due to imbalance in myocardial oxygen demand and
supply
o Demand: Heart rate, systolic blood pressure, wall tension/stress (preload
and muscle mass), contractility
o Supply: Coronary artery resistance and diameter, collateral blood flow,
perfusion pressure (flow from aorta to coronary artery, determined by LV end-
diastolic pressure)
 Most often 2/2 coronary atherosclerosis; consider vasospasm, embolism,
dissection

2. Presentation
 “Classic” chest pain: May be gradual, exertional, tightness/pressure/
squeezing/ heaviness, associated with nausea/vomiting/dizziness/sweating,
radiation down either arm or jaw (“toothache”)
 Beware atypical presentations in women, diabetics, elderly e.g. shortness of
breath, weakness, nausea/vomiting, palpitations w/o chest pain
 Relief with NTG, GI cocktail may not reliably differentiate ischemic vs.
nonischemic chest pain
 Stable angina: Brief chest pain, relieved with rest or NTG
 Unstable angina: New chest pain limiting activity, pain at rest (usually >20
min), pain with increasing frequency/duration/severity w/ -troponin
64
  NSTEMI: +Troponin, no ST elevation
 STEMI: +Troponin, ST elevation (vs. Prinzmetal’s angina)

3. Dx
 Hx and Exam
 IV, O2, monitor; EKG, CXR
 Trop + lytes ± coags
 Consider other ddx (see “Chest Pain” in High Risk CC chapter)

4. Mgmt
 ASA 325 mg PO (crushed); clopidogrel if allergic to ASA
 NTG (unless contraindicated e.g. low BP, tachycardia, RV infarct, etc)
 B-blocker only if hypertensive and no contraindications (e.g. low BP)
 Morphine

ACS management algorithm

65
 Cocaine Chest Pain
1. Pathophysiology
 Indirect sympathomimetic blocks reuptake of catecholamines
 Increased norepinephrine and epinephrine levels stimulates α1, α2, β1,
and β2 receptors; α-agonist activity causes both coronary and peripheral
vasoconstriction
 Sodium-channel blockade QRS prolongation, negative inotropy
 Dose-dependent vasoconstrictive effects + prothrombotic effect + increased
myocardial O2 demand increased risk of MI
o Most pts w/ cocaine-associated MI do not have severe CAD
 Chronic effects
o Accelerated atherogenesis
o LVH dilated cardiomyopathy

2. Presentation
 HTN, tachycardia, arrhythmias
 6% of pts w/ cocaine-associated chest pain (CACP) have +troponin
 At high doses, the negative inotropy can decrease LV fxn and cause heart
failure
 Massive overdose: May see hypotension 2/2 sodium channel blockade,
arrhythmias, myocardial ischemia

3. Dx
 Don’t just think ACS. Consider alternative dx e.g. crack lung, aortic dissection,
PTX, myocarditis, vasculitis
 EKG often difficult to interpret; high incidence of LVH, early repol; also some
pts w/ cocaine-associated MI will have normal or nonspecific EKG

4. Mgmt
 Overall similar to non-cocaine CP except in liberal use of benzos and NTG
 For severe HTN refractory to benzos (rare), can use phentolamine
 AVOID beta-blockers (including labetolol); can cause unopposed alpha
stimulation coronary and systemic vasoconstriction
 Hold ASA if suspicious for aortic dissection
 If must intubate, caution w/ succinylcholine (sux)
o Sux and cocaine both metabolized by plasma cholinesterase sux can
prolong cocaine effects, and cocaine can prolong paralysis from sux
o In pts w/ rhabdo, sux may worsen hyperkalemia and precipitate life
threatning arrhythmias

5. Dispo
 Similar to non-cocaine CP: Attempt to risk stratify, but most w/ CACP are
admitted because it is difficult to identify which pts are low risk

HTN
1. Pathophysiology
 Unclear for essential hypertension; may be r/t increased sympathetic neural
activity, increased angiotensin II activity, or decreased nephron mass

66
2. Presentation
 SBP > 140 and/or DBP > 90
 Often asymptomatic, incidental; may be associated with pain/anxiety in ED
 Malignant hypertension: Severe htn, diastolic >100-120, assoc w/ retinal
hemorrhages, exudates, or papilledema; may be associated with hypertensive
encephalopathy
 Hypertensive urgency = BP>200/110 without evidence of end-organ damage
 Hypertensive emergency/Malignant hypertension = elevated BP with evidence
of end-organ damage
Cotton wool spots Ischemia/Acute MI on EKG Acute RF: BUN/Cr
Linear retinal hemorrhage New LVH/LV failure New proteinuria
with pulmonary edema
Decreased visual acuity CHF (CXR or clinical) New hematuria
Severe headache/AMS Aortic dissection
(hypertensive encephalopathy)
Neurologic findings
 Consider secondary e.g. pre-eclampsia/eclampsia, renal dz (acute
glomerulonephritis)

3. Dx
 Recheck BP in both arms
 Exam: Mental status, Blurred vision, retinal hemorrhage, chest pain, dyspnea,
edema
 Labs: CBC, lytes, UA, lytes
 ECG, CXR, head CT for neuro symptoms, chest CT for r/o aortic dissection (if
CP/unequal pulses)

4. Mgmt
 Suggested approach

 Majority of patients with HTN urgency do not require acute tx, and BP can be
lowered with PO meds as outpt over 24-48h
SBP 140-159 2 months
160-200 2 weeks
> 200 Initiate therapy, recheck in 1-2 days
DBP 85-89 1 year
90-100 1 month
100-114 1 week
67
 > 115 Initiate therapy, recheck in 1-2 days
 For true HTN emergency, goal is to lower diastolic BP by 10-15% over first
hour, then by 25% over the next 6-12hours
 Pts are often volume depleted, and may require IVF to avoid hypotension
 Antihypertensives for malignant hypertension
Med Dose Notes
Esmolol 500 mcg/kg load Very short half life (HR > than BP)
over 1 min; Useful in aortic dissection
gtt 50-300 Short half life, good for cardiac pts
mcg/kg/min
Labetalol 20 mg IVP, max 300 Useful in CVA, avoid in CHF/cocaine
mg IV; gtt 0.5-3 Good for pregnant patients
mg/min
Hydralazine 10-20 mg q30 min Useful in preeclampsia/eclampsia
Nicardipine 2-5 mg bolus, drip Useful in CVA
2.5-15 mg/hr
Nitroglycerin 5-200 mcg/min Q3-5 min for desired effect; Good for
cardiac pts, usually used with other
meds
Nitroprusside 0.5-4 mcg/kg/min Easily titrated. Increased mortality in
post-MI pts

5. Dispo
 Dispo to ICU with central line if BP labile or requiring gtts
 Admit if severe symptomatic hypertension requiring IV meds

CHF
1. Pathophysiology
 Triggers/causes: Med non-compliance, MI, dysrhythmias (i.e. afib with RVR),
myocardial depressant drugs, toxins (cocaine), increased myocardial demand
from infection/trauma/dehydration/anemia, severe HTN, valvular dysfunction,
myocarditis, peripartum, vitamin deficiencies

2. Presentation
 Dyspnea, orthopnea, cough, fatigue
 Tachycardia, lower extremity edema, elevated JVP, hepatomegaly, S3, rales

3. Dx
 History and physical exam clues
 EKG may show LVH, strain, ischemia, or dysrhythmia
 CXR showing edema—though findings can be delayed
 BNP: Sensitivity 90%, specificity 74%
o May be low in acute pulmonary edema
o Falsely low in obese patients
o <100 rules out CHF fairly well, and >500 rules in a component of cardiac
failure. Gray zone not that helpful
o Must be adjusted for renal failure
68
  Troponin: Often sent to r/o ACS as cause of CHF, and to get an idea of
whether there is active demand ischemia
 Bedside echo to r/o effusion, give you a rough sense of overall contractility

4. Mgmt
 Noninvasive positive pressure ventilation (BiPAP) before intubation unless
patient is very altered/can’t tolerate (controversial thpy= consider small dose of
lorazepam for sympathectomy, anxiolysis to allow patients to tol. BiPAP)
 NTG: Drug of choice in critically ill CHF patients. At low doses is mainly a
venodilator  decreases preload; also increases coronary blood flow by
vasodilation. Start with SL 0.4 mg or nitropaste 1 inch; if gtt ready, may start at
20-50 mcg/min IV gtt, double q3-5 min up to max 200 mcg/min, titrate to SBP
and sx
 Captopril 6.25mg PO as tolerated by blood pressure. Not ideal for ED 2/2
difficulty titrating, but may consider
 Lasix 0.5-1 mg/kg IV (usually 40-80 mg), double dose if inadequate response
 Dopamine/dobutamine/norepinephrine gtt if hypotensive
 No Role for Morphine- increases intubation, ICU admission, mortality

5. Dispo
 Admit: All patients with abnormal VS, increased WOB which does not
improved with treatment, or lab abnormalities, or if cause of CHF is unknown or
untreated
 High mortality in hypotensive patient with pulmonary edema. Consider early
intubation and ICU admission if unstable, significant hypoxia, no improvement
with BiPAP

Aortic Dissection
1. Pathophysiology
 Risk factors: HTN (70-90%), connective tissue dz, 3rd trimester pregnancy,
congenital heart dz (coarct, bicuspid aortic valve), trauma, cocaine/meth, infxn
(syphilis, endocarditis)
 Classification
o Stanford type A = any involvement of ascending aorta
o Stanford type B = no involvement of ascending aorta
 Untreated mortality is ~33% by 24 hrs, 50% by 48 hrs, 90% by 1-3 months

2. Presentation
 Consider in any patient with pain in 2 compartments (neck and chest, chest
and abdomen) or pain and neuro deficit
 Pain is most common presenting sx
o Abrupt, maximal at onset
o Migrates as dissection propagates
o Radiates to jaw/neck (ascending/arch), back (descending)
 Possible neuro deficits
o CVA if carotid involvement
o Spinal cord deficits
 Other associated presentations
o Acute MI (if coronary artery involvement)

69
 o Aortic regurg, acute CHF
o Abdominal pain (if mesenteric vessel involvement)
o Flank pain, hematuria (if renal vessel involvement)
 Exam findings
o Unequal pulses
o Focal neuro deficits
o Aortic regurg murmur (type A)
o Tamponade (type A)
o Cold, pulseless extremity

3. Dx
 Upright CXR
o Mediastinum >8 cm or abnormal contour
o Displacement of trachea or esophagus rightward
o Depressed left bronchus
o Left pleural effusion
o Separation of calcified aortic intima from aortic contour
 EKG
o MI (if coronary artery involvement)
o LVH (HTN)
 CTA chest/abdomen (dissection protocol): Test of choice in ED
 TEE: Consider if too unstable for scanner

4. Mgmt
 Type B = Medical tx only: Control BP and HR to decrease risk of propagation
of dissection
o IV Esmolol gtt 50-300 mcg/kg/min titrated to HR of 60-80, then add
nitroprusside gtt 1-10 mcg/kg/min titrated to SBP of 100-120
o Or metoprolol 5 mg IV bolus vs. labetolol 20 mg IV bolus, repeat 40-80 mg
q10 min prn, max 300 mg, titrate to SBP 100-120; or labetalol gtt 0.5-3 mg/min
up to 300 mg total cumulative dose
 Type A = medical treatment as bridge to surgery

5. Dispo
 Must transfer SFGH pts to UCSF for CT surg; immediate CT surg consult at
UCSF
 Admit to ICU for close hemodynamic monitoring

Abdominal Aortic Aneurysm

1. Pathophysiology
 Most are infrarenal
 Risk factors: male, age >60, smoking, HTN, CAD/PVD, family history

2. Presentation
 Easy to miss!
 Sudden onset severe abdominal, back or flank pain ±syncope
 Retroperitoneal bleeding/hematoma (usually on left), may radiate to groin and
cause hematuria (misdx as kidney stone)
 May have dull low back pain radiating to legs (misdx as MSK)

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  May have LLQ pain w/ guaiac+ stool (misdx as diverticulitis)
 Ecchymosis on abdominal wall, flank, groin, perineum
 Femoral neuropathy (hip/thigh pain, quad weakness, decr patellar reflex) 2/2
hematoma compressing femoral nerve

3. Dx
 May feel large pulsatile mass in abdomen
 US may identify AAA, but does NOT tell you if it is ruptured!
 CTA: If pt stable enough, shows rupture and branch vessel involvement

4. Mgmt
 ABCDs, resuscitate
 Stat surgery (SFGH)/Vascular (UCSF) consult

5. Dispo
 If at SFGH, pt may require txf to UCSF if stable to survive transport

Endocarditis – see Infectious Disease chapter

Myocarditis
1. Pathophysiology
 Immune inflammation of myocytes, multiple causes, most idiopathic
o Viral: Coxasckie, Echovirus, Flu, HBV, EBV, HIV
o Chagas most common worldwide
o Hypersensitivity w/ eosinophilia: PCN, HCTZ, sulfa, doxorubicin, AZT,
methyldopa
o Misc: Toxo, strep, radiation, SLE, mono, cocaine, Kawasaki

2. Presentation
 Variable, range from non-specific disease  CHF and sudden death
o 60% of pts with recent viral syndrome
o 35% with chest pain
o 20% with fever, myalgias, HA, rigors, flu-like symptoms
o Dyspnea, palpitations, syncope
o CHF symptoms
o Peds: Cyanosis, poor feeding, respiratory distress, grunting, wheezing

3. Dx
 Physical exam
o Tachycardia out of proportion to fever
o Pericardial rub if pericarditis
o JVD, edema, rales, S3
 Workup
o Troponin (most specific), CBC, ESR (elev 60%).
o CXR: Usually normal, or CHF signs
o EKG: Sinus tach most common, ST elevation, low amplitude, Q waves, AV
block, BBB

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 o Echo:  EF, hypokinesis, global wall motion abnormality.

4. Mgmt
 Monitor
 Rule out tamponade
 Remove offending drugs
 Manage CHF and arrhythmias as appropriate
 Steroids and NSAIDs contraindicated in acute phase, discuss with consultant

5. Dispo
 Admit to cards for monitoring, med management

Pericarditis
1. Pathophysiology
 Causes
o Infectious: Viral (Coxsackie –most common), bacterial, fungal, parasitic
o Recent MI: Dressler’s syndrome)
o Malignancy: Leukemia, lymphoma, breast, melanoma
o Connective tissue: SLE, RA, sarcoid, amyloidosis, scleroderma
o Other: Radiation, hypothyroidsim, renal failure, cardiac surgery, aortic
dissection

2. Presentation
 Stabbing CP, worse w/ deep inspiration, positional – worse lying flat
 Sometimes SOB, dysphagia, low-grad temp
 Tachycardia, tachypnea
 Friction rub
 Hypotension if tamponade present (see below)
 Muffled heart sounds, pulsus paradoxus, Kussmaul sign

3. Dx
 CBC, Chem-7, consider ESR
 EKG
o Stage I: Diffuse STE and PR seg depression, with PR elevation in AVR
o Stage II: Resolution of STE and PR changes, Twave flattening
o Stage III: TWI
o Stage IV: Normalization of EKG changes
 Cardiac enzymes
 Blood cx if thought to be bacterial
 CXR (usually normal)
 Bedside echo (formal echo if concern for tamponade)

4. Mgmt
 Pain control with 600-800 mg ibuprofen, narcotics for most cases
o Avoid NSAIDs in post-MI patients

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  Do not anticoagulate post-MI pts (can cause hemorrhagic effusion)

5. Dispo
 Admit unstable patients, patients were there is concern for bacterial infection,
or patients who need emergent HD (uremic pericarditis)

Tamponade
1. Pathophysiology
 Pericardial effusion with increased pericardial pressure (usually due to acute
accumulation)  compression of chambers with decreased filling during
diastole (esp during inspiration)
o Chronic pericardial effusion may eventually cause tamponade with
accumulation of larger volume (e.g. >2L)
 Causes
o Trauma with hemorrhagic effusion
o Idiopathic
o Infectious: Viral, bacterial, mycoplasma, Fungal, parasitic, Infective
endocarditis with valve ring abscess
o Radiation
o Neoplasm: Metastatic (lung/breast ca, leukemia, melanoma), primary,
paraneoplastic
o Other: Myocarditis, dissecting aortic aneurysm, Dressler’s syndrome, early
infarction pericarditis

2. Presentation
 Most common misdiagnosis is heart failure; consider dx in any patient with
enlarged heart on CXR and symptoms
 Cardiogenic shock with hypotension, tachycardia
 Acute: Chest pain, tachypnea, shortness of breath
 Subacute: Chest discomfort/fullness, LE edema, fatigue

3. Dx
 Exam: Tachycardia, tachypnea, JVD, hypotension, muffled heart sounds,
pulsus paradoxus
 CXR: Cardiomegaly
 EKG: Low voltage, tachycardia, electric alternans
 Echo: Effusion, right atrial and ventricular diastolic collapse, IVC plethora

4. Mgmt
 Supplement preload with volume to temporize (500 mL NS)
 Pericardiocentesis: 16g needle at L paraxiphoid at 30° aimed to L shoulder, or
parasternal using US guidance
 Avoid positive pressure ventilation if possible (reduces cardiac filling)

5. Dispo
 ICU for hemodynamic monitoring

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 Overview of Valvular Diseases
1. Aortic stenosis
 Sx: Angina, syncope, CHF if severe
 Exam: Crescendo-decrescendo systolic murmur at RUSB, radiates to carotids
 Mgmt: DO NOT ABRUPTLY REDUCE PRELOAD (beware of NTG). Gently
diuresis if in failure. May require surgery if severe

2. Aortic Insufficiency
 Sx: Dyspnea, pulmonary edema
 Exam: Diastolic murmur at LUSB
 Mgmt: Surgery; or medical CHF tx (vasodilators, diuretics) if not surgical
candidate

3. Mitral Stenosis
 Sx: Dyspnea, pulmonary edema, A-fib
 Exam: Diastolic murmur at apex
 Mgmt: Valve replacement surgery or percutaneous valvuloplasty

4. Mitral regurgitation
 Sx: Pulmonary edema, A-fib
o Sometimes caused by papillary mm rupture during acute MI
 Exam: Holosystolic murmur at apex, radiates to axilla
 Mgmt: Nitroprusside for afterload reduction, dobutamine for inotropic support,
IABP if needed as bridge to surgical repair/replacement.

Approach to Dysrhythmias
1. General Approach
 Is the patient stable? If not, skip straight to ACLS (see Resuscitation
chapter)
 Fast or Slow?
 Regular or Irregular?
 Narrow or Wide?

2. Bradycardias
 Regular
o Sinus bradycardia: Consider meds (BB, CCB, amio), inferior MI, increased
vagal tone, hypoxia, increased ICP, sick sinus, hypothermia, hypothyroidism
st
o 1 degree AV Block: PR > 0.2 sec no intervention required
o Junctional escape rhythms: Slow, narrow, very regular rhythms without clear
P waves
o Ventricular escape rhythms: Slow, wide, usually regular rhythms without
clear P wave before every QRS
 Irregular
o 2nd degree AV Blocks
 Mobitz I (Wenckebach): Progressive increase in PR interval until a beat is
dropped. Block usually w/in AV node, occurs w/ inferior MI, myocarditis. Often
no tx required, can use atropine
 Mobitz II: Sporadic dropped beats, usually infranodal block in His-Purkinje
system. May occurs with anteroseptal MI. Needs PACEMAKER

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  Complete heart block: No relationship b/w P waves and QRS (AV
dissociation). Needs pacemaker
 Approach to Mgmt: For symptomatic bradycardias only
o Notes
 Rare to have patient symptomatic until rates are below 40 bpm. If
hypotensive and HR >40, look for other causes
rd
 Identify type 2 second degree and 3 degree block: These patients must be
admitted for permanent pacer evaluation
o Atropine: 0.5 to 1 mg IV q5 min (to a total dose 0.03-0.04 mg/kg)
 Ineffective in transplanted heart go straight to pacing
 Use with caution as can prcepitate VT or VF in MI patients, or potentially
worsen AV block
o Pacing
 Transcutaneous: Temporary
 Transvenous: When transcutaneous fails, or as bridge to permanent pacer

3. Tachycardias
 Narrow, regular
o Sinus tachycardia
 Consider pain, anxiety, fever / infection, hyperthyroidism, EtOH or benzo
w/d, PE, etc
 Treat underlying cause
o Atrial tachycardia
 Due to ectopic atrial pacemaker, increased automaticity, or digoxin toxicity
 Rate usually 150-250 and regular, beat-to-beat variability is possible,
accelerates and decelerates gradually
 May need BB, CCB or ablation of focus
o Atrial flutter
 Due to re-entrant circuit w/in the atrium
 Flutter waves w/ rate of 300 – best seen in inferior leads and V1; ventricular
rate of 150 if 2:1 block, 100 if 3:1 block (but rule of multiples of 300 does not
hold if pt on antiarrhythmic meds)
 May give adenosine to transiently slow the ventricular rate and allow you to
see flutter waves
 Difficult to treat medically since need large amounts of AV nodal blockade
(BB or CCB; amiodarone or digoxin if CCB or BB ineffective) or
cardioversion starting with 10-20 joules
o AVNRT
 Reentrant circuit through the AV node; set off by a PAC
 Tachycardia is on/off – no slowing or speedup
 P waves are absent (buried in the QRS complex) or retrograde; HR ~160-
200
 Block AV node w/ vagal stim, adenosine or other AV nodal blocking meds
(BB, CCB, digoxin)
o AVRT
 Due to accessory pathway (WPW etc.)
 Tachycardia is on/off – no slowing or speedup. short RP interval w/
retrograde P wave
 Need AV nodal blockade
o Junctional tachycardia

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  Due to ischemia, digoxin toxicity, cardiomyopathy
 Rate 100-140, P waves retrograde or absent (buried in QRS)
 Treat underlying cause
 Narrow, irregular
o Atrial fibrillation
 If unstable, need to cardiovert (see ACLS algorithm in Resuscitation
chapter)
 If stable, control rate and consider anticoagulation; some may be eligible for
cardioversion
 Rate control: Don’t mix CCBs and BBs!
 Diltiazem 10-20 mg IV over 2 min, repeat q15 min prn w/ 0.35 mg/kg or
25 mg. If unable to control rate w/ boluses, use gtt of 5-15 mg/hr. Watch for
hypotension
 Beta-blockers: Metoprolol 5 mg IV q5min x 3 or Esmolol IV bolus 500
mcg/kg, gtt 50-200 mcg/kg/min
 Amiodarone IV load 150 mg over 10 min then gtt at 1 mg/min x 6 hours
then 0.5 mg/min x 18 hours. May chemically cardiovert pt; good for pts w/
reduced EF as will not depress cardiac function
 Digoxin 0.5 mg IV load, then in 6 hours 0.25 mg IV q6h x 2. Slows rate by
incr vagal tone, use only in conjunction w/ other rate controlling agents. <ay
take hours for effect. Lower risk of hypotension 2/2 +inotropy
 Anticoagulation
 If AF present >48 hrs and pt is stable, pt needs to be anticoagulated for 2-
4 wks prior to cardioversion and 3-4 wks after cardioversion
 Or get a TEE: IF no atrial thrombus, may cardiovert right away, followed
by anticoag for 3-4 wks after cardioversion
 Cardioversion: Always followed by anticoagulation unless AF<48hrs.
 Electrical: Start w/ 100 J
 Chemical: May use amiodarone, sotalol, procainamide, propafenone,
or ibutilide
 Beware the incomplete history for the duration of symptoms
 Beware the low risk AF: Pt is low risk for embolism once echo has shown
absence of structural heart disease
 After cardioversion: Many pts need antiarrhythmic after cardioversion to
maintain sinus rhythm; usually use amiodarone
o Atrial flutter w/ variable block: May mimic A-fib on EKG. (See Atrial flutter)
o Multi-focal Atrial Tachycardia (MAT)
 Multiple ectopic atrial foci, usually assoc w/ pulmonary dz
 At least 3 different P wave morphologies and 3 different PR intervals
 Treat underlying cause
o Sinus rhythm w/ multiple PACs
 Look for Ps buried in the ST or T of the beats preceding pauses
 There may be a change in the T wave of the post-pause beat
 Wide, regular
o VT: If patient is crashing, or if not with typical BBB morphology, assume it’s
VT until proven otherwise
o SVT w/ BBB or rate-related aberrancy
o SVT w/ accessory pathway: May cause wide or narrow QRS, depending on
whether the retrograde conduction is through the AV node or the accessory
pathway

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 o Approach to Mgmt:
 If no pulses or very unstable, go to ACLS (see Resuscitation chapter)
 If SVT with aberrancy, treat underlying rhythm
 If in doubt, Amiodarone 150 mg IV over 10 min, may repeat to max of 2.2
g/24 hrs and prepare for synchronized cardioversion
 Wide, irregular
o If pulseless or VF, go to ACLS (see Resuscitation chapter)
o VF: Need immediate defibrillation, ACLS
o Polymorphic VT: Includes torsades. Given Magnesium sulfate 1-2 gram IV
if torsades
o A-fib w/ BBB (“A-fib w/ aberrancy): If there is typical LBB or RBB
morphology. Control rate (see Atrial fibrillation)
o Afib in WPW syndrome: Rare
 Cardioversion or procainamide 20 mg/min gtt (titrate to arrhythmia control,
hypotension, QRS widening >50%, or max 17 mg/kg) then 1-4 mg/min or
amiodarone 150 mg over 10 min then gtt at 1 mg/min x 6 hours then 0.5
mg/min x 18 hours
 DO NOT give digoxin, BB or CCB as these AV nodal blockers can increase
the rate of transmission through the accessory pathway and lead to VF

Pacemakers and Defibrillators

1. Pacemakers
 Nomenclature: Pacemakers are described by 3 letters - chamber paced,
chamber sensed, and response. The other classifications (programmability,
other functions) are less important in ED

I II III
Chamber Paced Chamber Sensed Response to Sensing
Atrium (A) Atrium (A) Triggers (T)
Ventricle (V) Ventricle (V) Inhibits (I)
Dual (D) Dual (D) Dual (D = T+I)
None (O)

 Troubleshooting pacemakers
o Complications post-pacemaker placement
 Early: PTX, tamponade, myocardial perf
 Late: Infection, lead thrombus, lead fracture, battery failure etc. Any cellulitis
over the generator insertion site is a serious bacterial infection and should be
considered high risk for endocarditis
o Functional failure
 Failure to pace (aka failure to output): Absence of pacemaker spikes on
EKG in the setting of bradycardia
 Failure to capture: Pacer spikes are not followed by atrial or ventricular
activation on EKG
 Failure to sense: Pacer spikes present at the wrong time or despite
adequate intrinsic heart rate
o Mgmt
 Get an EKG (look for pacer spikes/relation to QRS) and CXR (to see leads)
 Placing a MAGNET over the pacemaker turns off sensing function;
temporarily converts pacemaker to a fixed rate (usually ~70) and allows
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 assessment of whether the pacemaker is capturing. ONLY DO THIS if
absolutely necessary. Variable responses to this – for example, the pacing
function of an AICD is not affected by magnet placement.
 Always contact cardiology (EP) and/or device vendor to interrogate device if
you suspect pacemaker malfunction

2. AICDs
 Frequent/repeated shocks
o May be response to VT/VF or sensing malfunction (sensing of SVT or
muscle contraction)
o THE MAGNET deactivates the AICD
o Needs interrogation by cardiology (EP)
 CPR/defibrillation in pt w/ AICD
o CPR: Perform as usual; may feel a shock but it is not dangerous
o Defibrillation: Do not place the paddles close to AICD generator, otherwise
perform as usual
o AICD should be tested after cardioversion/defibrillation to ensure that its
function has not been altered

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 Dermatology
By Susan Brim Res ed. Bory Kea Faculty ed. Eric Suess

General
1. Approach to rashes
 Sick or not sick?: If the patient is toxic-appearing, febrile, or has abnormal vital
signs  evaluate, diagnose, and treat empirically in parallel to resuscitation as
you move forward with rash diagnosis
 History: Onset, migration/evolution of rash (e.g. vesicles  bullae), travel, new
medicines (go back at least 2mo), new exposure to chemicals/clothing/
detergents/environments, immunosuppression
 Exam: Undress the patient – examine all skin, also pay particular attention to
oral/genital mucosa, palms/soles

2. Derm Vocabulary
 Macule: Flat, circumscribed area of change < 1 cm
 Papule: Solid raised lesion < 1cm
 Nodule: Palpable, solid lesion > 1cm found usually in dermis or subcutaneous
tissue extending deeper than a plaque
 Patch: Flat, circumscribed area of change > 1 cm
 Plaque: Circumscribed elevated/raised solid lesion > 1cm
 Pustule: Circumscribed area containing purulent material
 Vesicle: Circumscribed serious fluid-filled lesion < 1cm
 Bulla: Vesicle > 1cm
 Petechia: Small non-blanching red/purple/brown macule, pinpoint,
hemorrhage from small capillaries, < 1cm

Erythematous rash

*Adapted from Murphy-Lavoie H and LeGros T. Emergency Medicine: A Peer

Reviewed Journal, 2010.

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**Nikolsky sign= lateral stroking of skin  separation of epidermis; SSS =
Scalded Skin Syndrome; TEN = Toxic Epidermal Necrolysis; TSS = Toxic Shock
Syndrome

1. Anaphylaxis/anaphylactoid response
 Cutaneous manifestations in 90% of cases
 Presentation: Generalized urticaria, pruritus or flushing, swollen
lips/tongue/uvula, laryngeal edema; CV (tachycardia, hypotension, shock), GI
(abdominal cramps, vomiting, diarrhea)
 Mgmt
o Airway management, IVF
o Remove offending agent if identified and possible
o Epinephrine IM 1:1000 (1mg/mL) give 0.3-0.5mg IM q5-15min (Peds
0.01mg/kg IM q5-15min)
o Epinephrine IV 1:10,000 (0.1mg/mL), 2-10 mcg/min titrated to BP (Peds
0.1-1mcg/kg/min titrate to BP)
o Glucagon 1-2mg IV for adults on beta-blockers
o Adjunctive: Benadryl 25-50mg IV, famotidine 20mg IV, albuterol,
solumedrol 120mg IV
 Dispo: Observe 4-6 hours for rebound anaphylaxis and d/c with epi pen if
improved/resolved; admit to ICU if no improvement or requiring epinephrine gtt

2. Kawasaki disease
 Childhood vasculitis of unknown cause
 Presentation: See diagnostic criteria below
 Dx: Classic needs 4 of 5 diagnostic criteria + fever (“CRASH and Burn”); may
have incomplete if <4
o Conjunctival injection: Bilateral without exudate
o Rash: Diffuse, polymorphous erythroderma
o Adenopathy: Cervical LAD >15 mm diameter, usually unilateral, one, painful,
non-purulent
o Strawberry tongue, or diffuse oral/pharyngeal mucosal erythema,
red/cracked lips
o Hands and feet edema, erythema, or desquamation with convalescence
o Burn: High fever ≥ 5 days
 Mgmt
o High dose ASA 80mg/kg/day PO in 4 divided doses initially
o IVIG 2g/kg over 8-12h
 Dispo: Admit to peds
 Complications: Coronary artery aneurysm is serious complication

3. Scarlet fever
 Associated with GAS pharyngitis
 Presentation
o Diffuse maculopapular “sandpaper” like eruption
o Starts head and neck and spreads
o Desquamation during convalescence
 Mgmt

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 o Same as streptococcal pharyngitis: PCN G IM 1.2 million U (25,000 U/kg) x1
or PCN VK 500 mg PO bid x10 days (12.5 mg/kg po qid x10 days)
 Dispo: D/c home

4. Scromboid
 Food-borne illness, classically from improperly managed fish e.g. tuna,
mackerel, skip-jack, bonito. Due to elevated biogenic amines e.g. histamine
 Presentation
o Within 1h of ingestion: Flushing, erythematous rash, palpitations,
tachycardia, sensation of warmth
o Less often: HA, blurred vision, resp complaints.
 Mgmt
o Benadryl 25-50mg PO/IV
 Dispo: D/c home, follow up w/ PMD/allergy to r/o fish allergy
 Reportable condition! Need to fill out morbidity and mortality form

5. Staphylococcal Scalded Skin Syndrome (SSSS)

 <5yo highest risk, newborns commonly present at 3-7days old
 Presentation: Abrupt fever, erythema of neck/axillae/groin with skin tender to
palpation. No mucosal involvement
 Mgmt
o IV fluid resuscitation
o Antistaphyloccocal antibiotic: nafcillin 50-200 mg/kg/day IV/IM div q6h (max
500 mg IV/IM q4-6h) or consider vancomycin 1 gram IV. May switch to
dicloxacillin 12.5-25 mg/kg/day PO div q6h (max 125-500 mg PO q6h)
o Analgesia, local wound care
 Dispo
o Well appearing children >1yo with min slough  outpt
o Infants/toxic kids  admit
o Adults very rare but high mortality  admit
o Course: Heals 10-14days without scarring

6. Toxic Epidermal Necrolysis (TEN)

 TEN is in a spectrum of disease with erythema multiforme to SJS to TEN, with
increasing toxicity
o TEN: >30% BSA involvement
o SJS to TEN: 10-30% BSA involvement
 Associated with sulfas (#1 cause), PCN, quinolone, antiepileptics, NSAIDs,
allopurinol; also assoc with graft vs host rxn and blood product transfusion
 Presentation
o Sudden onset diffuse erythema with tender skin and sloughing
o Face first and spreads down, massive skin sloughing, +mucosal involvement
o Toxic appearing
 Mgmt
o Supportive care
o D/c offending medicine
o No steroids
o Wound care: Don’t use sulfadiazine!! – sulfa containing)

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  Dispo: ICU admission, burn unit if significant skin sloughing

7. Toxic Shock Syndrome (TSS)

 Usually caused by Staph aureus producing exotoxin TSST-1
 May also be caused by Streptococcal TSS (GAS)
 Source can include abscess, tampon, nasal packing, wounds, postpartum
 Presentation
o Early macular rash, toxic appearing, shock, fever
o Early rash can be quite pale – look for erythema of mucous membranes
o Desquamation 1-2wk after illness onset
 Dx: Criteria include fever, HoTN, erythematous macular rash, 3 organ system
involvement and S. aureus infection
 Mgmt
o Supportive treatment: IVF, pressors
o Remove source
o Antibiotics: Clindamycin 600mg IV and Vancomycin15mg/kg IV
o Consider IVIG in severe cases
 Dispo: admit to ICU

Maculopapular rash

*Adapted from Murphy-Lavoie H and LeGros T, Emergency Medicine: A Peer

Reviewed Journal, 2010

1. Cutaneous drug reaction

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  Common drugs: aminopenicillins, sulfas, cephalosporins, allopurinol,
phenobarbitol, NSAIDs, quinolones, phenytoin, VPA, ACE inhibitors, thiazide
diuretics, beta blockers, OCP, phenothiazines, corticosteroids
 Mgmt: stop offending drug

2. Erythema multiforme (EM)

 Associated with infection and drug exposures
 Presentation
o EM Minor: Pruritic target lesions on extremities self ltd 1-2wk
o EM Major: Prodrome (URI, fever, malaise) then centripetally spreading non-
pruritic target lesion rash with mucosal involvement.
 Mgmt
o EM minor: Topical steroids, outpt derm f/u
o EM major: May need admission for supportive care, stop offending agent.
o No role for systemic steroids

3. Lyme Disease – see CDC site: www.cdc.gov/lyme

 Tick borne illness: Borrelia burgdorferi from Ixodes tick bite
 Presentation
o Erythema migrans (large target lesion) – spreads over days-weeks
o Secondary rash, fever, meningitis, AV node block, migratory arthralgias,
myalgia, Bell’s Palsy
 Dx: Clinical symptoms or biopsy of tick bite; consider testing if equivocal
o Serologic testing: Enzyme immunoassay (EIA) or immunofluorescence
assay (IFA) then IgM/IgG western blot for confirmation of positive tests
 Mgmt: Doxycycline100 mg PO bid
o Erythema migrans: Treat for 10-14 days
o Bells palsy, first degree heart block, arthritis: Treat for 21-28 days
 Dispo: Usually outpatient management and follow up
 Prophy after tick bite (Wormser GP et al, Clin Infect Dis 2006): Routine
antibiotics not recommended, but consider doxycycline 200 mg PO x1 (Peds 4
mg/kg PO x1) if
o Tick identified as adult or nypmhal I. scapularis attached for ≥36 h (based on
engorgement with blood or known exposure time) AND
o Prophy to be provided within 72 hours after tick removal AND
o Local rate of infection with B. burgdorferi ≥20% (New England, mid-Atlantic
states, Minnesota, Wisconsin) AND
o Doxycycline not contraindicated (not pregnant, >8 yo, no allergies)

4. Pityriasis Rosea
 No clear etiology, possibly viral
 Presentation: “Christmas tree” pattern of scaly lesions with possible salmon-
colored herald patch
 Mgmt: Supportive with antihistamine, emollients

5. Scabies
 Presentation: Pruritic, excoriated lesions commonly on hands in web spaces.
 Dx: Clinical diagnosis, may see mites on skin scrapings with microscopy

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  Mgmt: Permethrin 5% topical cream. Apply to skin and leave 8-12h before
washing off. May repeat in 1 week if mites reappear

6. Stevens-Johnson Syndrome (SJS)

 Usually related to drug but also infections, malignancies
 Presentation
o Prodrome fever, myalgia, malaise  rapid onset of rash (starts dorsa of
hand)
o Diffusely distributed bullous target lesions (+palm/sole/mucous membranes)
o Toxic appearing
 Mgmt: Stop offending agent, supportive care
 Dispo: Usually admit to ICU

7. Viral Exanthem
 Examples: Measles, rubella, fifths disease
 Self-limited, supportive care

Petechial rash

*Adapted from Murphy-Lavoie H and LeGros T, Emergency Medicine: A Peer

Reviewed Journal, 2010

1. General tips
 For petechiae/purpura not clearly explained by trauma or benign etiology
consider CBC, coags, blood smear

2. Disseminated gonococcal infection

 Presentation
o Sparse, peripherally distributed vesicles

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 o Associated urethritis/cervicitis/septic arthritis
 Mgmt: Ceftriaxone 1 gram IV
 Dispo: Admit

3. Henoch-Schonlein Purpura (HSP)

 Autoimmune systemic vasculitis affecting skin, kidneys, GI tract
 Mainly in school aged children
 Presentation
o Purpura (legs/buttocks/arms), abdominal pain, arthritis
o Rash can initially be erythematous/macular/urticarial appearing
o Hematuria 10-20%, vomiting/diarrhea/intussusceptions
 Dx: Check UA – no Cr needed unless abnormalities on UA
 Mgmt
o Most self limited with supportive care only
o Hydration/rest/analgesia and close outpt f/u
o OK to give NSAIDs unless renal failure/sig GIB
o Evidence unclear for steroids
 Dispo
o Home if pain controlled, no renal dysfxn/HTN, tolerating POs, no sig GIB,
normal mental status
o Generally weekly UA/BP measurements for 2months
o Admit if above criteria not met

4. Idiopathic (immune) Thrombocytopenic Purpura (ITP)

 May be associated with preceding viral infection
 Presentation: Isolated thrombocytopenia with no clinically apparent condition
 Mgmt
o Transfusion if life threatening bleeding
o Hematology consult for adjunctive treatment: Steroids, IVIG

5. Meningococcemia
 Neisseria meningitides
 Most common in young children and adolescents
 Presentation
o Preceding URI/flu-like symptoms
o Initial erythematous maculopapular rash on wrists/ankles then
spreads/petechial
o Toxic appearing, febrile, AMS, shock
 Mgmt
o Ceftriaxone 2 gram IV (+ vancomycin 1 gram IV ± ampicillin 2 grams IV)
o Steroids concurrent or prior to antibiotics
o Supportive care
 Prophy for contacts: Rifampin 600mg PO bid x 2 days or ciprofloxacin
500mg PO x 1
 Dispo: Admit, droplet/contact precautions

6. Rocky Mountain Spotted Fever (RMSF)

 Tick borne disease: Rickettsia rickettsii
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  Mostly April-September, mostly South Atlantic region and western south-
central states
 Presentation
o Fever, rash, myalgia, headache – can range mild to life-threatening
o Rash begins macular on wrist/ankle/forearm palm/sole/torso 
maculopapular  petechial
o 15% no rash (“spotless fever”)
o May appear toxic, febrile
 Mgmt
o Doxycycline 100mg PO q12h x 7-10d for adults, consider doxy for peds
>8yo, can give chloramphenicol 50-100 mg/kg/day div q6h (max 4
grams/day) for peds (not in neonates – gray baby syndrome) and pregnant
(avoid if near term)
o If unclear meningococcemia vs RMSF treat for both
 Dispo: Can d/c with outpt f/u for mild cases, admit if sick appearing

7. Purpura fulminans
 Associated with infection, pregnancy, massive trauma, end-stage malignancy,
heptatic failure, snakebites, transfusion reactions
 Presentation: Life-threatening disorder with fever, shock, subcutaneous
hemorrhage, DIC, organ failure
 Dx: Thrombocytopenia, schistocytes, elevated PT/PTT, decreased fibrinogen,
elevated D-dimer
 Mgmt
o Treat underlying cause, folate, vitamin K, FFP, cryoprecipitate, blood
products
o Emergent Hematology consult
 Dispo: admit to ICU

8. Thrombotic Thrombocytopenic Purpura (TTP)

 Inhibition of ADAMTS13 enzyme by circulating antibodies unable to cleave
von Willebrand factor multimers causing increased coagulation
 Presentation
o Clinical triad: Thrombocytopenia, hemolytic anemia, elevated LDH
o Pentad: Fever, thrombocytopenia, hemolytic anemia, neurologic deficits,
renal failure
 Dx: Mostly normal coags and fibrin, +schistocytes/helmet cells on smear
 Mgmt
o Plasmapheresis, FFP to temporize
o Emergent Hematology consultation
o Do not give platelets unless life-threatening bleed and after consultation with
Hematology; concern for precipitating additional thrombus
 Dispo: Admit to facility with plasmapheresis

Vesiculobullous rash

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*Adapted from Lavoie H and LeGros T, Emergency Medicine: A Peer Reviewed
Journal, 2010

1. Bullous Pemphigoid (D for deep blisters)

 Better prognosis/less oral involvement than pemphigus vulgaris
 Presentation
o Chronic autoimmune cutaneous blistering in elderly (also infant)
 Dx: Histopathology
 Mgmt: Consult dermatology, may include topical/oral steroids, tetracycline,
dapsone, immunosupressants
 Dispo: Outpatient management

2. Contact Dermatitis
 May result from a variety of irritants, commonly poison ivy/oak, nickel jewelry
 Presentation
o Papules/vesicles with erythematous base
o Pruritic, watch out for secondary infection
 Mgmt
o Oral antihistamines
o Topical steroid creams BID: hydrocortisone 1% cream or clobetasol 0.05%
cream for more severe cases (avoid on face, can cause hypopigmentation)
o Consider systemic steroids for severe cases with facial involvement, bullae
or large BSA involvement. Should taper slowly

3. Hand-foot-and-mouth disease
 Common in children
 Most commonly caused by Coxsackie virus A16
 Peak incidence Summer/Fall
 Presentation
o Oral lesions develop and then skin lesions including palms/soles
o Can be asymptomatic or pruritic
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 o Infants may have more diffuse distribution of lesions
 Mgmt: Supportive care. Self limited, usually 3-6days. PO challenge and
evaluate for dehydration in little kids

4. Herpes Zoster
 Varicella-zoster virus reactivation
 Presentation
o Usually prodrome with pain/paresthesia prior to rash eruption
o Painful, grouped, vesicular lesions in dermatomal distribution
o Usually resolves over 2-3 weeks
o Do not miss herpes opthalmicus (vesicles on tip of nose, check for corneal
ulcers) or Ramsay Hunt syndrome (facial nerve involvement/Bells Palsy,
vesicles on ear or TM, hearing loss)
 Mgmt: Should start therapy within 48-72h
o Valcyclovir 1 gram PO TID x 7days (or acyclovir 800mg 5x/day x 7-10
days) to prevent post-herpetic neuralgia
o Prednisone 40-60 mg/day (controversial benefit to steroids, may improve
symptoms)
o Pain control: NSAIDS and narcotics
 Dispo
o Most patients managed outpatient
o Admit patients with: Immunocompromised (transplant recipients in treatment
for graft rejection, advanced AIDS with OIs), disseminated disease
(involvement of multiple dermatomes, visceral organ), complications (e.g.
Ramsay hunt, Zoster ophthalmicus, resistance to acyclovir)

5. Necrotizing fasciitis
 Surgical emergency! Immediately consult Surgery if suspect this
 Presentation
o Severe spreading skin infection with possible crepitus, “dishwater” drainage
o Pain may be out of proportion to examination
 Mgmt
o Surgery consult ASAP for debridement
o Unasyn 3 grams IV or ampicillin 2 grams IV
o Clindamycin 600 mg IV for toxin inhibition
o ±Vancomycin 1 gram IV
 Dispo: Admit to OR for debridement  ICU

6. Pemphigoid Vulgaris (S for superficial blisters)

 Rare, age 40-60, associated with myasthenia gravis and thymoma
 Presentation
o Generalized mucocutaneous autoimmune blistering disease
o Triggers: Penicillamine, captopril, rifampin, stress
o Painful, flaccid bullae, often oral involvement, +Nikolsky sign
 Mgmt
o Steroids and immunosuppressive therapy
 Dispo: Admit if large areas of involvement

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7. Smallpox
 All lesions in same stage of development
 If suspect this immediately isolate patient and notify public health department

8. Varicella
 Adults at higher risk of varicella pneumonia and encephalitis
 Presentation: Pruritic lesions, lesions are in different stages
 Mgmt
o Usually supportive care, symptomatic treatment
o In pregnant patients consider treatment with acyclovir 800 mg PO 5x/day x7
days

Suggested Reading
 Murphy-Lavoie H, LeGros T. “Emergent diagnosis of the unknown rash, the
algorithmic approach.” Emergency Medicine: A Peer Reviewed Journal, March
2010
 Wormser GP, Dattwyler RJ, Shapiro ED, et al. The Clinical Assessment,
Treatment, and Prevention of Lyme Disease, Human Granulocytic
Anaplasmosis, and BAbesiosis: Clinical Practice Guidelines by the Infectious
Diseases Society of America. Clin Infect Dis. 2006; 43: 1089-134

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 Endocrine/Metabolic emergencies
By Kristin Berona, Res ed. Kennedy Hall Faculty ed. Susan Lambe
Philippa Soskin

Hypercalcemia
1. About/Pathophysiology
 98% total body calcium in bone
 50% of remaining calcium is physiologically active ionized calcium
 Parathyroid hormone 3 actions: 1) increases Ca resorption from bones, 2)
2+
2+
stimulates renal resorption of Ca , 3) stimulates renal conversion of Vit D2 to
2+
Vit D3, which then increases gut resorption of Ca
 “ParatHIGHroid hormone increases calcium”

2. Presentation
 Stones (nephrolithiasis), bones (osteolysis), groans (abdominal pain,
constipation, PUD, pancreatitis) and psychogenic overtones (anxiety,
depression, AMS)
 Most often present with abdominal symptoms: nausea, vomiting, abdominal
pain, constipation
 Polyuria, polydipsia (unable to concentrate urine)
 Cardiac manifestations >14mg/dL: PR prolongation, QT shortening, QRS
widening, BBB, bradycardia, dysrhythmias
 Acute onset and severe hypercalcemia more likely to be malignancy

3. Etiology
 90% of hypercalcemia from hyperPTH or malignancy
 Primary hyperparathyoidism (gland hyperplasia, adenoma, carcinoma,
familial)
 Malignancy: (>13mg/dL more likely cancer than PTH) Multiple myeloma, bone
metastases, paraneoplastic syndromes
 Other disorders: Thyrotoxicosis, Adrenal Insufficiency, pheochromocytoma,
TB, sarcoid, leprosy
 Increased absorption: Chronic kidney disease on CaCarbonate/Acetate for
phosphate binders, Milk alkali syndrome (metabolic alkalosis stimulates Ca
reuptake in distal tubule), hypervitaminosis D increases Ca absorption and bone
resorption, Crohn’s: inc uptake at terminal ileum
 Drugs: Lithium, thiazide diuretics, theophylline

4. Dx
 Corrected calcium = (0.8 * (4 - Pt's Albumin)) + Serum Ca
 Serum and ionized calcium, as well as phosphate levels
 Identify underlying cause: Reasonable for ER to send PTH levels as first step
to differentiate malignancy from primary PTH
 If normal PTH, can consider PTHrP, 25-hydroxyvitamin D (calcidiol), 1,25-
dihydroxyvitamin D, urinary calcium, per request of consultant/admitting team
 Order an ionized calcium if you are concerned (1.1-1.4 mmol/L)

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5. Mgmt
 Treat in ED if serum Ca >14mg/dL (considered severe, treat even if
asymptomatic) or symptomatic
 Normal Saline: Most hypercalcemic patient volume depleted, also helps dilute
Ca, may require up to 4L
 Consider loop diuretics, watch out for dehydration, only use after volume
repletion. E.g. Furosemide 20-40 mg IV
 Phosphate repletion if <3.0 (hypophosphatemia makes hypocalcemia more
difficult to treat b/c phosphate binds Ca). Treat ONLY via PO and keep Ca PO4
product <40 (otherwise crystals precipitate. Ca PO4 product = Ca x PO4)
 If very severe, or based on recs from oncology or endocrinology, may
consider:
o Bisphosphonates to inhibit osteoclast activity: Pamidronate 90 mg IV over 2
hours, or Zoledronic acid 4 mg IV over 15 minutes (onset 2-4 days)
o If VitD-mediated hypercalcemia, give glucocorticoids: Hydrocortisone IV
100–300 mg daily or Prednisone PO 40–60 mg daily for 3–7 days

6. Dispo
 If mild, asymptomatic, can D/C home with PMD follow up
 If symptomatic or severe, admit for work up

Hypocalcemia
1. About/Pathophysiology
 Refer to Ca pathophysiology in hypercalcemia

2. Presentation
 Usually asymptomatic
 Neuromuscular: Muscle weakness, cramps, perioral paresthesias, seizures,
tetany
o Chvostek's sign: Facial muscle twitching after tapping on facial nerve
o Trousseaus: Carpal spasm (flexion at wrist/extension at fingers) after BP cuff
inflated >3min
 Cardiac: QT prolongation, if severe CHF, bradycardia, dysrhythmias

3. Etiology
 PTH deficiency: Surgical removal, chronic renal insufficiency, hypo-
magnesemia (causes PTH insensitivity), meds, metastatic disease, autoimmune
 Vit D deficiency: Nutritional, chronic illness, renal insufficiency
 Miscellaneous: Sepsis, pancreatitis, hyperphosphatemia, massive
transfusion, medications (loop diuretics). Acidosis buffers/masks hypocalcemia
so NaHCO3 administration may provoke hypocalcemia

4. Dx
 Serum Ca level, corrected for albumin- (see calculation in hypercalcemia
section above, as Ca will be falsely low in hypoalbuminemia e.g. volume
overload, chronic illness, malnutrition or nephrotic syndrome)

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  Ionized Ca is accurate and is not biased by albumin
 Also obtain phosphate level to help elucidate etiology (if elevated, less
sensitivity to PTH)

5. Mgmt
 No need to treat in general unless severe/symptomatic
 Correct hypomagnesemia prior to treating hypocalcemia (Magnesium sulfate
1-2g IV over 10-20minutes followed by 1g IV/hr until Mg >1mg/dL)
 Acute IV repletion if carpopedal spasm, tetany, seizures, prolonged QT
interval, or asymptomatic patients with an acute decrease to ≤7.5 mg/dL: Ca
gluconate 1-2g IV over 10-20min. Pediatrics: 10% Calcium gluconate 10-
20mg/kg IV over 5min
 PO repletion if mild symptoms and Ca >7.5 (will likely not need to do in ER):
Ca CO3 500-1000mg TID between meals
 If due to renal failure: Primary MD may start Vitamin D or Calcitriol (active
form Vit D), but it does not need to happen in ER

6. Dispo
 Admit if severe as above; otherwise, outpatient management

Hyperkalemia
1. About/Pathophysiology
 98% total body potassium is stored intracellularly
 Normal serum values 3.5-5 mEq/L
 Mild 5-6mEq/L, mod 6.1-7mEq/L, severe >7mEq/L

2. Presentation
 Usually asymptomatic
 Neuromuscular: Cramps or weakness-->paralysis or tetany
 Cardiac: Palpitations, chest pain, syncope
 EKG findings: Peaked T--> prolonged PR--> widened QRS-->sine wave-->vfib
 Consider hyperkalemia as cause of bradycardia in renal patients!

3. Etiology
 Too much intake:
o Ingestion (usually have to have underlying renal failure so unable to excrete
efficiently)
o Iatrogenic (K supplements)
o Blood transfusions (high K content)
 Not enough excretion:
o Renal failure
o Type IV RTA (hyporeninemic hypoaldosteroneism)
o Medications: NSAIDS, ACE inhibitors, Cyclosporin, K-sparing diuretics
(spironolactone)
o Tubular defects (transplant, nephropathy, obstructive uropathy, chronic
pyelonephritis)
 Transcellular shifts

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 o Cell death: Rhabdomyolysis, intravascular hemolysis, tumor lysis syndrome
o Acidosis (H+ go inside cell, K+ comes out)
o Insulin deficiency
o Drugs: Beta blockers, digitalis, succinylcholine
 Pseudohyperkalemia: Blood sample hemolysis/tourniquet

4. Dx
 Consider all hemodialysis patients hyperkalemic until proven otherwise
 Lab testing: If unstable patient check K on VBG/ABG
 EKG findings as above

5. Mgmt
 Obtain STAT EKG because it will help determine treatment
 Cardiac Stabilization with EKG changes
o Calcium chloride or Calcium gluconate “1 Amp”= 1g IV STAT. CaCl2 has
3x elemental calcium and works faster but scleroses peripheral veins.
Consider CaCl2 if have good IV access, including central line
o Avoid calcium if on digoxin (“stone heart” or concern for cardiac tetany with
increase in intracellular sodium and calcium due to digoxin inhibition of Na-K
ATPase pump. Contraversial - contradicted by Levine et al J Emerg Med 2011)
 Temporizing measures: Stimulate Na-K ATPase pump
o Insulin: 10 units regular insulin IV given with D50W (1amp= 25g IV), recheck
sugar in 30min, watch for hypoglycemia
 Onset 10-20min, lasts 2-4 hrs
o Albuterol: 10-20mg per neb over 1 hour
 Onset 20-30 min, duration 2-4 hrs
 Caution in tachycardic cardiac patient
+ +
o Sodium bicarb: Dose 1amp=50mEq IV. (bicarb ion stimulates H /Na
exchange  stimulate Na-K ATPase pump. questionable effectiveness, only
give if concomitant acidosis, best in non renal failure patients)
 Elimination
o Kayexalate (sodium polystyrene sulfonate) 30-60g PO or 50g PR may
repeat q2 until BM. Exchanges Na for K in intestinal tract. 1g binds approx
1mEq K. Caution, may worsen pulmonary edema in fluid overload (Na load),
also associated with intestinal necrosis when dissolved in sorbitol
 Onset 1-2 hrs, duration 4-6hrs
 Do NOT give if going to dialysis – diarrhea during dialysis isn’t fun
o Furosemide 20-80mg IV(depends on renal function) only works if pt makes
urine
o Dialysis: Indicated urgently if ECG/conduction abnormalities, unstable
(hypotension), volume overload

6. Dispo
 ICU if unstable, arrhythmias; page Renal fellow and consult for urgent HD
 Tele if stable, no EKG changes but moderate hyperkalemia
 Consider D/C home if K<6, normal EKG, and has dialysis planned in 24 hours
 Review medication list prior to D/C

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7. Tips
 Can use VBG for more rapid repeat K if you think spurious/hemolyzed
 Page Renal fellow at UCSF or SFGH for dialysis

Hypokalemia
1. About/Pathophysiology
 Mild 3-3.5, mod 2.5-2.9, severe <2.5

2. Presentation
 Usually asymptomatic
 Neuromuscular: Vague myalgias, cramping to paralysis, hypoventilation
 Cardiac: Palpitations to arrhythmias
 EKG findings: Mild T wave flattening  small U wave  shorter ST segment
U wave larger, takes over T wave (V2-V3) atrial or ventricular arrhythmias.
Can also see wide PR and QRS. Hypokalemia does not prolong QT interval, but
if U wave present, T and U blend, and apparent prolongation of QT occurs

3. Etiology
 Inadequate intake: Malnutrition, alcoholism (with concurrent hypoMg)
 Increased excretion:
o GI: NG suctioning, emesis, diarrhea
o Renal: Type I or II RTA, hyperaldosteronism,
o Medications: Thiazides, loop diuretics, antibiotics(PCN), steroids, laxatives
o Other: Bartters and Liddle’s syndrome (you will not diagnose this in the ED)
 Transcellular shifts
o Metabolic or respiratory alkalosis
o Medications: Albuterol, insulin, risperidone, quetiapine
o Stress/illness: E.g. 50-60% of trauma patients 2/2 catecholamines
o Hypothermia
 Other: Familial hypokalemic periodic paralysis, hyperthyroidism, leukemia

4. Dx
 Serum potassium
 If suspect hypokalemia, check magnesium and phosphate as well
 If hypokalemic and on digoxin, check dig level because hypokalemia
potentiates dig toxicity

5. Mgmt
 If given as IV, give slowly, no greater than 10mEq/hour. Never give KCl as
IVP, check Cr before repleting! Lethal Injection Dose is 100 mEQ given as IVP
 3-3.5 mEq/L:
o Asymptomatic, healthy patients: no treatment needed, encourage PO intake
(K-rich foods e.g. bananas, papaya, prune juice, mango, orange, pear, raisins)
o Patients with cardiac disease: replete to serum 4mEq/L given risk of
arrhythmia e.g. KCl 20-40 mEq PO x1
 2.5-3mEq/L
o Oral KCl 20-40mEq/day (chronic supplementation: div BID/TID)

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 o Oral KCL elixir 40-60mEq/dose for faster elevation of serum K
o IV KCl 10-20mEq/hour (cannot exceed 10 mEq/hr via peripheral IV and
20mEq/hr via central line)
 <2.5mEq/L
o Requires IV KCL, still at rate 10-20mEq/hour, slow down to 5mEq/hr if renal
insufficiency or heart block
o Requires tele monitoring and recheck K q 1-3hours
o D/C IV and switch to PO as soon as reaches 3.5mEq

6. Dispo
 D/C healthy asymptomatic patients. Encourage K-rich foods and consider
decreasing K-wasting diuretics (thiazides, lasix)
 Ok to D/C pts that require daily oral supplementation as long as can obtain
repeat K check in 1-2 days with PMD
 <3mEq/L: Consider admitting patients for 24hr obs who are elderly, have
significant co-morbidities, or poor access to f/u
 <2.5mEq/L: Admit to tele

7. Tips
 If hypomagnesemic may be refractory to K repletion, replete Mg as well
 If hypophosphatemic (e.g. Type 2 RTA) may consider Neutra-Phos-K, 250mg
tab gives about 14mEq K, can given 250-500mg PO QID

Hypo- and hyper-magnesemia

1. About/Pathophysiology
 Normal range: 1.8-3.0 mg/dL

2. Presentation
 Hypomagnesemia (similar to hypocalcemia)
o Hyperreflexia, tetany, convulsions
o CV: Arrhythmias, prolonged PR and QT intervals, widened QRS, T-wave
flattening, U waves
 Hypermagnesemia
o Nausea, vomiting, weakness, decreased DTR, hypotension, respiratory
depression, cardiac arrest

3. Etiology
 Hypomagnesemia: malnutrition, alcoholism, TPN, cirrhoisis, GI losses,
thiazide and loop diuretics
 Hypermagnesemia (rare): iatrogenic, rhabdo, DKA, PTH abnormalities, tumor
lysis, laxative, antacid, or enema abuse, adrenal insufficiency

4. Mgmt
 Hypomagnesemia
o Only treat if severe, symptomatic, or cardiac patients: 2-4 g Magnesium
Sulfate IV, max dose 8g/day
 Hypermagnesemia

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 o IVF, Furosemide 20-80mg IV, Ca supplementation to antagonize/counteract
hypotension Calcium gluconate 100-200mg IV
o If unstable will need continuous Ca infusion and/or hemodialysis

5. Dispo
 If asymptomatic D/C home
 If symptomatic hypomagnesemia: similar to hypocalcemia, may treat and if
stable and close follow up D/C home
 Symptomatic hypermagnesemia: admit (ICU if unstable, HD needed, etc)

Hypo- and Hyper-phosphatemia

1. About/Pathophysiology
 Normal levels adults 3.0-5.0 mg/dL; neonates 4.0-7.0 mg/dL
 Serum Ca and PO4 levels inversely proportional
 Phosphate absorbed passively in gut, actively in kidney (activated by Vit D3);
PTH inhibits phosphate reabsorption in kidney

2. Presentation
 Hypophosphatemia
o Usually only symptomatic if <1.0
o CV: Decreased contractility, dysrhythmias
o Neuro: Seizure, coma
o Heme: Hemolysis,impaired immune system, thrombocytopenia
 Hyperphosphatemia
o Usually presents when Calcium phosphate product > 70
o Causes hypocalcemia (inversely related) so presents like hypocalcemia e.g.
paresthesias, tetany, seizure, and cardiac dysfunction

3. Etiology
 Hypophosphatemia: Decreased gut resorption (PO intake), renal wasting, or
cellular redistribution (DKA, AKA, severe malnutrition, malignancy, hyperPTH,
Vit D deficiency)
 Hyperphosphatemia: Decreased renal excretion (renal failure) or increased
intake

4. Mgmt
 Hypophosphatemia
o If mild asymptomatic no need to treat, encourage PO intake
o If symptomatic, mild-mod: KPhos 500mg PO QID (500mg Kphos=16mmol
phosphate and 24mEq potassium)
o If severe (<1) or unstable: Replete IV but need continuous cardiac monitoring
 Kphos 0.08-0.16mmol/kg IV over 6 hours
 If K>4.0 use NaPhos 0.08-0.16mmol/kg IV over 6 hours
 Hyperphosphatemia
o If mild, asymptomatic: No need to treat, restrict intake, PMD can start
phosphate binder such as Calcium or Renagel
o If symptomatic: IVF (NS), admit for monitoring

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5. Dispo
 Hypophosphatemia
o If asymptomatic/mild no need to treat and D/C home
o If mild symptomatic, treat, likely send home (based on stability,
comorbidities, and follow-up)
o If severe <1.0 start IV repletion and admit for cardiac monitoring and
treatment of underlying issues
 Hyperphosphatemia
o If asymptomatic/mild D/C home and f/u with PMD
o If symptomatic/severe admit

Hyponatremia
1. About/Pathophysiology
 Na < 130
 Water diffuses into the cell  cellular edema

2. Presentation
 May be asymptomatic, symptoms increase in severity as Na level decreases
 Nausea, headache, malaise, lethargy, confusion, agitation, seizures

3. Etiology
 Hypo-osmolar (<275)
o Hypovolemic – severe total body water loss
 UNa < 10: Extrarenal (GI, skin, drains, hemorrhage)
 UNa > 20: Renal (diuretics, osmotic dieresis, salt wasting, adrenal
insufficiency)
o Euvolemic
 Urine Osm < 100: Polydipsia, beer potomania
 Urine Osm > 100: SIADH, hypothyroidism, adrenal insufficiency
o Hypervolemic
 UNa < 20: CHF, cirrhosis, nephritic syndrome
 UNa > 20: Renal failure
 Iso-osmolar (275-290) = pseudohyponatremia
o Lab artifact due to increased protein and increased lipid states
 Hyper-osmolar (>290)
o Hyperglycemia [Corrected Na=Plasma Na + (0.016 x (serum glucose –100)]
o Mannitol, sorbitol, radiocontrast

4. Dx
 Serum electrolytes, BUN, creatinine
 Serum osmolality [=2(Na + K) + Glucose/18 + BUN/2.8 + ethanol/4.6]
 Urine osmolality, urine sodium
 TSH

5. Mgmt
 Guided by severity of symptoms, duration of illness, and volume status
 Treatment of underlying disease
 Hypovolemic
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 o Isotonic saline (0.9% NaCl)
o Correct at a max rate of 8-10 mmol/day
 Euvolemic
o Fluid restriction (1 liter/day)
o May give 3% NaCl + furosemide if symptomatic
 Hypervolemic
o Fluid restriction (1-1.5 liters/day)
o Diuretics (furosemide)
o Dialysis may be indicated in advanced renal failure
 Severely symptomatic (seizures)
o 3% saline 100 mL IV over 10-60 minutes, may repeat x1 after 10 minutes
(100 mL increases Na by ~2 mmol/L, increasing by 4-6 mmol/L is us. enough)
o Rule of sixes: increase by 6 mmol/L total in first 6 hrs for severe sx, no more
than 6 mmol/L per day (e.g. no further increase if seizure and increased by 6
mEq/L on first day). [Sterns et al, Am J Kidney Dis 56:774-779]
o Do not correct Na by more than 6-8 mmol/L within 24 hours, 12-18 mmol/L in
48 hrs, 14-20 mmol/L in 72 hrs. [Sterns et al, Semin Nephrol 29:282-299]
 Rapid correction of Na puts patients at risk for central pontine myelinolysis!

6. Dispo
 Consider admit if new, severe, and/or symptomatic

Hypernatremia
1. About/Pathophysiology
 Na > 145
 Usually a disorder of water imbalance rather than salt imbalance
 Water diffuses out of the cell  loss of cellular volume
 Reduced water intake: AMS, intubation

2. Presentation
 Nausea, weakness, irritability, restlessness, AMS, stupor, coma, seizures

3. Etiology
 Increased water loss
o GI: Vomiting, diarrhea, third spacing
o Renal: Osmotic dieresis, diabetes insipidus
o Dermal: Excessive sweating, severe burns
o Hyperventilation
 Increased sodium
o Increased intake: Salt tabs, sodium bicarb, hypertonic saline
o Increased reabsorption: Hyperaldosteronism, Cushing’s, congenital adrenal
hyperplasia, corticosteroids

4. Dx
 Serum electrolytes, BUN, creatinine
 Serum osmolality [= 2(Na+K) + Glucose/18 + BUN/2.8 + ethanol/4.6]
 Urine osmolality, urine sodium
 Neuroimaging for evaluation of AMS
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5. Mgmt
 Hypovolemic
o 0.9% saline infusion
 Euvolemic
o Oral fluids
o 0.45% saline
o Treatment for DI
 Hypervolemic
o Furosemide followed by hypotonic (0.45% saline) fluid infusion
o Dialysis may be indicated in renal failure
 Severely symptomatic
o Acute hypernatremia may be treated rapidly
o In chronic hypernatremia, care should be taken not to correct too quickly.
Free water (FW) deficits be corrected over 48 hours
o FW deficit = 0.6 x weight (kg) x [(current Na/4)-1]

6. Dispo
 Consider admit if acute, severe, and/or symptomatic

Hypothyroidism
1. About/Pathophysiology
 Dysfunction of hypothalamic pituitary thyroid axis: TRH  pituitary releases
TSH  thyroid makes T4  converted to T3 in peripheral tissues
 3-10x more common in females than males

2. Presentation
 Vague symptoms from hypometabolic state and tissue deposit of
glycosaminoglycans
 Dry/coarse skin, cold intolerance, puffiness, weight gain, constipation, slow
movements, hoarseness, decreased sweating, depression, menstrual
irregularity, myalgias/arthralgias
 Prolonged reflexes, hypothermia, peripheral neuropathy, bradycardia,
periorbital edema, pale dry skin, anemia
 Myxedema coma (the hypothyroid emergency!) =decompensated
hypothyroidism, not usually myxedematous and not comatose.
o AMS (coma to confusion), hypothermia, CV collapse (hypotension
bradycardia), hyponatremia/hypoglycemia

3. Etiology
 Primary hypothyroidism= thyroid gland failure
o Hashimoto’s autoimmune thyroiditis (anti TPO and anti thyroglobulin AB),
surgical resection, radiation, amyloidosis, iodine deficiency (rare in Western
countries), drug induced (amiodarone, lithium, IL-2)
 Secondary hypothyroidism = pituitary failure
o Sheehan's syndrome, pituitary neoplasm, pituitary surgery/radiation.

4. Dx
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  Send TSH (normal 0.5 and 5.0 mIU/L), free T4, chem panel
 High TSH, low freeT4= primary hypothyroid
 Low TSH, low free T4= secondary hypothyroid
 Look for precipitating event (infection, exposure, surgery, stroke) in myxedema
coma: CBC, CMP, CXR, EKG, blood cx, UA/UCx, consider CSF, cortisol level

5. Mgmt
 Myxedema coma
o ABC’s, supportive care
o Levothyroxine 300-500mcg IV
o Give stress dose steroids (Hydrocortisone 100mg IV) prior to levothyroxine
if concern for adrenal insufficiency. Treating with T4 can precipitate adrenal
insufficiency.
o Look for and treat precipitating event (e.g. infection  give abx)
 If mild and symptomatic hypothyroidism diagnosed in ER, may start
Levothyroxine 25-50mcg daily, need f/u with PMD closely (1-2 weeks) and
repeat TSH in 4-6 weeks
 PASSIVE rewarming only, with appropriate volume resuscitation. If warm too
quickly pts with vasodilate worsen CV collapse

6. Dispo
 Mild -mod hypothyroidism: D/C home f/u closely with PMD
 Acute decompensated hypothyroidism: Admit to ICU

7. Tips
 TSH/freeT4 performed in house UCSF Mon-Sat, turn-around time takes up to
24hrs (often less). SFGH available in house Mon-Fri. Communicate with
admitting team or PMD if admit/discharge patient before result returns
 If considering myxedema coma, better to treat than not treat. T4 is not active,
needs to be converted to active so no huge danger if given but not needed
 Consider early intubation and ventilation if myxedema coma (reduced
ventilatory drive and weak respiratory muscles).

Hyperthyroidism
1. About/Pathophysiology
 Hyperthyroidism is thyroid gland hyperfunction, which is different from
thyrotoxicosis, the state of increased metabolism and catecholamines. Thyroid
storm is the most severe manifestation of thyrotoxicosis (1-2% pts with
thyrotoxicosis progress to storm)

2. Presentation
 Symptoms: Anxiety, irritability, tremulousness, wt loss, palpitation, DOE, heat
intolerance, thin hair, irregular menses, diarrhea
 Signs: Goiter/nodules, perioribital edema/proptosis, tachycardia, atrial
fibrillation, widened pulse pressure
 Apathetic hyperthyroidism: Occurs in elderly, much more subtle presentation
with slow afib, depression, wt loss
 Thyroid storm 1-2% of patients with thyrotoxicosis: acute decompensation or
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 hyperthyroidism from infection, surgery, iodine contrast, MI, CVA, trauma, OD
o Fever, AMS, tachycardia/cardiac dysfunction/CHF, seizures

3. Etiology
 Overproduction of thyroid hormones: 60-80% of hyperthyroidism due to
Graves disease, (autoimmune TSH receptor antibodies), TSH secreting pituitary
adenoma, toxic nodular adenoma, gestational trophoblastic disease or molar
pregnancy (BHCG can stimulate TSH receptor). Also remember, acute phase of
Hashimotos can be hyperthyroid state
 Thyroiditis: Subacute often due to viral (often tender gland), post-partum, drug
induced (amiodarone, interferon-alpha, lithium, iodine)
 Exogenous thyroid hormone: Over-replacement or factitious use
 Ectopic foci: Metastatic thyroid carcinoma or struma ovarii (ovarian teratoma)

4. Dx
 Low TSH and elevated free T4
 Ddx: Sepsis, serotonin syndrome, malignant hyperthermia, NMS,
sympathomimetic intoxication, pheochromocytoma, panic attack
 TSH may be more sensitive marker of thyroid dysfunction than T3, T4 levels
 If considering thyroid storm, also send CBC, Chem10, blood and urine
cultures, CXR, EKG, UA, bedside glucose

5. Mgmt
 Thyrotoxicosis (stable): Start on beta-blocker (Propranolol 20-80mg PO TID)
for symptom relief in discussion w/ endocrinologist, f/u for definitive treatment
o Outpatient treatment options include radioactive iodine, antithyroid
medications methimazole (MMI) or propylthiouracil (PTU), or surgery
 Thyroiditis: NSAIDS for pain, Beta-blocker for tachycardia, may need steroids
e.g. Prednisone 40-60mg PO daily x 1 week with gradual tapering over 4
weeks (only start in discussion w/ PMD/endocrinologist)
 Thyroid storm
o ABC’s and supportive treatment: antipyretics, IV rehydration, glucose
monitoring
o Step 1) Block conversion T4 to T3: Propanolol 1mg IV q15min until PO
effective, Propanolol 60-80mg PO q4hrs; or Esmolol 250 to 500 µg/kg bolus,
then infusion at 50 to 100 µg/kg per min. Caution in CHF/Asthmatics
o Step 2) Block new hormone synthesis: Methimazole 25mg PO q 6hrs (per
feeding tube if cannot take PO) or Propylthiouracil 300-400mg PO q 6hrs,
some experts advocate loading dose 600-1000mg PO, consult endocrinology.
MMI is first line
o Step 3) Block release of thyroid hormones with Iodine: wait at least 1 hour
after administration of MMI or PTU before giving iodine
 Lugols 10% solution 10 drops PO q 6hour OR
 Saturated solution of Potassium iodide (SSKI) 5 drops PO every 6hours
o Consider steroids for adrenal insufficiency if refractory hypotension:
Hydrocortisone 100mg IV or Decadron 10mg IV
o Treat precipitating factor: infection, MI, etc

7. Dispo
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  Mild symptoms: Start BB, speak with PMD if possible, close follow up and
endocrine referral
 Moderate symptoms (new onset a fib, mild CHF, n/v/d): start BB, supportive
care, admit
 Thyroid storm: Admit to ICU, stat endocrine consult

8. Tips
 Thyroid storm has 30% mortality of treated patients (2/2 CV collapse, higher
mortality in younger pts), take very seriously
 Dopamine inhibits TSH secretion, steroids can lower TSH levels without
affecting thyroid function

Acute Adrenal Insufficiency

1. About/Pathophysiology
 Adrenal gland synthesizes glucocorticoids, mineralocorticoids, and androgens
 Glucocorticoid most important : increases CV contractility, increases GFR,
simulate gluconeogenesis, promote lipolysis, increases protein catabolism,
inhibits insulin and increases resistance, decreases production of inflammatory
cytokines

2. Presentation
 Acute: Shock, decreased response to fluid/pressors, hypothermia, n/v,
confusion, abdominal pain
 Chronic: Vague complaints of weakness, lethargy, anorexia, orthostatic
hypotension, GI disturbance, weight loss, hyperpigmentation, hypoglycemia,
hyponatremia, hyperkalemia

3. Etiology
 Most common cause in US is secondary insufficiency from chronic steroid
use then withdrawal
 Primary pituitary problems: Adenoma, metastases, hemorrhage, Sheehan’s
(postpartum pituitary necrosis), head trauma
 Primary insufficiency: Autoimmune adrenal atrophy, infection (TB, CMV,
histoplasmosis), congenital adrenal hyperplasia, adrenoleukodystrophy, adrenal
hemorrhage, amyloidosis, hemachromatosis, drugs (ketoconazole, etomidate).
 Relative insufficiency: Inadequate hypothalamic pituitary response to major
stress
o Most commonly encountered adrenal insufficiency in ED, 2% of population
o Usually patients on steroids chronically who are post-op, infection, trauma

4. Dx
 In ED it is a clinical diagnosis given history and clinical findings
 Labs: Electrolytes, CBC, TSH, free T4, infectious work up, look for underlying
cause
 Send random serum cortisol for admitting team before initiating treatment
o <15mcg/dL suggest adrenal crisis
o >35 mcg/dL unlikely adrenal insufficient
o Between 15 and 35 consider Cosyntropin test (not usually necessary in ED)
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  Send serum cortisol and ACTH (on ice)
 Administer Cosyntropin 0.25mg IV/IM x1
 30-45 minutes after administration send repeat cortisol and ACTH, if rise in
serum 9mcg/dL normal response, if less consider insufficient

5. Mgmt
 ABC’s including bedside glucose
 Do not wait for serum cortisol if there is strong suspicion! Treat empirically!
 Acute adrenal crisis
o Very sick/hypotensive: Hydrocortisone 100mg IV x 1  50-100mg IV q6hrs
 High dose hydrocortisone will have enough mineralocorticoid activity, but
can give Fludrocortisone 50mcg PO daily
o Sick but fairly stable: Dexamethasone 4-10mg IV q6hrs
 Relative adrenal insufficiency (patients on chronic steroids in mild-mod
illness): Double outpatient steroid dose

6. Dispo
 Admit all acute adrenal crisis
o Hypotensive or altered mental status: ICU
o Quick response to therapy with stabilized vital signs: tele vs. floor
 Known disease, mild symptoms, stable vitals, and good f/u, consider D/C

7. Tips
 Dexamethasone will not affect Cosyntropin test and does not have
mineralcorticoid activity, you may discuss with admitting team if time permits
which steroid they prefer. If worried about patient, give Hydrocortisone.
 Mineralocoticoid activity: Fludro (200x) > Hydrocortisone (1x) > Dex (0)

Diabetic Ketoacidosis
1. About/Pathophysiology
 Syndrome due to insulin deficiency and glucagon excess  hyperglycemia,
acidosis, dehydration, electrolyte imbalance
 Increased glucose  glucose in renal tubules  osmotic dieresis 
dehydration/electrolyte imbalance

2. Presentation
 Sx: Polydipsia, polyuria, polyphagia, weight loss, nausea, vomiting, abdominal
pain
 PE: Tachypnea, Kussmaul’s respirations, hypotension, orthostatic BP
changes, signs of dehydration, AMS/lethargy, acetone on breath, consider
cerebral edema, esp. in kids
 Watch K: May code from hypokalemia exacerbated by your treatment (insulin)!
 Cerebral edema: 57-87% of all DKA deaths due to cerebral edema in
kids. RFs: Younger, new onset, higher BUN, low pCo2, low pH, failure of Na to
rise appropriately

3. Etiology

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  Physical/emotional stressors (e.g. infection, MI, trauma, stroke, EtOH/drugs),
cessation of exogenous insulin intake

4. Dx
 Glucose: >350 mg/dL (though 18% may present with glucose <300)
 Serum electrolytes: Look for anion gap
o Na: Low 130s
o K: Often falsely elevated: 4.5-6 (but total potassium deficit expected)
 Often 3-5 mmol/kg down  so will eventually need 140-200 mEq K
o Bicarb: <10
 Serum ketones: High
 UA with urine ketones: Present
 CBC: Leukocytosis may be present
 ABG: Low pH

5. Mgmt
 Fluids
o If hypotensive: Rapid infusion of NS until SBP>80
o Not hypotensive: 1 liter/hour of NS for first 3-4 hours
o Change to ½ NS at 250-500 cc/hr, goal urine output at 1-2 ml/kg/hr
(careful not to administer too rapidly especially in elderly)
o Change to D5 ½ NS when BG 250-300 mg/dl
o Beware: Central lines in DKA have high incidence of thrombosis, avoid
unless absolutely necessary
o Peds: NS 10-20 cc/kg gentle boluses if unstable; otherwise replace fluid
deficit slowly over 48hours to avoid cerebral edema
 Start with NS, switch to ½ NS after 1-4h
 Estimate fluid deficit by exam/weight
 IV infusion rate = [(fluid deficit + GI losses – initial boluses)/48], or
1.5xmaintenance rate
 Insulin
o Bolus: Regular insulin 0.1 units/kg IV push (DKA in peds-> NO BOLUS!)
o Infusion: 0.1 units/kg/hr with q1 hour BG checks
o Stop infusion once BG reaches 250-300 mg/dL
 Potassium: Get the K! Must replete the K if less than 3.3
o Once K is 4.0-4.5, add KCl 20 mEq to each liter of IV fluid
o Check electrolytes q2  q3  q4
 Magnesium
o If low replete with Magnesium sulfate 1-2 g in first 2 liters
 Phosphate
o Usually unnecessary
o If PO4 < 1 mg/dL, replete with Potassium phosphate 20-30 mEq/L in
replacement fluids
 Acidosis
o pH > 7.0: Do not give bicarb
o pH < 7.0: Give NaHCO3 50 mEq in ½ NS with KCl 20 mEq/L over 1 hour. Do
not given bicarb in children or if suspect cerebral edema (bicarb= worsens
cerebral edema)

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  Cerebral edema: Treatment is Mannitol 0.25-1 g/kg bolus, or 3% NaCl 5-10
mL/kg over 30 minutes
 Caution with intubation! Don’t take away their respiratory drive unless
intubation is absolutely indicated. Consider giving Sodium bicarb 50 mEq just
before RSI, avoid excessive hyperventilation post intubation (decreases
intracranial blood flow and worsens cerebral edema) but also avoid
hypoventilation (loss of respiratory compensation for acidosis). Get ABG/VBG
prior, and aim for patient’s own pCO2 and prior RR.

6. Dispo
 Admit to ICU or step down

7. Tips
 Interpreting VBG vs. ABG: pH 0.05 lower than arterial pH, pO2 40-50 instead
of 100, and pCO2 about 5 higher than arterial pCO2 (45 rather than 40)
 Peds pearls: Avoid aggressive fluids (may trigger cerebral edema). No insulin
bolus. Avoid bicarb and central lines 2/2 edema and clots, respectively. Consult
peds endocrine fellow, obtain weight of child prior to calling.

Hyperglycemic Hyperosmolar State

1. About/Pathophysiology
 Diabetic decompensation  hyperglycemia, hyperosmolality, dehydration
(often 10-12 L down), and AMS. May progress to coma
 More deadly than DKA; patients often die of underlying dz, not hypertonicity.
 Decreased glucose uptake  hyperglycemia results in fluid shift from
intracellular to extracellular space  osmotic dieresis  hypotonic urine
 Unlike DKA, ketosis and acidosis generally minimal or absent
 Focal neurologic signs are common
 Often seen in elderly with decreased renal function

2. Presentation
 Sx: Thirst, polydipsia, polyuria, oliguria
 PE: Signs of dehydration, tachycardia, hypotension, orthostatic BP changes,
AMS (somnolence, focal neuro defecits, seizures)

3. Etiology
 Inadequate fluid intake (due to illness, stroke, dementia, etc) in diabetic
patients, medications
 Sometimes seen in non-diabetics (burns, dialysis, TPN/PPN)

4. Dx
 Glucose: >700 mg/dL
 Serum electrolytes: Na: 140s, K ~5, Bicarb >15, BUN >50
 Serum osmolality: > 350 mOsm/L [= 2(Na+K) + Glucose/18 + BUN/2.8]
 Serum ketones: Absent or low
 UA with urine ketones: Absent or low
 ABG: No or mild metabolic acidosis, pH > 7.25

105
5. Mgmt
 Fluids
o If hypotensive: Rapid infusion of NS until SBP>80
o Not hypotensive: 1 liter/hour for first 3-4 hours
o Change to ½ NS at 250-500 cc/hr, goal urine output at 1-2 ml/kg/hr
(careful not to administer too rapidly especially in elderly)
o Change to D5 ½ NS when BG 250-300 mg/dl
 Insulin
o Bolus: Regular insulin 0.05 - 0.1 units/kg IV push
o Infusion: 0.05 - 0.1 units/kg/hr with q1 hour BG checks
o Stop infusion once BG reaches 250-300 mg/dL
o Only start insulin when K >3.3
 Potassium
o K less depleted without acidosis but insulin therapy may make repletion
necessary. Add KCl 20 mEq to each liter of IV fluid if good renal function
o Check electrolytes q2h  q3h  q4h
 Sodium
o [Corrected Na = Plasma Na + (0.016 x (serum glucose – 100)]
o Correct with NS and ½ NS
 Magnesium
o If low, replete with Magnesium sulfate 1-2 grams in first 2 liters
 Phosphate – usually don’t need to replete
o If PO4 < 1 mg/dL, replete with Potassium phosphate 20-30 mEq/L in
replacement fluids

6. Dispo
 Admit to ICU or step down

Hypoglycemia
1. About/Pathophysiology
 Abnormally low blood glucose that causes symptoms

2. Presentation
 Autonomic sx (< 60 mg/dL): Tremor, anxiety, irritability, nausea, vomiting,
palpitations, trembling, hunger, sweating
 Neuroglycopenic sx (< 50 mg/dL): Inattention, headache, lethargy, dizziness,
blurry vision, agitation, focal neuro deficits, seizures, confusion  coma

3. Etiology
 Excessive exogenous insulin or excessive oral hypoglycemic; Psych (suicide
attempts, factitious, Munchausen’s by proxy) or accidental ingestion (kids,
“street valium” = sulfonylurea)
 Critical illness (sepsis, liver disease, renal failure, CHF)
 Tumors (insulinomas, non-islet cell tumors)
 Autoimmune (Lupus, Graves)
 Other: Alcohol, starvation

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4. Dx
 Insulinoma: Whipple’s Triad: (1) hypoglycemia sx present, (2) low BG, (3) sx
resolve when BG normalizes
 Blood glucose < 60 mg/dL
 Consider: LFTs
 For nondiabetic, draw blood sample prior to treatment for the following:
glucose, insulin, c-peptide, proinsulin, glucagon, growth hormone, cortisol, beta-
hydroxybutyrate, insulin antibodies, sulfonylurea drug level

5. Mgmt
 If patient able to eat: 15g of simple carbohydrate PO  eat a “complex” meal
 If unable to eat
o No IV: Glucagon SQ or IM (adults: 1mg, children: 0.5 mg, infants: 50 µg/kg)
o With IV: Dextrose IV bolus (adults: D50W 1 amp, children: D25W 2-4 ml/kg,
infants: D10W 5-10 ml/kg)
 Continued q30 minute BG checks for 4 hours after euglycemia achieved
 If unresponsive to original treatment, start continuous dextrose infusion (D5W
or D10W)
 Octreotide in sulfonylurea and insulinoma-related hypoglycemia: 50-100
µgrams SC q6 hours or IV infusion 100-125 µg/hour

6. Dispo
 May consider D/C if: Hypoglycemia fully/rapidly reversed w/o dextrose drip,
uneventful 4 hour ED obs with normal BG, tolerating PO, known etiology with
unlikely recurrence (short acting insulin), no major co-morbidities, patient
understands prevention and monitoring of hypoglycemia, follow-up with PCP
 Consider admit if: Oral hypoglycemic use, intermediate and long-acting
insulins, requiring dextrose drip to maintain BG, hypoglycemia non-reversible in
ED, hypoglycemia secondary to critical illness
o Always admit sulfonylurea ingestions/overdose!
 Psych consult for suicide attempts, factitious disorder, Munchausen’s

Alcoholic Ketoacidosis
1. About/Pathophysiology
 Starvation metabolism  FFA mobilized from adipose tissues  acidosis
 Low caloric intake  catabolic/ketogenic state
 Alcohol metabolism  NAD depletion  increased ketone body formation
2. Presentation
 Sx: History of binge drinking with stop, nausea, vomiting, abdominal pain
 PE: Tachypnea, tachycardia, signs of dehydration, acetone on breath, ?AMS.
 Hard to diagnose, have to have high index of suspicion. Suspect in daily EtOH
users who stopped drinking, are vomiting with dry mucous membranes +/-
abdominal pain

3. Etiology
 Usually occurs in chronic alcoholics after a binge  vomiting, decreased food
intake, dehydration
 Risk factors: Poor nutrition, liver disease, dehydration
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4. Dx
 Check electrolytes, BUN/Creatinine (AG metabolic acidosis, hypokalemia,
hypomagnesemia). May have normal or only slightly elevated lactate on VBG
 Glucose: Low to slightly elevated, no hyperglycemia
 UA with urine ketones: Present, but not on urine dip. Dip tests acetoacetate,
but AKA state increases reducing substances, and acetoacetate gets reduced
to beta hydroxybutyrate. Must test for this in serum.

5. Mgmt
 Hydration
o D5 ½ NS IV (give Thiamine 100 mg/ Folate 1mg/MVI first) preferred
o IV NS may paradoxically worsen acidosis from chloremic metabolic acidosis
 Potassium: Add KCl 20-30 mEq/L of fluids
 Glucose: PO if stable, IV if low sugar
 Magnesium
o If low, replete with Magnesium sulfate 1-2 grams IV
 Phosphate – usually don’t need to replete
o If PO4 < 1 mg/dL, replete with Potassium phosphate 20-30 mEq/L in
replacement fluids
 Acidosis: For pH<7.1, NaHCO3 1-2 mEq/kg IV
 Treatment of EtOH withdrawal

6. Dispo
 Consider admit if severe
 D/C if clinically well, decreasing/resolved anion gap
 Ketoacidosis may reverse in 12-24 hours if no underlying dz or complications

Suggested Reading
 Cooper, M and Stewart, Paul. Corticosteroid Insufficiency in Acutely Ill
Patients. N Engl J Med 2003; 348:727-34
 Gennari F. Hypokalemia. N Engl J Med 1998; 339:451-458
 McKeown, N et al. Hyperthyroidism. Emerg Med Clin N Am 2005; 23: 669–685
 Moffat et al. Hyperkalemia. BMJ 2009; 339:1019-1024
 Pimentel L and Hansen K. Thyroid Disease in the Emergency Department: a
Clinical and Laboratory Review. J Emerg Med 2005; 28: 201–209

108
 Environmental Emergencies
By Jake Miss Res ed. Adrian Flores Faculty ed. Judy Klein

Accidental Hypothermia
1. General
 Defined as core temperature less than 35° C
 Compensation to heat loss
o Conduction: Transfer of heat through objects in contact (wet clothes)
o Convection: Transfer of heat through fluids and gases
o Radiation: Transfer of heat between the body and its surroundings by
electromagnetic waves
o Evaporation: Transfer of heat through conversion of liquid to gas
(sweating/breathing)
 Temperature regulated by pre-optic nucleus in anterior hypothalamus
o 35° - 32° C (Mild)
 Vasoconstriction, shivering and basal/endocrine thermogenesis
o 32° - 29° C (Moderate)
 Shivering stops, progressive depression of basal metabolic rate
o 29° C and below (Severe/Profound)
 Autonomic and endocrine mechanisms are inactive
2. Clinical presentation of hypothermia
 Cardiovascular
o Initial tachycardia, then bradycardia, 50% normal at 28° C
o Decreased cardiac output; at 30° C 2/3 normal
o EKG: Osborn (J) wave
 Can appear at any temperature below 32° C
 Upright in aVL, aVF and lateral precordial leads
 Diagnostic but not prognostic

*from http://medicine.ucsf.edu/education/resed/ecg/hypothermia.html
o Dysrhythmias: Both atrial and ventricular are common in moderate to severe
hypothermia, heart block also possible
o Use caution when placing central line: the wire “tickling” the atria or
ventricles can be highly arrhythmogenic
o Avoid jarring the patient
 Core temperature afterdrop
o Decline in core temperature after removal from cold
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  Pathophysiology unclear but perhaps perfusion of cold extremities, counter
cooling of the blood until the temperature gradient is eliminated
o Loss of peripheral vasoconstriction leads to decreased MAP and PVR
 Anticipate hypotension during rewarming and aggressively fluid
resuscitate prior to external rewarming (bair hugger will warm, vasodilate
and drop pressure if the patient is not “tanked up” first)
CNS
o Progressive depression, variable
 34° C: Amnesia and Dysarthria
 33° C: Ataxia and Apathy
 32° C: Stupor, loss of papillary reflexes, agitation, hallucinations
 25° C: Loss of cerebral autoregulation, areflexia, coma
 19-20° C: Flat EEG
o Paradoxical Undressing
 Maladaptive, often in elderly
 Thought to be related to feeling of warmth created by loss of peripheral
vasoconstriction to skin in advanced hypothermia. Your skin is your
thermostat: if it feels warm, you feel warm.
 Renal
o Cold diuresis
 Decreased RBF, excrete glomerular filtrate, little nitrogenous waste
excreted  metabolic acidosis
 Independent of volume status
 Respiratory
o Initially stimulated, then decreasing proportionally related to decreasing
metabolism
o Respiratory acidosis and hypercarbia can occur due to hypoventilation
o Decreased airway protection and coughing
o Non-cardiogenic pulmonary edema, ARDS and apnea at <24° C
 Hematology
o Coagulopathy is grossly underestimated
 Fibrometers warm sample to 37°C then measure INR
 Clotting Times: symptomatic Factor IX deficiency occurs ≈ 25% of normal
 35° ≈ Factor IX level 39% of normal
 33° ≈ Factor IX level 16% of normal
 31° ≈ Factor IX level 2.5% of normal
o Bleeding time: Reflects platelet function
 37° ≈ Bleeding time 2.4min
 32° ≈ Bleeding time 5.8 min
o The only treatment is re-warming. If you give blood product, it just gets cold
and functions poorly

3. Treatment of hypothermia
 Cardiac arrest: “No one is dead until they are warm and dead”
o Even intermittent CPR in the field can be helpful
o One of the few times you would do CPR in the Wilderness
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  Hypothermia, lightning, drowning
o ACLS, aggressive rewarming/active internal warming until 30°C (86 °F)
o Have a high index of suspicion for hypothermia. Insist on rectal temp for
screening, then temperature sensing foley to monitor temperature during
resuscitation
 Don’t miss sepsis in a hypothermic patient with rigors
 Prevent further heat loss
 Labs
o FSBG, VBG/ABG (uncorrected for temperature), CBC, Chem 10, lipase (for
ischemic pancreatitis), coags
 Volume resuscitation
o NS (not LR) warmed to 40-42° or through a Level 1 or other fluid warmer
o Rewarming: Active vs. passive

*adapted from: Mulcahy and Watts. Emergency Medicine Practice. 2009

o Passive
 Non invasive, the treatment of choice for most mild hypothermia patients
 Remove wet clothing, cover patient with insulating material in favorable
atmospheric conditions. Shivering rewarms at 0.5° C /hr
 This will not work below 30-32° C: no shivering or inherent heat production
 Aim for rate of 0.5 - 2°C/hr
 Active
o Indications
 CV instability
 Mod/severe hypothermia = less than 32° C
 Inadequate rate or failure to re-warm passively
 Endocrine insufficiency
o External/non-invasive
 Bair hugger (1-2.5° C /hr): Most common at both UCSF/SFGH
 Warm bottles, heating pads, etc. are also available
o Internal/invasive
 Airway rewarming: Heated, humidified oxygen at 40-44 degrees (need
respiratory therapy to set up). Heats 1-2.5° C /hr
 Warmed IVF: Inline warmers at UCSF/SFGH, warms IVF to 40-42 degrees,
need short IV lines. Heats1-2° C /hr
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  Gastric/urinary irrigation: Not very effective due to small surface area of
these organs, generally not recommended
 Closed thoracic lavage
 Requires chest tube
 Place one chest tube per side and connect to a Y connector, with
connections to the level one warmer tubing and the pleurevac. Use clamp to
alternate lavage and drainage.
nd rd
 If no Y-connector, may place 2 chest tubes, one placed anteriorly 2 /3
th
ICS at MCL, the other in normal 5 ICS at PAL Warms 3° C/hr
 Peritoneal dialysis: Infuse and drain 2 L of dialysate (use warmed NS from
Level I) q20 mins, for total of 6L hours. Warms 1-3° C /hr
o Extracorporeal blood rewarming (these should happen in the ICU)
 Venovenous
 Hemodialysis
 Continuous AV rewarming: Easiest as lines can be placed in ED if machine
is available, not available at SFGH
 Cardiopulmonary bypass

Frostbite
1. General
 Occurs when tissue freezes (-0.55° C)
o Vs. Frostnip: Superficial injury with pain, pallor and anesthesia. Reversible
w/ warming
 Risk factors: Intoxication, trauma, improper clothing, physical de-conditioning,
malnutrition, fear, DM/atherosclerosis/anemia/hypotension, duration of exposure

2. Pathophysiology
 Pre-freeze phase
o Tissue temp drops below 10° C and cutaneous sensation is lost
o “Hunting response”: Cold induced, intermittent vasodilation at <10° C,
occurring in 5-10 minute cycles to attempt to protect the extremity
 Freeze-Thaw Phase
o Tissue freezing: Ice crystals form extracellularly first, drawing water out from
the cells, which collapse and die if more than 1/3 of cellular volume is lost
o Rapid freezing will cause ice crystal formation intracellularly, causing more
damage
o Vascular stasis and progressive ischemia
o Progressive microvascular collapse in venules then arterioles 
endovascular dysfunction dictates the amount of permanent damage
o Red blood cells sludge and form microthrombi causing worsening ischemia
3. Clinical features
 Early features
o Cold and pain at affected area
o Paresthesia and/or numbness with continued freezing
o Areas with blanching blends into areas of uninjured skin
 Late features
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 o White and waxy skin distinctly demarcated from uninjured tissue
o Woody tissue w/o sensation
o Progress to bruising and blistering, usually upon thawing
 Assessment of severity
Mild frostbite Severe frostbite
st nd rd th
1 degree 2 degree 3 degree 4 degree
Depth of Partial Full Skin and Skin,
frozen thickness thickness subcutaneous subcutaneous
tissue tissue tissue, muscle,
tendon, bone
Tissue Red or Red Blue/black Deep red/mottled
color hyperemic  black, mummy
Blistering None Clear Blood blisters, Profound
or necrosis blisters some necrosis necrosis
Edema Minor Significant Significant Minimal or none
*adapted from Hallam, et. al, BMJ 2010

4. Treatment of frostbite
 Rapid rewarming done only when there is no risk of re-freezing
 For transport, replace wet clothes with dry loose fitting clothes, and splint
injured areas
 NO RUBBING, AVOID MECHANICAL TRAUMA
 Protocol for rewarming
o Treat systemic hypothermia up to 34° C
o Immerse extremities in warm water at 40-42° C (104-108° F) manually
circulated until the extremities are pliable, and color/sensation have returned,
usually 15-30 mins
 After re-warming care
o Debride white blisters and treat topically with aloe vera q6h
o Leave hemorrhagic blisters intact and treat with aloe vera q6h
o Elevate affected part and splint as indicated
o Give TD vaccine
o Prophylactic abx controversial, but wounds should be monitored for infection
o Ibuprofen 400-600mg PO q12 hrs or ketorolac 30 mg IV q6h (to block
arachadonic acid pathway)
o Adequate analgesia with opioids as indicated
o Admit all but the most simple cases
o Take serial photos and get baseline x-rays, possible angiogram
o Consult surgery and orthopedics, but protect your patients from acute
surgery/amputation!
 “Frostbite in January, amputation in July”: Acute amputation not indicated
 Takes 60-90 days at least to determine extent of tissue loss
 May consider intra-arterial tPA in patients with high risk for multiple
digit/proximal amputations, no contraindications, presenting within 24 hours
(controversial) after d/w ortho/surgery. If given, dose as bolus 2-4 mg IA then
0.5-1 mg/hr via femoral or brachial artery, with follow-up angiograms
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 Other Cold Injuries to the Extremities
1. Non-Freezing Cold Induced Injuries (NFCI)
 Does not involve freezing of tissue, which distinguishes it from frostbite
 Occurs in temperatures near freezing point, often in muddy and wet weather
 Hikers, older adults and homeless people are at risk

2. Chilblains (aka: Pernio)

 Local irritation, pain, itching and red patches (papules) in areas exposed to
cold, dry conditions
 Plaques, vesicles and bullae may develop

3. Trench foot (aka: Immersion foot)

 Term originated in WWI (Trench Foot), and shipwrecked sailors in WWII
(iImmersion iInjury)
 Occur at temperatures 0-15° C (32-59° F)
 Caused by tight fitting boots, prolonged cold and wet exposure, leading to skin
breakdown, prolonged vasoconstriction and subsequent nerve and tissue
damage

4. General clinical presentation

 Pre-hyperemic phase
o Intense vasoconstriction: Sluggish cap refill and absent distal palpable
pulses
o Tissue appears blanched, yellow-white or molted, NO BLISTERS
o Muscle cramps and anesthesia are common
 Hyperemic phase
o Within hours of re-warming, extremities become hot, erythematous, painful
and swollen with bounding full pulses, but delayed cap refill
o Hyperalgesia, paresthesias common and progressively improve
o Ischemia, lots of edema, blisters, formation of eschars. Lasts 24 hours to 10
weeks
 Post-hyperemic phase
o Vague neurological sx with no physical signs. May last years
5. Approach to treatment
 Symptomatic relief and reversal of ischemia
 Rewarming vs cooling
o Core temperature should be raised while the extremities are kept cool
o Rapid re-warming of extremities will cause increased metabolic demand of
the damaged tissue causing increased edema, skin necrosis, tissue damage
and pain
o Elevate the effected extremities and expose to air
o Continue local cooling until pain improves, circulation has recovered and
hyperemia subsides
o Never rub the injured areas as this can worsening the extent of injury
 Prevention is key
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 Heat Illness
1. General
 Predisposing factors
o Extremes of age: very young and elderly patients
o Psychiatric patients
o Patients with chronic diseases
o Strenuous activity in heat in un-acclimatized patients

2. Heat Cramps
 Brief, intermittent and severe muscle cramps typically in fatigued muscles after
heavy work
 Related to copious sweating and salt depletion after copious hypotonic fluid
repletion
 Not associated with rhabdomyolysis
 Tx with PO or IV salt solutions and education

3. Heat Edema
 Lower extremity edema occurring in un-acclimatized patients, especially
elderly in sub/tropical areas, often associated with travel or more rigorous
activities than usual
 R/o other causes e.g. DVT, thrombophelbitis, lymphedema, CHF
 Diuretics are of no utility and sx should resolve after a few days of
acclimatization

4. Heat Syncope
 Basically hypovolemia (due to sweating) and vasodilation (decreasing thoracic
blood volumes) leading to syncope
 Often in elderly
 R/o other illness
 If no other causes of syncope, reassure and educate about hydration

5. Prickly Heat (aka. Miliaria rubra/lichen tropicus/heat rash)

 Acute inflammatory disorder of skin in hot/tropical climates
 Caused by blockage of sweat glands by macerated stratum corneum and
secondary staph infection
 Acute phase: intensely pruritic vesicles on an erythematous base
o Rash is usually confined to clothed areas and often area is anhdrotic
 Profunda stage: 7-10 days later, keratin plug fills vesicles  deeper
obstruction of sweat gland and vesicles form in dermis. Can persist for weeks
o Not pruritic and look similar to piloerection
 Treatment
o Chlorhexidine in light cream/lotion and antihistamines during acute phase
o Salicylic acid 1% can be applied to affected areas
o If diffuse, can try erythromycin
o Prevention with loose fitting clothes and avoiding continuous sweating

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6. Heat exhaustion/heat stroke
 Heat exhaustion: Early spectrum of heat stroke
o 2 major types, though usually presents as a mixed picture
 Water depletion 2/2 inadequate PO intake with progressive hypovolemia
 Salt depletion: Similar to heat cramps except systemic symptoms arise from
hypotonic fluid intake
o Clinical presentation
 Vague malaise, fatigue, headache, n/v, muscle cramps
 Core temperature may be normal or < 40 °C (104 °F)
 Intact mental status, no coma or seizures
 Dehydration: Tachycardia, orthostatic hypotension
 Hyponatremia, hypochloremia and low urine sodium and chloride
concentrations
 Heat stroke: Associated with 30-80% mortality, hallmark is mental status
change
o Damage is a function of temperature and also exposure time
o Failure of compensatory mechanisms of temperature regulation, leading to
severe hyperthermia and multisystem tissue damage and organ dysfunction
(always liver)
o Neurologic dysfunction (e.g. AMS) is a key symptom requiring aggressive
cooling
o Types
 Exertional: Young, healthy patients in setting of exercise. Assoc with
diaphoresis, hypoglycemia, DIC, rhabdomyolysis, ARF, marked lactic acidosis
and hypocalcemia
 Classic: Elderly or sedentary patients with predisposing factors or meds, in
setting of a heat wave. Assoc with anhidrosis, normoglycemia, mild ↑CPK,
mild coagulopathy, oliguira, mild acidosis
 Diagnosis
o Exposure to heat stress, endogenous or exogenous
o Signs of severe CNS dysfunction (ataxia, coma, seizures, delirium)
o Severe hyperthermia (core temperature may be above 40.5 °C (105 °F), but
may be lower if EMS cooled pt already, no strict cut-off)
o Hot skin common, sweating CAN be present so can have heat stroke and be
wet
o Marked transaminitis
 Differential diagnosis
o Malignant Hyperthermia (MH)
o Neuroleptic Malignant Syndrome (NMS)
o Other drugs: MDMA, cocaine, serotonin syndrome, alcohol withdrawal, ASA
o Seizures
o Endocrine: Thyroid storm, pheochromocytoma, DKA
o Sepsis and infection
 In addition to common infections, consider encephalitis, meningitis, malaria,
tetanus, typhoid
o CNS hemorrhage
 Treatment

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 o Both heat exhaustion and heat stroke should be treated with cooling, with
more aggressive interventions and monitoring for heat stroke
o Mild illness (heat exhaustion)
 Place in cool environment, assess volume status clinically, consider
sending labs for electrolyte abnormalities
 Rapid recovery usually follows fluid administration
 Young or otherwise healthy patients can be treated as outpatients,
otherwise admit
o Severe illness (heat stroke)
 IV, O2, monitor and invasive temperature monitor, labs
 May consider antipyretics like APAP or NSAIDs in undifferentiated
hyperthermia, but immediate cooling takes precedence in true heat stroke
 Goal: Actively cool to 38-39 °C (100.4-102.2° F), then stop measures to
avoid overshooting
 Cooling methods: Evaporation preferred. May also consider ice packs to
neck, axillae, groin, ice water immersion, cooling blankets. Consider
cardiopulmonary bypass in severe or resistant coma
 SFGH: Get a cooling blanket to place under the patient, then drape in a
sheet soaked in room temperature water and use a floor drying fan propped
up to blow air over the patient. Replace the damp sheet as needed by
soaking with fresh water. Also place ice bags at axilla, groin, neck while
protecting patient’s skin
o Fluid resuscitation
 Start at 1 liter and reassess. Pt is volume depleted, but once the systemic
vasoconstriction resolves, they will be much less volume depleted.
o Seizures: Treat with benzodiazepines to start as usual
o Metabolic derangements: Watch for rhabdo, DIC, renal failure and
electrolyte disorders and treat accordingly. Caution with rapid correction of
hyponatremia (risk of central pontine myelinolysis)
o Admit
Dysbarisms and Barotrauma
1. General
 Boyles Law: P1V1 = P2V2
o In seawater, every 33ft of depth = 1 atm of pressure
o At depth of 33ft, any gas filled structure has ½ V compared to the surface;
Conversely upon ascending from 33ft without exhaling it would have 2V
 Causes of serious injury
o Barotrauma to lungs on ascent, causing pneumothorax and arterial gas
embolism (large bubbles)
o Gas “bubbles” forming in vessels after too rapid an ascent = decompression
sickness (small bubbles)
o Occurs not only in diving ascent, but rapid ascent to high altitude as well
2. Barotrauma
 Descent

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 Clinical features Treatment
Otic barotraumas Pain, fullness, vertigo, Decongestants
(“ear squeeze”) conductive hearing loss
(can’t equalize mid ear)
Sinus barotraumas Pain over sinus, possible Decongestants
(“sinus squeeze”) nose bleed
Inner ear Sudden sensorineural ↑HOB, no nose-blowing,
barotraumas hearing loss, tinnitus, antivertigo meds, urgent
severe vertigo after forced ENT c/s
valsava
 Ascent
Clinical features Treatment
Pulmonary Dyspnea, CP, subQ air, Symptomatic care for
extra-alveolar air on XR pneumonediastinum
2/2 rapid or uncontrolled Drain ptx
ascent Does not need recompression
Arterial Neuro sx after uncontrolled ABCD, high flow O2, IVF
gas or rapid ascent, or with Immediate recompression
embolism pulmonary barotrauma (hyperbaric)
*Any neuro sx + pulmonary
barotraumas should be treated
as arterial gas embolism
*adapted from Tintinalli’s Emergency Medicine, 2011

3. Decompression Sickness – occurs minutes to hours after surfacing

Clinical features Comments
Type I: “pain- Joint and extremity deep Usually single joint (knees,
only” DCS pain, no ∆ w/ mvmt shoulders)
(“bends”)
Skin: mottling, pruritis, May get lymphatic blockage,
color changes will take days to resolve
despite recompression
Type II: Pulmonary: cough,
“serious” hemoptysis, dyspnea,
DCS substernal CP (“chokes”)
May get CV collapse
Neuro: truncal Tends to affect lower cervical
constriction  rapid and thoracic regions 
ascending paralysis scattered lesions, may see
autonomic dysfunction
Vestibular: vertigo, Usually after long, deep dives
hearing loss, tinnitus,
disequilibrium

118
 (“staggers”)
Type III: DCS II sx + stroke Present immediately after
combination syndrome/sx/symptoms ascent or surfacing,
of DCS and symptoms may
arterial gas spontaneously resolve
embolism
*adapted from Tintinalli’s Emergency Medicine, 2011

4. Treatment
 Any arterial gas embolism or “serious DCS” should be treated with 100% O2,
reperfusion with fluid resuscitation, and rapid recompression in hyperbaric
oxygen chamber (HBO)
 HBO Centers in SF
o St. Francis Memorial Hospital: 415-353-6700
 HBO Centers in Bay Area
o Travis Air Force Base, Fairfield: 707-423-3987,707-423-3286
o John Muir Medical Center, Walnut Creek: 925-947-3212
o Doctor’s Medical Center, San Pablo: 510-235-3483
Lightning Injuries
1. General
 1000 events/yr in US annually with 10-30% mortality and 76% risk of long term
sequelae
 Rare occurrence in the Bay Area
 Lightning to thunder time less than 30 second places you at risk for lightning
strike (though depends on surroundings: e.g. standing on a piece of iron in bare
feet vs. sitting in your car with rubber tires)
 Direct strike is often fatal

2. Pathophysiology
 Flashover
o When victim is struck, primary current arc travels outside the body
o Secondary current created by magnetic fields  cardiac, internal injuries
 Electroporation
o Lighting induced reorganization of cell membrane lipids creates pores,
leading to cell death
o Muscle and neurons are most affected
o May lead to respiratory arrest from CNS disruption or respiratory muscle
paralysis
 Keraunoparalysis: Neurological and muscle paralysis due to vascular spasm
and autonomic NS instability

3. Clinical
 Triage Keys
o Don’t get struck by lightning or electrocute yourself

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 o Treat the lightning victims in cardiac/respiratory arrest first as they have high
likelihood of survival given the proper care
 Orders: CBC, Chem 10, CK, UA, EKG
 Cardiac
o Dysrrhthymias: VF and asystole
o Tachycardia and hypertension
o Global mycocardial depression, vasospasm, pericardial effusion
o EKG: ST elevation, QT prolongation, T wave inversions. ST↑ 2/2 myocardial
cell death from lightning injury, usually not vascular ischemia
 Neuro
o Acute effects: Immediate onset
 Common: LOC, LE paralysis
 Other: Headache, confusion, AMS/amnesia
 Pupillary dilation or anisocoria can be caused by autonomic dysfxn in
comastose pt and unrelated to brain injury
 CT Scan for heat-induced coagulation of cerebral cortex, epidural, subdural,
ICH
o Prolonged effects: Delayed onset and permanent
 Seizures, AML, ataxia, parksonism, ataxia
 Vascular: Diffuse vasospasm, may get skin changes (white to blue to red) 2/2
cycles of vaso-constriction/-dilation w/ pallor, cyanosis and hyperemia
 Ophthalmic: Lightning induced cataracts, may be acute or delayed
 Auditory: TM rupture common due to blast effect
 Musculoskeletal
o Rhabdomyolysis, myoglobinuria
o Posterior shoulder dislocation
o Spinal fractures and other injuries can be caused by tetany or 2° trauma
 Cutaneous
o Lichtenburg figures: Pathognomonic for lightning strike. Ferning pattern,
disappears in 24h, not a true thermal burn
o Burns: Flash, punctate, contact, blistering, linear, superficial erythema
Drowning
1. General
 Often seen at UCSF from people at Ocean Beach
 4 leading cause of accidental death in US, 2 leading cause in patients
th nd

under 15 yrs old

 No longer use term “near-drowning”: any submersion injury is a “drowning”
regardless of outcome
 Diving reflex: Parasympathetic, thought to be protective. Bradycardia, apnea,
peripheral vasoconstriction, central shunting of blood flow
 Cold shock response: When submerged in water less than 10°C. Triggers
gasp reflex, hyperventilation, hypertension and dysrrthymias
 “Dry” drowning: Controversial term, may be up to 20% of all drowning.
Laryngospasm leading to hypoxia, hypercarbia, acidosis and eventual loss of
consciousness and cardiac arrest with no inhalation of water
 “Wet” drowning: Majority of injuries

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 o After initial laryngospasm passes, water aspirated into lungs, causing dilution
and washout of surfactant and impaired gas exchange
o Usually also swallow lots of water
o Can cause both pulmonary edema and ARDS pathophysiology
 Fresh water: Hypotonic, hemodilution, hemolysis and hyponatremia
 Salt Water: Hypertonic, hemoconcentration, hypernatremia and
hyperkalemia
 Treatment
o ABC’s, IV, O2, monitor, ATLS/ACLS as needed
o Treat associated conditions or those which contributed to drowning e.g.
spinal cord injuries, hypothermia, syncope, seizures, comorbidities
o Determine GCS and O2 sat
 If GCS > 13 and O2 Sat > 95% on RA, excellent prognosis for recovery.
Monitor for 4-6 hours for delayed pulmonary effects, but admit if GCS not
normal or any respiratory symptoms after observation
 If GCS < 13 or O2 Sat < 95% on RA, give O2, consider CPAP/intubation. If
Intubated, consider prophylactic abx for Aeromonas species. Get CXR, labs
(lytes, glucose), monitor acid/base, temp, and admit
o Pts presenting to ED in cardiac arrest after warm water submersion have
low probability of meaningful neurological recovery

Altitude Illness
1. General
 Intermediate altitude 1520-2440 m (5000-8000 ft)
 High altitude >2440 m (>8000 ft) is a hypoxic environment
 Very high altitude 4270-5490 m (14,000-18,000 ft)
 Extreme high altitude >5490 m (>18,000 ft)
 You will NOT see this at UCSF or SFGH
o San Francisco: 10m = 30ft, Mt. Tamalpais: 784m = 2,574ft
o Lake Tahoe: 1897m = 6,225ft, Top of Squaw: 2758m = 9,050ft, Top of
Kirkwood: 2987m = 9,800ft
o Everest Base Camp: 5360m = 17,590ft, Chomolungma (Everest): 8848m =
29,029ft or 8850/29,035

2. Risk Factors
 Rapid rate of ascent
 Sleeping at high altitude (hypoxia is maximal during sleep)
 Altitude above 2000m (6562 ft)
 Age >50 possibly protective
 Obesity
 Exertion at altitude
 Maximum elevation attained
 Previous AMS
 Duration of stay at altitude
 Cold Temperatures
 Living lower than 900m
 Not risk factors
o Gender: women tend to have less HAPE
121
 o Fitness Level, in shape not protective
o Tobacco use

3. Spectrum of disease
 Acute Mountain Sickness (AMS): Headache + 1 of following
o Anorexia/nausea/vomiting
o Fatigue/weakness
o Dizziness/lightheadedness
o Difficulty sleeping
o May see low O2 saturation, but no other physical exam findings
o *Symptoms may start 2-36 hours after arrival at altitude, will not resolve until
descent
 High Altitude Cerebral Edema (HACE): Acute mountain sickness + ataxia
and/or altered mental status. Less common below 16,000-17,000 ft
 High Altitude Pulmonary Edema (HAPE): 2 symptoms + 2 signs in setting of
recent travel to high altitude w/o CHF or PNA. May start 3-5 days after reaching
high altitude, depends on speed of ascent. 50% may have AMS/HACE
o Symptoms
 Dyspnea at rest (earliest sign, usually with crackles and tachypnea)
 Cough
 Weakness or decreased exercise tolerance
 Chest tightness and congestion
o Signs
 Crackles or wheezing in at least one lung field
 Central cyanosis
 Tachypnea
 Tachycardia
4. Prevention and treatment
 DESCENT is priority
 Oxygen, ?hyperbaric therapy via portable chamber en route, meds
Medication Indication Dosage
Acetazolamide  AMS, HACE prophy  125 mg po bid
(Peds: 2.5 mg/kg po q12h)
 AMS treatment  250 mg po bid
(Peds: 2.5 mg/kg po q12h)
Dexamethasone  AMS, HACE prophy  2 mg po q6h or 4 mg po q12h
(not for prophy in kids)
 AMS treatment  4 mg po/iv/im q6h
 HACE treatment  8 mg po/iv/im then 4 mg q6h
(Peds: 0.15 mg/kg po/iv/im q6h)
Nifedipine HAPE prophy/ 30 mg SR po q12h or 20 mg SR
treatment po q8h
Taladafil HAPE prophy 10 mg po bid
Sildenafil HAPE prophy 50 mg po q8h
Salmeterol HAPE prophy 125 mcg inhaled bid
*adapted from: Luks, et. al. Wilderness and Environmental Medicine. 2010
122
  Intubation for HAPE is rare
 Other therapies for HAPE
o ?Inhaled beta-agonists
o Trial of PDE-5 inhibitors
o Dexamethasone, lasix does not help in HAPE

Envenomations
1. General
 UCSF is the receiving center for any envenomation at the California Academy
of Sciences
 Check binder in the Fish Bowl with all of the protocols for every possible
envenomation or injury at the site as determined by Dr. Matt Lewin

2. Snake Bites
 Of 14 families of snakes, 5 are poisonous; rattlesnakes most common in US
 Snakes can strike accurately to about 1/3 of their body length
 20% of all bites are “dry” bites, with no venom injected
 In the Bay Area, Western Pacific Rattlesnakes are present
 Venom is a mixture: Cytotoxic, hemotoxic and neurotoxic toxins depending on
species
 Crotalinae: Rattlesnake, copperhead, cottonmouth, fer-de-lance
o Locally cytotoxic with swelling erythema, petechiae, ecchymosis and
hemorrhagic blebs, local compartment syndrome
o Systemic hemotoxicity: thrombocytopenia, coagulopathy, fasiculations and
possibly hypovolemic shock
o Treatment based on severity of symptoms, not body weight.
o Tx endpoint: Reversal of systemic symptoms, stop progressive edema/pain
o Consult poison center (1 800 222 1222) for exact dosing and guidance
o Repeat dose every hour until progression of symptoms is halted
o Caution with Mojave Rattlesnake: delayed neurological signs and symptoms
and minimal local bite injury, but must be treated aggressively with antivenom ,
with at least 4 vials of CroFab even with minimal symptoms
Severity of enveomation Initial dose (vials)
Antivenom Crotalinae CroFab
Polyvalent (Wyeth) (Protherics)
None or minimal None None
Mild (local pain/swelling) 5 4
Moderate (proximal 10 4-6
progression of swelling,
ecchymosis, mild
systemic sx)
Severe (hotn, 15 8
progressive swelling
and ecchymosis,
coagulopathy)
th
*adapted from Olson (Ed.). Poisoning & Drug Overdose, 5 Edition, 2007

123
  Elapidae: Coral snake, cobra, krait, mamba
o Systemic neurotoxicity is more predominant than local toxicity and can be
delayed
o Human envenomation is rare/difficult as snake has small, posterior fangs 
must chew victim
 General approach to snake bites
o Call poison control 800-222-1222
o Remove victim from vicinity of snake, wash area with soap and water and
remove any constricting clothing, rings or other jewelry
o Do NOT apply ice as this worsens local tissue effects 2/2 vasoconstriction
o Do NOT tourniquet
o Splint/immobilize extremity near heart level
o Do NOT cut over the bite or try to suck out venom with mouth. Suction in
general, even within first 15 minutes has not been shown to improve outcome
o Determine severity of bite and provide wound care
o Monitor for at least 6 hours. If no signs of envenomation then can be
discharged (except caution with Mojave Rattlesnake)
o Send labs: CBC, CK, coags, chem10, Type and Screen if bleeding, UA
o Monitor for respiratory muscle weakness and shock (mostly for elapid
envenomation). If present, Admit to ICU
o Administer antivenom if indicated, but needs to be species specific so try to
identify the snake. If antivenom not available in hospital, call SF ZOO 415-753-
7080 or California Academy of Sciences 415-379-8000

3. Spider bites
 Latrodectus: Black Widow. Ubiquitous in California
o Bite is usually initially painful, definitely painful locally in 30 to 120 mins
o Erythemetous, target lesion with possible central blanching
o At 3-4h, cramping of involved extremity, with centripetal progression to
chest, back or abdomen with “board-like” rigidity, weakness, headache,
paresthesias
o Can cause hypertension, diaphoresis, nausea, vomiting, tachycardia, may
mimic ACS or surgical abdomen and can last 1-2 days
o Treatment
 Clean wound, may use intermittent ice packs, tetanus if indicated
 Monitor 6-8 hours but may need pain control admission
 Labs to consider: Chem 7, Calcium, CK
 Morphine/hydromorphone as needed (may require high doses)
 Consider adding on IV Calcium or methocarbamol for cramping
 Equine-derived antivenin: Rapidly effective for symptoms, with small risk
of anaphylaxis/large risk of serum sickness. Consider in the very young, the
very old, the pregnant, significant autonomic dysfunction, pain refractory to
analgesics
 Loxosceles: Brown Recluse. Usually not found in California
o Classically cause “necrotic arachnidism”
o Initial bull’s eye lesion, 1-5cm, which then progresses to necrotic ulcer over
24-72 hours

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 o May take month or longer to heal with rare systemic symptoms
o Management: Only usual wound care has been shown to be effective, may
need referral to wound clinic or plastics clinic
 Tarantula: Imprecise name for many large spiders. Not toxic

Suggested Reading
 Hallam, et. al, Managing Frostbite. BMJ. 2010;341:c5864
 Luks, et. al. Wilderness Medicine Society Consensus Guidelines for the
Prevention and Treatment of Acute Altitude Illness. Wilderness and
Environmental Medicine. 2010; 21(2);146-155
 Mulcahy and Watts, Accidental Hypothermia: An Evidence Based Approach.
Emergency Medicine Practice. 2009; 11(1)
 Olson (Ed.). Poisoning & Drug Overdose, 5 Edition, 2007
th

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 Gastrointestinal Emergencies
By Margaret Salmon Res ed. Annemarie Sheets Faculty ed. John Stein

Acute Liver Failure and End-Stage Liver Disease

1. General approach
 Etiology: Most commonly due to alcoholic liver disease and viral hepatitis
o Chronic infection in 6-10 % of hepatitis B and 85% of Hepatitis C (70% of
these go on to develop chronic liver disease)
o Toxins: Amanita mushrooms, herbal remedies
o Idiosyncratic drug reactions: Acetaminophen, isoniazid
o Autoimmune disorders
o Metabolic: Wilson’s disease, hemachromatosis, acute fatty liver of
pregnancy, hereditary metabolic disorders
o Vascular disease: Budd Chiari, veno-occlusive disease
o Non alcoholic fatty liver disease (NAFLD)
 S/sx: Complications of advancing cirrhosis, portal hypertension and infection
o Hx: Anorexia, nausea, vomiting, fever, and abd pain, GIB, AMS, fatigue
o Exam: Jaundice, sallow complexion, palmar erythema, cutaneous spider
neve, parotid gland enlargement and testicular atrophy and gynecomastia.
Hepatomegaly with firmness or shrunken and grossly nodular (advanced
cirrhosis). Splenomegaly and ascites w/ portal hypertension.
 Mgmt
o Labs
 CBC with diff, complete metabolic panel with Ca, Mg, Phos
 Liver function tests AST, ALT, alkaline phos
 Hepatocyte synthetic function: Pt, PTT, INR and albumin
 Hepatocyte catabolic activity: direct and indirect bilirubin
 If fever: Lactate, 2x blood cultures, peritoneal fluid analysis
 If AMS: Ammonia + fever w/u
 Dispo: Assess admit criteria depending on presentation (see below)

2. Hepatic encephalopathy (HE)

 Etiology: 50 – 70% of patients with chronic liver disease have some AMS 2/2
hepatic encephalopathy with elevated ammonia levels
 S/sx: AMS
o Asterixis: a repetitive tonic-clonic wrist flexion elicited after forced wrist
hyperextension
 Mgmt
o HE is a clinical diagnosis. Ammonia levels do not correlate with extent of
AMS so not followed serially
o Other considerations: HE is a diagnosis of exclusion so look for the
precipitant cause. Rule out: SBP, traumatic SDH, hypoglycemia, Weinerke-
Korsakoff, hyper or hyponatremia, medication overdose, other infection or
volume depletion, sepsis, ARF, GIB
o Decrease ammonia load with lactulose 20 gm (30ml) PO or 300 ml PR
(diluted with 700cc of water or normal saline, retained for 30 min)
o Antibiotics such as neomycin and Riaximin are not routinely given in the ED
o Treat underlying/precipitant cause
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 o Cerebral edema in 75-80% of patients with grade IV HE  order non-
contrast head CT for Stage IV and consider it for Stage III
 HE Staging
o I: General apathy
o II: Lethargy, drowsiness, variable orientation, asterixis
o III: Stupor with hyper-reflexia, extensor plantar reflexes, tremor, aggressive
o IV: Coma, decerebrate posturing, dilated pupils
 Dispo: All pts with HE do not necessarily need to be admitted
o If on pre-transplant list, touch base with pre-transplant LTU, discuss dispo
o If post-transplant see “Post- transplant presentation.” If HE 2/2 acute hepatic
failure or patients with known ESLD presenting with stage III or IV
encephalopathy, then admit
o If new liver failure with HE, admit

3. Ascites / Spontaneous bacterial peritonitis

 Etiology: Ascites primarily due to splanchnic vasodilation, portal hypertension,
decreased serum oncotic pressure
o Risk factors for SBP: low protein ascites, T-bili >2.5mg/dl, GI bleed, UTI,
recent catheterization, previous SBP
 S/sx: Compromised respiratory function and/or abdominal discomfort 2/2
distention
o SBP: Fever in only 70%, abdominal pain <60%, encephalopathy 50%,10%
asymptomatic  low threshold for diagnostic paracentesis in ED
 Mgmt
o Check coags and platelets. If INR < 1.5, no significant thrombocytopenia, no
evidence of DIC, may do a therapeutic paracentesis. If elevated INR/low
platelets, d/w LTU or admitting team, may consider diagnostic paracentesis
only (using 20G syringe, remove 30 ml).
 Ultrasound guided has a high success rate, but no studies to date compare
the safety with blind paracentesis
 Do not remove more than 5 L, controversial how much/when albumin should
be replaced
o Body fluid labs: Albumin, total protein, cell count, gram stain, cultures, LDH
o Serum labs: total protein, LDH, blood cx
3
o Diagnosis of SBP: PMN>250/mm or WBC>1000/ml
 Positive gram stain in 5-20%, useful to rule in perforated bowel if
polymicrobial
o Abx: Ceftriaxone 1 gm IV
o Volume: given risk for hepato-renal syndrome, may need to resuscitate w/
albumin 25% 1.5 grams/kg up to 100 grams (usually given by admitting team).
 Dispo: All patients with ascites who present with fever and/or +diagnostic tap
need to be admitted

4. Gastroesophageal varices and hemorrhage

 Etiology: Varices 2/2 portal hypertension, leading to venous dilation in areas
with low venous pressures  collateral vessel formation in esophagus, stomach
o Esophagus prone to bleeding 2/2 superficial location, lack of supporting
connective tissue
 S/sx

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 o Hematemesis (“coffee-ground”), melena, or BRBPR (if brisk bleeding) in pts
with ESLD or possible liver dz (e.g. chronic alcoholic)
o Vague symptoms: Lightheadedness, generalized weakness or fatigue
o Caution: Vital sign abnormalities may be masked by co-morbidities and
meds (e.g. baseline hypotension 2/2 decreased intravascular oncotic pressure,
absence of reflex tachycardia 2/2 beta-blockers)
 Mgmt
o Massive bleed
 ABCD, IV, O2, monitor. Need two large bore (14-18 G) IVs, place NG tube
 Send cbc, coags, chemistries, lfts, type and cross
 Transfuse pRBCs, consider FFP and vitamin K if INR >2.0; Goal Hct >25,
platelets >50, INR<1.5. Consider activating “massive transfusion protocol” if
requiring >6 units pRBC with massive bleeding
 Consider DDAVP 0.3 mcg/kg IV q 12 hr 2x doses if platelets <50 (usually
not given in the ED)
 Octreotide 50 ug IV bolus, then 50 ug/h gtt
 Protonix 80 mg IV, then 8 mg/h gtt
 Ceftriaxone 2 g IV
 Early intubation if hemodynamic instability or altered mental status
 At SFGH, notify ICU, GI, IR and general surgery
 At UCSF, notify ICU and GI for endoscopy
 Consider Sengstaken-Blakemore tube if acute life-threatening bleeding from
esophageal or gastric varices when endoscopic hemostasis and
vasoconstrictor therapy are unavailable or not working. Located in ICUs at
Moffitt, in pixis room next to Trauma 1 at SFGH

o Minor bleed
 ABCD, IV, O2, monitor. Need two large bore (14-18 G) IVs, place NG tube
 Send cbc, coags, chemistries, type and screen
 Admit to MOD
 Dispo: Admit to ICU if requiring hemodynamic monitoring, transfusion,
emergent endoscopy, sclerotherapy, or banding. Otherwise admit if evidence of
bleeding for observation and serial blood draws

5. Coagulopathy
 Etiology: decreased ability to synthesize coagulation factors 2/2 liver failure
o GI tract is the most common site of bleeding
 Mgmt
o Send cbc, coags, chemistries, lfts, type and screen (cross if drop in Hct)
o Give vitamin K (PO if asymptomatic, IV if actively bleeding; see Hematology
chapter for dosing)

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 o Prophylactic administration of FFP is usually not recommended: May
interfere with assessments of liver function, may worsen cerebral edema
o Despite coagulopathy, ESLD pts are at high risk for thrombosis

6. Hepatorenal syndrome
 Etiology: ARF in preexisting chronic or acute hepatic failure w/ histologically
normal kidneys. Usually seen in pre-transplant patients (renal function often
recovers after liver transplantation). Renal failure in the cirrhotic patient is a
marker of extreme morbidity
 S/sx
o Type 1: Often 2/2 SBP; rapid rise in creatinine and decreased UOP. Median
survival < 1 month
o Type 2: Slower progression and less severe renal impairment
 Mgmt
o Labs: CBC, chemistries, lfts, coags, ua/ucx
o Review hx and list of medications. Look for reversible causes e.g.
intravascular volume depletion (prerenal azotemia), intrinsic renal disease
(drug induce interstitial nephritis), post renal obstruction or infection
o Ultrasound the bladder to r/o retention and kidneys to r/o obstructive
hydronephrosis
o If on transplant list, notify LTU. If not or if at SFGH, admit to MOD.
o Midodrine (oral alpha 1 agonist) and albumin 25% (usually ordered by the
admitting team)
o Blood urea nitrogen (BUN) concentration may not be sensitive to assess
renal function 2/2 decreased hepatic production of urea
 Dispo: Admit all new acute renal failure in setting of liver disease

7. Post TIPS complications

 Etiology: TIPS shunts blood away from liver to decrease portal htn, but also
further decreases liver detoxification. TIPS shunt may also malfunction or
thrombose
 S/sx: Worsening hepatic encephalopathy. Volume overload and/or
esophageal variceal bleed due to TIPS malfunction or thrombosis
 Mgmt
o CBC, chemistries, lfts, coags
o Resuscitate as above if e/o variceal bleed
o Ultrasound with doppler: Specify “evaluate recent TIPS, ensure patency and
good flow”
o Notify and discuss mgmt with service that did procedure
 Dispo: If unstable or evidence of infection admit. All others, d/w LTU or GI
team who did the procedure

8. Fulminate hepatic failure: Rapid, severe, and acute liver injury with impaired
synthetic function and encephalopathy in pts with normal liver or well
compensated liver disease
 Etiology: Acetaminophen, viral hepatitis (esp. hepatitis B), other toxins
(Amanita) – see “General approach” for full ddx
 S/sx: AMS 2/2 HE, coagulopathy, hypoglycemia and/or or markedly elevated
bilirubin
 Mgmt
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 o CBC, chemistries, lfts, coags, fibrinogen, t&c, viral hepatitis panel, APAP
level, iron levels
 R/o acetaminophen toxicity! If suspect ingestion, call poison control, draw
an APAP level at presentation and at 4 hours (from ingestion or from
presentation if unknown), start emperic NAC140 mg/kg PO or 150 mg/kg IV
(can stop later if APAP negative). Get time of ingestion and consider charcoal
if < 1 hr (see Toxicology chapter for more details)
 R/o Amanita phalloides mushroom poisoning. Call poison control, get time
of ingestion and consider charcoal if < 1 hr
 Consider viral etiology
o Consider non-con head CT if AMS: Cerebral edema in 75 -80% with grade
IV encephalopathy. Watch for signs of elevated ICP e.g. systemic
hypertension, bradycardia, and irregular respirations (Cushing's triad)
 Mannitol IV 1-2 gram/kg if increased ICP 2/2 cerebral edema
o Monitor for ARF which complicates acute liver failure in 30-50%
o Correct metabolic disturbances e.g. hypophosphatemia and hypoglycemia.
Alkalosis > acidosis in early stages of acute liver failure, often 2/2 mixed
respiratory and metabolic abnormality
o Pulmonary edema and pulmonary infections in 30%. Consider intubation in
respiratory distress but caution as high PEEP can worsen cerebral edema
o Call the Moffitt LTU service for consideration for liver transplantation
 Dispo: Admit to ICU (Moffitt for possible liver transplant)

9. Post-transplant presentation
 Etiology: Depends on the immediate operative course/complications. Consider
graft failure, infection, drug toxicities and ARF. GVHD is low on differential
 Mgmt
o CBC, chemistries, lfts, coags
o Abdominal ultrasound with doppler to evaluate graft for patency and flow
o Don’t order drug levels unless specifically requested by LTU as they need to
be drawn in early am before daily dosing. Levels are expensive and don’t help
with management
o Notify and involve post-transplant LTU in mgmt (they may have more lab or
imaging requests)
o Check medical record for operative course and complications

10. Vascular complications of the liver

 Portal vein thrombosis: 2/2 trauma, sepsis, pancreatitis, hypercoagulability.
Diagnosed by angiography
 Hepatic vein thrombosis (Budd-Chiari): Abdominal pain, hepatomegaly,
ascites. Diagnosed by doppler ultrasound
 Non-thrombotic veno-occlusive disease: pain after taking “medicinal tea,”
chemotherapy, or BMT. Diagnosed by doppler ultrasound

Surgical Abdomen
1. Acute mesenteric ischemia
 Etiology: Intestinal hypoperfusion
o SMA embolism (50%): Older pt with valvular disease, dysrhythmias, CHF,
recent MI, beta-blocker or digoxin use
o SMA thrombus (15-25%): Atherosclerotic disease
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 o Mesenteric venous thrombus (5%): Hypercoag states, prior DVT / PE, portal
HTN, abdominal infections, blunt abdominal trauma, pancreatitis, splenectomy,
malignancy in portal area
o Non-occlusive ischemia (20-30%): Post-operative, especially HD patients,
atherosclerotic disease, low-flow states, cocaine - 25% will have no pain or GI
bleeding
 S/sx: Findings neither sensitive nor specific
o Classic: Abd pain out of proportion to exam, pain with soft abdomen, or post-
prandial pain
o Chronic mesenteric ischemia (intestinal angina) may be constant or episodic,
consider in pts w/ mesenteric atherosclerotic disease
 Mgmt
o CBC, chemistries including Ca, Mg, Phos, VBG with lactate (usually
elevated, but normal does not r/o)
o Fluid resuscitate 0.9% NS, and keep NPO
o NG tube for decompression
o Early surgical consult if high index of suspicion
o Consider r/o AAA with bedside ultrasound
o KUB limited, useful only if e/o immediate free air. Classic “thumb printing
shows” in only <20%
o CT abdomen with angiography: Test of choice, sensitivity >95%. Look for
free air, dilated bowel, thickened wall, fat stranding
o Abx: Zosyn 4.5 gm IV (UCSF) or Ertapenem 1 gram IV (SFGH)
o Consider heparin if no contraindications but only after surgery consult (in
case going to OR)
o Avoid digoxin and vasopressors if possible as this will increase the ischemia
 Dispo: Admit to surgery. Consider ICU given ~50% mortality if diagnosed
within 24 hrs and >70% if diagnosis delayed. Patients will either receive
anticoagulation or go to OR for exploratory laparotomy vs. bowel resection

2. Small bowel obstruction (SBO)

 Etiology: Adhesions, mass/malignancy, volvulus, or incarcerated hernia
 S/sx: Abd pain or distention, decreased stool
 Mgmt
o CBC, lytes, coags, lactate, LFTs, lipase
o NG tube on suction for bowel decompression, NPO
o Fluid resuscitation
o Antiemetics (e.g. Zofran for nausea / vomiting
o Exam and palpate for hernia. If hernia is present and no pain at the site,
attempt to reduce it
o May consider abdominal series, looking for free air and air-fluid levels, but
usually need CT abdomen which has higher sensitivity and specificity, identify
anatomy, and can detect other pathology
o Surgery consult
 Dispo: Admit to surgery for bowel rest on NG tube, observation

3. Biliary disease
 Most common diagnosis in ED patients with abdominal pain > 50 years
 Etiology

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 o Stones: Most commonly 2/2 precipitation of cholesterol monohydrate crystals
due to imbalance of cholesterol: bile salt ratio and/or due to stasis (fasting pts,
diabetes, pregnancy, OCP use). Others include pigment stones (in hemolytic
anemia, cirrhosis, biliary tract infections) or mixed stones
o Infection: May be 2/2 obstruction due to stone, or may be caused by biliary
stasis in trauma or debilitated pts (acalculous cholecystitis)
 S/sx: RUQ/epigastric pain
o Biliary colic/acute cholecystitis: Postprandial upper abdominal pain that
radiates to the upper back. Murphy’s sign on palpation or ultrasound may be
elicited. ±Fever, nausea/vomiting with acute cholecystitis, may be difficult to
differentiate b/w biliary colic and cholecystitis
o Choledocholithiasis: Stone in common bile duct. Jaundice, ?clay-colored
stools, elevated direct bili, elevated alk phos. May be associated with gallstone
pancreatitis
o Cholangitis: Infection of the biliary tree
 Charcot’s triad: Jaundice (80%), fever (95%), abdominal pain (90%)
 Reynold’s pentad: Charcot’s triad + shock and AMS
 Management
o CBC, lytes, LFTs, lipase. Bcx if febrile/suspect infection
o NPO; NS bolus if needed, then maintenance; analgesia
o Bedside US: Look for stones, pericholecystic fluid, thickened gallbladder wall
or dilated common bile duct
o Formal US: >98% sensitive for stones. May be requested by surgery,
consider if bedside US unclear or for confirmation
 Formal hrs: UCSF 8am to 7:30pm M-S, SFGH 7:30am to 5pm M-S
o Consult surgery if evaluation c/w possible cholecystitis; admit to medicine for
GI evaluation if concern for choledocholithiasis/cholangitis
o If evidence of acute cholecystitis/cholangitis, start abx: Zosyn 4.5g IV at
UCSF or Ertapenem 1gram IV at SFGH
 Dispo: Admit to surgery unless pain is under control, pt is afebrile, and no
evidence of obstruction/cholecystitis on labs or scan. If d/c’ed, f/u in surgery
clinic

4. Appendicitis
 Etiology: Obstruction of appendix lumen with fecolith or other material causing
inflammation, ischemia  necrosis and suppuration
 S/sx: RLQ pain, pain migration from epigastric or periumbilical  RLQ, abd
wall rigidity, pain before vomiting, and positive psoas sign. Anorexia is not a
useful symptom
 Mgmt
o CBC, chemistries (consider lft/lipase to r/o biliary dz, ua)
o IV fluid bolus, then maintenance
o Analgesia
o If young male pt w/ classical sx, consult general surgery w/o imaging
o CT abdomen preferred in adults and non-pregnant women. Order US in
pediatric patients and pregnant women.
o Zosyn 4.5 gram IV (UCSF) or Ertapenem 1gram (SFGH) IV
 Dispo: Admit if e/o appendicitis. If suspicious, but well-appearing and benign
exam, consider D/C home with abdominal exam in 12-24 hours in ED

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 Non-Surgical Abdomen
1. Acute pancreatitis
 Etiology: EtOH and gallstones most common in US (80%). Also consider
ARVs, steroids, sulfa, thiazide / loop diuretics, trauma, pancreatic mass
 S/sx: Epigastric pain, may be generalized, may radiate to back. Associated
with nausea and vomiting
 Mgmt
o CBC, lytes, LFTs, lipase, Ca, Mg, Phos, Serum LDH (for Ranson’s criteria)
 Ranson’s criteria at admission: Age >55, WBC >16k, glucose >200 mg/dL,
AST >250, LDH >350
o NPO w/ IV fluids
o Analgesia
o Antiemetics
o Consider Foley to monitor I&Os
o Bedside U/S to eval for stones and CBD dilation
o Consider CT abdomen “pancreatic protocol” to eval for necrosis,
hemorrhage, cysts
 Dispo: Consider ICU if unstable. Admit to medicine. If obstructive pancreatitis,
consult GI for possible MRCP or ERCP. Consider surgery consult if gallstone
pancreatitis

2. Diverticulitis
 Etiology: Acute inflammation of the diverticula
 S/sx: LLQ pain and tenderness
o 20% of patients have no abdominal tenderness
o Older, HIV+, and immunocompromised patients are at increased risk for
perforation
 Mgmt
o CBC, lytes, LFTs, stool guaiac
o CT abdomen with IV contrast
o NPO w/ IV fluids, analgesia
o If febrile / ill-appearing, give zosyn or cipro + flagyl
 Dispo
o Admit if unable to take PO, multiple co-morbidities, extensive fat stranding,
free air, or large areas of inflamed colon
o Otherwise D/C home with clear liquid diet which can be advanced after 2-3
days if improving
o Give strict precautions: Return if ↑ pain, fever, or unable to tolerate PO
 Approx. 25% of patients diagnosis with diverticulitis for the first time with have
complicated diverticulitis (perforation, obstruction, abscess, or fistula). Nearly all
complicated cases will require surgery

Other GI complaints
1. Diarrhea
 Definitions
o Acute (<14 days): viral, tox, traveler’s diarrhea
o Persistent (>14 days): consider parasites, bacteria, HIV-related illness,
meds, allergies, systemic disease (DM)
o Chronic(>30 days): food allergies, radiation enteritis, malabsorption,
inflammatory bowel disease
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 Etiology: Loose or frequent stools due to increased water content, stool
content, or gut motility. Most community or traveler’s diarrhea associated with
salmonella, shigella, campylobacter, E coli O157:H7
o Infectious
 Viral gastroenteritis e.g. Norwalk, rotavirus in day care
 Bacterial: Campylobacter, Clostridium perfringens, E coli O157:H7, ETEC,
Salmonella, Shigella, Staph aureus, Vibrio
 Other: Giardia, Cyclospora, Cryptosporidium
o Inflammatory: Crohn’s, ulcerative colitis; appendicitis
o Malabsorption: Celiac disease, lactose intolerance
o Vascular: Ischemic bowel disease
o Tox/Meds: Antibiotics (consider C diff), chemo/radiation, htn meds
o Functional: Irritable bowel syndrome, fecal impaction, obstruction
o Other: Food allergies, colon cancer, hyperthyroidism
 S/sx: loose or frequent stools, nausea/vomiting, ±fever/chills, signs of
hypovolemia
o Evaluate duration of symptoms, quality/quantity/frequency of stools, travel
hx, occupation, day care exposure, recent diet (raw/undercooked meat or
seafood, milk), sick contacts, sexual contacts, new meds
o Red flags: Severe dehydration, bloody or febrile diarrhea; Diarrhea in infants,
elderly, or immunocompromised pts
 Mgmt
o Hydration: PO if tolerated, IV if severe
 Oral rehydration solution: 6 tsp sugar, ½ tsp salt, 1L water
o Supportive care
 Small frequent meals. No evidence-based data to suggest BRAT diet
(Banana, Rice, Apple sauce, Toast) is better than normal diet
 Antimotility: e.g. Immodium, Bismuth: Symptom relief for non-bloody, non-
inflammatory diarrhea in non-immunocompromised, afebrile pts. Avoid in pts
with inflammatory pathogens (delayed clearance of pathogens  risk of toxic
megacolon)
 Abx: Bactrim (in peds), ciprofloxacin, or levofloxacin x5 days may
decrease course by 1-2 days in traveler’s diarrhea, shigella, Campylobacter.
Avoid in EHEC 2/2 increased risk of hemolytic uremic syndrome, and in
salmonella due to increased risk of carrier state. Metronidazole x7-10 days if
suspect Giardia or x10 days C. difficile
o Limit testing
 No test for toxogenic diarrhea
 Consider CBC and electrolytes if ill-appearing, febrile, severe abdominal
pain, bloody diarrhea (r/o HUS, look for eosinophilia) ; lower threshold for labs
if immunocompromised, elderly, infants/pediatric
 Stool cx if fever, bloody diarrhea, diarrhea >7 days, suspect possible
outbreak (salmonella, shigella, campylobacter, E coli O157:H7). Overall low
yield – positive in 1.5-5.6% cases
 Stool ova and parasites: consider if diarrhea >14 days,
immunocompromised, or those unresponsive to abx, suspected outbreak,
recent travel to foreign countries/wilderness
 Fecal WBC neither sensitive (42%) nor specific (63%), but may suggest
inflammatory if consistent with hx
 Fecal lactoferrin: Sensitivity 66%, Specificity 75% for inflammatory diarrhea

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  C diff: test only if >1 yo, passage of ≥3 unformed stool in ≤24 consecutive
hours and recent abx exposure (96% have abx use within 14 days). Very
sensitive. Do NOT repeat test if prior hx of C diff as test may be positive for
weeks, or if recent negative test (1.7% gain if test repeated within 7 days)
o Immunocompromised: consider crypto, microsporidium, MAC, lymphoma,
Kaposi sarcoma
o Reportable diseases
 Within 1 hr: Cholera, scromboid, E coli O157:H7, hemolytic uremic
syndrome, shiga toxin, other suspected foodborne illness or outbreaks
 Within 1 working day via fax or phone: Campylobacter, Cryptosporidium,
listeria, Salmonella, Shigella, Typhoid fever, Vibrio, Yersinia
 Dispo
o Most can be d/c’ed if able to tolerate PO, afebrile, VS normal. Usually
diarrhea is self-limited even without meds
o Consider admit if immunocompromised (and need for further w/u), ill-
appearing with abnormal vital signs despite hydration
o Consider referral for colonoscopy if rectal bleeding, persistent diarrhea, or to
r/o colon ca in elderly

4. Perianal diseases
 Etiology: Infected anal crypt glands. Pilonidal cysts are due to infected hair
follicles near the gluteal cleft
 S/sx: Anal pain, ±pain with defecation, possible fever/malaise. Pus drainage if
spontaneously draining
 Mgmt
o Distinguish perianal (in the perianal skin) vs. perirectal abscess (through the
sphincter). In general, perianal abscesses should be drained in the ED with
local anesthesia, while perirectal abscess requires surgery consult and
drainage in OR
o Frequent sitz bath to keep wound clean after drainage
o Consider abscess culture if hx of multiple abscesses requiring multiple
courses of antibiotics, diabetes, immunosuppression
 Dispo
o Perianal abscesses may be d/c’ed home after I&D, plan f/u in wound clinic
(SFGH) or with PMD/urgent care in 2 days
o Most do not need antibiotics after I&D; consider abx if diabetes,
immunosuppression
o Consult surgery for mgmt of perirectal abscess

Suggested reading
 Burg MD, Hovanessian H. Diarrhea: Identifying Serious Illness And Providing
Relief. Emergency Medicine Practice 2005; 6(7):

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 Gynecological emergencies/Sexually transmitted infections
By Bory Kea Res ed. Susan Brim Faculty ed. Susan Promes

General
1. Approach to abdominal pain with possible gynecologic etiology
 History
o Sexual history
o Vaginal discharge/bleeding
o Last menstrual pain
o Lower abdominal pain or pain radiating to lower back suggests possible gyn
etiology
 Physical exam
o General abdominal exam, CVAT, RUQ
o Pelvic
 External: Lesions, visible discharge
 Speculum: Vaginal vault, cervix
 Bimanual: CMT, ovaries, check for palpable mass
 Consider US depending on indication
 Order a pregnancy test on any woman of child-bearing age

STI: Sexually Transmitted Infections

1. General tips
 Most up-to-date resources regarding STIs: http://www.cdc.gov/std/treatment
 For therapy in pregnancy patients, consult Lexicomp or d/w gyn

2. Bacterial vaginosis – polymicrobial

 Sx: White/gray discharge with fishy odor
 Dx: Need at least 3 or 4 clinical criteria
o Homogeneous, thin, white discharge that smoothly coats the vaginal walls
o Presence of clue cells on micro, pH of vaginal fluid >4.5
o Positive whiff test
o Gram stain
 Mgmt
o Metronidazole 500 mg PO BID x 7 days (Tell patient to avoid ETOH)
o Clindamycin 300 mg PO BID x 7 days
o Intravaginal gel, creams, and ovules
o Partner treatment: No
o Treatment during pregnancy mandatory to decrease rate of PROM

3. Trichomoniasis vaginalis
 Sx
o Men: Asymptomatic or non-Gonococcal urethritis
o Women: Diffuse, malodorous, yellow-green vaginal discharge with vulvar
irritation,“strawberry cervix”, friable cervix
 Dx
o Wet Mount: Sensitivity 60%–70%

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 o OSOM Trichomonas Rapid Test or Affirm™ VP III: Sensitivity >83% and a
specificity >97%
 Mgmt
o Metronidazole 2 g PO x 1 OR 500 mg BID x 7days (Tell patient to avoid
ETOH)
o Tinidazole 2 g PO x 1
o Partner treatment: Yes
o Avoid sex until therapy complete AND asymptomatic

4. Vulvovaginal candidiasis
 Epidemiology: 75% of women at least 1 episode, 40% with >1 episode
 Sx: Pruritus, vaginal soreness, dyspareunia, external dysuria, and abnormal
vaginal discharge
 Dx: Clinically by signs/symptoms
o Exam: Vulvar edema, fissures, excoriations, or thick curdy vaginal discharge
o Wet mount: Saline, 10% KOH or Gram stain yeast or pseudohyphae
(spaghetti and meatballs appearance)
o Lab testing: Culture or other test positive for a yeast species
o Classification
 Uncomplicated
 Sporadic or infrequent VVC, AND
 Mild-to-moderate VVC, AND
 Likely to be C. albicans, AND
 Non-immunocompromised women
 Complicated
 Recurrent VVC, OR
 Severe VVC, OR
 Non-albicans candidiasis, OR
*Note: In patients with recurrent or severe candidiasis, consider DM or
immunosuppression and check glucose/CBC, may need six months
suppressive therapy with fluconazole
 Mgmt
o Fluconazole 150mg PO x 1
o Intravaginal treatments: Over the counter treatments such as Clotrimazole
or Monistat
o Partner treatment: N/A

5. Chlamydia trachomatis
 Epidemiology: Over 1.2 million incidence reported per year
 Sx: Dysuria, discharge
o Women: 80%-90% HAVE NO SYMPTOMS
o Men: 25% HAVE NO SYMPTOMS
 Dx: Urine, endocervix, vagina or rectal
 Mgmt
o Azithromycin 1 gm PO x 1
o Doxycycline 100 mg PO BID 7 days
o Erythromycin base 500 mg PO QID x 7 days
o Partner treatment: Seek evaluation; if not, antibiotics for partner
o Avoid sex x 7 days
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 o Re-test: 3 mo
 Complications: PID and infertility

6. Neisseria gonorrhea
 Epidemiology
o Women: UP TO 80% HAVE NO SYMPTOMS
o Men: Usually symptomatic
 Sx
o Localized: Cervicitis or urethritis with discharge
o Disseminated
 Skin: Petechial or pustular acral lesions
 Joint: Asymmetrical arthralgia, tenosynovitis, or septic arthritis
 Rare: Perihepatitis, endocarditis or meningitis
 Dx
o Gram stain: Intracellular Gram-negative diplococcic
o Culture, nucleic acid hybridization tests, and NAAT
o Swab all sites for disseminated
 Mgmt
o Genital and pharyngeal
 Ceftriaxone 250 mg IM x 1 OR
 Cefpodoxime or cefixime 400 mg po x 1, but poor pharyngeal penetration
o Disseminated – admit
 Ceftriaxone 1gm IV/IM q 24h PLUS treatment for chlamydia
o Quinolones NOT recommended given high resistance in California
o Partner treatment: Seek evaluation; if not, antibiotics

7. Pelvic Inflammatory Disease

 Epidemiology: In the USA 750,000 women experience an episode of acute
PID each year.
 Sx: abdominal pain, vaginal discharge, nausea/vomiting, fever
 Dx: CDC definition: No other cause for illness other than PID AND CMT OR
adnexal tenderness OR uterine tenderness
o To increase specificity, include the following criteria
 T>101°F (>38.3°C)
 Mucopurulent discharge
 High quantity of WBC on wet mount
 Elevated ESR or CRP
 Positive cervical discharge culture with: N. gonorrhoeae or C. trachomatis
 Mgmt
o Outpatient
 Ceftriaxone 250 mg IM x 1 OR
 Cefoxitin 2 g IM with probenecid 1 g PO x 1 OR
 Other injectable 3rd generation cephalosporin
 Plus doxycycline 100 mg PO BID x 14d
 For any of the above: can also add Metronidazole 500 mg PO BID x 14 d
 Indications for admission:
o Surgical emergency cannot be excluded
o Tubo-ovarian abscess
o Pregnancy

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 o Severe illness (nausea, vomiting, high fever)
o Unable to follow or tolerate outpatient regimen (ie pediatric population)
o Failure to respond to outpatient therapy
 Complications
o Salpingitis/Tubo-ovarian abscess
o Fitz-Hugh Curtis: RUQ pain, jaundice with PID
o Ectopic pregnancy
o Infertility
 Special populations
o Intrauterine device
 Increase risk in the first 3 weeks of insertion, but afterwards believed to
protect against PID as forms a cervical mucus plug (Grimes 2000)
 Remove only if absolutely necessary, and in discussion with gynecology if
available as it’s expensive
o Pregnancy: Rare in this population—cervical mucus plug thought to be
protective

Table 1. Urogenital ulcers

Infection Bug # Tender Edge Base Lymph
nodes
Chancroid Haemophilus Many Marked Soft Dirty Tender,
ducreyi Fluctuant

Granuloma Klebsiella Many None Serpiginous Beefy red, Erosive

inguinale granulomatis white granulation lesions
Dono- tissue overlying
vanosis lymph
nodes
Painless
Lympho- Chlamydia One None Soft Eroded Tender
granuloma trachomatis, papule
venereum type L1, L2,
L3
Herpes Herpes Many Marked Soft Clean Tender
simplex virus
Syphilis Treponema One None or Indurated Clean Indolent
pallidum mild

8. Chancroid (Hemophilus ducreyi)

 Sx: Painful genital ulcer with regional lymphadenopathy
 Diganosis: Based on clinical presentation
o May diagnose without PCR testing if able to exclude syphilis and HSV
 Mgmt
o Azithromycin 1 gram PO x 1
o Ceftriaxone 250 mg IM x 1

9. Granuloma inguinale (Donavanosis)

 Epidemiology: Endemic in tropical and developing areas, rare in US

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  Sx: Painless erosive lesion overlying lymph nodes
 Dx: Donovan bodies seen on dark-staining of tissue crush preparation or
biopsy
 Mgmt: Doxycycline 100mg BID x 3 weeks or until lesions resolved

10. LGV: Lymphogranuloma venereum

 Epidemiology: Caused by Chlamydia trachomatis, L1, L2 or L3 serotype
 Sx: Painless ulcer, localized inguinal lymphadenopathy
 Dx: Culture, DIF, or nucleic acid detection
 Mgmt: Doxycycline 100mg PO BID x 3weeks
 Complications: Proctocolitis leading to chronic, colorectal fistulas and
strictures

11. Herpes
 Epidemiology: Two types but not exclusive to these locations, increasing
cross-over
o Type 1: Non-genital areas (eyes, ears, mouth)
o Type 2: Urogenital area
 Sx
o Primary infection
 More severe than recurrent infection
 Often accompanied by systemic symptoms (constitutional)
o Recurrences: Less frequent, less painful
o Severe HSV
 Hospitalization
 Disseminated infection
 Pneumonitis
 Hepatitis
 CNS complications
 Mgmt: HSV
o Episodic: Acyclovir 400 mg TID x7-10 days or Valacyclovir 1 gram PO BID
x7-10 days
o Suppressive: Acyclovir 500 mg PO BID, Valacyclovir 1 gram PO Daily
o Partner treatment: If with discordant partners, suppressive therapy
recommended
o Consistent condom use and avoidance of sexual activity during recurrences
 Special Populations
o Co-Infected with HIV
 Increased shedding
 Suppressive therapy may be useful, but no clear data
o Pregnancy
 No increased risk of birth defects during first trimester with treatment
(Stone, KM 2004)
 30-50% transmission if acquires HSV near time of delivery

12. HIV
 Epidemiology
o 1.2 million with HIV in US; 1 in 5 unaware of infection
o High incidence among men who have sex with men, African Americans
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 o Injection drug use, commercial sex workers also at risk
o Transmission from needlesticks: 0.32% parenteral, 0.09% mucocutaneous
 Sx
o Primary infection: Fever, painful mucosal ulcers, pharyngitis, nontender
lymphadenopathy, maculopapular rash, myalgias, headache, nausea,
anorexia, weight loss. Symptoms may last up to 1 wk, labs with lymphopenia,
thrombocytopenia
o Unexplained AMS
o Thrush
o Disseminated zoster
o Aseptic meningitis
o Opportunistic infections e.g. candidiasis, pcp, toxoplasmosis, Cryptococcus,
CMV
o New cytopenia without cause
o Kaposi’s sarcoma, B cell lymphoma, oral hairy leukoplakia
 Dx
o Screening in the ED
 Rapid HIV: >99% sensitive and specific, used at SFGH
 Standard testing: Enzyme immunoassay screen followed by western blot
confirmation for positive tests
 Consent: Document verbal consent on order form and in chart
 Mgmt
o New diagnosis
 UCSF: Rare as tests usually ordered on admitted patients. Enlist help from
social work
 SFGH: Page PHAST (Positive Health Access to HIV Services and
Treatment) service at 443-3892. For questions on HAART, page HIV consult
service at 443-4601
o Post exposure prophylaxis: Must start within 24 hours
 Call 415-353-7842 (UCSF) or 415-469-4411 (SFGH) to discuss with
needlestick hotline
 AIDS
o CD4: Ask patient, look in chart. If not available, estimate CD4 <20 if absolute
lymphocyte count <950. Helps predict susceptibility to opportunistic infections
 Early >500: Associated with bacterial pna, TB, herpes
 Late <200: Fungal infections, malignancies, toxoplasmosis
 Very late <50: MAC, CMV, histoplasmosis, CNS lymphoma, cryptococcus
o Viral load: Used to monitor therapy
o Opportunistic infections (OI)
 PCP: Most common OI
 Dry cough, dyspnea, fatigue, fever
 CXR with b/l infiltrates, elevated LDH
 Treat with high dose bactrim 5 mg/kg IV; Pentamidine if allergic
 Steroids if PaO2 <70, A-a gradient >35
 Prophylaxis: Bactrim 1 DS PO daily if CD4 <200 and to prevent reinfection
post PCP
 Cryptococcus: Rare if CD4 >100
 Insidious, fever, ha, nausea, ams
 LP: Increased OP, increased protein, WBC <20/mL, normal glucose. Can
send CSF or serum CrAg (Serum sensitive >95%)
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  Treat with amphotericin 0.7 mg/kg IV + flucytosine 25 mg/kg PO qid
 Prophylaxis: Fluconazole 100-200 mg/day if CD4 <50
 Toxoplasmosis: CD4 <100
 Most common cause of focal intracranial mass
 HA, N/V, seizures, focal neuro deficit, AMS
 CT/MRI: Ring enhancing lesions
 Treat with pyrimethamine 200 mg then 50-100mg/day PO + sulfadiazine
4-8 grams/day (100 mg/kg) PO + folinic acid 10 mg/day PO

13. Syphilis: Treponema pallidum

 Epidemiology: Virulent, highly motile, penetrates mucous membranes and
abrasions
 Sx
o Primary (6weeks, infectious): Painless chancre (localized disease)
o Secondary (6mo, highly infectious)
 Disseminated disease with constitutional symptoms
 Maculopapular rash
 Condyloma lata
o Tertiary (years later)
 Gummas
 Aortitis (infarct of vasovasorum)
 Neurosyphilis: Tabes dorsalis, altered mental status
 Argyll robertson pupil
o Congenital
 Early: HSM, hepatitis, pneumonia, rash, blood dyscrasia, cartilage
abnormalities, condyloma lata
 Late: Saddle nose, Hutchinson teeth, blindness, fetal malformation, and
sabre shins
o Latent: Lacking signs or symptoms, but positive serologic testing
 Dx
o Biopsy or direct microscopy on dark field
 Call lab medicine resident if between 8am-5m
o Serologic: RPR (more sensitive if lesion > 1 week)
o T. pallidum particle agglutination [TP-PA]
 Mgmt
o Adults: Benzathine Penicillin G 2.4 million units IM x 1
o Peds (Congenitial < 1 month old): Benzathine Penicillin G 50,000 units/kg
IM or admission for IV penicillin
o If allergic to penicillin, use tetracycline 500 mg PO qid x14 days (early) or
doxycycline 100 mg bid x28 days (late latent)
o Complications associated with treatment: Jarish Herxheimer phenomenon:
Patient develops a rash caused by a release of endotoxins during treatment as
bacteria dies causing an allergic appearing response

14. Expedited Partner Treatment (i.e. Rx for partner as well as patient)

 Permissible in 27 states currently, including California
 Decreases persistent or recurrent infections in women
 Cost-saving
 Data does not support use with men who have sex with men

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 Testing of Sexually Transmitted Infections
Test Sex Culture Source Instructions
SFGH: F Endocervical swab (Pink-BD ProbeTec) 1. Remove excess
Chlamydia mucous from the cervical
Gonorrhea os with the large-tip, swab
and discard
2. Insert the small-tip
UCSF: F swab into the cervical
Chlamydia canal and rotate for 15-
only 30secs
3. Withdraw swab-Avoid
contact with vaginal
mucosa
4. Break the shaft of swab
at the score mark
5. Tightly recap the tube
containing the swab
M Urethral (Blue-BD ProbeTec) 1. Insert the swab 2-4cm
into the urethra and rotate
for 15-30secs
2. Withdraw swab and
place the blue cap/swab
into transport tube
3. Tightly recap the tube.

UCSF: F Cervix (Culture Swab) 1. Insert swab in cervix

Gonorrhea and twirl gently for 3-5s.
Low 2. Place swab in charcoal
prevalence transport media

M Urethra (Culture Swab) 1. Insert swab and twirl

gently
2. Place swab in charcoal
transport media

SFGH: Both Urine (Yellow GenProbe) 1. No voiding 1hr prior to

Gonorrhea/ collection
Chlamydia 2. 20-30 mL of FIRST part
of stream into sterile cup
Both 3. Transfer into YELLOW
UCSF: Gen Probe collection tube
Chlamydia 4. Fill out SFDPH
only* requisition form
At UCSF, same except:
*Gonorrhea 1. 15-20ml into sterile cup
coming 2. Refrigerate until sent
soon in-house

143
HSV Both Ulcer (Culture swab) 1. Swab base of eroded
H.Ducreyi ulcer
2. Place in tube
3. Mark on requisition,
rule out H.ducryi or HSV

Tricho- F High vaginal (InPouch TV) 1. Collect sample from

monas high in the vaginal canal.
2. Twirl swab in (InPouch
TV) top portion of pouch
3. Do not break
connection into bottom
pouch
4. Roll Top of pouch twice
and fold yellow tabs over

Bacterial F Vaginal 1. Collect vaginal

Vaginosis discharge on cotton swab.
Yeast 2. Place swab in black top
specimen tube (without
charcoal)
3. Place 2-3 drops of NS
in specimen tube
Or
1. Smear vaginal
discharge on a glass slide
2. Place slide in urine
specimen container

Gynecologic Pain
1. Acute etiologies
 Physiologic dysmenorrhea: colicky lower abdominal pain related to the start
of menstrual cycle
o Mgmt: NSAIDS
 Ovarian Torsion: Enlarged ovary (usually secondary to large or multiple cysts)
twisting on itself, in women of childbearing age, threatening blood supply to
ovary and subsequent necrosis
o Epidemiology: Incidence of 7%, more common on the right
o Sx: Acute onset of unilateral pelvic pain, twisting/sharp sensation as torses,
nausea/vomiting
o Dx: Urine pregnancy test, CBC, Doppler pelvic US
o Mgmt
 2 large bore IVs
 Anti-emetics and analgesics
 Emergent Gyn consult
 Definitive treatment: Surgery
 Ovarian ruptured cyst: Rupture of a corpus luteum cyst usually pre-
menstrual. Must rule out appendicitis if on the right and normal US
o Cause: Mechanical, sexual activity
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 o Sx: Acute onset of pain
o Dx: Pelvic ultrasound showing minor free fluid near ovarian cyst, with a
negative b-hCG
o Mgmt: Pain control, does not cause significant hemorrhage
 Mittelschmerz: Mid-cycle lower abdominal pain thought due to the extrusion
of ova
o Sx: Pain may be acute and then subside within a few hours or last 2-3 days
o Dx: Mid cycle, normal pelvic exam, and negative b-hCG, and/or negative
ultrasound if prolonged pain

2. Chronic etiologies
 Endometriosis: Growth of endometrial tissue outside of the uterus, causing
cysts and adhesions in the pelvis
o Epidemiology: Approximately 30 years old
o Sx: Dysmenorrhea, dyspareunia in a cyclical fashion with hormonal surges
o Mgmt: Analgesics, follow-up with Gynecology or primary care doctor on
possible hormonal medications
o Complications: Infertility and occasional cyst rupture with severe bleeding
 Fibroids (leiomyomas): Benign tissue growth of the myometrium but can
grow large causing torsion or infarction of the tumor
o Epidemiology: 20-40% of women will be diagnosed with one, but only a
fraction requiring treatment
o Sx: Asymptomatic if small, but can cause heavy and painful periods,
dyspareunia, urinary frequency/urgency
o Dx: History of fibroids with similar pain, or exclusion of other diseases based
on history and exam, and ultrasound showing fibroid causing pain
o Mgmt: Analgesics, if suspect torsion or infarction, get US and Gyn consults;
if not, then outpatient follow-up with Gynecology
o Complications: Infertility, pre-mature labor, miscarriage
 Psychological: May occur post-trauma or of unclear etiology, usually
managed by gynecology and pain management

Vaginal Bleeding
1. Vaginal bleeding related to menses
 For vaginal bleeding in pregnancy, see obstetrics chapter
 Unstable: Resuscitate first, ask later
o 2 IVs, O2, monitors, T&C, Rh status, CBC, Upreg, bedside US
 History: Is the patient pregnant? LMP? Perimenopausal? How many pads per
hour or in 24hr period?
 Exam: Pelvic exam unless patient greater than 20 weeks to locate placenta.
See obstetrics chapter if pregnant. Determine source of bleeding: vulva, vaginal,
cervical or above the os. Clots or profuse bleeding
 Differential
o Period associated bleeding: Menorrhagia, abnormally heavy and/or
prolonged periods
o Dysfunctional uterine bleeding: Heavy period without clear etiology may be
due to hormonal imbalance. Diagnosis of exclusion
 Mgmt: Medroxygprogesterone (Provera) 10mg PO daily for 10 days

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  Refer to primary care doctor or gynecology, may need endometrial biopsy or
US to rule out malignancy

2. Bleeding unrelated to pregnancy or periods

 Differential
o Trauma: May be occult, thorough exam and history, repair
o Post-operative: Bleeding after gynecology procedure. Resuscitate and
consult
o OCP issues: May cause breakthrough bleeding, or hormonal imbalance
o Cervical polyp/cancer: 90% are squamous cell carcinomas. Bleeding occur
post-coital or metorrhagia (intermenstrual bleeding), exam showing ulcers,
nodules, or friable tissue.
o Uterine carcinoma: An adenocarcinoma presenting in post-menopausal
women, with heavy and frequent vaginal bleeding with a normal physical exam
o Other: Thrombocytopenia, anti-coagulation disorders or drugs
 Dx: CBC, pregnancy test if less than 60yo, type and screen if only minor
bleeding, type and cross if heavy bleeding (more than 1 pad per hour for 4 hrs)

146
 Ear/Nose/Throat and Dental Emergencies
By Hangyul Chung-Esaki, Deepa Res ed. Swati Singh Faculty ed. Guy Shochat
Ravikumar, Kristin Kuzma

Ear
1. Foreign body
 Presentation: May be asymptomatic or c/o pain, discharge, decreased
hearing, fullness, nausea/vomiting
 Ddx: Impacted cerumen, otitis externa, TM perf, hematoma, tumor
 Mgmt
o Insects should be killed prior to removal with 1% lidocaine or mineral oil
o Try removal of inorganic objects with irrigation, suction, wire loop, curette,
right angle hook, or alligator forceps depending on object
o Caution with button battery or vegetable matter – do NOT use irrigation
(battery may cause liquefaction necrosis, vegetable matter will swell)
o Superglue method: Apply glue to blunt end of cotton swab, hold still for 60
sec, remove object
 Tips
o Consider procedural sedation
o Consider ENT consult or even delayed removal by ENT if anticipate
difficulty/complications or TM perforation
 Disposition: F/u with PCP in 1wk, return if persistent discharge, bleeding, pain
 Complications: Perforated TM, ossicle disruption, external auditory canal injury

2. Hearing Loss
 Presentation: Acute vs. gradual, assoc sx (tinnitus, vertigo, neuro sx)
 Diagnosis: Check TMs, neuro exam
o Rinne: Comparison of air vs. bony conduction
 Conductive hearing loss: Bone > air (negative)
 Normal/sensorineural hearing loss: Air > bone (positive)
o Weber: Put tuning fork in mid-forehead
 Unilateral conductive hearing loss: Loudest in affected ear
 Unilateral sensorineural hearing loss: Loudest in unaffected ear
o Modified Weber w/o tuning fork: Ask pt to hum
 Conductive hearing loss: Lateralize to affected ear
 Sensorineural hearing loss: Louder in unaffected ear
 Ddx: Infectious (viral, bacterial meningitis), vascular (stroke), metabolic,
conductive (FB, otitis, trauma), neoplasm, meds, trauma (temporal bone fx)

3. Impacted cerumen
 Presentation: Hearing loss, otalgia, fullness, itching
 Mgmt: Remove cerumen only if symptomatic or interfering with exam
o Cerumenolytics: Use if no infx, perf, or otologic surgery. Use Mineral oil or
Hydrogen peroxide, Docusate, Cerumenex 2-3x for 3-5 days. A good
strategy when hard cerumen is present!
o Irrigation: Use warm NS or water diluted 1:10 Hydrogen peroxide
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  CI: Unilateral deafness, perforated TM, chronic middle ear infection,
previous surgery to middle ear, previous pain with irrigation
o Curette and suction: Only under direct visualization
 Disposition: D/C home, advise mineral oil 10-20 min/wk for prevention.
Consider ENT referral if severe pain, chronic impaction, unable to remove,
pus/necrosis

4. Vertigo: see general approach to vertigo in high risk CC chapter

 DDx: BPPV, labyrinthitis, labyrinthine infarction/ischemia, vestibular neuritis,
meniere’s dz central causes of vertigo (consider MRI/CT to evaluate posterior
circulation)
 Peripheral vertigo overview
o Spontaneous vestibular nystagmus: Unilateral, horizontal, suppressed with
visual fixation
o Positive head thrust test: Inability to maintain visual fixation with rapid
rotation of head 15 degrees
o Gait appears “unstable” but able to ambulate
o Symptomatic supportive therapy: Antiemetics (Zofran), antihistamines
(Meclizine, Benadryl, Dramamine), benzodiazepines (Valium/Ativan),
anticholinergics (Scopolamine)
 BPPV
o Diagnosis: Dix hallpike
o Mgmt: Epley maneuver (perform slowly for less patient discomfort and
nausea), supportive
 Labyrinthitis: Inflammation of inner ear, mostly viral after uri
o Mgmt: Hydration, supportive. Steroids (Prednisone 60 mg x5 days with 5
day taper). Acyclovir in HSV, abx in bacterial labyrinthitis
 Meniere’s dz: “Endolymphatic hydrops” with fluid build up
o Presentation: Fluctuating sensorineural hearing loss, aural fullness, nausea
o Mgmt: Treat symptoms. Possible diuretics. Outpt ENT referral
5. Otitis externa – see Infectious Disease chapter

6. Otitis media – see Infectious Disease chapter

7. Perichondritis
 Due to trauma (e.g. piercing) or severe otitis externa spreading to auricular
cartilage, usually strep or staph, pseudomonas (recent piercing)
 Presentation: Local pain +/- purulent drainage, ?cartilage deformity with
edema and erythema along pinna
 Ddx: Consider auricular cellulitis, relapsing polychondritis (autoimmune,
involves cartilage of respiratory tract and aorta, cartilage lacking in ear)
 Mgmt: Eliminate foreign body, drain abscess if present, debridement of
necrotic cartilage
o Abx: Pseudomonal coverage. Ciprofloxacin 750 mg PO q12h or IV
 Disposition: ENT c/s for debridement
 Complications: Deformity (“cauliflower ear”)

8. Temporomandibular joint (TMJ) disorders

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  Dislocation
o Anterior dislocation of condyle, often with yawning/laughing or trauma.
Predisposition due to anatomy (fossa and anterior articular eminence
mismatch), weak TMJ ligament capsule, TMJ syndrome, torn ligaments
o Presentation: Inability to close mouth, palpable condyle in front of articular
eminence, muscle spasm
o Diagnosis: Clinical, though consider XR to r/o fx if trauma
o Mgmt: Closed reduction with sedation. Grab mandible with both hands,
thumb inside mouth on ridge of mandible next to molars, downward pressure
then push posterior-superior into temporal fossae
 Alternative: Passive stretch. Interesting technique from England:
http://www.youtube.com/watch?v=Kp8AzHIC0hM
o Disposition: D/C home, NSAIDs/muscle relaxants for pain, warm compress
to area x24 hrs, avoid jaw opening, soft diet x1 wk. If recurrent, apply Barton
bandage (ace wrap around top of head and mandible), OMFS f/u
 TMJ syndrome
o Due to trauma, psychological tension, habits (bruxism, clenching), anatomy.
o Presentation: Unilateral facial pain, increases during day/with use (vs. TMJ
arthritis which improves during day), can trigger headache; associated with
clicking, popping and snapping; otalgia, tinnitus, decreased hearing
o Diagnosis: Palpable spasm of masseter muscle and internal pterygoid,
reproducible pain with pressure below ear and forward along mandibular
condyle. Jaw deviation to affected side, +/- trismus, myofascial spasm
o DDx: Temporal arteritis, otitis media, dental abscess, cluster headache,
migraine, trigeminal neuralgia
o Mgmt: Moist heat compress 4-5x/day for 7-10 days, soft puree diet x2 wks,
analgesics
o Disposition: Refer to dentist, periodontist for occlusive therapy (e.g. bite
plates) or intra-articular steroid injections if persistent, or surgical mgmt

Nose
1. Epistaxis
 Anterior bleed (Kisselbach’s plexus: anterior ethmoidal arteries, superior labial
br of facial artery), posterior bleed (posterior ethmoidal artery, sphenopalatine
artery)
o Local: Trauma, URI, nose picking, allergies, decreased humidity, nasal
polyps, foreign body, irritants, nasopharyngeal mucormycosis, ICA aneurysm,
postop, chlamydial rhinitis neonatorum. Significant proportion of posterior
bleeds due to vascular pathology such as aneurysm and thus need ENT f/u
o Systemic: Nasal vessel atherosclerosis, anticoagulation/bleeding
dyscrasias/vit K or folic acid deficiency, pregnancy, hereditary hemorrhagic
telagiectasia (Rendu-Osler-Weber), liver dz, ICA aneurysm rupture, DM,
alcoholism, chronic nephritis, chemo, thrombocytopenia
o Idiopathic
 Diagnosis: Visualize with nasal speculum, differentiate anterior (Kiesselbach’s
plexus) vs. posterior (blood in posterior oropharynx, persistent bleed despite
anterior packing)
 Mgmt: ABCs – consider airway issues if massive bleed
o First have the patient blow out clots from the nose
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 o Afrin 2-4 puffs in each nostril for vasoconstriction
o Direct b/l pressure with minimal gauze padding and preferably between
thumb pad and flexed index finger over Kiesselbach’s x10 minutes without
stopping to look. If fails, blow clot one time and repeat one time
o If pt is unable to hold pressure for 10 minutes, place nose clip for pressure
(tape 2 tongue blades in middle, place nose in b/w blades)
o If site of bleeding identified, may apply silver nitrate for chemical
cauterization (apply for 4-5 sec), only use on one side of septum
o Pledgets: Soak cotton in 1:1 4% topical lidocaine and 1:1000 epinephrine,
phenylephrine, or oxymetazoline
o Packing
 Rhino-rocket: Soak in water for 30 seconds. Place into nostril parallel to
floor. Inflate with 10-15 cc air. Leave in for at least 48hrs, give abx for toxic
shock prophy with staph coverage (Augmentin, Clindamycin)
 Merocel: Apply bacitracin for lubrication and place in nostril
o Posterior bleed: Trial of Nasostat/Epistat or foley (12-16 Fr, inflate with 15 cc
saline). ENT consult for endoscopic cautery/arterial ligation if persistent bleed
 Disposition: D/C home if controlled, advise moisturization with humidifiers,
vaseline/bacitracin and no picking or blowing nose despite clot sensation. ENT
consult/admit if uncontrolled with coagulopathy, complications, or posterior
bleed requiring packing

2. Foreign body
 Often asymptomatic, may have occlusion, purulent/bloody nasal discharge.
 Trial of removal by blowing nose with occlusion of unaffected nare, positive
pressure into unaffected nostril, mouth-to-mouth breathing by parent to child
 Tools: Alligator forceps, Katz extractor/5-6fr foley, Schunkt-neck catheter
(suction with umbrella), super glue (see Ear: foreign body). Do NOT irrigate
 Abx: Amoxicillin or Clindamycin if infection or for prophy if long-standing FB
 Call ENT if: Button batteries/magnets, infection, delayed presentation, failed
removal
 Complications: Epistaxis, pulmonary aspiration with posterior dislodgement,
infection (sinusitis, periorbital cellulitis), ulceration/burns/septal perforation
(magnets, button batteries)

3. Sinusitis
 Pathophys: Inflammation of paranasal sinuses.
 Etiology: Most commonly post-URI 2/2 ciliary dysfunction, may lead to
bacterial suprainfection (strep pneumo, H flu, anaerobes). Pseudomonas in HIV,
CF, nasal tubes. Fungal including Rhizopus, Mucor, absida in DKA; also
consider aspergillus (mycetoma “fungal ball” and allergic fungal sinusitis).
Autoimmune, allergic
 Presentation
o Acute: <4 wks. Nasal discharge, congestion, facial pressure, dental pain,
fever, HA, cough, decreased smell. Severe sx >7-10 days increases risk of
bacterial. Peds associated with otitis, FB
o Subacute: 4-12 wks; Chronic: >12 wks
 Diagnosis: Sx >7 days with 2 Major or 1 Major + 2 minor

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 o Major: Facial pain/pressure, purulent nasal discharge, F, congestion,
obstruction, hyposmia/anosmia
o Minor: HA, cough, fatigue, halitosis, dental pain, ear pain/pressure
o Exam with mucosal hyperemia, crusting, facial pain
o Consider fungal in toxic, immunocompromised pts with black/brown
discharge with gray/necrotic mucosa
o If rhinitis, consider cocaine, CSF rhinorrhea, foreign body/neoplasm
 Mgmt
o Mild (no F, mild pain), <7 days: Likely viral, support with Oxymetazoline
(Afrin) 0.05% nasal spray BID X 3d (use <3 days to avoid rebound
vasodilation), pseudoephedrine 30-60mg PO QID. Consider anti-allergy meds
e.g. diphenhydramine 25-50mg QID, cetirizine (Zyrtec) 10mg qDAY,
fexofenodine (Allegra) 60mg BID
o Severe, >7 days: Amoxicillin 500 mg PO TID x7-10 days (high dose: 1 g
PO TID; peds: 45 mg/kg/d div bid or high dose 90 mg/kg/d div bid x10-14
days). If allergic, Bactrim DS bid X 10d
o Refractory after treatment x7days: Azithromycin 500 mg pox1 then 250 mg
x4 days (peds:10 mg/kg PO daily then 5 mg/kg po daily) or Augmentin
875/125 mg po bid x7-10 days (high dose 2000/125 mg po bid; peds: 80-90
mg/6.5 mg/kg/d po div bid x10-14 days). Levaquin 500mg po X 10d if allergic
o In HIV+: Treat for 21 days
 Disposition: D/C home with return precautions – HA, AMS, vomiting. ENT
referral if sx >1 mo
 Complications: Periorbital cellulitis, meningitis, osteomyelitis, cavernous sinus
thrombosis, intracranial abscess. Potts Puffy Tumor (extension into cortical
bone)

Throat
1. Abscesses and infections – see Infectious Disease chapter for specifics
Fascial space/ Clinical Diagnosis and Disposition
anatomic area presentation Treatment
Peri-apical abscess Acute or chornic Periapical lucency on Refer to dental
odontalgia; pain panorex/CT;
with percussion; no I&D/analgesics/
visible swelling Antibiotic
Subperiosteal Vestibular, palatal, Stab incision to Dental/oral
or sublingual alveolar bone,I&D, surgery referral
swelling/fluctuance analgesics/antibiotic 24-48h
Buccal space Massive cheek Analgesics/antibiotics; OMFS c/s for
swelling palpable fluctuance I&D
Masticator spaces; Severe trismus CT may confirm. May OMFS c/s,
submasseteric, need fluid resus hospitalize if
pterygomendibular, trismus,
temporal toxicity, or
severe
dehydration

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Sublingual, Swelling Airway, iv antibiotics, OMFS c/s,
submandibular, fluid resus prn likely
submental space hospitalization
unless well
localized
Ludwig angina “brawny edema”, Stabilize airway, broad STAT OMFS or
upper airway spectrum abx ENT c/s,
obstruction with prepare for OR
stridor
Parapharyngeal Pharyngeal bulging, CT for localization and OMFS c/s (if
infections; Lateral, dysphagia, trismus, extent, lateral neck XR odontogenic),
Retropharyngeal nuchal rigidity with may show ENT c/s for
space prevertebral retropharyngeal peritonsillar or
involvement thickening pharyngeal
IV abx (clinda or pcn G I&D, admit
+ flagyl)
Mediastinitis Chest pain, severe Wide mediastinum on Admit
dyspnea, systemic CXR, gas or fluid on
toxicity CT scan, IV abx
Cavernous Sinus Ocular pain, orbital CT or MRI may Admit
Thrombosis edema, retinal confirm
hemorrhages; CN
III, IV, V, VI deficits
th
*adapted from Harwood-Nuss’ Clinical Practice of Emergency Medicine, 5
edition. Oral and Maxillofacial disorders

2. Foreign body
 Often due to ingestion or aspiration
o Most often due to food aspiration (nuts/carrots/popcorn)
 Presentation: Choking, gagging, dysphagia, wheezing
o Kids may have delayed presentation with wheezing or coughing, with
unilateral breath sounds on exam
o 60% children may present with mild or no sx
o Consider in ddx for new onset croup or asthma with sudden onset wheeze
 Diagnosis
o Consider anteroposterior and lateral neck radiographs
o CXR may be helpful but is often normal
 May see unilateral hyperexpansion, lobar atelectasis or post-obstructive
pneumonia
o Consult ENT for bronchoscopy for laryngeal FB
o Consult GI for endoscopy to retrieve esophageal FB
 Mgmt: Removal of foreign body
 Disposition: Admit for FB removal/obs if not able to clear spontaneously
 Complications: Recurrent unilateral pneumonia/wheezing

3. Tracheostomy care and complications

 Bleeding: From superficial, thyroid, carotid arteries, anterior jugular veins,
brachioecephalic artery. Tracheoarterial fistula presents weeks out from
innominate artery erosion – 50-75% mortality! Often has sentinel bleed
precursor (hemoptysis, mild bleed).
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  Fistula: Tracheoesphageal 2/2 posterior wall perf with trach or erosion, assoc
w/ percutaneous dilational tracheostomy. Cuff leak, food aspiration, abdominal
distention, copious secretions. Arrange for bronchoscopy
 Infection: Cellulitis, drainage, tracheitis, bronchitis, pna, sepsis
o Periostomal cellulitis: Outpt abx
o Watch for mediastinitis, mediastinal abscess, paratracheal abscess, esp if
s/sx systemic infx, or pain with breathing/swallowing. If present, treat with IV
abx (resp flora, MRSA coverage)
 Obstruction: Usually present w/ resp distress. Check for mucous/secretions,
blood. Check placement, give high flow oxygen, apply saline to loosen
secretions and suction. Clean inner cannula, consider replacing tube if
persistent distress, cuff leak, tube fx
 Stenosis: Not symptomatic until lumen decreased to 50-75%, often due to
pressure necrosis, ulceration, and granulation tissue formation. Usually needs
bronch, referral to ENT
 Other: Ptx, pneumomediastinum, air leaks, dislodgement, false passage, tube
fx with aspiration, decannulation
 Replacing trachs
o Indications: Cuff rupture/leak, complete or partial obstruction
o CI: Recent trach (within 1 wk), caution in coagulopathy, plt <50k
o Materials: Same size trach tube + 1 size smaller tube, BVM, lubricant
o Preoxygenate pt. Supine position, extend neck. Prep new tube with lubricant,
and insert obturator. Thread cloth tie into one side of tube. Insert a red rubber
catheter or bougie through old trach tube. Remove old trach ties and sutures,
grab stay sutures and remove old tube. Insert new tube over rubber catheter or
bougie using seldinger technique. Remove obturator and catheter/bougie,
connect to ventilator/BVM, confirm position (BS, ETCO2, CXR). Secure ties

4. Approach to obstructive airway

 ABC! IV, O2, monitors. Chin-lift, jaw thrust. Prepare for difficult airway
including bougie, fiberoptic, potential crich
 Consider racemic epi nebs (0.5 mL of 2.25% in 2 mL NS), Solumedrol 125
mg IV for hypersensitivity/ croup, trial of Heliox for temporizing measure (but
only 20% O2 delivered)
 Magill forceps or suction tube for foreign body retrieval, or push FB into
brunchus if unable to remove for ventilation
 Ddx
o Foreign body: Usually supraglottic; smaller objects may pass subglottic.
Subglottic items have intermittent obstruction, worse with head-down position,
localized wheezing if in bronchus
o Infections: E.g. Ludwig’s angina, RPA/parapharyngeal abscess, epiglottitis.
Start early IV abx
o Hypersensitivity: Anaphylaxis, HAE, ACE-I
o Anaphylaxis: Start early solumedrol 125 mg IV, epinephrine 0.3 mL 1:1000
SQ, diphenhydramine 50 mg IV
o HAE: FFP to supply C1-esterase inhibitor
o Hemorrhagic disorders: Hematomas 2/2 anticoagulants. FFP, vit K
o Mass: Extrinsic compression e.g. esophageal distention, mediastinal tumors
(SVC syndrome) or direct (neoplasia e.g. laryngeal CA, Kaposi sarcoma, etc)

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5. Neck masses
 Ddx
o Congenital: Brachial cleft cyst, thyroglossal duct cyst, dermoid cyst, cystic
hydromas, torticollis, thymic masses, teratomas, lymphagioma, laryngocoele
o Inflammatory/Infectious (esp in peds): Adenitis (bacterial e.g. strep/staph;
viral e.g. hiv, ebv, hsv; fungal e.g. coccidiomycosis; parasitic e.g.
toxoplasmosis), cat-scratch dz, tularemia, local infection, sialoadenitis,
thyroiditis, MAC, M. tb
o Benign: Mesenchymal tumors (lipoma, fibroma, cystic hygroma, neural
tumor), salivary gland mass, vascular (hemangiomas, AVM, lymphangiomas,
aneurysm)
o Neoplastic/Malignant: Sarcoma, salivary gland tumor, thyroid/parathyroid
tumors, lymphoma, metastasis
 Mgmt: Most masses are inflammatory. Could try empiric abx x2 wks, consider
screening CXR and CBC and PPD. Imaging if higher suspicion. ENT referral if
mass persists >2 wks, growing, fixed, matted cervical LN, or masses in
parotid/thyroid

Dental Emergencies
1. General information
 SFGH and UCSF have OMFS residents available 24 hours a day who can
help with many dental emergencies. UCSF also has adult and pediatric dentistry
on call
 Outpatient Referral Resources for the uninsured: Healthy San Francisco does
not provide dental care but has a good resource guide
http://www.healthysanfrancisco.org/files/PDF/HSF_Dental_Vision_Resource.pdf
 “The Dental Box” at SFGH contains the materials for many dentalgia related
problems. It is located in the EMS radio room, on the top left shelf

2. Anatomy
o Deciduous teeth number 10 maxillary and 10 mandibular, normal dentition
consists of a central incisor, lateral incisor, canine, and two primary molars
o Permanent teeth from 1 to
32, starting with the upper
right third molar/wisdom tooth
(1) to the upper left third
molar (16) to the lower left
third molar/wisdom tooth (17)
to the lower right third molar
(32).
o Counting Shortcut: Front
incisor R to L will always be:
#8 to #9

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 3. Nerve blocks: See Procedures chapter

4. Microbiology
o Common bacteria causing dental abscess
include the fusobacteria and provetalla, and
peptostreptococci, and microerophillic
streptococci
o Actinomyces is an invasive organism that
presents as a mass or ulcer Commonly infects
the bone many patients with chronic oral
infections Characterized by history of recurrent
infection that responds to a short course of
antibiotic and then recurs

5. Non-traumatic oral complaints

 Dentalgia (toothache): Facial pain often 2/2
dental issues, however consider sinusitis, deep
cervical space infection trigeminal neuralgia,
polymyalgia rheumatica/giant cell arteritis,
sialoadenitis, arthritis, otitis media/externa
o Dental caries and Periapical Abscesses
 Etiology: Common bacteria include fusobacteria, provetalla,
peptostretococci, microaerophilic streptococci
 Presentation: Pain localized to tooth, may radiate to ear, jaw, eye. Sensitive
to percussion. Variable sensitivity to cold and heat
 Diagnosis
 Periapical abscesses confined to alveolar bone
 Tooth may not have obvious caries
 Severe pain on percussion may indicate an apical abscess. May cause
palpable swelling in vestibule but not amenable to I&D
 Complications: Subperiosteal spread to deep fascial planes, osteomyelitis,
Abscessed anterior maxillary teeth can cause periorbital swelling or cavernous
sinus thrombosis via facial veins
 Mgmt
 Nerve block may help, but may be difficult to anesthetize infected tissue.
Local apical block may help if pain is isolated. Use mix of lido with epi and
bupivicaine can last until seen by dentist in the morning
 NSAIDS and opoids in limited amount with referral to dentistry

6. Periodontal abscess/parulis
 Etiology: Oral microbes such fusobacteria, provetalla, peptostretococci,
microaerophilic streptococci
 Diagnosis: Palpate vestibule for fluctuance and tenderness
 Mgmt
o Use a nerve block or supraperiosteal infiltration for anesthesia
o Anesthetic with epinephrine for hemostasis and prolonged anesthesia
o I&D with stab incision + blunt dissection with mosquito hemostats through
periosteum. Caution for wisdom teeth periodontal abscess/pericoronitis I&D –
avoid deep dissection (infects deep cervical spaces or lacerate internal carotid)

155
 o Rinse with saline. Consider Penrose drain secured with 4-0 silk suture if
large absces. Pencillin VK 500 mg PO QID x7-10 days. Referral to dentist or
OMFS in 24 to 48 hours for drain removal or for removal of wisdom teeth

7. Dry socket (post extraction periosteitis)

 Etiology: Removal of blood clot (e.g. rinsed off) after teeth extraction with
exposed bone. Us. 3-5 d post procedure. Food particles may also become stuck
under the open mucosa. Need to compare to and R/O alveolar osteomyelitis
(Alv.Osteo p/w F/C/ leukocytosis, surrounding teeth/bone sensitive to palpation)
 Mgmt
o Gently rinse socket with saline in a syringe with an angiocath catheter to
remove food particles
o SFGH: Eugenol soaked Gelfoam and dental cotton rolls available in dental
box. Dip cotton in Eugenol and pack socket
o UCSF: Apply lidocaine jelly and then pack with sterile idodoform gauze
soaked in lidocaine jelly
o Oral pain medications and repack with 2% viscous lidocaine q6 h prn
o Consider penicillin VK 500 mg PO QID for signs of infection
o Refer to general dentist for further treatment, needs repacking in 24h

8. Post–extraction hemorrhage
 Etiology: Spitting, swishing, sucking on a straw  dislodges clots. Also,
anticoagulants e.g. ASA, Coumadin, Plavix, or diseases that impair hemostasis
 Diagnosis: Remove all packing material in socket. Use saline rinse with
suction to view location of bleeding
 Mgmt
o Create large tight ball of gauze and have patient clench down for 20 minutes
o If bleeding continues inject lidocaine1% with 1:100,000 epinephrine until skin
blanches. Then reapply pressure
o If bleeding continues, call OMFS (may replace sutures or place Surgicel to
create a clot matrix)
o Blood clots may take 3 hours to stabilize in patients on platelet therapy or
anticoagulants. Have pt hold pressure for 1 hour, then re-examine
o Send patient out with strict instruction to avoid food for 3 hours, avoid
swishing, spitting, or using a straw for 7 days

9. Acute necrotizing ulcerative gingivitis (Trench mouth)

 Etiology: Seen in immunocompromised patients e.g. untreated HIV, peds,
particularly those under stress or poor dental care and nutrition. Caused by
fusiform bacteria and spirochetes
 Presentation: Sudden onset of tender bleeding gums, metallic taste, woody
sensation in teeth, systemic symtoms of fever and malaise
 Diagnosis: Pronounced hallitosis, gray pseudomembrane over bleeding gums,
blunted or scooped out interdental papillae, leukocytosis and
lymphadenopathy. May extend into deep tissues (cancrum oris) or the tonsils
and pharnyx (Vincent's angina). Consider gram stain and culture, facial x-ray for
bone extension, HIV test
 Mgmt
o Penicillin VK 500 mg PO qid or Clindamycin 300 mg PO q6h x7
days. Rinse twice daily with warm saline (1/2 teaspoon of salt in 1 cup of
156
 water), 0.12% chlorhexidine, or dilute 3% hydrogen peroxide (mixed half
and half with water)
o Viscous lidocaine may provide temporary relief
o Advise against smoking and carbonated beverages
o Refer to dentistry

10. Traumatic dental emergencies

 General principles
o Control hemorrhage with gauze/pressure
o Subluxed tooth: Tap individual teeth  movement or blood around tooth
 Mild: Soft diet for several days.
 Significant: Need immobilizationx10 to 14 days. If no dentist available have
pt bite on a piece of gauze, get periodontal pack (Coe-Pak). Mix 1:1 resin and
catalyst. Mold over anterior and posterior subluxed tooth along with 2-3 teeth
on either side. Have pt close mouth while mixture hardens. Works for 24 to 48
hours, but MUST avoid warm liquids. Refer to dentist as soon as possible.
o Avulsed tooth: displaced from periodontal attachment. handle by crown,
avoid injury to periodontal ligament, gentle rinse tooth w/ saline w/o wiping
root/ligament
 Adult tooth: Dental emergency – c/s OMFS. Re-implant: suction/irrigate
socket with saline, rinse tooth w/ milk/saline, place in socket. Ask pt to bite
down on moist gauze. Apply splint with adj teeth. If unable to replace, store
tooth in saline/milk/Hank’s solution to prevent periodontal ligament necrosis
(w/in 60-90 min)
 Peds: For primary dentition, dentist f/u in 1-2 wks. Do not replace 2/2 risk of
ankylosis
 Reimplant: Best if within 30 minutes, roots untouched. Lose 1% success for
every minute tooth is out of socket
 Liquid diet for 1 week then soft diet for 2 weeks. Avoid warm liquids. See
dentist as soon as possible
 Tooth Fractures
o Anterior teeth fx graded by Ellis grading system
Anatomy Treatment

enamel (chalky white) smooth sharp edges with emery

Ellis I
*0-3% pulp necrosis risk board, f/u with dentist

enamel + dentin
dry tooth with gauze, apply CaOH/dry
(yellow/pink)
Ellis II metal foil or plastic enamel bond. soft
*1-7% pulp necrosis risk
mech diet, dentist f/u 24-48h
assoc pain/temp sensitivity

pulp involvement
(pink, visible blood) treat like Ellis II (cover with moist cotton,
Ellis III *10-30% pulp necrosis risk, or Cavet e.g. temp root canal sealant),
assoc severe pain/temp liquid diet, urgent dental f/u
sensitivity

157
 alveolar bone fx with tooth need to dx/preserve tissue and repair
Alveolar involvement. mucosa. Dental emergency  c/s
fx assoc with high impact trauma OMFS (arch bar stabilization) +
TMJ at risk for dislocation antibiotics b/c this is open Fx!
 Oral soft tissue Injury
o Consider salivary gland trauma if injury involves parotid or penetrates near
the angle of the mandible. Failure to repair  stenosis or fistula formation
o Repair large tongue lacs to avoid scar tissue to preserve speech/ swallowing
o Diagnosis: Wipe all saliva from Stenson’s duct across form second molars.
Look for rapid re-accumulation of saliva
o Mgmt
 Perform all dental stabilization prior to soft tissue repair
 Consider OMFS consult if suspect salivary duct compromise
 Small tongue lacerations < 1 cm do not need repair
 Anesthesia: Consider lingual block, as well as local injection
 Close mucosa with 4-0 absorbable suture, but gingival and tongue
lacerations should use 4-0 black silk. For children 4-0 absorbable chromic is a
good choice. Remove intraoral non-absorbable sutures in 7 days
 For tongue lacerations, close in layers to reduce tension, using absorbable
suture for deep sutures
 For through and through lacerations involving skin and mucosa, suture
mucosa first, irrigate thoroughly to remove oral flora. Place subcutaneous
sutures with absorbable, then superficial with 6-0 or 7-0 suture. Remove in 3-
4 days
 Antibiotics should be given for intraoral or through and through repairs
 Saline rinse 6 times a day
 Recheck in 48 to 72 hours for infection

158
 Hematology/Oncology
By Sarah Gertler Res ed. Adrian Flores Faculty ed. Esther Chen

Blood products
1. General
 CMV neg, irradiated products for BMT patients and those undergoing
myeloablative chemo.
 CMV neg for peds <4 mo, pregnant women, heart/lung organ transplant
recipients, CMV neg cirrhotics who are going to receive a liver soon, and severe
HIV who are CMV neg (for full list see UCSF or SFGH transfusion guidelines)
 Always complete a blood consent prior to transfusion (unless emergent)
 Emergency blood release
o UCSF: Call blood bank 3-1313
o SFGH: Notify clerk/nurse, or call 6-8584

2. pRBCs
 1 unit = 250-350mL, should raise hct 3 pts (hgb by 1 g/dL)
 Peds: 10-15mL/kg, should raise hgb by 2-3 g/dL (3mL/kg raises hgb 1 g/dL)
 Indications
o Hgb <6 g/dL
o Hgb < 7-8 g/dL AND symptoms related to anemia (consider hgb<10 in a
symptomatic pt with cardiac hx). Give over 4 hours in CHF.
o Patient with active, severe hemorrhage with hypovolemia/metabolic acidosis
(e.g. trauma, GIB) – see Massive Transfusion Protocol
 Washed pRBCs if h/o severe allergic transfusion reactions
 UCSF: All pRBCs are leukoreduced

2. Platelets
 1 “six pack” = 1 apheresis unit = 250-300 mL, should raise count by 30-50 K
 Peds
o 1 adult unit (“6-pack,” 250mL) for kids >20-25 kg, should raise plts by 50-
100K
o 1 pediatric unit (125mL) for kids 10-15 kg (or 1 ped unit/10kg)
o 1 “quad pack” unit: (50-75mL) for kids <10 kg
 Indications
o <10k even if not bleeding, without TTP or HIT
o <20k if mucositis or fever
o <50k if actively bleeding or pending invasive procedure/surgery
o <75k if actively bleeding + uremia
o <100k if major bleeding (head/spine/eye/airway)
 Contraindications: TTP, heparin-induced thrombocytopenia, ITP unless severe
bleeding due to thrombocytopenia
 Consider DDAVP in dysfunctional platelets (vWD, uremia)

3. FFP
 1 unit= ~200–250 mL of anticoagulated plasma with approximately 400-500
mg (~ 2.0 g/L) of fibrinogen
 Peds: 10-15mL/kg, should increase clotting factors 10-20%
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  Transfuse 10-15 ml/kg FFP (average dose 3 units in Adult), lasts 4-6 hours
 Indications
o Active bleeding AND INR> 1.5
o After massive transfusion
o Urgent warfarin reversal
 Vitamin K as 5-10mg PO to 10mg IV over 30-60 min (see below)
o Factor deficiencies (if specific factor is unavailable)
o Procedures requiring INR correction e.g. LP, surgical procedures
o Special cases: TTP awaiting exchange transfusion, severe angioedema in
C1-esterase deficiency, antithrombin III deficiency in patients refractory to
heparin
o INR of FFP is approx. 1.6; cannot correct below this with FFP alone

4. Cryoprecipitate
 1 unit (12–15 mL) = ~80 units of Factor VIII, 200 - 350 mg of fibrinogen, von
Willebrand factor, Factor XIII
 Usually given in pools of 5-10 units. Raises fibrinogen 75 gm/dL
 Peds: 1 unit/2-5 kg
o 1 adult dose (10 units) for kids >20 kg should increase the various factors
from 40-100%
 Indications
o Active bleeding AND fibrinogen level <100 mg/dL (DIC)
o Von Willebrand’s disease
o Hemophilia A (if specific factor is not available)
o Factor XIII deficiency
o Uremic bleeding

5. Bebulin (Prothrombin Complex Concentrate)

 Contains factors II, VII, IX, X
 For life threatening bleeding with warfarin e.g. intracranial hemorrhage
 Usual dose 35-50 units/kg IVP (round up to nearest vial, available in 500,
1000, 1500 unit vials)

6. rhVIIa (recombinant factor VII, aka Novoseven)

 Replacement factor for hemophiliacs; consider in warfarin reversal but use in
trauma is controversial
 Usual dose 15-90 mcg/kg IV push

Massive Transfusion Protocol

1. Indications to consider
 Unexpected massive hemorrhage accompanied by hypovolemic shock and/or
metabolic acidosis
 Patients requiring >4 units of blood during the first hour of resuscitation, or
pediatric patients requiring >20mL/kg of PRBC’s in the first hour of resuscitation
 Decreasing hct & Hgb with continued blood loss or coagulopathy

2. Product protocols at each site

 SFGH: Must be activated by an attending (Surgery, Anesthesia, or ED); Call
blood bank 6-8584

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 o 4 units pRBC
o 4 units FFP
o Cryoprecipitate and platelets need to be ordered separately
 UCSF: Call blood bank 3-1313
o 4 units pRBC
o 4 units FFP
o 1 unit platelets
o Cryoprecipitate needs to be ordered separately, consider if fibrinogen <100
 Pediatrics (<50 kg)
o 4 units pRBC
o 2 units FFP
o 1 unit platelets
o Cryoprecipitate needs to be ordered separately, consider if fibrinogen <100
 Massive transfusion side effects
o Hyperkalemia, lactic acidosis, hypocalcemia, hypothermia, coagulopathy

Transfusion Complications
1. If you suspect a transfusion reaction
 Stop the transfusion, draw a fresh purple top, send the unused blood and
tubing to the blood bank

2. Acute hemolytic transfusion reaction

 Anti-A/anti-B or allo-antibodies to other red cell antibodies cause hemolysis of
donor RBCs
 Presentation: Fever, chills, flank pain, dyspnea, hypotension, ARF, DIC
o May also occur in delayed fashion, 3-14 days after transfusion, from a newly
formed allo-antibody
 Mgmt: STOP the transfusion, hydrate with IVF (goal UOP 100-200 ml/hr),
consider lasix and bicarb for renal protection

3. TRALI (Transfusion related acute lung injury)

 Donor antibodies attack recipient WBCs, leads to complement activation,
noncardiogenic pulmonary edema
 Presentation: Respiratory distress, within 1-6hr, usually with edema on CXR
 Mgmt: Stop transfusion, supportive care, consider intubation (treat similar to
ARDS)

4. TACO (Transfusion associated circulatory overload)

 Volume overload due to blood products
 Presentation: Dyspnea, hypoxia, bilateral infiltrates, elevated BNP, other signs
of volume overload
 Mgmt: Stop transfusion, treat like CHF (oxygen, nitrates, lasix, bipap)
 Prophylaxis: Slower transfusion rates (e.g. 4 hours/unit), lasix in between units

5. Febrile nonhemolytic transfusion reaction

 Presentation: Fever > 1 C, during or up to 4 hours after transfusion
o

 Mgmt: Stop transfusion, give anti-pyretics

o Consider bacterial contamination of product (most common with plts)

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 o Send blood cx if other signs of shock, and send remaining product to lab for
bacterial culture

6. Allergic reactions
 Presentation: Mild urticaria to anaphylaxis (due to preformed antibodies)
 Mgmt
o Mild reactions: Stop transfusion, give anti-histamines. If symptoms resolve,
may consider re-starting, but stop if symptoms recur. May consider steroids
o Severe reactions: stop transfusion and treat as anaphylaxis
 Prophylaxis in patients with prior history: Give washed pRBC

7. Infection
 Bacteria (cultured apheresis platelets) 1: 75,000
o Bacterial contamination: Fever, chills, rigors, arthralgias
o Mgmt: STOP transfusion, send product for culture
 HIV: 1: 2 million
 Hepatitis B: 1: 300,000 (unvaccinated)
 Hepatitis C: 1: 2 million

Sickle Cell Disease

1. Pain crises (vaso-occlusive crisis)
 Pts often require high doses of narcotic, and have pain protocols written in
conjunction with their PMDs- check the patient’s chart
 Labs: CBC, reticulocyte count to r/o aplastic crisis
 Mgmt
o At UCSF once patient’s have been cleared of acute medical problems, can
often be transferred to Mt. Zion for pain control
o Consider admission if the patient requires more than 3 doses of analgesia

2. Acute chest syndrome (ACS)

 Due to pulm infection (mycoplasma/chlamydia>pneumococcus now), fat
emboli, rib infarction, iatrogenic (excessive hydration/narcotics)
 Presentation: New infiltrate on CXR + any one of the following: Chest pain,
fever, cough, wheezing, tachypnea, SOB, fever
o Fever/cough most common in kids
o Chest pain, SOB, chills most common in adults
 Infiltrate defines disease: 1 positive confirms disease, 1 negative cannot
exclude the disease
 Mgmt: O2, antibiotics (3 gen cephalosporin for pneumococcus + macrolide
rd

for mycoplasma/chalmydia), begin bronchodilators/ consider transfusion, and

hospital admission

3. Other
 Who gets admitted
o Inability to control pain (most common indication)
o Sequestration (acute anemia, hypotension, shock in kids with spleens)
o Hemolytic crisis (severe anemia with nml/elev retics and jaundice)
o Megaloblastic crisis (folate deficient) or aplastic (parvo b19)
o Stroke/TIA

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 o Priapism
o Acute abdomen
o Acute Chest vs. Pna vs. PE, MI
o Retinal vessel disruption
o Infections with encapsulated bacteria (if not immunized)
 If these patients need transfusion, alert the blood bank, as blood needs
special screening

Supratherapeutic INR
1. If no significant bleeding
 INR < 5: Hold warfarin, restart warfarin when INR is therapeutic
 INR 5 - 9: Hold warfarin, ± give vitamin K 1-5 mg PO, recheck in 24hrs
 INR ≥ 9: Hold warfarin, give vitamin K 5-10 mg PO, recheck INR in 24hrs,
may repeat dose

2. If serious or life-threatening bleeding AND any INR prolongation due to

warfarin
 Hold warfarin
 Give FFP (lasts ~4-6hrs) and/or Bebulin (lasts 4-6hrs)
 Vitamin K 10 mg IV is the fastest, but risk of anaphylaxis (see below)
 May consider rhVIIa (Novoseven, lasts 1-2hrs)
 Follow INR frequently (q2-4hrs) until INR stable and bleeding controlled

3. Vitamin K
 PO is the preferred method of administration, it is predictable, safe, effective
 IV is effective, but must be given over 30 minutes, and recommended only in
cases of severe bleeding as it has a risk for anaphylaxis
 Subcutaneous is unpredictable and not recommended
 Speed of reversal
o 1-5 mg decreases INR in 24-48 hrs
o 5-10 mg decreases INR in 24 hrs

Oncology
1. Admitting patients with malignancy
 UCSF
o CRI (Cancer Research Institute) is for patients with liquid tumors. D/w heme-
onc fellow first, then call CRI hospitalist
o Solid tumor patients go to internal medicine, or the appropriate specialty
service (e.g., urology, ENT, GYN)
 SFGH: Most cancer patients go to medicine, with the exception of specialty
services, as above

2. Neutropenic fever
 Generally defined as ANC<500, or 500-1000 if recent chemotherapy, and
o
temp>38 C
 Mgmt
o Adults
 Call heme-onc fellow (UCSF)
 Labs: CBC with diff, lytes, T&S, Bcx x2, CXR, u/a & urine culture, DFA

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  Consider CT/LP if altered
 Broad spectrum antibiotics with pseudomonas coverage ASAP (Cefepime 2
grams IV + Vancomycin 1 gram IV)
o Pediatrics
 Call heme-onc fellow (UCSF)
 Labs: CBC with diff, lytes, T&S, CXR, DFA, UA (but don’t cath), Bcx x1
(from CVC if present, or peripheral culture)
 Antibiotics within 60 minutes of presentation (Ceftazidime 50 mg/kg IV or
Cefepime 50 mg/kg IV, max 2 grams; d/w heme-onc fellow)

Suggested reading
 UCSF transfusion guidelines
http://labmed.ucsf.edu/labmanual/mftlng-mtzn/test/info/4bb.html
 SFGH transfusion service/blood bank procedures
http://labmed.ucsf.edu/sfghlab/test/TransfusionServiceBloodBankProcedures.ht
ml
 Stramer SL. Current Risks of Transfusion-Transmitted Agents: A Review. Arch
Pathol Lab Med 2007; 131: 702-707.

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 Infectious Diseases
By Swati Singh Res ed. Margaret Salmon Faculty ed. Rachel Chin

General Info
1. Online resources
 Institution specific recommendations: http://www.ucsf.edu/idmp
 Hopkins antibiotic guide: http://hopkins-abxguide.org

2. Blood cultures
 Almost always draw 2 sets of blood cultures & a urine culture prior to giving
antibiotics
 Exception: Bacterial meningitis – give antibiotics right away
 Draw three sets of cultures if you suspect endocarditis
 Request “time to positivity” on cultures if patient has an indwelling line

3. Sepsis
 If you suspect infection, identify sepsis early (2 SIRS criteria plus documented
infection)
o T>38°C or < 36°C
o HR > 90
o RR >20
o WBC > 12, < 4, or > 10% immature bands
 Sepsis management goals (see algorithm in Resuscitation section)
o Aggressive volume resuscitation
o IV antibiotics
o Pressors for additional BP support
o Consider stress dose steroids e.g. hydrocortisone 100 mg IV in potentially
adrenally suppressed patient (on chronic steroids at home)

CNS Infections
1. Meningitis
 Presentation
oFever, neck stiffness/ nuchal rigidity, AMS, HA, photophobia, lethargy,
vomiting, sz; ill appearance, petechial rash, papilledema
o95% of bacterial meningitis has ≥2 of HA, fever, neck stiffness, AMS
oTriad of fever/neck stiffness/AMS <66% but absence of all 3 has sens 99%
o15% w/ focal findings, 20-50% w/sz at some point in illness
oKernig’s and Brudzinski’s signs specific but not sensitive; infants, elderly, and
immunosuppressed may not show meningeal signs
oJolt accentuation: If HA + F, ↑HA w/ horizontal head rotation at 2-3x/sec.
Sens 97%, spec 60% for CSF pleocytosis, small study (Uchihara et al, 1991)
 Etiology
oBacterial: Tends to be acute (<1 day)
Age Bugs
<1 mo GBS, E. coli, Listeria monocytogenes
1–3 mo GBS, S. pneumoniae, H. influenzae, N. meningitidis, GN bacilli
>3 mo S. pneumoniae, N. meningitidis, H. influenzae, neonatal pathogens
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Adult Strep. pneumoniae, Neisseria meningitides
*Listeria: immuno-compromised, elderly patients, & alcoholics
oViral: Subacute (1-7d). Enteroviruses (coxsakievirus, echovirus)>HSV
oFungal: Subacute/chronic (>1wk), lethargy, wt loss, night sweats; low-grade
temp, chronic ill appearance. Cryptococcus, coccidiodomycosis
 DDx: Encephalitis, SAH, migraine, dural venous sinus thrombosis,
pseudotumor cerebri, temporal arteritis
 Dx
oBlood cx, CXR, UA (for r/o simultaneous infection)
 ↓Plt in meningococcal dz
oLumbar puncture – see High risk CC chapter
 Mgmt
o Steroids before abx/LP if suspect bacterial (pneumococcal or H flu) or ↑ICP,
AMS
 Dexamethasone 10 mg (0.15 mg/kg) PO/IV, first dose 10-20 minutes
before antibiotics!
 Unclear evidence for age <6 wks
 Decreases vanco penetration of BBB, consider adding/substituting rifampin
600mg IVx1
 Do not given if neutropenic
o Abx
Age Drugs
<4wks [Cefotaxime 50 mg/kg IV or gentamicin 2.5 mg/kg IV] + ampicillin
100 mg/kg IV; consider acyclovir 20 mg/kg IV if ill-appearing, CSF
pleocytosis, or immunocompromised to cover HSV while awaiting
PCR
Peds [Ceftriaxone 50 mg/kg IV or cefotaxime 50 mg/kg IV] + vancomycin
>4wks 20 mg /kg IV; consider ampicillin 100 mg/kg IV if age <2 yo
Adult Vancomycin 1 gram (15-20 mg/kg) IV + Ceftriaxone 2 grams IV
*Add ampicillin 2 gram IV if age >50, immunocompromised
*Recent neurosurgery or skull penetrating injury: replace ceftriaxone
for cefepime 2 grams IV for pseudomonal coverage
 Herpes meningoencephalitis: Acyclovir 20 mg/kg IV
 If PCN/cephalosporin allergic: Substitute Ceftriaxone w/ Aztreonam 2g IV,
Ampicillin with TMP-SMX 5mg/kg IV
 Dispo: Admit with droplet/respiratory precautions for suspected bacterial
meningitis
 Exposure prophylaxis for all close contacts
o Illness w/in 48-72hrs of colonization, ↑risk 500-800X but NNT 1/200k (high
risk of tendon rupture 2/2 prophy vs. developing dz)
o Need to get droplets in mouth/nose to be contagious
o Ciprofloxacin 500mg PO X 1 (Ceftriaxone 250mg IM in peds <15 yo or
125mg IV if pregnant)

2. Encephalitis
 Presentation
o HA, neck stiffness, AMS (confusion, agitation, behavioral/ personality Δ,
emotional outbursts, cognitive deficits, altered, amnesia, Wernicke’s aphasia,
166
 psychosis), papilledema, hemiparesis, paresthesias, sz, temporal lobe auras
(odors, images, sounds), myoclonus
o Fever, AMS, focal neuro & sz more common (vs somnolence/lethargy in
meningitis)
o Think HSV in pt w/“Ψ” personality changes c/o HA
 Etiology
o HSV1: 10-20% of viral encephalitis; also consider equine, VZV, influenza,
west nile
o 50-70% of encephalitis will not have identifiable pathogen
 Dx
o CT head w/ and w/o contrast
o CSF: RBC>500 or xanthochromia in atraumatic tap raises concern for HSV
o Send CSF for HSV1/2 pcr, save extra CSF for further studies (d/w Neuro)
o Neuro consult
 Mgmt
o HSV/VZV: Acyclovir 10mg/kg IV over 1 hr q8hrs w/copious IVF to avoid
crystalluria and renal failure
o If AIDS w/CD4<100, consider CMV tx w/ ganciclovir 5mg/kg q12 &
foscarnet 90mg/kg q12hr. D/w pharmacy as dosing varies
o Dispo: Admit for further w/u of AMS

3. Cerebral abscess
 Presentation
o Mild HA progressing slowly over weeks
o 50% w/nuchal rigidity & fever, ±focal
 Dx: CT w/ and w/o for ring enhancing lesions
 Mgmt
o Ceftriazone 2 grams IV q12h + metronidazole 500 mg IV q12h ±
vancomycin 1 gram IV
o Consider toxoplasma gondii if immunosuppressed, add pyrimethamine 200
mg po then 50-100 mg/day OR sulfadiazine po 4-8 grams/day + folinic acid
10 mg/day po
o Consider neurosurg c/s, esp for large abscess, post-surgical
 Dispo: Admit

ENT Infections
1. Bacterial tracheitis
 Presentation: Secondary infection after viral URI, or recent procedure or
intubation with sudden worsening, high fever, stridor, cough, toxic appearance
 Etiology: S. aureus, S.pneumonia, S.pyogenes, M.catarrhalis, H.influenzae,
anaerobes
 DDx: Epiglottitis, pharyngitis
 Dx
o Method of choice bronchoscopy
o Culture/gram stain of mucopurulent secretion
o Neck radiographs not needed but can show subglottic narrowing of trachea
or irregular tracheal margins
 Mgmt
rd
o Unasyn 3 grams IV, or combination of 3 generation cephalosporin
(Ceftriaxone) with Clindamycin, consider Vancomycin
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  Dispo: OR for sedation, intubation, bronchoscopy

2. Epiglottitis
 Rarely seen in children since H. influenza type B vaccination
 Presentation: Sore throat with dysphagia/odynophagia & fever, ± drooling,
stridor, dyspnea, hoarseness; often sitting up, leaning forward, mouth open,
head extended, & panting, tripoding with inspiratory stridor
 Etiology
Age Organism
Adult H. Parainfluenzae, GAS, S. Pneumo, H. flu, S. Aureus
Adult Pseudomonas, H. Parainfluenzae, GAS, S. Pneumo,
Immunocompromised H. flu, S. Aureus
Peds S. Aureus, Strep, H. flu,
oAlso consider viruses, fungi
 DDx: PTA, RPA, pharyngitis, anaphylaxis
 Dx
oLabs: Leukocytosis
oImaging: X-ray of lateral neck shows enlarged epiglottis (“thumbprint”), but
not sensitive nor specific
oAdults: Direct visualization by fiberoptic laryngoscopy shows cherry red
epiglottis. Only attempt this exam with a plan for managing a difficult airway,
including cricothyroidotomy as direct laryngoscopy can cause
sudden/unpredictable airway obstruction
oChildren: Only interrogate the airway in the OR
 Mgmt
oMinimize airway manipulations, prepare for diff airway including crich kit as
above. Sit up pt, DO NOT LAY PATIENT FLAT, humidified O2
oCeftriaxone 1 gram q24h, Vancomycin 1 gram IV +/- Clindamycin 900 mg
IV or Metronidazole 500 mg IV
oSteroids: Methylprednisolone 125 mg IV
 Dispo: Likely ICU/OR for airway monitoring/management

3. Ludwig’s Angina
 Presentation
oFever/chills, drooling, mouth pain, meningismus, dysphagia, odynophagia,
trismus (parapharyngeal space), edema of upper midline neck & floor of mouth
oRapidly spreading “woody” cellulitis of bilateral submandibular space, may
enlarge/elevate/displace tongue, causing airway compromise and spread into
parapharyngeal/retropharyngeal/mediastinal space
oStridor, difficulty managing secretions, & cyanosis are late signs
 Etiology
oPolymicrobial oral flora withhemolytic streptococcus, oral anaerobes
(bacteroides), staph. GN if immunocompromised
oContinguous spread from periodontal infx (2nd or 3rd mandibular molar teeth),
or from PTA/suppurative parotitis
 DDx: PTA, cellulitis, epiglottitis, pharyngitis, lemierre’s
 Dx

168
 oClinical: Tender, symmetric, hard induration in submandibular area,
±crepitus, tongue swelling, erythema of oropharynx
oBlood cx to help identify organism in case of bacteremia
oCT: Evaluate extent of spread, surgical planning
 Mgmt
o Airway: Anticipate difficult airway, consider early intubation if rapidly
worsening edema/dyspnea. May need fiberoptic/crich/trach, consult anesthesia
and ENT early
o Broad spectrum IV abx: Cover staph/strep/anaerobes, GN if immunocompr
o High dose pcn G (12 million U/d) or Unasyn 3g q6h or Clindamycin 600-
900 mg IV q8h
o If MRSA: Vancomycin 1 gram (15-20 mg/kg) IV q12h
o Immuno-compromised: Consider Meropenem 1 g IV q8h or Imipenem 500
mg IV q6h or Zosyn 4.5 g IV q8h with Vancomycin
o Consider surgery for drainage/debridement if unresponsive to abx in 24h,
tooth extraction if able to identify source
 Dispo: Admit to ICU with ENT consult, monitor for airway compromise,
mediastinitis

4. Otitis externa aka swimmer’s ear

 Disruption of squamous epithelium in trauma or prolonged water exposure.
 Presentation: Pruritis, fullness, otalgia, hearing loss, mucopurulent discharge
 Etiology: Pseudomonas, staph; fungal assoc with chronic or in DM,
immunocompromised, tropical climates (aspergillus)
 Ddx: Consider Ramsay Hunt, furunculosis (well-circumscribed infx of canal
with staph, needs I&D + abx), auricular cellulitis
 Dx: Clinical
 Mgmt
o Mild with visible TM: Water, saline, 2% acetic acid (Vosol otic HC 4 gtts)
q6h x7-10days for cleaning
o Ciprofloxacin otic HC or Ofloxacin otic HC 4 gtts q12h x7-10 days or
Neomycin/polymyxinB/hydrocortisone 4 gtts q8h x7-10days. May need to
place a gauze wick to facilitate antibiotic entry and pus drainage
 Neomycin/polymyxinB/hydrocortisone may cause dermatitis, avoid if
perforated TM
 Dispo: D/C home with abx if mild with return precautions (sx should improve in
48-72h), consider admission if severe invasive otitis externa with treatment
failure
 Complications: Malignant or invasive otitis externa (aka skull base
osteomyelitis)  spread to temporal bone, assoc with high mortality (often in
elderly, immunocompromised, DM, AIDS), involves pseudomonas

5. Otitis media
 Assoc with Eustachian tube dysfunction 2/2 URI or congestion 2/2
barotrauma, tumor, allergies
o OME: Otitis media with effusion, serous accumulation
o AOM: acute otitis media, infection
 Presentation

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 o Adults: Otalgia w/ fluid accumulation, hearing loss, aural fullness vertigo,
low-grade fever
o Peds: Ear tugging, irritability, poor feeding, fever (Follow Fever Algorithm)
 Etiology
o S. pneumoniae, H. influenzae, M. catarrhalis, Group A Strep, viral
o Chronic disease more assoc with pseudomonas, staph
 DDx: Middle ear mass, mastoiditis, herpes zoster oticus (Ramsay Hunt),
bullous myringitis (mycoplasma), squamous cell carcinoma, fungal
 Dx: Clinical
o OME: Hx + middle ear effusion (bulging TM, limited mobility with pneumatic
otoscopy, air-fluid level, otorrhea)
o AOM: Hx + middle ear effusion (bulging TM, limited/absent TM mobility/air-
fluid level/pus behind TM, otorrhea)+ inflammation (TM erythema, otalgia)
 Mgmt
o Analgesia
o OME: Decongestants, antihistamines or nasal steroids for assoc allergic
rhinitis/nasal swelling. Resolves over 12 wks. Myringotomy if persistent
effusion or need to improve hearing (but CI if related to CA/radiation)
o AOM
 Adults: Consider abx as studies done on SNAP are in peds pop, especially
if severe disease (Mod-severe otalgia, F>39, meeting all 3 dx criteria)
 No prior abx: Amoxicillin 500 mg po tid x5-7 days
 Risk for drug resistant S pneumo: high dose Amoxicillin 1 g PO
TIDx5-7 days
 Failure of treatment (no↓sx in 2-3d)/T>39/mod-severe otalgia): high
dose Amoxicillin/clavulanate 2000/125 mg po q12h x7 days
 PCN all: Azithromycin 500 mg po x1 then 250 mg po x4 days or
Doxycycline 100 mg po bid x5-7 days or Levofloxacin 750 mg po daily x5
days or Moxifloxacin 400 mg po daily x7 days
 Consider imaging: Fine-cut temporal bone CT for chronic infection if
concern for middle ear mass, cholesteatoma, or mastoid erythema
 Peds
Age Certain* Diagnosis Uncertain Diagnosis
< 6 mo Antibiotics Antibiotics
6 mo – 2 yo Antibiotics Severe: Antibiotics
Non-severe: obs/SNAP
> 2 yo Severe: Antibiotics obs/SNAP
§
Non-severe : obs/SNAP
*Certain diagnosis requires meeting all three diagnostic criteria (acute onset +
middle ear effusion + inflammation)
§
Nonsevere = T <39°C in last 24 hours & mild otalgia
SNAP = Safety-Net Antbiotic Prescriptions
 Treat all <6mo and others with certain diagnosis
 Consider obs x48h or SNAP if non-severe illness AND uncertain diagnosis
in 6mo-2 yr, or >2 yr with non-severe illness
 Obs or SNAP only feasible if parent/caregiver is reliable, agreeable, and
able to return for follow-up

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  First line: Amoxicillin 40-45mg/kg BID, max 1g/dose
 Failure of treatment (no↓sx in 2-3d)/T>39/mod-severe otalgia:
Amoxicillin-clavulanate 45 mg/kg BID (max 1.5g/dose)
 Can give ceftriaxone 50mg/kg IM/IV outpt X 1-3 doses if unable to tol PO
 If PCN allergic: Azithromycin 10 mg/kg q24h POx1 (max 500 mg) then 5
2
mg/kg PO q24h x4 days (max 250mg) or clarithromycin 7.5mg/kg (max
1g/d) X 5d
 Total duration of treatment: 10 days for ≤5yo or severe disease; 5 days in
>5 yo with mild/moderate disease
 Dispo: Home. Follow up in 3-5d especially if <2 yo, risk factors for recurrence
o Consider ENT referral if recurrent, prolonged, or complications
o Unresolved unilateral effusion needs ENT eval for mass blocking the
Eustachian tube
 Complications: Mastoiditis, meningitis, TM perforation, suppurative
labyrinthitis, FN paralysis, brain abscess, lateral sinus thrombosis, subperiosteal
abscess, petrous apicitis
o Complications assoc with bony infx 2/2 osteomyelitis or cholesteatoma,
thrombophlebitis, or through congenital dehiscence
o Perforated TM: Pus/bloody drainage with subsequent pain relief
 Mgmt: PO abx + Ofloxacin otic HC 4 gtts q12h x7-10 days
 Avoid topical aminoglycosides/alcohol, neomycin/polymixin
B/hydrocortisone
 Outpt audiogram and ENT f/u if persistent hearing loss
 Chronic perforation >6 wks ±pus drainage needs f/u with ENT
5. Parotitis (suppurative): Acute unilateral induration/edema of parotid
 Due to obstructing sialolith/neoplasm, stasis, decreased salivation
(anticholinergics), poor oral hygiene/intensive dental cleaning, malnutrition,
immunocompromised (elderly, DM)
 Presentation: Firm swelling with erythema, esp pre and postauricular region.
pain, trismus, dysphagia, f/c. may express pus from duct
 Etiology: Polymicrobial with staph, oral flora, some GN (Klebsiella in DM)
 Ddx: Sialolithiasis, neoplasm, nonsuppurative parotitis
 Dx: Clinical. Send pus for culture, esp if performing needle aspiration. CT may
show stone, tumor, or abscess, most sensitive. May use US to see
stone/abscess
 Mgmt: Hydration, IV abx x10-14d
o Vancomycin 15-20 mg/kg q12h
o Metronidazole 500 mg IV q6-8h or clindamycin 600-900 mg q6-8h
o (consider Zosyn 4.5 g q6h, imipenem 500mg q6h or meropenem 1 g IV q8h
in immunocompromised)
 Dispo: Oral abx for PO tolerating pts with no e/o systemic illness,
hospitalization & parenteral abx for inability to tolerate PO liquids,
immunocompromised, no improvement with outpt mgmt in 48 hrs
 Complications: Neck swelling, respiratory compromise, facial bone osteo,
Lemierre’s syndrome, FN palsy, sepsis
 Nonsuppurative parotitis

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 o Viral: E.g. mumps, influenza, coxsackievirus, EBV, lymphocytic
choriomeningitis virus, paraflu, HSV, CMV, HIV. Often b/l, assoc with
prodromal period, no pus from duct
o Noninfectious: Collagen vascular dz, cystic fibrosis, alcoholism, DM, gout,
uremia, sarcoidosis, ectodermal dysplasia syndromes, familial dysautonomia,
sialolithiasis, tumors, drug-related disorders

6. Peritonsillar cellulitis/abscess (quinsy)

 Extension of tonsillitis into peritonsillar space forming abscess, esp in
teens/young adults, immunocompr, DM
 Presentation: Fever, odynophagia, unilateral sore throat, otalgia. Muffled
voice, trismus, unilateral uvula deviation, soft palate fullness/edema, +/-
drooling.
 Etiology: Polymycrobial (GAS, oral anaerobes e.g. Bacteroides). Abscess with
fluctuant, swollen tonsil
 Ddx: Epiglottitis, RPA, pharyngitis
 Dx: Clinical, may be difficult to differentiate cellulitis vs. abscess
o Consider U/S w/ endocavity probe to diagnose and also localize site for
needle aspiration – anesthetize first with topical/injected/nebulized lidocaine
o Send strep cx, gram stain/cx of pus from abscess
 Mgmt
o IV abx: Clindamycin 600-900 mg q8h or Ampicillin/Sulbactam 3g q6h or
Piperacillin/Tazobactam 4.5 g q8h, +/- Vancomycin IV 15 mg/kg q12h
o PO abx: Augmentin 45 mg/kg or 875 mg bid or Clindamycin 15 mg/kg or
300-450 mg q6h or Linezolid 20 mg/kg or 600 mg bid, total 14 days
o Steroids: Mixed evidence. Decadron 10 mg IV
o If abscess: Drainage via needle aspiration vs. I&D. Similar success
 Needle aspiration: Apply 2% viscous lidocaine topical, get good light
source. Inject 1% lidocaine into area, aim posterior-medial with 18-20 g
needle, insert 2 cm deep and aspirate (use “needle guard” by cutting needle
cap 2 cm from tip, replace cap onto needle). AVOID internal carotid artery!
May require repeat aspiration in 4-10% but less invasive
 I&D: Usually by ENT. May cause pulm aspiration of pus, more bleeding
o Tonsillectomy if: Upper airway obstruction, recurrent pharyngitis/PTA, failure
of abscess resolution
 Dispo
o D/C if able to tolerate PO, no airway compromise
o F/u in 24-36 h esp if no pus aspirated, return for dyspnea, trismus,
meningismus, bleeding
 Complications: Airway obstruction, aspiration PNA, sepsis, IJ thrombosis/
thrombophlebitis, carotid artery rupture/pseudoaneurysm, mediastinitis, nec
fasc, rheumatic fever (2/2 GAS)

7. Pharyngitis
 Presentation: Sore throat
 Etiology
o Bacterial: Grp A strep, Neisseria gonorrhea, C. diphtheria
o Viral: EBV, HSV, influenza, rhinovirus, coxsackievirus A
 Ddx

172
 o Acute: Consider RPA, PTA/cellulitis, supraglottitis/epiglottitis, noninfectious
(stevens-johnson syndrome, pemphigus, angioedema).
o Chronic: GERD, OSA, fungal (candida), chronic sinusitis with postnasal drip,
chemical irritants, glossopharyngeal neuralgia, CA (pharyngeal, lingual,
tonsillar), monomyelocytic leukemia, thyroiditis
 Dx: Clinical. Assess for assoc sx, trauma, trismus, facial pain, meningismus,
infectious contacts, etc
o Centor criteria for Grp A strep: 1) Tonsillar exudates, 2) Tender anterior
cervical adenopathy, 3) Fever, 4) No cough
o If 3-4 criteria, PPV GAS 40-60%, if 0-1 criteria, NPV GAS 80%
o Rapid strep: Sn 70-90%, Sp 90-100%. Negative does not R/O strep
o Strep culture: Sn 90%, Sp 95-99%
o Strep serology: ASO titers for rheumatic fever, but not useful for strep
pharyngitis
 Other
o Diphtheria: Grey-white pharyngeal pseudomembrane
o EBV: Palatal petechiae, splenomegaly, posterior cervical adenopathy.
Atypical lymphocytosis (>=10% of total lymphocytes), heterophile ab (high
st
false neg during acute phase, up to 25% 1 wk, consider if persistent sx), EBV
serology (Sn 97%, Sp 94%, use only if need to confirm EBV). Suspect in pts
with rash after ampicillin/amoxicillin
o Lateral neck XR: Consider if suspect epiglottitis in sick pt (thumb sx, thick
epiglottic/aryepiglottis)
o CT neck: Evaluate deep space neck infection (peritonsillar, retropharyngeal,
parapharyngeal abscess), difficult if unable to lie flat
 Mgmt: Symptomatic in most, abx for abscess/strep
o Gargles: Salt water, Magic mouthwash (1:1:1 of 2% lidocaine, Benadryl
12.5 mg/5mL, Maalox, swish/gargle/spit 1-2 tsp q6h prn)
o Consider steroids if severe pain or if difficulty taking po – Decadron 10 mg
(0.6 mg/kg) PO/IV x1
o NSAIDs, analgesics
o Abx for strep: PCN G IM 1.2 million U (25,000 U/kg) IMx1 or PCN VK 500
mg PO bid x10 days (peds 12.5 mg/kg po qid x10 days). If PCN all:
Clindamycin 300-450 po tid x10 days
 Dispo: Admit if sx of upper airway obstruction or immunocompromised,
epiglottitis or RPA; o/w D/C home if able to tolerate po

8. Stomatitis
 Presentation: Infectious mouth and throat lesions
 Etiology: Usually viral
o Enteroviral (e.g. herpangina/hand foot mouth dz/Coxsackie): Oral lesions ±
fever, rash, abd pain, diarrhea
o Herpes (herpes simplex gingivostomatitis): Painful oropharyngeal lesions,
recurrent, high fever during primary infection
o Adenovirus: Acute pharyngitis with fever and tonsillar erythema
o EBV/CMV: Exudative pharyngitis with fevers, malaise
 Ddx: Behcet disease, oral cancer, cicatricial pemphigoid
 Dx: Clinical, viral culture is gold standard. Consider enteroviral PCR; also
Tzanck smear for herpes
 Mgmt
173
 o Supportive care with acetaminophen/ibuprofen, topical analgesics, oral
rehydration
o Viscous lidocaine not recommended (risk for toxicity)
o Mixture of diphenhydramine and Maalox for local pain relief
o Consider IV rehydration for PO intolerance due to pain
o Systemic antiviral therapy for severe dz (acyclovir)
 Dispo: Admit and give IV acyclovir 5 mg/kg q8h for immuno-compromised pts
 Complications: Rare. Viral meningitis, meningoencephalitis, myocarditis,
sepsis; prognosis for primary HSV infx beyond fetal/neonatal period good, latent
infections (less severe) can occur later

Cardiovascular Infections
1. Endocarditis
 Risk factors: Congenital or acquired valvular disease, prosthetic valves, IVDU,
poor dental hygiene, hemodialysis, DM, previous endocarditis,
immunocompromised
 Presentation: Classic triad (fever, murmur, anemia) is insensitive
o Fevers, malaise, chest pain, heart murmur SOB
o Arthralgias, myalgias, back pain, cough, neuro symptoms, weight loss, night
sweats
o Vascular, septic emboli, Roth’s spots, janeway lesions, splinter
hemorrhages, osler’s nodes
 Etiology: Staph aureus, Strep viridans, Enterococci most common
o IVDU: Staph aureus, Strep viridans, Pseudomonas, Fungi
o Community-acquired, native valve: Strep viridans, Staph aureus,
enterococcus, <5% HACEK (Haemophilus, Aggregatibacter, Cardiobacterium,
Eikenella, Kingella) gram negative rods
o Prosthetic valve : <1 month Staph epidermidis, >1month Staph aureus
o Elderly: Enterococci; with GI process – Strep bovis
o Immunocompromised/critically ill: Fungi, pseudomonas
 Ddx: Pneumonia, CHF, Septic Arthritis, Meningitis
 Dx: Maintain high-suspicion given vague and varied presentation
o Modified Duke Criteria rarely helpful in ED
o Labs: CBC, ESR, UA, Cr/BUN, Blood cx x3
o EKG: New AV blocks, complete heart block, AMI, bundle branch blocks.
o Echo: Valvular mass, new valvular regurgitation, intracardiac abscess,
dehiscence of prosthetic valve
o CXR: Multiple b/l pulmonary infiltrates (septic emboli)
o CT chest w contrast: septic emboli, abscesses, necrotic lesions
 Mgmt: Empiric antibiotics: Vancomycin 15mg/kg IV + Gentamicin 1mg/kg IV
(+Rifampin 600mg PO for prosthetic valve)
 Dispo: Admit to cardiology for IV abx, serial blood cultures, and surgical
evaluation

2. Myocarditis, pericarditis – see Cardiovascular chapter

Pulmonary Infections
1. Pneumonia
 Presentation: Fever, cough, SOB, purulent sputum, dyspnea, pleuritic CP
o Clinical features and exam may be lacking in altered/elderly patients
174
 o Peds
 Tachypnea is most sensitive predictor for dx
 Infant: Lethargy, poor feeding, apnea, flaring/grunting/tachypnea, vomiting,
diarrhea, dehydration, bradycardia/shock (may p/w no resp sx but just fever,
dehydration, tachypnea)
 Chlamydia causes afebrile pneumonitis w/staccato cough/rales in otherwise
well infant (occurs in 2wo-2mo), may have conjunctivitis
 Child: Malaise, HA, fever/chills, tachypnea/hypoxia/cough  WOB, pleuritic
CP
 Etiology
Age Organisms
Neonatal E. coli, GBS, S. aureus, Listeria monocytogenes, C.
trachomatis. Bacterial > viral
3 wk–4 mo C. trachomatis, S. pneumoniae, viruses
6 wk–4 yr S. pneumoniae, B. pertussis, RSV, Influenza
≥4 yr S. pneumoniae, Mycoplasma pneumoniae,
Chlamydia pneumoniae, Influenza
* Mycoplasma most common in 5-15yo
Adult CAP Outpatient S. Pneumoniae, C. Pneumoniae, Mycoplasma,
Legionella, H. flu, Viruses
Adult CAP Inpatient C. Pneumoniae, H. flu, Klebsiella, Legionella,
Wards Mycoplasma, S. Aureus, S. Pneumoniae, Viruses
Adult Healthcare Enterobacter, E. coli, H. flu, Klebsiella, MRSA, S.
Associated (HCAP) Pneumoniae
Adult ICU or Structural C. Pneumoniae, H. flu, Legionella, Mycoplasma,
Lung Disease Pseuodomonas, S. Aureus, S. Pneumoniae
oPseudomonal risk factors: Structural lung disease (CF, bronchiectasis),
repeated severe COPD exacerbations requiring frequent steroid/abx, recent
mech vent, recent broad-spec abx, advanced HIV
o Health-care associated pneumonia: Nursing homes or extended care
facilities; hospitalization for 2 or more days in acute care facility in past 90 days
of infection; HD within 30 days; IV antibiotics, chemotherapy, or wound care
within 30 days of infection. At risk for MRSA and pseudomonas
 DDx: COPD, Asthma, Bronchitis, PE, CHF, ACS, Pneumothorax
o Consider pertussis if <2 mo
 Dx
o Leukocytosis with left shift
o CXR with focal consolidation or patch interstitial infiltrates
o Lactate to evaluate for severe sepsis (PNA #1 cause of sepsis)
o Blood cx x2 prior to antibiotics for following conditions* or if admitting
*ICU admissions, alcohol abuse, cavitary lesions, chronic liver disease, pleural
effusion, leukopenia, asplenia
 Mgmt
oAdult: Antibiotics must be administered <6 hoursfrom triage time; if delayed
due to atypical presentation, must document “diagnostic uncertainty”

175
Condition Treatment
Community Doxycycline 100 mg PO bid x7-10 days OR
acquired Azithromycin 500 mg PO then 250 mg po daily x4 days
pneumonia – *If recent abx: Levofloxacin 750 mg PO daily x5 days OR
outpatient
Amoxicillin 1 gram PO TID + Doxycycline or
Azithromycin as above
Community Ceftriaxone 1 gram IV + Doxycycline 100 mg PO/IV (to
acquired cover atypicals)
pneumonia (CAP) – *Severe PCN allergy: Levofloxacin 750mg IV
inpatient
Healthcare- SFGH: Doxycycline 100 mg PO/IV +
associated (HCAP) Cefepime 1 gram IV + Vancomycin 1 gram IV
*see above for *If ICU-bound, substitute Doxycycline with Azithromycin
definition 500 mg IV
*Severe PCN allergy: Levofloxacin 750 mg IV +
Tobramycin 5 mg/kg IV + Vancomycin 1 gram IV

UCSF: Vancomycin 1 gram IV + [Levofloxacin 750 mg IV

OR Zosyn 4.5 grams IV OR Cefepime 2 grams IV]
±Azithromycin 500 mg IV
*Consider adding Doxycycline (floor) or Azithromycin (ICU)
if not using levofloxacin
*Severe PCN allergy: Aztreonam 2 gram IV +
Vancomycin 1 gram IV ± [Doxycycline 100 mg IV/PO OR
Azithromycin 500 mg IV]
ICU patients Vancomycin 1g IV (to cover MRSA) +
Azithromycin 500 mg IV +
Ceftriaxone 1 g IV
*If severe PCN allergy: Vancomycin 1g IV + Levofloxacin
750 mg IV
Pseudomonas risk Zosyn 4.5 grams IV OR Cefepime 1 gram IV
factors *SFGH has Cefepime only
Aspiration Levofloxacin 750 mg IV; consider anaerobe coverage
*GPCs, GNR, (Clindamycin 450-900 mg IV) if not improved or foul
anaerobes smelling sputum
Note: Do not initially treat aspiration pneumonitis with
abx.
o Peds
 Inpatient – see table below
 Ampicillin 50 mg/kg IVq6h
 Azithromycin 10 mg/kg q24h POx1 (max 500 mg) then 5 mg/kg PO q24h
x4 days (max 250 mg)
 Ceftriaxone 50 mg/kg IV q24h (do not use if age <2mo)
 Erythromycin 5-10 mg/kg IV q6h
 Gentamicin 2.5 mg/kg IV q8h
 Vancomycin 15 mg/kg IV q6h
176
 Age Common bacteria Abx*
Birth-4wks GBS, E coli, Listeria Amp + gent or amp/cefotaxime
1-3 mo S aureus, H flu, S pneumo, Ceftriaxone (add erythromycin if
Chlamydia suspect Chlamydia)
3 mo-5 yrs S pneumo, Mycoplasma, S Ceftriaxone (add macrolide if
aureus, H flu suspect mycoplasma)
5-12 yrs Mycoplasma S pneumo, Macrolide ± ceftriaxone
*Add vancomycin if very ill to cover resistant strep or staph aureus
 Outpatient treatment of CAP
 1-4 mo: C. trachomatis pna – azithromycin 10 mg/kg q24h POx1 (max
500 mg) then 5 mg/kg PO q24h x4 days (max 250 mg)
 4mo-4yrs: Amoxicillin 80-100 mg/day div BID (max 2g/day) x7-10 days or
Cefdinir (14 mg/kd/day, max 600 mg/day) or Clindamycin (30-40
mg/kg/day div q6-8h, max 1-2 g/day)
 ≥5 yrs: Azithromycin 10 mg/kg x1 day (max 500 mg) then 5 mg/kg q24h
PO x4 days (max 250 mg)
 Dispo
o Adult: Use clinical picture, comorbidities, age, clinical tools. All clinical tools
should be used with caveat – patient must be reliable, no other significant
comorbidities (immunosuppressed, structural lung disease)
 Well appearing, no comorbidities, no hypoxia/tachycardia, single lobe
involvement, reliable pts may be discharged home; Otherwise consider admit
 CURB-65: Confusion, Uremia ≥20 mg/dl, RR ≥30, BP (SBP <90 or DBP
≤60), Age ≥65
# Factors 0 1 2 3 4
30 day mortality 0.7% 2.1% 9.2% 14.5% 40%
Site of care Outpatient Floor Floor vs. step down ICU
 PSI (aka “PORT score”): Uses comorbidities, age.
Go to www.mdcalc.com/psi-port-score-pneumonia-severity-index-adult-cap/
Points <51 51-70 71-90 91-130 >130
Class I II III IV V
30 day mortality 0.1-0.4 0.6-0.7 0.9-2.8 8.2-9.3 27.0-31.1
Site of care Outpatient Obs/short stay Floor ICU
 SMART COP: Consider ICU admission if ≥5 points
 SBP <90 (2)
 Multilobar infiltrates on CXR (1)
 Albumin <3.5 g/Dl
 RR: <50 yo – ≥25; ≥50 yo – ≥30 (1)
 Tachycardia ≥125 (1)
 Confusion - new (1)
 Oxygen low: <50 yo – PaO2 <70, SaO2 <93%, PaO2/FiO2 <333; ≥50 yo –
PaO2 <60, SaO2 <90%, PaO2/FiO2 <250 (2)
 pH <7.35 (2)
# Points 0-2 3-4 5-6 >7
Risk of IRVS Low Moderate (1 in 8) High (1 in 3) Very high (2 in 3)
*IRVS = intensive respiratory or vasopressor support
o Peds: Admit if <3mo, hx of apnea/cyanosis/desat w/crying/feeding/exertion,
lung dz, prematurity, toxic/dyspneic/hypoxic (<92% sat), severe WOB, not
tolerating PO, empyema or other complications, not improved in 1-2d after tx
177
 GI infections
1. Appendicitis
 Presentation: Anorexia, acute onset periumbilcal pain migrating to RLQ, fever
 Etiology: Bacteroides, Enterobacteriaceae (E. Coli, Klebsiella, Proteus)
 DDx: Torsion, diverticulitis, cystitis, ectopic; Yersinia ileocecitis
 Dx: CT abdomen with contrast vs US (in young thin pts, female, peds)
 Mgmt: NPO, IV fluids, analgesia, Surgery consult
o UCSF: Zosyn 4.5 grams IV
o SFGH: Ertapenem 1 gram IV
 Dispo: Admit to surgery

2. Cholecystitis
 Presentation: RUQ or epigastric abdominal pain, nausea/vomiting, +Murphy’s
sign, worse with eating, fever
 Etiology: Bacteroides, Clostridium, Enterobacteriaceae, Enterococcus
 DDx: Pancreatitis, cholangitis, hepatitis, mesenteric ischemia, PUD
 Dx
o Leukocytosis, elevated alk phos/t bili
o US: Shadowing stones, sonographic murphy’s (pressure applied with probe
with gallbladder in view causes tenderness), gallbladder wall thickening (> 4
cm), pericholecystic fluid, common bile duct enlargement (4-5 mm + 1 mm for
every decade of life over 50)
 Mgmt: NPO, IV fluids, analgesia, Surgery consult
o UCSF: Zosyn 4.5 grams IV
o SFGH: Ertapenem 1 gram IV
 Dispo: Admit to surgery
 Cholangitis: Admit to medicine, consult GI for ERCP

GU Infections
1. Lower tract infections (e.g. cystitis/UTI)
 Presentation: Dysuria, frequency, urgency, nausea, hematuria, suprapubic
abdominal pressure/pain. No fever or flank pain
oUncomplicated UTI: Female, nonpregnant, nondiabetic, no other major
comorbidities with brief duration of symptoms (<7days)
oComplicated UTI: All men, pregnancy, DM, all patients with anatomic
abnormalities, comorbidities, indwelling stents/catheters/foleys, calculi,
obstruction, neurogenic bladder, spinal cord injury, immunosuppression,
 Etiology
Age Bug
Adult Uncomplicated Enterobacteriaceae (E. coli, Klebsiella),
Enterococci, Staph. saprophyticus
Adult Complicated + Pseudomonas
Pediatric E. coli, Proteus, Staph. saprophyticus, enterococci
Uncomplicated
Pediatric Complicated + Pseudomonas
 DDx: STI, kidney stone, diverticulitis, vaginitis, appendicitis
 Dx: Urine analysis
o Upreg in all women of child-bearing age
178
 o Always send urine culture in children & men, but no routine cx for first
presentation of uncomplicated UTI
oNo white cells on UA: Consider periurethral herpetic infx in females
 Mgmt
oUncomplicated UTI: Nitrofurantoin 100 mg po BID x5-7 days (do not use in
renal failure), cephalexin 500 mg qid x7 days. May consider bactrim DS 1 tab
po BID x3 days if no previous abx tx (caution due to high resistance)
oComplicated UTI: Consider cephalexin 500 mg qid x7 days or ciprofloxacin
500 mg PO BID x 5-14 days or consider admission for IV abx if suspect
resistant organism
oPeds: Cephalexin 10-25 mg/kg PO q6-8h x 5 days (if >3yo)
 General IV abx: Ceftriaxone 1 gram IV, levofloxacin 500 mg IV, or
gentamicin 3-5 mg/kg IV
 ESBL: Ertapenem 1 gram IV; may use meropenem 2 gram IV if concern
for serious urosepsis or pseudomonal risk factors; avoid imipenem 2/2
decreased seizure threshold
 Enterococcus: Ampicillin 1 gram IV q6h or amoxicillin 500 mg PO q8h
oFor symptomatic relief, consider phenazopyridine (Pyridium) 200 mg PO
TID x 2-3 days (will turn urine and other secretions orange, avoid contact
lenses). Use >2-3 days increases risk of methemoglobinemia
 Dispo: Usually home if no evidence of pyelonephritis or urosepsis

2. Upper tract infection (e.g. pyelonephritis)

 Presentation: Cystitis symptoms, plus fever, chills, nausea, vomiting, flank
pain. May have a history of frequent or resistant UTIs. +CVA tenderness, +/-
suprapubic pain on exam
o Older or male pts do not have to have flank pain or cystitis sx
 Etiology: Similar as UTI
 Ddx: Renal stone, AAA/dissection, acute glomerulonephritis (casts in urine),
papillary necrosis (fever, flank pain, gross hematuria w/o infection, consider in
sickle cell)
 Dx
o Labs: BUN/Cr, UA, UCx, consider imaging if concern for obstruction (e.g.
infected stone)
 Mgmt
o Outpatient: Cephalexin 500 mg PO qid x10-14 days (ok for pregnancy) OR
ciprofloxacin 500 mg po bid x10-14 days OR [Bactrim 1 DS po bid x14 days
+ ceftriaxone 1 gram IV x1]. DO NOT USE NITROFURANTOIN
o Inpatient: Ceftriaxone 1 gram IV or Ertapenem 1 gram IV (if concern for
ESBL); consider Zosyn 4.5 gram IV if concern for pseudomonas/health-care
acquired
o Peds: Cephalexin 10-25 mg/kg PO q6-8h x10 days then adjust based on
st st
culture results. Can give 1 dose ceftriaxone 50 mg/kg IV/IM or 1 dose
cephalexin in ED
o Supportive care: Antipyretics, antiemetics, and IVF
 Dispo
o Admit if ill-appearing, pregnant, unable to take PO, comorbidities (single
179
 kidney, renal txp, old age); otherwise d/c home
o Peds: Return for admission if persistent fever/vomiting despite tx X 48h. If <3
mo age or recurrent, f/u with PMD to R/O reflux/anatomic abnormality

Skin infections
1. Cellulitis
 Presentation: Redness, warmth, tenderness, edema
 Etiology: Staph & strep
 DDx: Erisypelas, abscess, necrotizing fasciitis, osteomyelitis, DVT, gout
 Dx: Clinical
 Mgmt
o Outpatient
 Cephalexin 500 mg PO qid + bactrim DS 2 tabs PO bid x10 days OR
 Cephalexin 500 mg PO qid + doxycycline 100 mg PO bid x10 days OR
 Clindamycin 300-450 mg PO TID x10 days (better compliance, but less
MRSA coverage)
o Inpatient
 Vancomycin 1 gram IV
 Clindamycin 600-900 mg IV PLUS [Zosyn 4.5 gram IV OR Ertapenem 1
gram IV] if concern for necrotizing fasciitis
 Surgery c/s ASAP if concern for necrotizing fasciitis
 Dispo: Home unless there are signs of systemic toxicity, homeless/unreliable/
immunocompromised with severe disease. Admit to ICU if concern for
necrotizing fasciitis

2. Necrotizing fasciitis: see Dermatology chapter

Bone & Joint

1. Septic arthritis
 Presentation: Red, hot, swollen, painful joint with pain on ROM & ttp
 Etiology
Category Bugs
< 5 years S. aureus, GBS, Hib, gram- negative bacteria
> 5 years S. aureus, GAS
Adolescents & adults S. aureus, Streptococcus, Enterococcus, GNR,
(including prosthetics, IVDA) N. gonorrhoeae, C. trachomatis
Sickle cell anemia Salmonella
 DDx: Gout, pseudogout, osteomyelitis, rheumatoid or osteoarthritis flare,
trauma
 Dx
o Labs: CBC with leukocytosis, ESR (>30 in 95%), CRP (elevated in 98%); XR
to evaluate for osteo
o Arthrocentesis: Send for gram stain, culture, cell count, crystals. Do not tap if
prosthetic/post-op, overlying cellulitis
 Cultures positive in 90%
 WBC >50k-100k, 75% PMNs (though caution – MRSA has been isolated
with lower WBCs)

180
  Crystals do not rule out septic joint – gout predisposes joint for infection
 Mgmt
o Ortho consult
o Ceftriaxone 2 grams IV + Vancomycin 1 gram IV
o Add pseudomonal coverage if prosthetic joint: Zosyn 4.5 grams IV instead of
ceftriaxone or gentamicin, ciprofloxacin
 Dispo: Admit to ortho for washout

Antibiotic Coverage
Gram Negatives Gram Positives Anaerobes
Cephalosporins Vancomycin (IV) Metronidazole (IV & PO)
Beta-lactamase inhibitors (IV Linezolid (IV) Carbepenems
& PO)
Flouroquinolones (IV & PO) Daptomycin (IV) Beta-lactamase
inhibitors
Carbepenems Chloramphenicol (IV)
Aminoglycosides Clindamycin (IV & PO)

Drug Gram + Gram - Anrb/Atyp Notes

Penicillin Strep Lesser (-) Anaerobes No B.Frag
Ampicillin Enterococcus poor *Amp DOC
Amoxicillin Listeria* Listeria
Nafcillin Strep / Staph NONE NONE “Staph
hunter”
Meropenem Strep / Staph Lesser (-) Anaerobes Big gun at
/ Ecoccus- Greater (-) UCSF –
weak least
resistance
Penicillins

Ertapenem Strep / Staph Lesser (-) Anaerobes Holes:

Greater (-) Pseudo-
monas,Acine
-tobacter
Ampicillin/ Strep / Staph Lesser (-) Anaerobes No activity
Sulb(Unasyn) for C.
Amox/Clv Enterococcus difficile
(Augmentin)
Pipercillin/ Strep / Staph Lesser (-) Anaerobes No activity
Tazobactam Enterococcus Greater (-) against C.
difficile
Aztreonam NONE Lesser (-) NONE OK in true
Greater (-) PCN allx
Cefazolin Strep / Staph Proteus/E. NONE
Ceph

coli/ H.flu/
Klebsiella
181
 3 Cefotaxime Strep / Staph Lesser (-) Poor anrb Holes:
3 Ceftriaxone Serratia SPACE
bugs
3 Ceftazidime Strep / Staph Lesser (-) Ceftaz – Ceftaz –
4 Cefepime Greater (-) anaerobes poor
Strep/Staph
/B.frag
2 Cefuroxime Strep / Staph Lesser (-) Anaerobes Hole: B.frag
2 Cefoxitin Strep / Staph Lesser (-) Anaerobes B.frag ~
30%
resistant
1 Cephalexin Strep / Staph Proteus / Poor anrbe
E. coli /
Klebsiella
3 Cefixime Strep sp. Lesser (-) Poor anrbe
(weak)
Levofloxacin Strep / Staph Lesser (-) Atypicals Moxi – not
Moxifloxacin / Listeria Greater (-) for UTIs,
Ciprofloxacin MRSA & Legionella anaerobic
Ecoccus coverage
FQs

weak ok
Moxi -
Stenotroph
omonas
Azithromycin Strep / Staph Legionella Atypicals Strep –
Clarithromycin / Listeria / Neisseria resist
Erythromcyin H. flu growing;
Staph –
MACs

weak
Holes:
MRSA,
poor gram
(-)
Doxycycline Strep/ CA- Lesser (-) Atypicals Holes:
Minocycline MRSA Legionella Anaerobes* B.frag,C.diff
/Listeria Proteus
Tigecycline Strep/Staph/ Lesser (-) Anaerobes Increased
MRSA/ Serretia/E mortality in
Tets

Ecoccus bacter hosp. infx

Listeria
Amikacin Staph/Listeria Lesser (-) None Holes:
Tobramycin Gram (+) Greater (-) Acineto-
AG

Gentamicin synergy only bacter

182
 Metronidazole NONE NONE Anaerobes C.diff
D.O.C.
Clindamycin Strep/Staph/C NONE Anaerobes
A-MRSA
weak
Vancomycin Strep/Staph/ NONE C.diff
MRSA/
Ecoccus/List
Linezolid Strep/Staph/ NONE NONE Need ID
MRSA/VRSA/ approval
VRE
Potent Potables 

Ecoccs /
Listeria
Daptomycin Strep/Staph/ NONE NONE Holes: PNA
MRSA/VRSA/ tx, lung infx
VRE source
Ecoccs / Need ID
Listeria approval
Septra Strep/Staph/ Lesser (-) NONE Holes:
MRSA/ weak group A
Listeria S.maltophi strep
lia-d.o.c pharyngitis
or E.
faecalis
Nitrofurantion
Strep/Staph/ E.coli NONE For Urine
MRSA/Ecocc infx only!
us/VRE
*Antibiotic charts courtesy of Zlatan Coralic
The Legend
Greater (-) Lesser (-) Anaerobes Atypicals
Serratia H. influenza Actinomyces Chlamydophila
Pseudo-monas E. coli B. Frag M. pneumoniae
Acinetobacter Neisseria Clostridium (not diff) Mycobacterium
Citrobacter Proteus Peptostreptococcus
Enterobacter Klebsiella
*Abbreviations: DOC – drug of choice, allx – allergy, CA-MRSA – community
acquired MRSA, VRSA – Vanco resistant Staph, VRE – Vanco resistant Ecoccus

Suggested reading
 Uchihara T, Tsukagoshi H. Jolt accentuation of headache: the most sensitive
sign of CSF pleocytosis. Headache. 1991; 31(3): 167

183
 Neurology
By Joe Freeman Res ed. Hangyul Chung-Esaki Faculty ed. Bill Whetstone

Altered Mental Status

1. AEIOU TIPS
 A: Alcohol (Vit B12, thiamine deficiency), Arrhythmia
 E: Encephalopathy (infection, hepatic, HTN), Endocrinopathy
(hyper/hypothyroid, hyper/hypocortisol), Electrolytes (hyper/hypoNa,
hyper/hypoCa, hypophosphatemia)
 I: Insulin (hyper/hypoglycemia)
 O: OD, O2 (hypoxemia, hypercapnia, severe anemia/hemorrhage, ↓O 2 to brain
 ↓cardiac output, CO poisoning)
 U: Uremia
 T: Trauma, Tumor (lesions w/mass effect, hydrocephalus, cerebral edema),
Temperature (hypo/hyperthermic)
 I: Infection, Inflammatory (TTP, vasculitis)
 P: Psych (dx of exclusion)
 S: Stroke (esp large hemispheric, brainstem), SAH/SDH/EDH/ICH, Sz (post-
ictal, non-convulsive status, complex partial), Shock

2. Coma
 “Don’t” coma cocktail: Fingerstick→1 amp (50cc/25g of glucose)
D50W(except infants) O2, Narcan (0.4-2mg IV/IM), Thiamine 100mg IV (if
malnourished/chronic EtOH, consider Wernicke’s)
 Level of arousal: Automatisms like coughing/swallowing→little significance;
response to voice (name loudly, clap hands), non-noxious stimuli (rub shoulder),
noxious stimuli (supraorbital pressure, pinch shoulder, nail bed pressure, pinch
limbs); all help find lateralizing signs
 Respirations
o Hyperventilation (metabolic derangement→sepsis, hepatic encephalopathy,
DKA, ↑ICP, mid-brain injury)
o Cheyne-Stokes (steady ↑→↓size of breaths→apnea, seen in diffuse cerebral
impairment→bilateral infarcts, HTN encephalopathy, CHF, metabolic
derangements, also sign of impending herniation w/supratentorial mass)
o Apneutic (end-inspiratory pause 2-3s) & ataxic (irregular size &
rate)→brainstem lesion
o Apnea (brain death vs deep metabolic coma)
 Pupils
o Equal & reactive: Intact midbrain
o Small & reactive: Metabolic encephalopathy→opioids, thalamic lesions,
bilateral hemisphere lesion, bilateral pons damage
o Pinpoint: Opiod OD, pontine lesion
o Large/mid-position & fixed: Midbrain insult, herniation, sympathomimetic,
anticholinergic, toxin
o Unilateral & dilated: Ipsilateral CN III palsy/midbrain lesion→uncal herniation
 Motor
o Flexor in arms & extensor in legs (decorticate)→less severe supratentorial
derangement
184
 o Extensor in arms/legs (decerebrate)→more severe supratentorial
derangement
o If flexor→extensor, suggest possible herniation

3. Delirium
 ↑Risk: >65yo, visual/hearing loss, hx EtOH, neuro dz (stroke, dementia), HIV,
ESRD, ESLD, terminal illness, depression
 Mortality 22-76%, often unrecognized in elderly
 Eval: R/o depression, mania & acute psychosis, infection, EtOH, medications;
consider ACS, urinary obstruction, fecal impaction, pain (commonly overlooked)
Delirium Dementia Psychiatric
Attention level Fluctuates Normal ±normal
Onset Sudden Gradual ±gradual
Level of Decreased Normal Normal
consciousness
Thought Disorganized Normal ±disorganized
process
Hallucinations Transient Only in advanced Sustained
disease
Delusions Transient Only in advanced Sustained
disease
Course Fluctuates over Gradually ±stable
course of hours progressive

Vertigo
1. Quick tips
 See High Risk CC chapter for approach in evaluation of “weakness/dizzy”;
consider other differential diagnoses before anchoring
o Neuro: Stroke/TIA, vasovagal presyncope, carotid sinus hypersensitivity
o CV: Dysrhythmia, hypovolemia, anemia
o Endocrine: Electrolytes, hypoglycemia
o Tox: Medication related side effects/overdose
o Other: Infection, Hyperventilation Syndrome
 3 most important aspects of neuro exam: Focal findings, gait, nystagmus
 Peripheral vs. central vertigo
Peripheral Central
Vertigo Acute, intermittent, severe, Progressive, constant, mild nausea,
intense n/v, provoked by no Δmovement
movement
Nystagmus Always; unidirectional ±if have, ±bidirectional (but
(horizontal, rotary but no vertical►central), no latency, no
vertical), latency 2-40s, fatigue, not decreased w/fixation,
fatigability, inhibited by Δdirection w/gaze
ocular fixation
Sx ±hearing loss/tinnitus Diplopia, rare hearing loss/tinnitus
(Meniere) (except acoustic neuroma),
brainstem/cerebellar findings
Gait Refusing to walk 2/2 fear of Willing to walk but unable to
severe sx
o Note: End point nystagmus→few beats when go far lateral is WNL
185
 o Timing
 Seconds: Likely BPPV
 Min-hrs: Vertebrobasilar TIA, migraine, partial sz, Meniere’s
 Hrs-days: Vestibular neuronitis, ischemia, MS
 Evaluate for cerebellar (vertebrobasilar) ischemia: 1/4 of pts with risk factors
(DM, smoking, HL, HTN, A fib, vascular dz) & acute vestibular syndrome
diagnosed w/ cerebellar infarct. Brain stem signs e.g. diplopia, dysarthria,
dysphagia, focal neuro-sensory/motor; infarct in inferior cerebellum rare,
presents w/ vertigo, nystagmus, postural instability.
 Mgmt
o Peripheral: Meclizine (25mg PO), diazepam (2-4mg IV/5-10mg PO),
diphenhydramine (25-50mg IV/PO)
o Central: Evaluate for posterior circulation stroke, consider neuro c/s
 Dispo
o Home if peripheral vertigo and healthy, <50yo, classic hx, no HA, no
AMS/focal, no vascular disease
o Consider imaging with CT head or MRI/MRA (early ischemia, 4 vessel
patency) and neuro c/s if concern for central with +HA/focal neuro findings, or
elderly

Facial Droop
1. Quick tips
 1 : Check FSBG
st

 2 : UMN vs. LMN (strength of eye closure/eyebrow elevation/forehead

nd

wrinkle→spared in UMN)

2. Stroke (until proven otherwise) – see Stroke section

 If UMN lesion or any other focal neuro sx (weakness, decreased sensation,
diplopia, dysarthria)

3. Bell’s palsy
 Gradual onset, painless. often noticed incidentally, unilateral taste loss of
anterior 2/3rds, hyperacusis; may be preceded by sensation of fullness
in/behind ear
 Bell’s phenomenon: Eye rolls back in head w/attempts to close the lid; can be
abrupt
 Bell's vs stroke
o Bell’s: LMN  forehead muscle weakness (no wrinkle), intact sensation
o Stroke: UMN  no forehead muscle weakness (wrinkle) ± sensation defect
depending on how large of area is hit
o Both: Facial (eyelid/cheek) weakness
 Highest incidence >70yo (also at risk for stroke, but often other findings); 60-
75% of all unilateral facial paralysis; ↑risk if pregnant
 Etiology: “AL with a STD”→AIDS, Lyme, Sarcoid, Tumor, DM; but most
commonly 2/2 Herpes (50% w/viral prodrome)
 Exam: Paralysis of upper & lower facial segments but no other neuro deficits;
do a full neuro exam (esp CN VI & VIII, CT scan if concern for stroke/AMS
 Mgmt (start tx w/in 1wk, best if w/in 3d)
o Prednisone 60mg qDAY X 5-7d, then taper 10mg/day (unless 2/2 Lyme)

186
 o Valcyclovir 1000mg PO TID X 7d (only for severe cases)
o Artificial tears, tape eyelid before sleeping
 Prognosis: Resolves completely w/ tx in 80% w/10% slight asymmetry & 10%
significant asymmetry

Headache
1. Quick tips - see High Risk CC chapter for general approach and management

2. Intracranial Hemorrhage
 Presentation
o Acute onset, HA, n/v (2/2 ICP), meningismus (2/2 intraventricular blood)
st
o Clinical deterioration may occur with hematoma expansion (usually 1 3 hrs)
or cerebral edema (24-72hrs)
o Depressed/LOC (large hematoma, increased ICP, direct compression RAS);
contralateral sensory/motor deficits
 Location
o Putamen (most common): Contralateral hemiplegia/sensory/conjugate gaze
paresis, homonymous hemianopsia, aphasia, neglect, apraxia, ±lethargic;
most common 2/2 HTN
o Cerebellar: Severe ataxia/vertigo/nystagmus, dysarthria, dysmetria ±↓LOC,
ipsilateral gaze palsy/facial weakness/sensory loss, no hemiparesis
o Thalamic: Contralateral sensory>motor; most common 2/2 HTN
o Pontine: Severe HA, hyperventilation, pinpoint pupils, no oculovestibular
reflex, decerebrate posturing; most common 2/2 HTN
o Lobar: Seizure, dense contralateral homonymous hemianopsia (occipital),
contralateral plegia/paresis of leg w/ arm sparing (frontal); most common 2/2
amyloid (esp in atraumatic elderly pts)
 Risk factors: HTN, EtOH, cerebral amyloid angiopathy; more common in older,
men (esp >55yo), blacks, Japanese
 Mgmt
o Coumadin associated bleed: Reverse potential coagulopathy immediately
 Vit K 10mg PO/SC (or IV diluted in NS over 1 hr)
 Bebulin 30-50U/kg (rounded up to next vial size; have pharmacy calculate
as each vial may vary)
 If stable w/minor bleed and not too high INR, may give FFP 10 ml/kg over
90min instead of Bebulin
 Consider 6 pack plts if hx of ASA or plavix
o Surgical evacuation: Cerebellar hemorrhage >3cm or clinical deterioration,
ICH w/accessible AVM, clinically deteriorating young pt with lobar hemorrhage;
often determined case by case
o Treat hyperthermia and hyperglycemia aggressively
o ICP mgmt
 ICP monitoring in pts w/GCS≤9, neuro deterioration 2/2 ↑ICP, ICH score≥2
*ICH score: 30d mortality ≥70% if ICH score≥3
GCS ICH volume IVH Infratentorial ICH Age
3-4 2 ≥30 1 Yes 1 Yes 1 ≥80 1
5-12 1 <30 0 No 0 No 0 <80 0
13-15 0

187
  Treat BP if >220/120 (2/2 uncontrolled HTN, stress, Cushing response-
HTN, bradycardia, irregular respirations) w/ labetalol 5-20mg IV q15min PRN
OR nicardipine gtt 0-15mg/hr
 Don't use nitropaste/venodilators as may increase ICP
 Antiemetics to avoid emesis
 Other: HOB to 30º (decreases ICP 5), hyperventilate to PaCO2 of 30 if
impending herniation, mannitol 0.25-1g/kg IV, furosemide 20-100mg IV
o Sz prophylaxis: Phenytoin load 20 mg/kg; consider levetiracetam
o 30-50% mortality, 20% independent@6m, 1/3 of non-traumatic enlarge w/in
24 hrs

3. Subarachnoid hemorrhage
 Presentation: Thunderclap w/acute onset (onset more important than
severity), often during exertional activities (sex, coughing, wt lifting),
meningismus, n/v, photophobia, ±sz, AMS, syncope (50%); ±low-grade fever
(blood is pyretic)
 Hunt-Hess Scale
o I: Asymptomatic/mild HA (70% survival)
o II: Moderate-severe HA, nuchal rigidity, no focal deficits(60%)
o III: Confusion, drowsiness, mild focal deficits(50%)
o IV: Stupor, hemiparesis (40%)
o V: Coma, moribund appearance, posturing (10%)
 30-50% have sentinel HA days-wks before SAH (usually 2-3 days)
 ↑Risk w/smoking, EtOH, drugs, HTN
 ↑Risk berry aneurysm w/FHx, coarctation of aorta, polycystic kidney dz,
Marfan, Ehlers-Danlos, AVMs
 Dx
o CT head: 5% sens w/in 6-24hrs, 80% at 3d, 50% at 7d
o LP if neg CT as CT angio not yet considered sufficient alone; ↑RBC in CSF
(but hemolyzed by 6-12hrs; xanthochromia peaks at 2d, gone by 2 wks)
 Mgmt
o If need to intubate→post-intubation sedation w/ midazolam or propofol (avoid
long-term NM blocking agents to monitor exam)
o Use nimodipine 60mg q 4hrs X 21d in H+H I-III to decrease vasospasm,
±phenytoin 13-15mg/kg IV at <40mg/min for seizure prophylaxis
o Goal SBP<140 (for unsecured aneurysms, unless suspect elevated ICP or
vasospasm)
 1st tx pain/anxiety
 Labetalol 5-20mg IV q15min PRN OR nicardipine gtt 0-15mg/hr
 Manage ICP as in “Intracranial hemorrhage” above;
o Antiemetics to avoid emesis which can ↑ICP
o No PO meds for possible surgery (pts need higher pressures s/p surgical
clipping/coiling)
o Definitive tx: Neurosurgical clipping (>7mm if unruptured) vs endovascular
coiling

4. CNS infections e.g. meningitis, encephalitis, abscess – see Infectious

Disease chapter

5. Pseudotumor cerebri/Idiopathic intracranial HTN

188
  Presentation
o Young, obese, ♀, childbearing age, OCPs, steroids, tetracycline, vit A,
Accutane, thyroid dz
o Moderate intensity daily/constant HA & visual c/o; HA classically worse on
awakening then improves during day; often general HA w/intracranial noise
(waterfall/blowing), CN VI palsy
 Etiology: Increased intracranial pressure with normal CSF
 Dx
o Exam: ±Normal; papilledema, Δvisual fields (peripheral vision), ±CN VI palsy,
no focal deficits (besides CN II/VI)
o CSF: Opening pressure>25 in lateral decubitus w/legs straight; normal/low
CSF protein/cell count
o CT: No mass/ventricular enlargement on CT head
 Mgmt
o Neuro consult
o Acetazolamide (start 1g PO→4g PO)
o Prednisone 60-100mg PO w/slow taper
o May require multiple LPs
o If severe sx/visual loss→VP shunt/optic nerve sheath fenestration
 Major complication is blindness from optic nerve compression

6. Cerebral edema & ↑ICP

 Presentation
o ↓MS, papilledema, unilateral blown pupil, progressive focal deficit, impaired
up gaze (CN 6 palsy)
o Cushing’s triad: bradycardia, respiratory depression, hypertension (2/2
brainstem compression)
st
o Leg spasticity may be 1 sign of ↑ICP
 Etiology: HTN encephalopathy, venous sinus thrombosis, CSF
(hydrocephalus), cerebral edema, global hypoxia, infection, mass (ICH, SDH,
EDH, tumor, abscess)
 Dx: Clinical (e.g. Cushing’s triad or e/o herniation in pts with traumatic brain
injury, stroke, mass, etc) – see Trauma chapter for herniation patterns
 Mgmt
o ↓ICP by elevating HOB to 30º
o Mannitol 50-100g IV q3-5hrs. Need to check serum osm & serum Na qdose,
hold if Sosm>320 or Na>150; caution w/renal failure/heart failure/pIV
(extravasation is bad)
o Hypertonic saline 3% NaCl 10-40 mL/hr to max Na 150
o 27.5% NaCl ‘bullets’ 10-20 cc over 5 min via central line if mannitol and 3%
fail
o Intubate w/hyperventilation goal pCO2 25-30 (prevents acute herniation short
term; save for dire situations as brief effect w/worse rebound-brain adjusts
buffering after 1-6hrs w/ sudden drop in pH with ICP spike when
hyperventilation stops)
o ↑MAP via NS if hypovolemic, pressors (neo if tachy, dopamine if brady)
o Tx hyponatremia aggressively as it can worsen edema and ↑ICP

7. Tumor

189
  Presentation: Worse when lying down/head forward, awakens pt from sleep,
worse upon awakening
 Etiology: Most common 2/2 mets from lung/breast
 Dx: CTH vs MRI (severity of HA not predictive)
 Mgmt:
o Dexamethasone 10mg IV then 4mg IV q6hr if edema or severe sx
o Neurosurgery c/s

8. Temporal arteritis
 Presentation: >50yo, HA (throbbing, frontotemporal, 85%), temporal
artery/scalp tenderness (70%, ±nonpulsatile), jaw claudication (65%)
 Etiology: Associated with polymyalgia rheumatica
 Dx: 3/5 of age>50, new localized HA, temporal artery TTP/↓pulse, ESR>50
(95%), bx
 Mgmt
o Prednisone 60-80mg/d for 1-2 yrs (start immediately if suspect dx so no
vision loss 2/2 ischemic optic neuritis
o Biopsy by optho/vascular w/in 3 days
o NSAIDs for pain

9. Trigeminal neuralgia
 Presentation: Electric shock-like pain V2/V3>>V1 distribution, unilateral (R>L),
trigger sites (tapping on side of face), last only secs
 Etiology: Trigeminal nerve compression (trauma, vessel aneurysm, tumor, etc)
 Mgmt: Anticonvulsant (carbamazepine 200mg/d or lithium), analgesia

10. Sinusitis – see Ear/Nose/Throat and Dental chapter

11. Migraine
 Presentation
o Classic (30%): Unilateral throbbing HA ± aura (Δvision that moves→jagged
lines, white spots, geometric shapes), n/v, blurred vision, photophobia; no focal
unless complicated migraine; sleep/quiet/dark helps, ±FHx, lasts hrs-days (4-
72hrs) w/diurnal variation (most occur w/in 6 hrs of certain time), HA begins
during or <60min after aura; slow onset
o Common migraine: Can be just about anything (incl neck pain, diffuse HA,
occipital HA)
o Auras: visual (most common)→scintillating scotoma, Δvisual field;
motor→hemiparesis, ophthalmoplegia, aphasia; sensory→hemiparesthesia,
dysesthesia; brainstem (basilar migraine)→vertigo, ataxia
o Migraine markers: ice cream HA, motion sickness, hangover HA, childhood
episodic n/v/abd pain
o 90% nausea, 75% vomit at some point, 20% loose BM, 80% hypersensitivity
of special senses
 Etiology: Unknown
o Identify triggers e.g stress, menses, OCP, pregnancy, chocolate, EtOH (esp
red wine), caffeine, hard aged cheese, MSG, nitrites, Δcircadian rhythm
 Mgmt

190
 o Abortive for mild-mod: Simple analgesics (NSAIDs e.g. naproxen 500mg
q8h has better BBB penetration than ibuprofen and lasts longer)
o Moderate-severe
 Prochlorperazine (compazine) 10mg IV/IM over 2 min, may repeat in 1 hr,
also good for n/v (Watch for akathisia)
 Droperidol 2.5mg IV; black box for prolonged QT  check ECG before,
place on monitor X 1hr
 Metoclopramide 10mg IV, may repeat in 30min
 Chlorpromazine 10mg IV/IM, may repeat 1 hr
 Sumatriptan (Imitrex) 6mg SC, may repeat in 1 hr, follow w/25mg PO to
prevent recurrence or 100mg PO as initial dose, onset 10-15m but ↓efficacy
as ↑time onset. CI in ACS risk pt & ergot w/in 24hrs
nd
 Fiorecet 1-2 tab at onset and can take 2 dose after 4 hrs, max 6/24hrs, 2
days/wk
 Reglan 10mg PO/IV
 Toradol 30mg IVx1
o For acute migraine w/vertigo can use sumatriptan or nifedipine gel cap
(bite off cap, suck out fluid, hold under tongue, lie down for 1 hr) or midrin po
1-2 tab at onset, then 1 capsule each ½ hr until relieved or 2 caps per hr, max
10/HA, 2 days/wk
o Prophylactic: βB, TCA, CCB, anticonvulsant
 Status migrainosus: Dihydroergotamine 1mg IV/IM q8hrs
w/metoclopramide 10mg IV before for antinausea (n/v common SE)
o May be fatal if used in undiagnosed SAH so do NOT use in ED w/o neuro
c/s; CI: triptan w/in 24hrs, ACS risk pt
 CI in pregnancy & CAD: DHE, sumatriptan, methysergide
 Never use triptans & ergots together
 Caution if 1 “migraine” >35yo (73% have 1 attack by 30yo) – r/o other
st st

causes
 Use of analgesics >10days qmonth can increase HA
frequency/duration/intensity

12. Tension headache

 Presentation: Dull, aching, bilateral, nonpulsating, not worse w/exertion, slow
onset in neck/occiput that worsens throughout day w/fluctuations that last
hrs/days; associated stress/muscle strain
 Mgmt: Abortives e.g acetaminophen 1g, ibuprofen 400-800mg, naproxen
500mg PO TID, indomethacin 25-100mg PO TID; midrin 1-2 tab@onset, 6 per
HA, 24 per month total

13. Cluster headache

 Presentation
o Usually ♂ 20-50yo, 50% w/EtOH sensitivity during attack
o Sudden onset unilateral stabbing eye/supraorbital/temporal pain
o In “clusters” (80% several attacks/day X hrs for up to 6-8wks, 15% chronic
w/>1yr long bouts)
o Severe pain, worse in particular season, diurnal (happen at same time every
day, like clockwork, often early AM)
o Cranial autonomic sx (30% w/Horner’s during/between bouts)
o Conjunctival injection, lacrimation, eyelid edema, miosis, ptosis
191
 o Nasal congestion, rhinorrhea
o Forehead & facial swelling, sense of restlessness/agitation
 Mgmt
o Sumatriptan 6mg SC (tx of choice)
o High flow O2 @ 15L/min X 15min (2/3 of pts respond)
o Intranasal cocaine/lidocaine (to anesthetize sphenopalatine region)
o Prednisone 60mg X 10d then 1 wk taper (try to avoid if possible)
o Prophylactic: CCB, ergots, lithium; consult neuro for f/u

14. Chronic subdural hematoma

 Presentation
o Sx onset >2wks s/p trauma (often occult)
o More common in elderly/EtOHics (brain atrophy)
o HA, unilateral weakness (50%), AMS, dementia
 Dx: CT head
 Mgmt: Supportive, correct coagulopathy, NSG for evacuation
 Consider subdural hygroma (collection of blood-tinged fluid in dural space,
density on CT=CSF) in ddx

15. Internal carotid/Vertebral artery dissection

 Presentation
o Most common cause of stroke<45yo
o Internal carotid: Unilateral anterior neck pain or HA around eye/frontal area,
±abrupt onset, ipsilateral Horner’s, contralateral CVA
o Vertebral: Occipital/posterior neck pain w/CVA
 Etiology: H/o neck manipulation/chiropractic/trauma
 Dx: MRI/MRA is best (less so CTA)
 Mgmt: Vascular/surgery c/s, anticoagulation for stroke prophylaxis

16. Cerebral venous sinus thrombosis

 Presentation: Vague/varied, HA, AMS, focal neuro, papilledema, sz
 Etiology: Adjacent local infection, trauma, hypercoagulability (pregnancy,
OCPs)
 Dx: MRV first choice; CT/MRI only helpful if positive (does not r/o)
 Mgmt: Heparin, catheter-based thrombolysis if severe sx

17. Post-LP headache

 Presentation
o W/in 1-7days
o Worse w/upright, better w/flat positioning
 Etiology: Incidence related to size/needle type
o 20G cutting needle:40%; 25G cutting needle:5%; 22G atraumatic needle:4%
o Use an 18g as the trocar to get through skin & soft tissue then thread
atraumatic needle through 18g
 Mgmt: Analgesia, IVF, caffeine 500 mg IV, blood patch (anesthesia c/s)

18. Other causes

 CO Poisoning, Glaucoma, HTN encephalopathy, traumatic bleed (epidural,
subdural hematoma)

192
 Seizure
1. Quick Tips
 Check immediate FSBG in all pts w/seizure
 Don’t delay steroids/abx If thinking meningitis; LP can be done later
 Most common cause of sz is treatment non-compliance
 Lactate should clear spontaneously w/in 1 hr
 Always perform 2º survey for injury e.g. posterior shoulder dislocation

2. Presentation
 Post-ictal (~15-30m), abrupt onset/termination, stereotyped behavior, lack of
recall, non-provoked, purposeless movement, incontinence
 Eclampsia: From >20wks up to 4wks postpartum
 Phenytoin tox: Gait ataxia (tandem walk), nystagmus
 Pediatrics – see Pediatrics chapter

3. Etiology
 CNS injury: Stroke, bleed, CA/tumor/abscess, encephalopathy, hypoxia, TBI
(10% risk with ICH, coma/amnesia >1 day)
 Drugs/tox: Cocaine/meth/speed/PCP, anticholinergics, EtOH, demerol, benzo
w/d, PCN, lidocaine, heavy metals, CO, mushrooms, toxic EtOHs
o Intentional OD: ASA, theophylline, INH (tx B6), TCA, lithium,
diphenhydramine, amphotericin, bupropion; supratherapeutic phenytoin/
carbamazepine
 Metabolic: Hyperthermia, hypoNa (<120, esp if rapid); hyperNa (>160),
hypoCa (<7.5), uremia, hepatic encephalopathy, hypoglycemia (<45),
hyperthyroidism; inborn errors of metabolism in kids; HHS, low Mg, low Phos,
 Infectious: Meningitis, herpetic encephalitis, 3º syphilis, parasitic CNS
(neurocysticercosis), toxoplasmosis, abscess; febrile sz In kids
 Inflammatory: Vasculitis (SLE, Polyarteritis Nodosa)
 Degenerative CNS: Neurofibromatosis, tuberous sclerosis, Sturge-Weber, HIV
 Other: Eclampsia, migraines
 Idiopathic seizure disorder: New epilepsy, breakthrough, low drug levels 2/2
noncompliance, ∆ drug metab

3. Dx
 CT head noncon: if obvious head trauma or persistent AMS, 1 seizure
st

 1 time sz w/return to baseline: FSBG, UPreg, CBC, Chem-10. May consider

st

Utox/HIV/VDRL/RPR
o If HA & fever or persistent AMS: CT/LP
 Known epileptic w/no Δsz pattern & complete recovery: Check drug level &
FSBG, outpt f/u
o R/o infection if therapeutic anticonvulsant level
o If therapeutic & no evidence of infection, consider EKG (cardiogenic
syncope), chem-10 (metabolic), ± Utox, CK/UA (myoglobinuria), LFTs (tox/liver
dz/uremia)

4. Mgmt
 If first time sz with identifiable, reversible cause, usually no anticonvulsants,
but need f/u
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 o Advise NO driving, bath/swimming, operating hazardous machinery, other
activities where sz may harm
o Fill out DMV reporting form. Must be sz-free X 6mo to get license back
st
o Unprovoked 1 sz: 2 yr recurrence 40%
 Phenytoin ↓risk25%; long term if the pt has epilepsy, ↓frequency. Highest
nd st
risk of 2 sz 1 3-6m
 If seizing
o O2 face mask, place on side (↓aspiration), suction airway (but don’t try to
insert), NPA/(OPA)
o Ativan 2mg IV or Ativan 5mg IM (max 8mg) or Valium PR 20mg (only lasts
~30min)
o Most seizures stop even before meds, consider status algorithm if >5 min,
consider phenytoin/fosphenytoin 20 mg/kg IV load
 Fosphenytoin can be loaded faster
 PO phenytoin load: 500 mg q1hr x2
 Status epilepticus: see Resuscitation section

5. Seizure type
 Generalized: Involves entire cerebral cortex. LOC; clonic (jerking), tonic (rigid),
tonic-clonic, myoclonic, atonic; incontinence, apnea/cyanosis, post-ictal
 Absence: Staring spells, rhythmic blinking, no incontinence, cease abruptly
w/o patient recall, minimal post-ictal. In kids, resolves w/age; rare in adults
 Focal: Sz w/o LOC, can occasionally progress to generalized
o Simple partial: Motor/sensory/autonomic sx only
o Complex partial: Impaired consciousness but no LOC, +post-ictal, may retain
higher cortical fxn during sz (driving, playing musical instrument); automatisms
(lip smacking, repeated phrases, frank psychosis)

Stroke/TIA
1. Quick tips
 Activating stroke protocol
o UCSF: “CODE stroke” on pagerbox or 443-COMA (2662)
o SFGH: 443-NERV (6378)

2. Presentation
 Sudden focal weakness/numbness, AMS, dysarthria
 Other sx: Dizziness (vertigo), ataxia, Δvision
 TIA: Sx<24hr (80% <30min). 20% of TIAs have recurrent stroke in 1-3mo
(50% w/in 2 days), 50% in 1yr
 Localization
o 70% strokes are anterior circ (MCA or its branches), 25% of strokes<65yo
Vascular Major Finding Other Findings
territory
Anterior Contralateral weakness AMS, ↓judgment, preservation, primitive
cerebral (leg>arm, face), minimal reflexes (gasp, suck), incontinence
artery sensory

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Middle Contralateral weakness Homonymous hemianopsia, gaze
cerebral & numbness of preference (towards size of infarct).
artery face/arm>leg Receptive/expressive aphasia
(dominant hemisphere), neglect (non-
dominant hemisphere), inattention
Superior Contralateral face/arm ↓Sensation contralateral face and
MCA weakness, Broca’s extremities, hemineglect
apahsia
Inferior Wernicke’s aphasia, Wernicke’s may appear as delirium;
MCA upper outer visual field check visual fields to r/o stroke
loss
Lacunar Pure motor OR pure Clumsy hand-dysarthria syndrome;
artery sensory most commonly basal ganglia, putamen,
thalamus, internal capsule; often during
sleep
Posterior Contralateral visual field Memory loss, homonymous
cerebral loss, contralateral light hemianopsia, misc Δocular/visual
artery touch/pinprick loss; (cortical blindness)
minimal weakness
Vertebro- Vertigo (hallmark), Spasticity, syncope/drop attacks,
basilar crossed→ipsilateral CN nystagmus, dysarthria dysphagia,
artery & contralateral diplopia, loss of pain/T on ipsilateral
weakness face & contralateral body
Distal Crossed: Pain & Ipsilateral Horner’s, gait/limb ataxia,
vertebral temperature (ipsilateral vertigo, nausea, hiccups, dysarthria
or on face, contralateral on *aka Lateral medullary/Wallenberg
posterior body) syndrome
inferior
cerebellar
artery
Basilar Locked in syndrome Lateral gaze weakness
artery
Cerebellar Sudden inability to Lateralizing dysmetria (finger nose
artery walk/stand, HA, n/v finger), dysdiadokokinesis (poor rapid
cerebellar findings alternating movements)

3. Dx
 Exam (as above in localization)
o Posterior fossa (midbrain, pons, medulla, cerebellum): Impaired
consciousness, ipsilateral face/eye weakness w/ contralateral hemiparesis
(crossed defects), slurred speech, disequilibrium
o Putamen or thalamic hemorrhage: most common of HTN bleed; contralateral
hemiparesis (esp if putamen), sensory loss (esp in thalamus), conjugate gaze
paresis, aphasia

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 o Pontine hemorrhage: Coma, pinpoint pupils, quadriplegia, autonomic
instability
o SAH: Sudden onset of thunderclap, n/v, lethargy; usually no focal deficits
 Labs: Cbc, chem10, coags, T&S, UA, ECG; CXR, guaiac (for tPA)
 Immediate CT head noncon to r/o hemorrhagic (15%); most acute ischemic
will not have any findings on noncon
 CTA head for ischemic stroke: Bypass Cr if no renal failure or tPA eligible
o Immediate: Normal
o Hyperacute (1-6hrs): 25-50% normal, 25-50% hyperdense artery, mild
parenchymal hypodensity
o Early acute (6-24hrs): Sulcal effacement (early mass effect), loss of
gray/white differentiation, low density in basal ganglia
o Late acute (1-3d): Wedge of low density in arterial distribution/GM/WM,
increased mass effect
o Early subacute (4-7d): Persistent mass effect or edema, ±gyral enhancement
w/contrast
o Late subacute (1-8wks): Resolving mass effect, persistent gyral
enhancement
o Chronic (months-yrs): Atrophy & encephalomalacia; increased size of
ventricles, no enhancement
o Other: Tissue at risk (↑MTT, ↑CBV) vs. infarct (↑MTT, ↓CBV)
 Consider MRI if posterior stroke or if requested by neuro (MRI w/ DWI, FLAIR
+MRA if no CTA)
o Acute stroke: Restricted diffusion (bright) on DWI, dark on ADC 1 h post
stroke

4. Mgmt
 Stroke
o Rapidly assess airway, last seen normal, FSBS, activate stroke protocol
o Hemorrhagic: see Intracranial Hemorrhage under “Headache”
o Ischemic: Determine tPA eligibility by calculating NIHSS score during initial
assessment/stroke code, assessing inclusion/exclusion criteria
0=alert and responsive; 1=arousable to minor
1a. Level of Consciousness
stimulation; 2=arousable only to painful
(LOC)
stimulation; 3=reflex responses
1b. LOC Questions: Ask patient's 0=both correct; 1=One correct; 2=Neither
age and month. Must be exact. correct.
1c. Commands: Open/close eyes,
0=both correct; 1=One correct; 2=Neither
grip and release non-paretic
correct.
hand.
0=normal; 1=partial gaze palsy; abnl gaze in
2. Best gaze: Horizontal
one or both eyes; 2=forced eye deviation or
extraocular movement by
total paresis which cannot be overcome by
voluntary or doll's eye.
doll's.
0=no visual loss; 1=partial hemianopia,
3. Visual field: Use visual field
quadrantanopia, extinction; 2=complete
threat if necessary. If monocular,
hemianopia; 3=bilateral hemianopia or
score field of good eye.
blindness.

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4. Facial palsy: If stuporous, 0=normal; 1=minor paralysis (normal looking
check symmetry of grimace to face, asymmetric smile); 2=partial, 3=complete
pain. Paralysis (lower face). paralysis (upper and lower face).
5. Motor arm: Arms outstretched 0=no drift; 1=drift but does not hit bed;
90º (sitting) or 45º (supine) for 10 2=some antigravity effort, but cannot sustain;
sec. Encourage best effort, note 3=no antigravity effort, but even minimal
paretic side. movements count; 4=no movement at all;
6. Motor leg: Raise leg to 30º X=unable to assess due to amputation, fusion,
supine for 5 sec. etc.
0=no ataxia (or aphasic, hemiplegic); 1=ataxia
7. Limb ataxia: Check finger-
in upper or lower extremity; 2= ataxia in upper
nose- finger; heel-shin; score only
and lower extremity; X=unable to assess as
if out-of-proportion with paresis.
above.
8. Sensory: Use safety pin. Check 0=normal; 1=mild to moderate unilateral loss
grimace or withdrawal if but patient aware of touch (or aphasic,
stuporous. Score only stroke confused); 2=total loss, patient unaware of
related losses. touch. Coma, bilateral loss.
9. Best language: Describe 0=normal; 1=mild-mod aphasia
cookie jar picture, name objects, (comprehensible); 2=severe aphasia (almost
read sentences. May use no information exchanged); 3=mute, global
repeating, writing, stereognosis. aphasia, coma.
0=normal; 1=mild-mod slurred; 2=severe,
10. Dysarthria: Read list of words unintelligible or mute; X=intubation or mech
barrier
11. Extinction/neglect:
0=normal, none detected (or visual loss alone;
Simultaneously touch patient on
1=neglects or extinguishes to double
both hands, show fingers in both
simultaneous stimulation in any modality;
visual fields, ask about deficit, left
2=profound neglect in more than one modality.
hand.
 Admit to ICU: tPA, need for gtt (BP mgmt), ICH, risk of deterioration
(cerebellar bleed)
 TIA: Risk stratify, d/w Neuro
o ABCD2 score: 2day stroke risk 0-3points 1%, 4-5points 4%, 6-7points 8%
 Age>60yo
 BP>140/90
 Clinical features (unilateral weakness-2 points, speech impairment w/o
weakness-1 point)
 Duration (>60min-2 points, 10-59min-1point)
 Diabetes
 If 0-3ptsconsider d/c home after neuro consult with expedited outpt f/u; all
others get admitted

5. tPA for ischemic stroke

 Inclusion for 0-3hrs: ≥18yo, neg CT head for bleed, <3hr sx/last seen normal
 Inclusion for 3-4.5 hrs: ≤80yo, NIHSS≤25, CT head noncom
w/hypodensity<1/3 MCA territory
 Exclusion
o Significant edema/midline shift/SAH on CT head

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 o Prior ICH from untreated source, AVM, aneurysm, CA
o Sustained BP>185/100 despite tx
o Coma/severe obtundation
o Fixed eye deviation
o Complete hemiplegia
o Minor/isolated sx (NIHSS≤4 (flexible especially if stuttering))
o Sz at onset of stroke
o INR>1.7, LMWH w/in 24 hrs or PTT>40, plt<100k, hct<25%
o Serum glucose <50 or >400 mg/dL
o Prior stroke/head injury w/in 3months
o Arterial puncture at non-compressible site or LP w/in 7d
o Major surgery/trauma w/in 14d, septic embolus, pericarditis/thrombus/
aneurysm 2/2 MI w/in 3months
o STEMI
o Pregnancy
o GI/GU hemorrhage w/in 21d
o Additional exclusion for 3-4.5hrs: INR>1.3, hx of recent stroke if diabetic
(relative)
 If 3 to 6-8 hrs, consider IA tPA or embolectomy
 Dose: 0.9mg/kg IV tPA (max 90mg); bolus 10% of dose, give remaining 90%
over 1 hr; NO foley for 4 hrs, no NG for 24 hrs; no ASA/Heparin/LMWH x24 hrs
 BP s/p tPA: Maintain BP<185/110 (consider placing a-line). If BP >230/140
despite tx with labetalol/nicardipine, d/c tPA
 If clinically worsen on tPA, suspect bleedSTAT CT head, check coags, give
FFP 2 UNITS q6hrs X24hrs, bebulin 35 units/kg IVP, 1 apheresis plt unit
 30% relative, 12% absolute increase in good outcome @ 3m &1yr but risks of
3-6% ICH 2/2 tPA vs 1% placebo but 50% of complications die (still overall
mortality rate is similar)

6. Adjunctive Treatment
 HTN: Tx only if>200-220/120, MAP>120, aortic dissection/MI/CHF/ARF/HTN
encephalopathy, ICH, or tPA
o Lower slowly & <20mmHg total
o Labetalol 10-15mg IV q15min (max 150 mg) or gtt 2-4mg/hr or nicardipine
5-15mg/hr gtt (titrate q5-15 min by 2.5 mg/hr, max 10 mg/hr)
o If sx worsen w/hypoTN, start phenylephrine 0-400mcg/min
o No nitrates/hydralazine if giving tPA
o Esmolol 500 mcg/kg IV load over 1 min then gtt 50-300 mcg/kg/min,
consider for HR if also MI/end-organ damage
 Fluids: Goal euvolemic; no D5W/D5½ NS - worsens cerebral edema 2/2
excess free water and exacerbates ischemic brain injury w/hyperglycemia
 Glucose: Goal <170; independent risk factor for poor outcome
 Vomiting: Common (esp vertebrobasilar, hemorrhagic), frequent suctioning,
NGT, Zofran

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 Obstetrics
By Dina Wallin Res ed. Susan Brim Faculty ed. Susan Promes

General
1. Leading causes of pregnancy related maternal death
 Embolism (PE or amniotic fluid)
 Hemorrhage
 Pregnancy induced hypertension
 Infection
 Idiopathic cardiomyopathy
 Ectopic pregnancy is #1 non-traumatic cause of death
 Trauma is #1 non-obstetric cause of death
o Screen for domestic violence!

2. Physiologic changes in pregnancy

 CV
o Increased cardiac output, increased pulse (90-100)
nd rd
o BP initially decreases by 2 trimester, then returns to baseline by 3
trimester
o Decreased CVP
o ECG changes (LAD, Q in III and aVF, flat/inverted T in III)
 Respiratory
o Increased RR, tidal volume, O2 consumption
o Decreased FRC
o Respiratory alkalosis
o Normal VBG for pregnancy: 7.4-7.47/ 28-36/40-50/18-22
 Heme
o Increased blood volume, increased WBC
o Decreased platelets and RBC
o Increased thromboembolic risk
st nd rd
o Hct: 1 tri- 35-46, 2 tri- 30-42, 3 tri- 34-44
 Renal
o Increased GFR  decreased BUN/Cr

3. Resuscitation of the pregnant patient

 IV, O2, monitor
 Airway – edema and friable mucousa
 Breathing
 Circulation: L lateral decubitus position or manual displacement of uterus
 Fetal monitoring (if after 24 wk): Normal FHR 120-160 bpm
 Perimortem C-section: Ideally within 5 min of maternal arrest. Continue CPR
during procedure and a little bit after
o Immediate OB and Peds/NICU consult
o Tools: Scalpel, Mayo scissors, toothed forceps, needle holder, needle and 0
or 1 chromic sutures, Richardson retractors
o Vertical midline incision, remove infant, double clamp and cut cord, remove
placenta, oxytocin

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 First Trimester
1. First trimester bleeding
 History: LMP, G/P/past ob/gyn hx, amount of bleeding (#pads/hour), sexual
history, trauma (e.g. foreign bodies)
 Differential: Ectopic preg, SAB, implantation, cervicitis, BV, gestational
trophoblastic disease, vaginal wall or cervical lesions, non-vaginal source (i.e.
rectal)
st
o 20% have 1 trimester bleeding! 50% of these will go on to SAB
 Mgmt
o ABCs, consider large bore IV, hemodynamic status assessment. May have
normal VS despite large blood loss; paradoxical bradycardia in ectopic
o US to evaluate for presence of IUP
o UA/UCx, UPreg, CBC, +/- type & screen, serum quantitative b-hCG (should
double q 2days in early pregnancy). UPreg is 99.4% sensitive; may get false
negative with dilute urine (SG < 1.015) or if you don’t wait at least 5 min for test
to develop
o Rhogam within 72 hours if Rh- in all cases
 GA <12 wks: 50 mcg IM
 GA >12 wks: 300 mcg IM
 Ectopic pregnancy
o Sx: Abd pain, abnormal vaginal bleeding, missed menses, shoulder pain
(peritoneal free fluid); VS usually normal (may have paradoxical bradycardia)
o Risk factors: PID, IVF, tubal surgery, IUD, previous ectopic, smoking, TAB in
previous 2 wk
o Dx: Pos Upreg + no IUP on US = early ectopic until proven otherwise
 UA, quantitative hCG in all; CBC, Rh, type & screen
 Discriminatory zone: IUP should be visible on formal trans-abdominal US
when hCG is >5,000-6,000; on transvag US if >1,000. Bedside US may be
less sensitive (operator dependent)
 Quantitative hCG should increase by at least 66% per 48h in IUP
2
o Mgmt: Gyn consult for surgical vs. medical (methotrexate 50 mg/m IM x1-3
doses) therapy
 Spontaneous abortions (SAB): Abdominal pain, vaginal bleeding
o Threatened: Os closed, US with IUP
 Mgmt: Serial hCG, pelvic rest, f/u in 48h (don’t need bedrest)
o Complete: Os closed, US with empty uterus
o Incomplete: ±Os closed, ±products of conception (POC) visible in
cervix/vaginal vault, US with thickened irregular endometrium
o Mgmt: Ring forceps to remove POC if visible & send to lab for pathology,
GYN consult if brisk bleed or need for manual uterine aspiration (MUA)
o Inevitable: Os open, VB, US—expulsion of gestational sac
 Mgmt: Needs ob/gyn f/u; consult if excessive bleeding for possible MUA
o Septic: ±Os closed, tender uterus, CMT, vag d/c, US—thickened irregular
endometrium, ±POC
 Mgmt: OB/Gyn consult, evacuate uterus, consider admit
o Blighted ovum: ±Os closed, variable sx, US—empty gestational sac
 Gestational trophoblastic disease
o Sx: Vaginal bleed, nausea/vomiting (hyperemesis), pre-eclampsia or
eclampsia (often prior to 24 wk GA), passage of grape-like cluster material, PE
from trophoblastic cells
200
 o More common in Asians, h/o prior molar preg, age >44
o hCG and uterus size may be greater than expected by gestational age
o US: “Snowstorm” appearance
o Mgmt: Oxytocin 10 units IV at 20-40 miliunits/min for hemorrhage, Gyn c/s
for D&C

2. Hyperemesis gravidarum
 Persistent vomiting, loss of >5% pre-pregnancy wt, often ketonuria
 Onset between 4-10 wk GA
 Dx of exclusion after considering pyelonephritis, appendicitis, biliary disease,
pancreatitis, tox, CNS disturbance
 Mgmt: IVF, antiemetics: metoclopramide 10mg IV (category B), odansetron
4mg (category B), vit B6 25mg PO 3x Daily.
 Admit pts with unstable VS, intractable vomiting despite aggressive tx,
persistent electrolyte abnormalities or ketosis, loss of >10% pre-pregnancy wt

3. Post-abortion complications
 Retained POCinfection, persistent bleeding several days post procedure
 Uterine perforation
 Bleeding: hemorrhage 2/2 atony, previously undiagnosed coagulopathy,
cervical lacerations
 Amniotic fluid or pulmonary embolism, DIC
 Mgmt: IV, fluids, CBC, type & screen, Rh, quantitative hCG; BCx if febrile;
fibrinogen, fibrin degradation products if suspect DIC; pelvic ultrasound
o hCG should fall 66% within first 48h, but may decline slowly over weeks
o Mild infection: Doxycycline 100 mg BID x 10 days + metronidazole 500 mg
TID x 7 days
o Serious infection: Cefoxitin 2g QID or cefotetan 2-3 g + Doxycycline 100 mg
BID (Tell patient to avoid ETOH)
 Suspected toxic shock syndrome: Clindamycin and imipenem-cilastatin

Second/Third Trimester
1. Second trimester bleeding
 Often results in loss of pregnancy
 Supportive care: Involve OB early, anticipate severe hemorrhage

2. Third trimester bleeding

 Placenta previa: Placenta over os. Painless bleeding
 Placental abruption: Placental disruption from uterine wall. Pain, +/-bleeding
(usually dark), hypovolemia, fetal distress
o Risk Factors: Trauma, maternal HTN, tobacco and cocaine use,
thrombophilia, AMA, multiparity, prior SAB or abruption
 Other: Bloody show (blood tinged cervical mucus plug at start of labor), small
placental separation, vaginal/cervical trauma, lower genital tract infection,
cervical polyps, hemorrhoids
 Mgmt
o AVOID pelvic exam for possible previa
o Labs: CBC, PT/PTT/INR, fibrinogen if suspect DIC (nl 400-450 mg/dL), type
& cross, Rh, Kleihauer-Betke test (does not need to be done in ED)

201
 o Ultrasound: NOT sensitive for abruption
o OB consult for fetal & maternal monitoring
o ±Rhogam, IVF and PRBCs PRN

3. Pregnancy induced hypertension

 HTN after 20 wk GA (if prior to 20 wk, considered chronic HTN)
 Spectrum: PIH, pre-eclampsia, eclampsia, HELLP (Hemolysis, Elevated Liver
enzymes, Low Platelets)
o General guidelines for BP control in pregnancy
 Goal SBP 140-150, DBP 90-100
 Hydralazine 5 mg IVP over 1-2 min then 5-10 mg q 20 min up to 4x.
Convert to PO once stable (usually 10-25 mg QID)
 Labetalol 10-20 mg IV q10-15 min up to 300 mg
 Nifedipine 10 mg PO q 30 min up to 50 mg
 Nitroprusside (for refractory hypertension)
 Avoid ACEI
o Pre-eclampsia
 RF: Nulliparous, AMA, multiple gestation, obesity, FHx, previous pre-E, DM,
thrombophilia, HTN/renal disease
 Sx: HA, blurred vision, epigastric/RUQ pain, edema, HTN, proteinuria,
elevated creatinine
 Mgmt: Control BP, fetal monitoring with supplemental O2 if e/o fetal distress,
OB consult. Delivery if severe (definitive treatment)
o Eclampsia: Elevated BP + seizure
 Place in L lateral decubitus
 Ativan 2 mg IV, other seizures meds prn
 Give Magnesium 4-6 g IV over 5 min, then 2 g/hour (*if no IV access: 10 g
IV (50% solution) in 2 buttocks).
*Watch for toxicity: Flushing, lost DTRs, respiratory depression, paralysis,
cardiac arrest. Antidote: Calcium gluconate 1 g IV
 Control BP as above
 Paralyze and intubate if in status epilepticus

4. Chorioamnionitis
 Fever, maternal and fetal tachycardia, uterine tenderness
 > 16 wk GA
 Mgmt
o Labs: Blood cx, cervical and vaginal cx for GBS, E. coli, Chlamydia,
gonorrhea
o Treat with ampicillin 2 grams IV/gentamicin 1.5 mg/kg IV
o OB consult for admission

Peri-/Post-Partum
1. Precipitous Delivery
 Sx: Nausea/vomiting, abdominal cramping or pain, back pain, urinary urgency,
stress incontinence, urge to defecate, anxiety
 Hx: Contractions, vaginal loss of fluid, vaginal bleeding, Ob/gyn hx, Surg Hx
 Exam: Estimate size/position of fetus, sterile manual vaginal exam except if
bleeding. If rupture of membranes perform a sterile speculum exam)

202
 o Nitrazine paper will turn from yellow to blue in presence of amniotic fluid.
May see “ferning” on glass slide after allowing fluid to air-dry
o Determine cervical effacement, dilation, station, presentation
 Mgmt
o General: IV, maternal and fetal monitoring, transfer to L&D if possible
o Labs: CBC, type & screen, Rh, antibody screen.
 If no prenatal care, send rubella titer, RPR, HIV, hepatitis panel
 Very preterm (22-34 wk): If fetus expected to survive, postpone delivery
o IVF (500 cc bolus, then 125 cc/h)
o Tocolysis (d/w OB): Magnesium, indomethacin, terbutaline, nifedipine
 Normal delivery: Dorsal lithotomy position, universal precautions, pushing with
contractions and resting between; panting, avoid pushing once crowning
o Equipment: Radiant warmer, towels, scissors, 2 clamps, bulb suction,
neonatal airway and vascular access equipment
o Nitrous oxide and opiate analgesia PRN
 Opiate analgesia may cause neonatal respiratory depression
o Clamp cord with 2 clamps 4-5 cm apart, with proximal one 5-10 cm from
neonate’s abdomen; cut between clamps
o Resuscitate infant per neonatal resuscitation protocol (see Resuscitation
section)
o Gentle traction on placenta to deliver placenta
 Shoulder dystocia: Emergent OB consult, drain maternal bladder, hip
hyperflexion, suprapubic pressure. Try Rubin (push anterior shoulder to head)
or Reverse screw (push posterior shoulder to head) to put baby in oblique
plane. Also try placing pt on all fours
 Nuchal cord: If cannot slip cord over neonate’s head, double clamp and cut,
expedite delivery
 Breech: Emergent OB consult, may need c-section. DO NOT PULL BABY!
 Cord/limb presentation: Trendelenburg/pelvis up, push baby back in  OR
ASAP for c-section!
 Cord prolapse: May present w/ fetal bradycardia. Emergent OB consult and
prompt vaginal exam  lift fetal presenting part off of cord  C-section

2. Amniotic fluid embolism

 Mortality 60-80%
 70% occur during labor; may also occur after SAB or TAB, or spontaneously in
nd rd
2 or 3 trimester
 Dyspnea and hypotension assoc with labor or abortion
 Severe: Cardiac arrest, DIC, multiorgan failure
 Mgmt: ABCs, Mgmt of DIC, inotropes

3. Postpartum hemorrhage
 May have falsely reassuring VS (“normal BP” due to compensated shock)
 Most commonly due to uterine atony
o Risk factors: Multiple gestation, multiparity, macrosomia
o Mgmt
 Abdominal and vaginal exam
 IVF, T&C, blood products as needed
 Uterine massage

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  Oxytocin 10 units IM or 40 units IV
 Methergine 0.2 mg IM/IV q2-4hr prn (not in HTN or pre-eclampsia due to
worsening hypertension and risk of stroke)
 Other causes: Vaginal or cervical laceration, uterine rupture, retained POC,
placenta accreta (implantation into myometrium), uterine inversion (with
excessive traction on cord), coagulopathy (including DIC)

4. Postpartum fever
 Differential: Endometritis, wound infx (including necrotizing fasciitis), septic
pelvic thrombophlebitis, breast engorgement, mastitis (as well as UTI, URI,
PNA, etc)
 Detailed OB hx (including vag d/c or bleeding); focused exam of genital tract,
wounds, breasts, urinary and respiratory systems
o CBC, BCx, UA/UCx; consider CXR, ultrasound, CT
 Endometritis: Clindamycin 900 mg IV + gentamicin 1.5 mg/kg IV or Unasyn
3 grams IV, Zosyn 4.5 grams IV; admit
 Pelvic septic thrombophlebitis: Anticoagulation, empiric antibiotics (Unasyn 3
grams IV or Zosyn 4.5 grams IV), admit
 Mastitis: Dicloxicillin 500 mg PO qid, cephalexin 500 mg PO qid, or
clindamycin 300 mg PO qid x10-14 days, breast emptying (may continue
feeding unless abscess). If abscess, I&D and stop breast feeding
 Engorgement: May cause breast pain and mild fever in first 2-4 days. Abx not
necessary

5. Stroke
 Risk peaks at 6 wk postpartum
 Risk factors: Pre-eclampsia, chronic HTN, DM, hypotensive episodes
 Cortical venous thrombosis: 1-4 wk postpartum
o Symptoms: HA, lethargy, vomiting, sz, gradual onset hemiplegia
o Mgmt: Neuro consult, supportive care
 Postpartum cerebral angiopathy
o Symptoms HA, vomiting, sz, focal neuro signs
o CTA with segmenatal narrowing of cerebral arteries
o Resolves spontaneously

6. Cardiomyopathy
 97% present in first 2 months postpartum
 Risk factors: Advanced maternal age, multiparity, twin gestations
 Presentation: Dyspnea, orthopnea, rales, renal insufficiency, abnormal but
nonspecific EKG, CXR with cardiomegaly and pulmonary edema
 Mgmt: Rule out other causes of failure, manage CHF

Common Complaints in the Pregnant Patient

1. Headache
 Most common cause: Muscle contraction (tension) HA. May tx with Tylenol
 18-86% of migraines abate during pregnancy
 Differential: Brain tumor (usually enlarge during pregnancy), pseudotumor
rd th
cerebri (3 -5 month GA), central venous thrombosis, SAH, pre-eclampsia

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2. Jaundice
 Cholestasis of pregnancy: Well-appearing, pruritic pt. >24 wk GA
o Risk factors: AMA, multiple gestation, winter months
o Diagnosis: Dilated canaliculi on US
o Increased risk for preterm delivery, meconium, IUFD
 Acute hepatitis: May occur throughout pregnancy
o Hepatitis E more aggressive in pregnant pts
o Hepatitis B can be vertically transmitted
 Acute fatty liver: Rapid liver failure, coma, seizures, hypoglycemia, DIC. >24
wk GA
o Rare. More common in primiparous, twin gestations
o Sx: N/V, flulike sx, RUQ pain; leukocytosis, low platelets, low fibrinogen,
elevated coags, transaminitis (though <1000)
o CT and US usually normal; dx is through liver biopsy

3. Appendicitis
 Occurs in same rate as nonpregnant women, but perforation rate is higher
o Most common surgical emergency in pregnancy
 As pregnancy progresses, appendix moves cranially, may rest near kidney
 Labs with leukocytosis, pyuria without bacteriuria in urine
 Consider US, MRI before CT

4. Pulmonary embolism
 Manage as in nonpregnant patient—heparin (avoid warfarin)

5. UTI (see Infectious disease chapter)

 Common during pregnancy: 2/2 Smooth muscle relaxation and increased
bacteria

6. Breastfeeding
 Medication safety: Check Lexicomp or LactMed (http://toxnet.nlm.nih.gov then
click “LactMed”)
 Caution in breastfeeding (Ito et al, NEJM 2000)
o Analgesics: Meperidine, oxycodone
o Antidepressants: Fluoxetine, doxepine, lithium
o Antiepileptics: Phenobarbital
o Antibiotics: Tetracycline
o Benzodiazepines: Diazepam, alprazolam
o CV: Amiodarone, atenolol, sotalol
 CT scans: UCSF uses omnipaque. No risk for infants, ok to breastfeed

Suggested reading
 Challoner K, Incerpi M. Nontraumatic abdominal surgical emergencies in the
pregnant patient. Emerg Med Clin North Am. 2003; 21(4): 971-83
 Cusick SS, Tibbles CD. Trauma in pregnancy. Emerg Med Clin North Am.
2007; 25(3): 861-72
 Ito S. Drug Therapy for Breast-Feeding Women. N Engl J Med 2000; 343:
118-126

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 Promes SB, Nobay F. Pitfalls in first-trimester bleeding. Emerg Med Clin North
Am. 2010; 28(1):219-34
 Stead LG. Seizures in pregnancy/eclampsia. Emerg Med Clin North Am. 2011;
29(1): 109-16

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 Ophthalmology
By Hemal Kanzaria Res ed. Patrick Lenaghan Faculty ed. Brian Lin

UCSF/SFGH Logistics
1. UCSF
 Slit lamps usually hide in the hallway outside room 21 or in the family waiting
room in the ED; the Tonopen and indirect ophthalmoscope are usually in the
clear cabinet in the gold side charting room

2. SFGH
 Slit lamps are usually in Zone 4. The Tonopen and Woods lamp are kept in
the drawer next to the main clerking area (between Zone 1 and Zone 2)

Anatomy of the Eye

th
*from Rosen’s Emergency Medicine, 7 ed.

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 Evaluating the eye
1. History
 Pain: Aching, burning, throbbing, itching, foreign body sensation
 Mechanism/context: Trauma/foreign bodies, viral syndrome, migraines
 Discharge: Watery vs. purulent, unilateral vs. bilateral
 Vision changes: “Curtain or veil” obscuring visual field, flashing lights, halo
around lights
 Associated symptoms: Redness, photophobia, headache, neuro symptoms
 Co-morbidities: HIV status, diabetes, hypertension
 Contact lenses/glasses
 Tetanus status

2. Exam
 “AVVEEPPP” mnemonic
o Anterior chamber: Flare (on slit lamp), hyphema (blood), hypopyon (cells)
o Visual acuity (see Snellen chart on next page)
o Visual fields by confrontation
o Extraocular movements
o External exam: Periorbital skin, eyelids (evert to check for foreign body), slit
lamp exam
 Slit lamp: Check for corneal abrasion, flare
o Pupils
o Pressure: Normal <21 mm Hg
 Always calibrate tonopen prior to use (see instruction manual at each site)
 Store tonopen with condom cover. Change to new cover prior to use
 Anesthetize patient with 0.5% proparacaine gtt
 Measure pressure by lightly tapping cornea multiple times until the “beep.”
Check error range after measurement – should be <5%
o Posterior compartment: Exam fundus including optic disc, macula, fovea

208
*place four feet away from patient

209
 Infectious/Inflammatory Conditions
1. Stye or hordeolum
 Etiology: Acute staphylococcal infection 2/2 blockage of lid margin glands or
hair follicles of the eyelid
o External to eyelid: Stye
o Internal to eyelid: Abscess of meibomian gland
 Presentation: Eyelid pain, tearing, lid mass
 Evaluation
o Exam: Eyelid edema (usually smaller than a chalazion), erythema, tender to
palpation
 Mgmt: Warm compresses for 10 minutes 4/day. Topical antibiotic ointment
(e.g., erythromycin bid) to lash line and affected area
 When to refer: Routine if no resolution after 3-4 weeks for I+D

2. Chalazion (CHalazion’s are CHronic)

 Etiology: Subacute to chronic inflammation that occurs spontaneously or may
follow a stye 2/2 blocked meibomian gland
 Presentation: Non-painful discomfort of eyelid, tearing, lid mass
 Evaluation
o Exam: Eyelid mass (usually larger than a stye), erythema, non-tender to
palpation
o Mgmt: Same as for stye/hordeolum (see above)
o When to refer: Routine if persistent or recurring lid mass for I+D, or steroid
injection, or to r/o malignancy

3. Blepharitis or meibomitis
• Etiology: Inflammation of the eyelid margin or eyelash follicles due to staph
infection, seborrheic blepharitis, or meibomian gland dysfunction
• Sx: Pruritis, foreign body sensation, mild pain, crusting around the eyes upon
awakening
• Evaluation
o Exam: Crusting along eyelashes or dry flaky lashes. Eyelid margins may be
red or thickened, with red, pitted, or ulcerated margins with loss or misdirection
of lashes. Conjunctival injection and mild mucous discharge may be present
• Mgmt: Warm compresses x 10-15 min 2-4/day, daily cleaning of eyelids and
lashes. If severe, topical antibiotic ointment (erythromycin or bacitracin) to
eyelids
• When to refer: Routine or within 1-2 weeks for cases of chronic unilateral
blepharitis to r/o malignancy

4. Acute conjunctivitis
• Definition: Conjunctival inflammation as a result of infection, allergy, or toxins
• Etiology
o Viral: Usually adenovirus, possible herpes simplex virus (HSV)
o Bacterial: Commonly S. aureus, S. epidermidis, S. pneumoniae, and H. flu
(especially in children)

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 o Allergic: Type 1 IgE-mediated hypersensitivity to pollen, animal dander, or
dust
• Sx
o Viral: Itching, burning, foreign body sensation, tearing
o Bacterial: Eye redness, purulent discharge with matting of eyelid
o Allergic: Bilateral intense itching, tearing, nasal congestion, redness
• Evaluation
o History
 Viral: Concurrent URI sxs w/ involvement of the other eye days later.
Patients with HSV conjunctivitis may have h/o perioral cold sores
 Bacterial: Involvement of other eye within 48 hours, purulent discharge
developing within 1-2 days of onset. If onset is hyperacute with significant
discharge (and genital involvement in adults), suspect gonococcal
conjunctivitis
 Allergic: Atopy, seasonal symptoms
o Exam
 Viral: Normal vision. Possible lid swelling and erythema, scant watery
discharge, can get occasional chemosis and small subconjunctival
hemorrhages
 Bacterial: Debris on lids and lashes, diffuse beefy conjunctival redness,
mild-moderate white-yellow purulent discharge, and no tender preauricular or
submandibular lymph node (often present in gonococcal conjunctivitis)
 Allergic: Eyelid edema and erythema, conjunctival injection, watery or
mucoid discharge, mild to significant chemosis
 Mgmt
o Non-herpetic conjunctivitis: Self-limited, resolve in 10-14d. Highly contagious
so advocate frequent hand washing, avoid touching eyes, shaking hands,
sharing towels, swimming in pools
o Bacterial conjunctivitis: Broad spectrum topical antibiotics (e.g., polytrim gtt
1 gtt to eye q3h x7-10 days, gentamicin, or tobramycin). If cause is H. flu,
amoxicillin/clavulanate 875/125 mg po bid. Should see ophtho in 2-3 days
o Allergic conjunctivitis: Remove offending allergen or dilute allergen using
artificial tears, cold compresses, and OTC combination antihistamine-
vasoconstrictor eye drops
 When to refer: Emergent if there is suspicion of gonococcal conjunctivitis,
routine if considering use of ocular steroids or in refractory cases

5. Superficial keratitis & corneal ulcer

 Etiology
o Infectious: Usually bacterial (Staphylococcus, Pseudomonas, Streptococcus,
Moraxella, and Serratia). Can be fungal, Acanthamoeba keratitis, HSV,
atypical mycobacteria
o Non-infectious: Severe dry eye, topical anesthetic abuse, residual corneal
foreign body or rust ring
 Sx: Pain, redness, acute unilateral blurred vision, photophobia, discharge if
infection is present
 Evaluation
o History: Trauma, poor lid apposition, contact lens wear, corneal foreign body,
corneal surgery

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 o Exam
 Decreased visual acuity if a central ulcer is present
 Pinpoint pupils in infectious keratitis, conjunctival injection
 Discharge may be mucopurulent (bacterial) or watery (viral)
 Haziness or focal white opacity of the cornea, and a hypopyon can
distinguish this entity from conjunctivitis
o Fluorescein staining: Epithelial defect surrounding dense white infiltrate.
Dendrites suggests HSV keratitis
o Herpes simplex can cause dendritic or geographic ulcer, or diffuse punctate
th
keratitis with fluorescein staining. Think Zoster if see vesicles in 5 CN
distribution (Hutchinson’s sign is nasociliary nerve involvement, 2 branches go
to eye and nose)
 Mgmt
o Topical and/or oral antibiotics, anti-fungals, or anti-viral (e.g., topical
trifluridine) and cool compresses for symptom relief
o For HSV in immunocompromised, or for zoster with ocular involvement,
admit for 5 mg/kg q8h
o Topical fluoroquinolones (e.g. levofloxacin 0.5% or moxifloxacin 0.5%1-2
gtt q2h while awake x2 days then q4-8h x5 days) for corneal ulcers
o Do NOT patch the eye 2/2 risk of pseudomonas infxn. Do NOT start steroid
eye drops
 When to refer: Emergent if suspect bacterial or viral keratitis. Within 12-24 hrs
for all corneal ulcers

6. Preseptal (periorbital) cellulitis

 Etiology
o Skin infection arising from an eyelid and periocular tissue anterior to the
orbital septum, most commonly from S. aureus, S epidermidis, streptococcus,
anaerobes > H. flu
o Associated with URI, may originate from hordeolum, chalazion, insect bites,
and trauma
 Sx: Eyelid and periorbital tenderness, redness, edema, mild fever, excessive
tearing
o Consider DDx: Orbital cellulitis, subperiosteal abscess, orbital abscess,
cavernous sinus thrombosis, dacroadenitis/cystitis, chalazion, contact
dermatitis, herpes zoster, herpes simplex
 Evaluation
o Exam: Eyelid erythema, edema, warmth, and tenderness. No change in
visual acuity, no proptosis, no restricted or painful EOM (if present, concerning
for orbital cellulitis). Eye itself is usually normal but may have mild conjunctival
injection
o Studies: Labs are not useful. Consider CT scan of orbits with contrast or MRI
if there are signs of orbital involvement (not needed for uncomplicated
preseptal cellulitis)
 Mgmt: Clindamycin 300 mg PO q6h x5 days to cover MRSA or bactrim DS 2
tabs bid+ augmentin 875/125 mg PO bid x7-10 days. Hospitalization and IV
antibiotics may be indicated for patients who appear toxic, age < 6 years, or if
refractory to oral antibiotics

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7. Postseptal (orbital) cellulitis
 Etiology: Infection of the orbital soft tissue posterior to the orbital septum,
usually from extension from other sites of infection (sinuses, teeth, lacrimal
gland/duct), from trauma or recent surgery, or seeding from bacteremia.
Typically polymicrobial, though S. aureus, S pneumoniae, anaerobes are
common; H flu in unimmunized, and mucormycosis in DM/immunocompromised
 Sx: Fever, URI sxs, eye redness, pain, facial pressure
 Evaluation
o Exam: Decreased vision, (+) afferent pupillary defect (optic neuropathy) in
severe cases. Proptosis and restricted, painful EOM. Eyelid edema, erythema,
warmth, and tenderness. Conjunctival chemosis and injection
o Labs: Can consider labs/cultures though diagnosis is clinical and
radiographic
o Studies: CT of orbits and sinuses +/- contrast usually confirms sinusitis or
orbital abscess
 Mgmt: Admit. Broad spectrum IV antibiotics with anaerobic coverage e.g.
vancomycin 15-20 mg IV bid + [Zosyn 4.5 IV q6h OR Unasyn 3 g IV q6h OR
clindamycin 600-900 mg IV tid), emergent ophtho consult

8. Iritis or anterior uveitis

 Etiology: Inflammation of anterior segment of uveal tract. Linked with HLA-B27
and seronegative arthropathy. If traumatic iritis, symptom onset within 3 days of
trauma
 Sx: Unilateral pain, photophobia, blurred vision, redness, tearing
 Evaluation
o Exam: Mildly to moderately reduced vision, constricted poorly reactive pupil,
(direct and consensual) photophobia. Discharge is watery if present, diffuse
redness but mostly perilimbal, cell and flare on SLE and hypopyon
 Mgmt: Topical cycloplegic (homatropine 2% 1-2 gtts, tropicamide 1% 1-2
gtts) for mild to moderate inflammation, topical steroids per ophtho
 When to refer: Emergent (should be seen by ophtho within 24-48 hrs)

9. Endophthalmitis
 Etiology: Inflammation of the aqueous or vitreous humor, typically infectious in
etiology; usually occurs post-surgery > penetrating ocular injury >
hematogenous spread
 Sx: Headache, pain, photophobia, vision loss, discharge
 Evaluation
o Exam: Erythema and eyelid swelling, conjunctival/scleral injection, chemosis,
hypopyon, e/o iritis
 Mgmt: Immediate ophtho c/s for aspiration of vitreous, intravitreal Abx and
steroids, IV abx, admission
 When to refer: Immediate

10. Papilledema
 Etiology: Increased ICP causing bilateral optic nerve edema; found with
malignant HTN, pseudotumor cerebri, intracranial tumors, hydrocephalus.

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  Sx: Headache, nausea, vomiting due to elevated ICP; visual symptoms are
often absent
 Evaluation
o Exam: Fundoscopic exam shows blurred disk margins, cup is diminished,
nerve head can be elevated with vascular congestions; can see flame shaped
hemorrhages adjacent to nerve head
o May use ultrasound as adjunct (see Ultrasound chapter)
 Mgmt: Treat underlying etiology, consult ophtho, neuro, NSx as appropriate

Eye Trauma
1. Subconjunctival hemorrhage
 Etiology: Rupture of conjunctival vessels from trauma, increased venous
pressure related to Valsalva, HTN, spontaneously
 Sx: Unilateral eye redness, usually asymptomatic
 Evaluation
o Exam: Normal vision, sharply circumscribed subconjunctival hemorrhage
with underlying sclera completely obscured
 Mgmt: Reassurance; should resolve spontaneously in 2 weeks.
 When to refer: Emergent if there is suspicion of globe rupture (360 degrees of
bullous subconjunctival hemorrhage). Routine referral if hemorrhage persists or
is recurrent for evaluation of hematologic or neoplastic dz

2. Corneal abrasion
 Etiology: Trauma from contact lens or any foreign body
 Sx: Redness, pain, photophobia, tearing, foreign body sensation, discomfort
with blinking, eyelid spasm
 DDx: Corneal or conjunctival foreign body or laceration, burn or keratopathy,
herpes simplex keratitis
 Evaluation
o History: Scratching or hitting the eye (direct injury from finger, paper, contact
lens, make-up brush, foreign body, work related etc.)
o Exam: Normal visual acuity (can be decreased if central abrasion or
associated iritis), eyelid edema, conjunctival injection. Evert eyelids to search
for foreign body if history is suggestive or if vertical/linear lesions seen on
fluorescein stain. Pain relief with topical anesthetic helps confirm diagnosis.
SLE to eval for cells/flare, full thickness laceration; negative seidel test.
Fluorescein staining shows corneal epithelial defect
 Mgmt: Pain relief with cyclopegic agent (cyclopentolate or homatropine),
topical NSAIDs, and/or narcotic. Do not give topical anesthetics (slows healing,
risk of ulcers)
o Non-contact lens wearer: Topical antibiotics (e.g., erythromycin ½” ribbon
2-6x day, polytrim 1 gtt q3h x7-10 days) to prevent infection. If abrasion is
secondary to fingernails or organic matter, prescribe a fluoroquinolone (see
below)
o Contact lens wearer: Antibiotic to cover Pseudomonas (e.g., tobramycin
0.3% 1-2gtts qid x5 days; ciprofloxacin 0.3%, levofloxacin 0.5%, or
moxifloxacin 0.5%1-2 gtt q2h while awake x2 days then q4-8h x5 days), d/c
contact lens use

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  When to refer: Urgent/24-48 hrs if no improvement in 2 days, if visual acuity is
markedly decreased, or if there is a large central abrasion.

3. Corneal laceration
 Etiology: Trauma from fingernails or foreign body
 Sx: Pain out of proportion to exam findings, decreased visual acuity, tearing,
FB sensation
 Evaluation
o History: Ask about work environment
o Exam: Conjunctival injection, SLE to identify corneal laceration, full
thickness corneal lacs can lead to misshaped iris, hyphema, decreased visual
acuity, shallow anterior chamber, bubbles in the anterior chamber. Seidel test
will be positive. However, small corneal lacs can close spontaneously, leading
to a negative seidel test
o CT orbit if suspected penetrating injury, though even this has low sensitivity
 Mgmt: Consult ophtho immediately if concern for full thickness laceration with
globe penetration; place protective shield over eye, instruct pt to limit EOM.
Give systemic antiemetics/analgesics to reduce pressure on the globe. Pt will
need Abx and Td update
 When to refer: Immediate if full thickness

4. Corneal or conjunctival foreign body

 Etiology: usually small foreign body (e.g. metal or wood/leaf particles)
 Sx: Pain, redness, tearing, foreign body sensation, blurring, photophobia
 Evaluation
o History: Trauma (working with metal on metal, power tools or weed-
whackers). Ask about safety goggle use
o Exam: Inspect for foreign body. Conjunctival injection, eyelid edema, and
foreign body +/- rust ring. SLE for cell and flare. Hyphema suggests globe
perforation. Fluorescein staining w/ vertical linear corneal abrasions (“ice rink
sign”) suggest FB under the upper eyelid
 Mgmt: Topical anesthetic (proparacaine 0.5% 1-2 gtts) before attempting to
remove foreign body with saline irrigation or moistened cotton-tipped applicator.
May use 25 gauge needle bevel up to remove superficial FBs under
magnification (slit lamp). Full thickness FBs should be removed by ophtho.
Apply antibiotic ointment (e.g., erythromycin ½” ribbon 2-6x day, polytrim 1 gtt
q3h x7-10 days), update Td, cycloplegics, analgesics prn
 Follow-up
o Corneal foreign body: f/u in 24 hrs
o Conjunctival foreign body: f/u as needed
 When to refer: Emergent if there is suspicion of globe rupture; NEVER remove
foreign body in the setting of suspected ruptured globe. Urgent/24 hrs if foreign
body is in conjunctival location or if not vision threatening

5. Eyelid lacerations
 Evaluation: Thorough exam as even a small laceration can have severe
underlying ocular injury
 When to refer

215
 o Full thickness lacerations (through the orbital septum): May require multiple
layer repair to achieve the best cosmetic result. Increased r/o cellulitis which
you should suspect if you see orbital fat into the laceration
o Damage to the medical canthus, especially of the lower lid as this may
involve the lacrimal drainage system and requires specialized repair. Suspect
when the wound affects the lid margin between the puncta and medial one
third of the eyelid. Ophtho will take to the OR within 24-36 hrs and in the
meantime pt should be on oral keflex 500 mg qid or topical erythromycin ½”
ribbon 2-6x day
o Wounds to the medial and lateral canthi may also interrupt canthal tendons
and improper repair can result in shortening of the palpebral fissure
o Deep transverse lacerations of the upper lid may involve the levator
mechanism. Look for ptosis
o Lid margin lacerations may involve the tarsal plate and require special care
in repair. If more than 1mm of the tarsal plate is lacerated, three-layer closure
is necessary (skin, orbicularis muscle, tarsus/palpebral conjunctiva). < 1 mm
lacs at lid edge can heal spontaneously. Partial thickness lid lacs not involving
the above structures can be repaired in the ED
o Delay of 48-72 hours won’t compromise outcome of most eyelid lacerations

6. Hyphema: RBCs layered or suspended within the anterior chamber

 Etiology: Trauma, coagulopathy, or anticoagulant use. Can be spontaneous
(e.g. sickle cell dz)
 Sx: Pain, acute unilateral blurred vision, or asymptomatic
 Evaluation
o Exam: Measure intraocular pressure. Measure the height of the collection of
blood (red- or black-colored) present within the anterior chamber
 Mgmt
o Protect the eye with an eye shield, limit reading/TV
o Elevate HOB for blood to settle + to prevent occlusion of trabecular
meshwork
o In consultation with ophtho, dilate pupil to prevent pupillary activity
o Control IOP (d/w ophtho)
 Topical beta blockers: Timolol 0.25% or betaxolol 1 gtt bid
 Mannitol IV 1.5-2 grams/kg over 30-60 min
 Topical alpha agonists: Dipivefrin 1 gtt bid or brimonidine 1 gtt tid
 Carbonic anhydrase inhibitors: acetazolamide 500 mg PO or IV. Do not
use in sickle cell pts
 Mild oral non-aspirin analgesics (e.g., acetaminophen) if pain is present until
specialist is seen
 Antiemetics, sedatives prn as adjuncts to limit increase in IOP
 When to refer: Emergent given risk of re-bleeding, dispo per ophtho

7. Penetrating injury to the eye

 Etiology: Suspect globe penetration in any puncture or laceration of the eyelid
or periorbital area, as any projectile injury has potential to penetrate the eye
 Sx: Sudden sharp pain, local redness, blurred vision, photophobia
 Evaluation

216
 o History: Sharp trauma to eye or face, recent fall, working with metal on
metal, power tools or weed-whackers and then feeling a strike to the eye
o Exam: Normal or decreased visual acuity, limited extraocular movements,
low intraocular pressure, tear shaped or irregular pupil, shallow anterior
chamber, hyphema, + seidel test. May see scleral perforation, subconjunctival
hemorrhage, corneal laceration, or lens dislocation. Vitreous hemorrhage may
obscure view of the retina. Don’t measure IOP (given risk of extruding
intraocular contents)
o Studies: CT of the orbit (avoid MRI if metal foreign body suspected)
 Mgmt: Avoid any pressure on the globe, elevate the HOB, protect the eye with
an eye shield. Ophtho consult immediately for surgical repair, start IV Abx,
update tetanus, give symptom relief with antiemetic, analgesic, keep NPO
 When to refer: Emergent

8. Retrobulbar hematoma
 Etiology: Severe blunt trauma to the orbit
 Sx: If conscious, will c/o pain, proptosis, decreased vision
 Evaluation
o Exam: Measure IOP if globe rupture is not suspected.
o Imaging: CT of orbit
 Mgmt: Consider lateral canthotomy for IOP > 40 mm Hg, consult ophtho
immediately
 When to refer: Emergent

9. Traumatic iritis (see iritis above)

10. Chemical Burns

 Sx: Redness, pain, blurry vision, eyelid spasm
 Evaluation
o History: Chemical exposure to the eye including alkali (e.g., cement, lye,
plaster powder, oven cleaner, drain cleaner, airbag powder, fresh lime), acids,
solvents, detergents, and irritants (e.g. mace). Alkalis (liquefaction necrosis)
are more dangerous than acid (coagulation necrosis)
o Exam (do after irrigation): Dependent on burn severity and time elapsed
st rd
since exposure. 1 to 3 degree periorbital skin burns, chemosis, conjunctival
hyperemia or blanching, subconjunctival hemorrhage, corneal edema or
corneal opacification
 Mgmt: Immediate irrigation of the eye with normal saline or water for at least
30 minutes. Then, check pH in the inferior fornix using litmus paper. Continue
irrigation until pH is neutral (6.8-7.5). Can use topical anesthetic prior to
irrigation for pain control. Finally, instill topical antibiotic (e.g., erythromycin ½”
ribbon 2-6x day, polytrim 1 gtt q3h x7-10 days). Update Td
 When to refer: Emergent for any pt with corneal clouding or epithelial defect;
Urgent if no corneal or anterior chamber findings

11. Thermal/ultraviolet keratopathy

217
  Sx: Bilateral moderate to severe pain, foreign body sensation, redness,
tearing, photophobia, blurred vision, and eyelid spasm all worsening 6-12 hrs
after the exposure
 Evaluation
o History: Extensive exposure to UV light through welding, skiing, or sun lamp
without the use of protective goggles
o Exam: Pupils small and sluggishly reactive. Presence of eyelid edema,
conjunctival injection, and diffuse corneal haze or edema depending on
severity
o Fluorescein staining: Punctate epithelial defects on corneal surface suggest
increased severity
 Mgmt: Double patch eyes for pain relief x 24 hours and dim lighting. Antibiotic
ointment (e.g., erythromycin ½” ribbon 2-6x day, polytrim 1 gtt q3h x7-10
days), cycloplegic eye drops and/or oral analgesics prn for pain. Recovery in
usually 12-24 hours
 When to refer: Urgent/24-48 hrs

Painful Visual Reduction/Loss

1. Angle-Closure Glaucoma
 Etiology: Increased IOP from blockage or reduced aqueous humor outflow
through the trabecular meshwork. Can lead to optic neuropathy and blindness
 Sx: Pain, acute unilateral blurred vision, colored halos around lights
(monocular), unilateral headache, photophobia, nausea, vomiting, diaphoresis
 Evaluation
o History: Age 55-70 years, women > men, far-sighted, eyes with narrow
angles, positive family history. Precipitating events include pupillary dilation
e.g. darkened room, stress, or dilating drugs like anticholinergic or
sympathomimetics
o Exam: Decreased visual acuity. IOP ~60-80 mm Hg (normal 10-21 mm Hg).
Fixed, midposition (4-6 mm) pupil. Conjunctival injection, cloudy cornea,
affected eye feels harder than unaffected eye by palpation through closed lids
 Mgmt: Lower IOP by blocking aqueous humor production of promoting outflow
o Topical beta blockers: Timolol 0.25% or betaxolol 1 gtt bid
o Topical alpha agonists: Dipivefrin 1 gtt bid or brimonidine 1 gtt tid
o Carbonic anhydrase inhibitors: acetazolamide 500 mg PO or IV
o Parasympathomimetic miotic agent: pilocarpine 1-2 gtt tid/qid
o Mannitol 1.5-2 g/kg IV
o Surgical intervention may be necessary
 When to refer: Emergent

2. Optic neuritis
 Etiology: Optic nerve demyelination that is idiopathic or from MS, childhood
vaccination or infections (e.g., measles, mumps, chickenpox, EBV, herpes
zoster), contiguous meningeal inflammation, granulomatous inflammatory dz
 Sx: Subtle or profound vision loss over hours (rare) to days (common) that is
usually unilateral but may be b/l. Pain with EOM, loss of color vision
 Evaluation
o History: Age 18-45 years. Previous similar episodes

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 o Exam: Decreased visual acuity, visual field defects, decreased color vision,
red desaturation. + APD. Optic disc may appear normal or swollen and
edematous (i.e., papillitis)
o Studies: Consider CBC, RPR, FTA-ABS, ESR, and CRP for atypical cases.
st
MRI of brain and orbits with gadolinium and fat suppression if this is the 1
episode or if atypical
 Mgmt: Controversial. IV corticosteroids may shorten symptom course and
decrease pain
 When to refer: Urgent to ophtho and neuro

Painless Visual Reduction/Loss

1. Central or Branch Retinal Vein Occlusion (CRVO or BRVO)
 Etiology: Thrombosis of CRV causing venous stasis, edema, and hemorrhage.
Risk factors include HTN, DM, HLD, glaucoma, vasculitis, hypercoag state
 Sx: Subacute onset but painless visual loss can be severe
 Evaluation
o Exam: Decreased VA, + APD. Optic disk edema and diffuse retinal
hemorrhages (“blood and thunder” fundus)
o Labs: Consider labs, hypercoag w/u, ophtho and neuro consult.
 Mgmt: No specific therapy
 When to refer: w/in 48–72 hours

2. Central or Branch Retinal Artery Occlusion (CRAO or BRAO)

 Etiology: Emboli (carotid or cardiac) causing occlusion of a retinal artery
vessel. Others include thrombosis, hypercoagulation disorders, giant cell
arteritis, trauma, sickle cell disease, vasculitis
 Sx: Sudden, painless, monocular loss of vision. Often preceded by amaurosis
fugax
 Evaluation
o Exam: Visual acuity decreased to counting fingers or light perception only, +
APD. Pale fundus, cherry red spot on the macula (fed by choroidal vessels)
thus appearing hyperemic compared to ischemic retina
o Studies: Consider labs, carotid artery doppler ultrasound, EKG,
echocardiography
o Ophtho and neuro consult
 Mgmt: Not evidenced based. Consider ocular massage - 10 seconds on, 10
seconds off, and repeat for a total of 5 minutes, which may dislodge the
embolus; consider hyperventilation into a paper bag can induce a respiratory
acidosis and subsequent vasodilation
 When to refer: Emergent

3. Retinal detachment
 Sx: Flashing lights, floaters, a “curtain” or “shade” obscuring field of vision,
peripheral and/or central visual field loss
 Evaluation
o Exam: Visual acuity and visual field testing may be abnormal depending on
location of detachment. May be difficult to see on direct fundoscopic exam.

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 o Ultrasound: Echogenic undulating membrane in posterior globe, protruding
into the vitreous
 Mgmt: Surgical repair
 When to refer: W/in 24 hours, assure good followup, can be d/c in middle of
night

Common Ophthalmic Medications Used in the ED

Type Name Indication Cautions Usual Dose
Mydriatic- Cyclo- Short-term Glaucoma; 0.5% in peds,
cycloplegic pentolate mydriasis and higher 1 gtt; 1% in
(Anticholinergic) cycloplegia for concentrations adults, 1 gtt;
examination in peds can onset 30 min,
cause agitation duration 24 h
Tropicamide Short-term Glaucoma 1-2 gtt of 0.5%
mydriasis and or 1% solution,
cycloplegia for onset 20 min;
examination duration 6 h

Homatropine Intermediate- Glaucoma, 1-2 gtt 2%

term pupil avoid in peds solution; onset
dilation, 30 min;
cycloplegia, duration 2–4 d;
treatment of for iritis 1-2 gtt
iritis bid

Naphazoline Conjunctival Use <72 h 1 gtt tid-qid

and congestion/ only; avoid in
pheniramine itching narrow angle
glaucoma; htn;
do not use with
contact lenses
in place.
Mydriatic- Olopatadine Allergic Do not 0.1% solution,
cycloplegic conjunctivitis administer 1 gtt bid, onset
(Antihistamine) while contact of action 30–60
lenses are min, duration
present 12 h
Tetracaine Anesthetic for Sensitivity to 0.5% solution,
ophthalmic eye ester-type 1-2 gtt; onset
solution examination, anesthetics; no of action 1 min,
foreign body prolonged use; duration 30
removal delays healing min
Topical Proparacaine Anesthetic for 0.5% solution,
anesthetics eye 1-2 gtt; onset
examination of action 20 s,
foreign body duration 15
removal min

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 1
Antibiotics Erythromycin Conjunctivitis Not the agent /2" applied to
ophthalmic of choice for lower eyelid
ointment contact lens bid-qid
wearers
Ciprofloxacin Conjunctivitis, Solution: 1-2
corneal gtt when
abrasion if a awake q2h for
contact lens 2 d; ointment,
1
wearer /2” to lower
eyelid tid x2 d

Tobramycin Conjunctivitis, 0.3% solution,

corneal 1-2 gtt q4h;
abrasions if a 0.3% ointment,
1
contact lens /2” to lower lid
wearer bid-tid
Gentamicin Conjunctivitis, 0.3% solution,
corneal 1-2 gtt q4h;
abrasion if a 0.3% ointment,
1
contact lens /2” applied to
wearer lower lid bid-tid
*adapted from Tintinalli’s Emergency Medicine

Acknowledgements
The author would like to especially thank Martha Neighbor M.D. and Tina Ku
M.D. A significant portion of this chapter has been adapted from their previous
work.

Suggested reading
 Shingleton BJ and O’Donoghue MW. Blurred vision. NEJM 2000; 343: 556-
562
 Leibowitz HM. The red eye. NEJM 2000; 343: 345-351
 Walker Richard A, Adhikari Srikar, "Chapter 236. Eye Emergencies"
(Chapter). Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler
GD: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e:
http://www.accessmedicine.com/content.aspx?aID=6387273

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 Orthopedics
By Marianne Juarez Res ed. Jake Miss Faculty ed. Michelle Lin

General tips
1. Ortho consults
 Need pt’s name, MRN, phone number, type of insurance when calling for
consult or for follow-up
 Sample script: “Hi, we have a consult we’d like you to see. The patient is a __
<age, gender, MRN> with concern for ____ <fracture, septic joint, compartment
syndrome, etc>, PMH significant for ____ <e.g. immunosuppression, diabetes>”
 Contacts
o UCSF ortho consults 443-5621
 Hand: 885-3825
 Peds: 353-2967
 Spine: 353-2739
 Sports clinic: 353-7566
o SFGH ortho consults 719-2475
 SFGH ortho clinic @ 3M: 206-8673
o SFGH hand consult
 Before 5pm: Plastics 1877-9008
 After 5pm: Rotates between trauma R2 and ortho. See on-call sheet
o SFGH spine: Rotates between ortho and neurosurg. See on-call sheet

2. History
 Mechanism, associated injuries
 Timing (previous injury/fracture/surgery)
 Splinted/casted
 Any associated neurologic changes/deficits (weakness, sensory changes)
 Pertinent co-morbidities: Diabetes, smoking, IV drug use, infection, any
medical condition that increases operative/anesthesia risk
 Specific elements
o Upper extremities: Right or left hand dominance, occupation, fight bite
o Spine: Sensory/motor changes, bladder/bowel function
o Lower weight: Ability to bear weight

3. Fracture Description (for imaging and decision rules see Radiology chapter)
 Location
 Open vs. Closed
 Simple vs. Comminuted
 Displacement and alignment
 Articular surface involvement

4. Physical Exam
 Observe
o Gross deformity, erythema, swelling, ecchymosis, fractures, blisters
o Open fracture, visible tendon/muscle/bone/pus
 Palpate
o Crepitus, step-offs, effusion/able to express fluid
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 o Tenderness (hurts when palpated) v. pain (hurts at baseline)
 Range of Motion (ROM)
o Flexion/extension, guarding; dorsi- and plantar-flexion for ankle
 Sensation
o SILT = sensory intact to light touch
o 2-point discrimination for hand with a paper clip (<5 mm is normal)
o Hand nerve distribution
 outer part of thumb = radial
 thumb side of index finger = median
 outer edge of pinky = ulnar
o Elbow: Median and ulnar nerve
o Shoulder: Axillary nerve = over the deltoid
o Acetabular: Sciatic nerve = posterior leg
o Hip: Femoral nerve = anterior leg
o Femur: Peroneal = antero-lateral lower leg and dorsum of foot
o Knee: Peroneal and tibial = postero-medial lower leg, plantar surface of foot
 Motor
o 5 = full strength and resistance in full range of motion
o 4 = decreased strength in full range of motion
o 3 = full range of motion against gravity
o 2 = full range of motion with gravity eliminated
o 1 = some muscle/tendon contraction visible or palpable
o 0 = paralysis
 Vascular: Pulses, capillary refill
 Reflexes (for spine complaints)

Specific Injuries
1. Septic Joint
 Antibiotic history, fever, ROM (both passive and active), major risk factors
(DM, rheumatoid arthritis, joint surgery with hardware)
 NPO until seen by ortho
 Labs
o CBC
o ESR: Normal values = male >10mm/h, female 0-15mm/h
o CRP: Normal <6.3mg/L
o Pre-op labs if significant concern to prep for possible OR washout
 Joint Fluid: Stat gram stain, cell count, culture. Concern if WBC >50K or
positive gram stain
o Do not tap if e/o surrounding cellulitis to avoid seeding infection into joint
space

2. Compartment Syndrome
 Pertinent history: Mechanism of injury, anticoagulation/bleeding diathesis,
immobilization (cast/splint)
 Findings: First pain, then usually numbness/tingling, pain w/ passive
movement
 Diagnosis: Mostly clinical, though may use pressure measurements
o Compartment pressure measurements: >30 mmHg concerning. Also
[diastolic bp (DBP) – CP] <20 concerning (limited perfusion)

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  Management
o Elevate, ice, pain meds
o Uni or bi-valve cast, remove splint
o Ortho c/s asap for possible fasciotomy

3. Open fracture
 Suspect in any fracture with laceration or abrasion above the skin
o GSW with fractures are considered “Open”
 If grossly open, gently but copiously irrigate the exposed bone and realign/
reduce fracture especially if signs of distal neuro/vascular compromise
 Explore wound, consider probing to evaluate for drainage of bloody “marrow”
 higher risk injury!
 Administer immediate antibiotics
o Gram positives: Cefazolin 1 gm IV
o Anerobe/gram negative coverage if grossly contaminated: Gentamicin
5mg/kg IV
 NPO and prepare for OR
o Exception: Finger open fx distal to MCP may be managed in the ED with
copious irrigation, loose sutures, and antibiotics
 Open Fracture
o Grading
 I: <1 cm wound & minimal soft tissue damage, low energy mechanism,
clean wound
 II: >1cm with mild to moderate soft tissue injury
 III: Extensive soft tissue damage including muscle, skin, & neurovascular
structures with periosteal stripping, a traumatic amputation or with arterial
injury that requires repair
Grade I & II Grade III (a & b) Vascular Injury (Grade III c)
Farm Injury
Soil Contamination
S. Aureus, + Gram Negatives + Anaerobes (like Clostridium)
Polymicrobial, S.
Epidermidis

4. Dislocations
 Shoulder: Simple dislocations are reduced by us in the ED.
o Need analgesia, consider local intra-articular lidocaine injection (10-20 mL of
1% lidocaine or 4 mg/kg max) vs. procedural sedation
o Many techniques, should be familiar with at least 2
 Traction-countertraction
 External rotation
 Scapular rotation
 Snow-bird (boot-strap method)
 Stimson (passive, hang weight on hand)
o Obtain axillary lateral X-rays post-reduction. *Scapular Y is not adequate for
ortho to assure full reduction, instead Valpeau (“reverse axillary”) is an option
o Sling the pt, recommend daily limited shoulder range of motion exercises to
prevent frozen shoulder
 Elbow: Will need ortho consult and sedation
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  Hip: Should be reduced immediately. Longer time out of joint increases risk of
avascular necrosis. Should get ortho involved especially for artificial hip joints
 Patella: Extend knee extension and apply mild medial palpation. Place in knee
immobilizer after reduction
 Knee: High concern for vascular injury. Obtain CTA even if the knee is already
reduced on exam. Document initial ABI’s on arrival
 Ankle: Usually done with ortho consultation, often has associated fractures
 Digits: Axial traction and guide back in anatomic position. Splint or buddy tape

5. Clavicle fracture
 99% do not need intervention
 Concern for conversion to open fracture if skin-tenting
 Mgmt: F/u with ortho as outpt, place in sling with early shoulder ROM to avoid
frozen shoulder

6. Fracture eponyms
 Boxer’s: Neck of the 4 or 5 metacarpal, often from punching someone or
th th

something
 Chance: Lumbar vertebral fracture involving body, posterior spinous
processes, and pedicles. Associated with lap seat belts and bowel injury in blunt
trauma
 Colles: Distal radius fracture with dorsal displacement. Most common wrist
fracture in adults
 Galeazzi: Fracture of radial shaft with dislocation of distal radioulnar joint
 Jones: transvere fracture of 5 metatarsal base, 15mm distal to the proximal
th

end of the bone, beyond the peroneus brevis

 LisFranc: Fracture dislocation at tarsometatarsal joint
 Maisonneuve: Fracture of proximal 3 of fibula associated with medial
rd

malleolar fracture and deltoid and syndesmosis disruption

 Monteggia: Fracture of ulnar shaft with dislocation of the radial head
 Smith: Distal radius fracture with volar displacement. Opposite of Colles fx

Splinting
1. General considerations
 Materials: Orthoplast vs. plaster. Use plaster if need closer molding
o Plaster: Ensure adequate layers of plaster and padding. Plaster is
exothermic so more layers = need more protection. Also use extra padding to
protect pressure/contact points e.g. elbow, prominent bony areas
 Upper extremity splints: 8-10 layers of plaster with 4-5 layers of padding w/
extra at any
 Lower extremity splints: 12-15 layers of plaster with 8-10 layers of padding
 Use bias and not ACE wrap for acute injuries to avoid subsequent over-
compression with swelling
 Indications: Fractures (even occult e.g. Salter Harris I, scaphoid), sprains, joint
infections, tenosynovitis, lacerations over joint

2. Commonly used types of splints

 Upper extremity
th th
o Ulnar gutter splint: 4 /5 prox. phalanx and metacarpal fx
225
 st nd
o Radial gutter splint: 1 /2 prox. phalanx and metacarpal fx
o Dorsal or volar hand splint: Soft tissue hand/wrist injuries (sprains, carpal
nd th
tunnel), wrist fx, 2 -5 metacarpal fx. Dorsal splint is more stable
o Thumb spica splint: thumb fx's or scaphoid fx
o Finger splint vs buddy taping for distal/middle phalanx fx's, sprains
o Sugar tong (or reverse sugar tong): distal radius or ulnar fx
 Lower extremity
o Bulky jones: Layers of padding applied with ace wrap. Used for short term
immobilization of soft tissue and ligament injuries
o Knee immobilizer: Uses Velcro, good for knee injuries
o Posterior ankle splint: Distal tibia/fibula fx, tarsal/metatarsal fx
o Stirrup ankle splint: Great for ankle sprains, other fx which need more
support. Allows less inversion/eversion, less plantar flexion. Aircast is similar,
can be worn inside a shoe
o Hard shoe: Foot fx e.g. Jones fx

Acknowledgement
The author would like to thanks to Jun Matsui of the Orthopedic Surgery
Department. A significant portion of this chapter has been adapted from her
previous work

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 Pediatrics
By Joe Freeman Res ed. Hangyul Chung-Esaki Faculty ed. Andrea Marmor,
David Duong

UCSF ED Logistics
1. Who to call for advice
 Peds Sr Resident: 353- 8185. If busy, call the Peds hospitalist at 353-8038

2. Who to call for admissions

 General peds: Admit to purple/orange team via calling the Sr resident at 3-
8185 (write the team color and the peds attending on your bed request sheet).
 Heme/onc: Red team. Page peds heme/onc fellow.
 DOTS (dialysis & organ transplant): for all pts who have transplants or are on
the transplant list. Page peds renal or GI fellow.
 NICU: <30days old. Call Sr Resident.
 PICU: Call PICU fellow (3-8039) and Sr peds resident.
 Cards: Call peds cards fellow (443-HLHS).
 Surgical specialties: Call the adult services (except peds surgery and peds
urology, all others have no peds specific ED consults)

SFGH ED Logistics
1. Who to call
 6M urgent care clinic: 8838, 6933
 Peds res pager: 1877-1689 (batch pager for R2/3)
 719-KIDS for apnea, seizure, non-traumatic non-babies
 Baby code: 719-BABY (OB chief, anesthesia, R3)

2. Logistics
 Peds is automatically called for peds trauma activations (they carry a trauma
pager) and should also be called for peds medical codes
 When to consult peds (for non-trauma)
o Age <5: Mandatory consult. Ideally, peds would like to be involved ASAP if
age <2 and/or critically ill
o Age 5-12: Should call peds, but optional consult (i.e. can notify prior to
discharge if otherwise well-appearing vs. early involvement if pt is ill and needs
admission)
o Age >12: At attending discretion
o Sicker, younger patients should get early peds involvement in a timely
fashion
o Also consider peds for help with CPS, social, and with help in diagnosis,
management, disposition
 No PICU at SFGH – all admitted kids (trauma, ortho, etc) are co-followed by
peds (e.g. primary team trauma, peds as consultant) unless admitted for
observation/ MRI for head trauma (admit to peds)
 When/how to transfer child to UCSF: For kids that require special treatment
only available at UCSF (PICU level medical care, extracorporeal membrane
oxygenation (ECMO), certain specialists, etc). Discuss case with peds consult
or peds chief resident, if they agree transfer is necessary they will call the UCSF
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 Access Center (353-1611, to arrange for a bed/peds attending admission/
ambulance transport)

Peds Code/Resus (see Resuscitation chapter for algorithms)

1. Hints
 See resuscitation chapter for age-appropriate vital signs
 Most common cause of pediatric cardiac arrest is progressive hypoxia
(respiratory) or hypovolemic shock (90% 2/2 PEA, asystole, bradycardia).
 Tachycardia with prolonged cap refill = compensated shock, treat
aggressively!
 Minimum SBP→2Xyr+70
 Aggressive fluid resuscitation is key: 20cc/kg of isotonic fluid at a time, repeat
frequently until HR and perfusion respond
 HyperK→CaCl 20mg/kg (max 1g)
 HTN crisis→nifedipine 0.25-0.5 mg/kg PO/SL (max 10 mg), hydralazine 0.1-
0.2 mg/kg IM/IV q4-6h (max 20 mg), nitroprusside 0.5-3 mcg/kg/min IV gtt
 Hemorrhagic trauma: 20cc/kg NS X 2, then 10-15cc/kg pRBC

2. Intubation/sedation
 Airway
Neonate <2 yo 2-6 yo 6-12 yo >12 yo
ETT Uncuffed: (age/4) + 4; Cuffed: Use 0.5 size smaller
Depth: Tube should be 3xsize deep at the lips
Blade size Miller 0 Miller 1 Miller 1-2 Miller/Mac 2 Miller 2-3/Mac 3
o Crich is contraindicated <5-8yo; use transtracheal jet vent with 14 G instead
o Decompress stomach with NGT if difficult to bag
o Initial vent settings: VT 10-12cc/kg (8-10cc/kg asthma), RR (age appropriate,
infant~20-30, ped 16-20), FiO2 100%, PEEP 3-5, Ppeak 20-30
o If difficult IV access, IO preferred; otherwise, drugs which may be
administered via ETT drugs: NAVEL
 Atropine 0.02-0.03mg/kg
 Epinephrine 0.1mg/kg of 1:1000, 0.01mg/kg of 1:10,000
 Valium 0.1-0.2mg/kg
 Lidocaine 2mg/kg, 1mg/kg
 All meds should be flushed w/5-10cc NS & 5 ventilations
 Medications (for full details see Procedures chapter)
Versed Fentanyl Sux Roc Etomidate Ketamine
0.05-0.1 mg/kg 1 mcg/kg (IV) 1.5 1 0.3 mg/kg 0.5-2
(IV) 1.5 -2 mcg/kg mg/kg mg/kg (IV) mg/kg
0.2-0.5 mg/kg (IN) (IN) (IV) (IV) (IV)
o Procedural sedation
 Brevital: Contraindicated <3yo
 Ketamine: Contraindicated in <3mo, seizure disorder, increased ICP

3. Fluid resuscitation
 Oral hydration
st
o Mild/mod dehydration: 5-30cc q5-15min w/goal 10cc/kg in 1 hr. If tolerated,
can continue at home. Goal to replace deficit w/in 4 hrs
o if vomit w/PO: Give Zofran 0.15mg/kg PO/IV, wait 30-60m then retry

228
 o IV hydration: NS in 20 cc/kg boluses until HR/cap refill respond or urine
produced; convert to PO before DC
 Maintenance Fluids
st nd
o 4cc/kg/hr for 1 10kg + 2cc/kg/hr for 2 10kg + 1cc/kg/hr thereafter
o Use D5¼ NS for <2yo, D5½ NS for >2yo
 Blood products
o pRBC 10-20cc/kg (↑2-3 hg)
o FFP 10-15cc/kg (↑10-20% clotting factors)
o Platelet (↑50-100,000 plt)
 1 adult unit (250 mL, single donor apheresis) if >20-25 kg
 1 pedi unit (half adult or 125 mL) if 10-15 kg
 1 quad pack (50-75 mL) if <10 kg

Neonatal Resus (see Resuscitation chapter for algorithm)

1. Hx
 Timing of delivery
o Mother hx: Primigravid? Estimated delivery date? Was the prior labor
short/long?
o Single vs multiple births?
o Need to push? (~delivery in 30-60m)
o Infants: ↑Risk of distress w/thick meconium, fetal distress, crash c-section,
premature

2. Assessment
 If meconium present and infant is not breathing, intubate and suction X2 below
cords. If unable to intubate quickly, proceed to steps below.
 Airway: Bulb suction mouth then nose
 Breathing: Warm & dry infant (warmer) and stimulate (rubbing back or tapping
toes) for 30 sec; if still apneic, HR <100, or cyanotic→continue resus
o Use blowby O2 only if e/o central cyanosis. (do not give supplemental O2 if
not hypoxic/cyanotic, may be detrimental)
o BVM if apnea, HR<100; BVM at 40-60 breaths/min; often have closed mouth
so use bottom of mask to push mouth open a little bit via the chin
 DO NOT BVM diaphragmatic hernia. Intubate immediately and place OGT
to decompress stomach
o ETT
 Intubate if no success w/ BVM, congenital diaphragmatic hernia, extreme
prematurity (<28 weeks) or extremely low birth wt (<1kg)
 Use 00 miller for <34 wks, 0 miller for newborns
 Tube size: “30 wks 3-0, 35 wks 3.5, 40 wks 4-0”
 Depth: 3X size
 Positioning: Larynx is anterior. If cords not visible, place blankets under
shoulders to line up w/big head
 Circulation: HR via apical pulse w/stethoscope or palpate umbilical
stump/brachial artery
o If HR<60 despite BVM w/100% O2 & CPR X30s OR no HR, cannulate
umbilical vein for access
 Administer epinephrine 0.01mg/kg of 1:1000 OR 0.1cc/kg 1:10,000 (ETT:
0.1mg/kg or 1cc/kg of 1:10,000)
 Give volume: 10cc/kg NS/LR/pRBC
229
  May also try bicarb 2mEq/kg of 0.5mEq/mL 4.2% soln, narcan 0.1mg/kg
o Start chest compressions if HR <60 after 30s BVM w/100% O2. Encircle
chest w/hand w/thumbs just below nipple line and push 1/3-1/2 of chest depth
at 120/min (compression:ventilation 3:1 w/pauses for ventilation)

3. APGARs (see Resuscitation chapter)

 Determined at 1,5,±10min
o Normal: 7-10
o Needs minor resus/support if 4-7
o Full neonatal resus if ≤3

Respiratory
1. Foreign body aspiration
 Acute onset coughing, choking, wheezing, Δvoice, dysphagia, stridor
 Most common cause is food; most commonly misdx as asthma/URI
 Consider CXR: Bilateral decubs or inspiratory/expiratory for hyperinflation,
mediastinal shift, atelectasis but may be nl (12-25%)
 Tx: If coughing/making sounds then let them try to cough it out. if unconscious,
give 5 back blows, 5 chest blows for infants vs. Heimlich for peds
 Consider trial of bronchodilators
 If stable, and classic history, rigid bronchoscopy by peds pulmonary

2. Asthma
 Albuterol neb: 2.5mg (use 1/2 if <1 year of age), ipratropium 0.25mg x3
 If impending airway compromise: methylprednisone 2mg/kg IV loading dose
then 0.5mg/kg q6hrs, magnesium sulfate 25-75mg/kg slow IV push (max 2g)
 Outpt steroids
o Prednisone 1-2mg/kg PO (max 60-80/d, crushed in syrup)
o Prednisolone 1-2mg/kg PO (tastes best) X 5d
o “IV” dexamethasone 0.6mg/kg, max 16mg PO q24-48hrs X 2
 On discharge, provide rx for 2 albuterol canisters (1 for home, 1 for school)

3. Pneumonia – see Infectious Disease chapter

4. Bronchiolitis
 Lower resp tract infection in <2yo (most severe <6mo +↑apnea risk) w/↑resp
effort/hypoxia/wheeze
 Peaks winter/spring
 Often 1-3d hx of URI
 Tachypnea, retractions/nasal flaring, prolonged expiratory wheeze, course
lung sounds/crackles, diffuse ‘washing machine’ exam
 RSV>>>parainfluenza/etc (rapid antigen test rarely changes management)
 Dx: XR only to R/O other dx→hyperinflation, peribronchial thickening
 Tx: Usually self-limited w/resolve 3-10d, antipyretics, IVF (if needed), nasal
suctioning
o Consider trial of albuterol or nebulized epinephrine 3-4cc 1:1000 or
racemic epinephrine 0.05cc/kg diluted in 3cc NS given over 15m
o Impending/arrest: try steroids, heliox, nebs of hypertonic saline, CPAP,
intubation
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  Admit: Need for IV fluids/frequent albuterol, persistent ↑WOB, hypoxia
(O2<92%), comorbidities (including prematurity)

5. Croup/laryngotracheobronchitis
 Viral infection of upper airway: Stridor, barking cough (seal-like, infants/young
kids), hoarseness (older kids/adults)
 Mostly fall/winter; most common 6mo-3yo (rare>6yo); most commonly seen in
ED 10p-4am b/c worse at night
 Mostly parainfluenza
 ±Viral prodrome (cough, coryza); often see w/URI sx
 Concern is subglottic narrowing so keep child calm in ED
 Soft-tissue neck (often not necessary):steeple sign (supraglottic narrowing,
also helps r/o other causes of stridor), CXR (r/o PNA/FB) if indicated
 Tx: Neb epinephrine if stridor at rest, or trial of humidified/cool mist O2 if not
o Mild: steroids - dexamethasone 0.6mg/kg (max 10mg) PO/IV/IM X1
o Mod/severe (stridor at rest): racemic epinephrine 0.05mL/kg (max 0.5mL)
of 2.25% SOLN diluted to 3cc total volume neb X 15m & dexamethasone
0.6mg/kg (max 16mg) PO/IV/IM
 If stridor at rest or severe obstruction: observe 2-3 hrs for epinephrine to wear
off before DC
 Admit: No improvement in ED, or need for >1 dose of epinephrine. Pts usually
present at nadir (>day 2-3), should improve steadily from then on

6. Stridor
 Infectious: Epiglottis, croup, bacterial tracheitis, PTA, RPA, Ludwig
 Medical: Anaphylaxis, angioedema, laryngospasm, tumor
 Other: Trauma, FB, burn, caustic ingestion

7. Epiglottis
 ‘Hot potato’ voice, stridor, drooling, neck extension
 Tx: Ceftriaxone 50mg/kg IV/IM BID (max 2g), ±vancomycin 15-20 mg/kg IV,
racemic epinephrine neb q20min prn, dexamethasone 0.6mg/kg (max 10mg)
IV/IM X1, ICU admission
 Visualize airway/intubate ONLY under anesthesia
 If pt is old enough let them use Yankauer suction catheter
 May be difficult to intubate but easier to bag-valve mask

8. Bacterial tracheitis
 Bacterial superinfection of trachea→rapid/severe resp sx
 Median age 4yo, more common in kids than epiglottitis
 Typically preceded by viral URI X few days, fever, rapid & severe stridor
w/toxic appearance, +/-cough, raspy/horse voice
 Difficult to diagnose: Soft-tissue neck XR may show subglottic narrowing, dx
only by bronchoscopy s/p intubation in OR
 Abx: Ceftriaxone 50 mg/kg IV/IM or clindamycin 10 mg/kg IV q8h ±
vancomycin 15 mg/kg IV

9. Pertussis (see algorithm below)

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*From Michelle Lin’s Paucis Verbis: Pertussis algorithm

 Vaccine only ~80-90% effective (TdaP now starting at 11 years)

 Most common <3mo, 7-9yo, teenagers
 Persistent (>2 wks) spasmodic severe whooping cough w/gasp after attack
(±posttussive emesis) but <6mo may not whoop, just staccato cough with apnea
 No fever (vs PNA)
 3 stages
o Catarrhal: x7-10d, rhinorrhea, lacrimation, mild cough

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 o Paroxysmal: 1-4wks, ↑frequency/strength of cough, whooping inspirations
w/cough paroxysms
o Convalescent:↓Sx but cough can persist for several months
 WBC 20-60k, pertussis kit for nasopharyngeal swab X 10s for PCR/cx
 Tx: Azithromycin 10 mg/kg q24h POx1 then 5 mg/kg PO q24h x4 days (only
really helps if catarrhal stage), albuterol 2.5mg neb qhr to ↓paroxysmal
coughing
 Admit: <6 mo or ill-appearing
 Droplet precautions X 7d; tx high risk contacts (infant, pregnant, person in
contact w/high risk) and finish vaccinations; return to school s/p abx course
 Empirically tx all suspected of pertussis infection

Fever Without a Source

(*adapted from lectures of Dr. Marmor)
1. Neonate (0-28d), T>38
 SBI/UTI: E coli, GBS>>S. aureus, Listeria, Salmonella
 CBC, blood cx, cath UA/UCx, LP
 Tx: Ampicillin + gentamicin IV or ampicillin + cefotaxime IM/IV (look up
dosing based on age/wt on ucsf.edu/idmp)
o If ill-appearing or CSF pleocytosis: ±Acyclovir 20 mg/kg IV and CSF HSV
PCR (also consider HSV w/vesicular rash/non-traumatic bloody
LP/↑↑↑AST/ALT/mom hx (esp if vag delivery w/active lesions)
 Admit all regardless of w/u

2. 1m-3m, T>38
 SBI/UTI: E coli/GBS/S pneumo>>N mening, H flu
 CBC: If WBC>15 or <5, get blood cx & give ceftriaxone 50 mg/kg IM/IV
 Cath UA/Ucx
o Treat for pyelo if +LE/nitrites
o Admit if very young or not tolerating PO
 LP if irritable/lethargic
 Strongly consider LP if giving abx
 F/u as outpt next day if abx given or admit if unable to assure f/u

3. 3m-36m, T>39
 Vaccinated against pneumo
o UA recs same as unvaccinated
o No blood cx or abx if well-appearing w/≥3 doses vaccine
o Partially vaccinated: Still low risk but if <3 doses & <7mo may have ↑risk
o Close outpt f/u for all
 Unvaccinated against pneumo (<2 doses vaccine)
o UA for all ♀<24mo, circumcised boys<6mo, uncircumcised boys <12mo
w/fever>48hrs, circumcised 3-6mo w/fever>48hrs
o Neg UA only r/o UTI in low risk (girls/uncircumcised>12mo,
circumcised>6mo), otherwise send UCx
o CBC if T>39.5 (if WBC>15 or <5→blood cx & ceftriaxone IM/IV)
o LP if irritable/lethargic
o Strongly consider LP if giving abx
o Close outpt f/u for all

233
 st
o 1 dose of abx for UTI (presume pyelo) need to be given in ED

Abdominal Pain/GI Bleed

1. Appendicitis
 Atypical presentation common
 Diffuse abd tenderness, decreased PO’s, refusal to walk
 30-60% of <6yo will have perf
 More common when >2yo, peak 9-12yo
 Diagnostics
o 96% with WBC >10, left shift >75% neutrophils; however, caution in kids with
normal WBCs
o May be assoc with sterile pyuria
o Alvarado score

 1-4: Appy unlikely

 5-6: Possible appy
 7-8: Probable appy
 9-10: Very probable appy
 Caution: 0-8% patients with score <5 had appendicitis, especially in kids
<10 yo
o If no nausea, RLQ pain, difficulty walking, rebound tenderness, or absolute
PMN <6,750 = negative LR 0.058 (Kharbanda, Pediatrics 2005)
o Perform ultrasound first: sensitivity and specificity 90-95%, positive LR 17.2-
49.5, negative LR 0.01-0.14
o CT if ultrasound inconclusive: Limited CT of appendix sensitivity 95-100%

2. Intussusception
 Most common cause of obstruction in 2mo-5yo; peaks in toddlers
 Hallmark is intermittent abd tenderness (pain lasts few minutes 10-20min
apart) OR inconsolability OR lethargy. ± fever, v/d (soon after onset of pain)
 Abd is benign b/t episodes of crying/fussiness/inconsolability→abd distention
w/RUQ sausage-like mass (95% at ileocecal junction), currant-jelly stool (late
finding, heme+ stool almost always)
 Diagnosis: US 100% Sn/Sp; upright abd XR: ±bowel obstruction
 Diagnosis/treatment: Air-contrast (safer)/barium enema dx & tx (~80-90%; CI
is peritoneal, <3mo, consult surg before performing)
 Other tx: NPO, IVF/transfusion (often p/w life-threatening dehydration/
anemia), IV abx

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3. Malrotation/volvulus
 Neonate (80% <1yo) w/bilious vomiting, ±abd distention, irritability/lethargy,
FTT, GIB/hematochezia
 Dx: Abd XR→double bubble, pneumatosis intestinalis, nonspecific bowel
obstruction, cecum L of midline (but nl does not r/o); Upper GI series
 Tx: NPO, NGT, hydration, surg consult
 Bilious emesis in neonate is malrotation until proven otherwise
 ↑Risk of diaphragmatic hernia, abd wall defects, duodenal atresia,
Hirschsprung, intussusception

4. Incarcerated/strangulated hernia
 Groin/testicular pain w/scrotal swelling/fullness, ±hx of inguinal fullness
w/standing/coughing that resolved w/lying down
 Dx: ±US for small intestine vs hydrocele vs epididymitis vs tumor
 Tx: Manual reduction if <12hrs (ice pack over hernia, benzo for procedure),
surg consult if any signs of systemic illness

5. Meckel’s diverticulum
 0-2yo (up to 10yo) most often p/w painless LGIB in <5yo (most common
cause of lower GIB in peds), ±obstruction or w/LLQ pain/mass & melena
 Dx: Technetium-99m nuclear scan to find heterotopic gastric mucosa (needs
to be bleeding)
 Tx: T&C X 10cc/kg (↑risk of abrupt brisk GIB)
 Rule of 2’s: Present first 2 yrs of life, 2% of population, 2% are symptomatic, 2
in long, 2ft from ileocecal valve, 2 types of epithelium (gastric, pancreatic)
6. Hirschsprung’s disease
 Neonates: >48hrs before passage of meconium, abd distention, recurrent
bilious vomiting
 Older kids: Chronic constipation, early satiety; 4♂:♀; nearly all dx by <2yo
 ↑Risk w/Down syndrome, FHx
 Dx: Barium enema/bx
 Tx: IVF, NGT, rectal tube
 Complication: Hirschsprung’s enterocolitis (toxic megacolon)

7. Foreign body ingestion

 Common in 6mo-3yo; >50% coins
 Once past the esophagus (~30% spont) and stomach, majority will safely pass
through rest of GI tract
 70% of those that get stuck will be lodged at the thoracic inlet of esophagus or
cricopharyngeous muscle (C6)
 Gagging, vomiting, drooling, coughing, dysphagia, refusal to eat, wheezing
 ↑Risk of complications w/ length>3-5cm (if>1yo) or >2cm (if <1yo) or
diameter>2cm & should consult for possible removal
 Dx: CXR/soft tissue neck XR (if coin will see face if in esophagus or rim if in
trachea), ±esophagram (↑risk aspiration)
 Tx: Can obs 12-24hrs if round/noncorrosive/asymptomatic/no hx of
esophageal dz/ingestion<24hrs ago, ±glucagon 0.5 mg or 20-30 mcg/kg (≤20
kg) or 1 mg (>20 kg) IM/IV/SQ or diazepam 0.04-0.3 mg/kg IM/IV or nifedipine
0.25-0.5 mg/kg PO/SL (max 10 mg) or NTG
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  Can take 3-8d to get out on average (up to 4 wks)→daily/weekly XR if concern
 Button battery: Remove if lodged in esophagus (liquefaction necrosis/rupture
w/in 4-6hrs) or if in stomach>48hrs

8. Anal fissure
 Along with milk protein allergy, most common cause of GIB in infant
 Usually occurs with constipation, visible on exam

9. Milk protein allergy

 Usually presents < 3 mo of age, often microscopic
 Can occur in breastfeeding infants if mother is drinking milk

Blue Baby
1. Neonatal cyanosis & shock
 R/O sepsis, seizures
 If suspected CHD: PGE1 0.05-0.1mcg/kg/min to keep a possible PDA open
(SE: apnea, hypoTN, hypoglycemia)

2. Apnea/Acute Life-threatening Event (ALTE)

 Frightening apneic episode w/Δcolor/muscle tone/MS/choking
o Periodic breathing: ≥3 pauses, each lasting >3 seconds, <20 seconds of
normal breathing in between
o Pathologic apnea: apnea ≥20 sec with bradycardia, hypotonia, cyanosis, or
other compromise
 Hx
o Central (no effort) vs obstructive (chocking/gagging/abd wall movement)
apnea
o Asleep/eating/playing right before event, recent illnesses, rx, hx of SIDS,
birth hx/wt gain/developmental milestones
 If there is an etiology, it’s usually apparent with good H and P
 Selected labs as indicated by H and P: Consider RSV/pertussis, chem, CXR,
UA, cx, ECG); if <1m, get cx, abx & LP if concern for CNS lesion/infection
 Admit if < 4 wks of age, concern for NAT, or recurrent apnea
 Ddx
o GI: Most common, GERD w/bronchospasm, intussusception, volvulus
nd
o Neuro: 2 most common, sz, CNS bleed, tumor
rd
o Resp : 3 most common, OSA, airway abnormality, foreign-body
o Cardiac: Arrhythmia, congenital heart dz
o Metabolic: Dehydration, electrolyte, inborn error, endocrine
o Infectious: Meningoencephalitis, sepsis, RSV, URI, pertussis, croup, PNA
o Non-accidental injury

3. Congenital cardiac defects

 Blue baby 5 T’s:*Tetralogy of Fallot, *transposition of great vessels, *tricuspid
(pulmonary) atresia, total anomalous pulmonary venous return, truncus
arteriosus (*=tx w/PGE1)
o Tetralogy of Fallot: Prone to ED presentation when PDA closes (loss of L to
R shunt). Presents w/in 1 wk old, most common cyanotic defect

236
 o Transposition of great arteries/total anomalous pulmonary venous drainage
& truncus arteriosus present at 2-6 wks old 2/2 ↓pulmonary vascular resistance
(transposition may present immediately after birth to 1 wk w/low O 2, cyanosis,
resp distress in ♂)
 Pink baby (SOB, CHF sx) 3 D’s: VSD (most common congenital heart abnl),
ASD, PDA (to-and-fro machinery-like murmur, treat with indomethacin)
 W/u: Pulse ox pre- (R arm) & post- (either leg) ductal & BP UE>LE
(coarctation), 100% O2 (“hyperoxia”) test (pO2<100mmHg suggests cardiac,
pO2>150mmHg suggests non-cardiac/pulmonary), EKG, CBC, CXR, ±echo
 Tx
st
o If presents w/in 1 wk of life, think tetralogy. Tx w/ IV PGE1 0.05-
0.2mcg/kg/min (s/p peds cards consult if possible). SE: apnea ~10% so
st
strongly consider intubation if transporting, most common w/in 1 hr
o CHF: Furosemide 0.5-1mg/kg IV, enalapril 0.005-0.01mg/kg IV,
±dobutamine gtt
o Tet spell: Usually<3yo, 2/2 exertion of feeding/straining/crying →
squatting/knees to chest, IVF boluses, morphine 0.1mg/kg IV/IM/SQ, O2,
phenylephrine 0.1mg/kg IV/IM

Jaundice
1. Kernicterus/hyperbili toxicity
 Lethargy, poor suck/feeding poorly, tremor, extensor rigidity, sz
 Ddx
o Botulism (has jaundice, no fever/high-pitched cry)
o Tetanus (both ±retrocolis (neck backwards)/opisthotonus (arching of trunk
backwards)
o G6PD, other metabolic disorder
 Tx: Exchange transfusion

2. Well newborn with jaundice

 Check direct/indirect bili, CBC to assess if hyperbili is 2/2 hemolysis.
o If anemic, check Coombs, blood smear, Mom and baby’s ABO/Rh, retic
count)

3. Useful info
 Sepsis in neonates often p/w jaundice but rare in well-appearing jaundiced
infants
 Unconjugated hyperbilirubinemia in neonates ±physiologic but conjugated
hyperbili always pathologic
 Use newborn hyperbilirubinemia assessment calculator (uses hrs since birth &
t bili) to determine if phototx vs exchange transfusion
 Jaundice after 1 week of age: Think breast milk, G6PD, sepsis, metabolic

Limp
1. Osteomyelitis
 Most common 0-5yo, femur & tibia most common; majority S aureus
 Fever, malaise, bone pain, ±swelling/TTP
 CBC, ESR, blood cx, XR (periosteal elevation/bone destruction takes 10-21d),
MRI is most sensitive/specific

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  Tx: Ortho consult, abx (vancomycin 15 mg/kg IV q6h, ceftriaxone 50 mg/kg
IVq24h)

2. Septic arthritis
 Most common<3yo but can occur any age
 Hip>knee>elbow
 Febrile, toxic-appearing, flexed/externally rotated/abducted hip, pain w/ROM,
±warm/swollen/erythematous
 Dx: XR/US for effusion. arthrocentesis, wbc/esr/crp
 Tx: Abx
o Birth to 3 mo: Cover staph, GBS, GN bacilli with vancomycin 15 mg/kg IV
q6h + [gentamicin 2.5 mg/kg (IBW) IV q8h or cefotaxime 50 mg/kg IV q8h]
o >3 mo: staph and strep. Vancomycin 15 mg/kg IV q6h
 Admit

3. Toxic/transient synovitis
 3-10yo, acute or chronic hip/thigh/knee pain
 Most common cause of unilateral hip pain in 3-10yo
 ±Febrile, non-toxic appearing, limited ROM
 Dx: Wbc/esr/crp nl, hip XR neg (±effusion), get US to r/o effusion (if
effusion→need to tap to r/o septic arthritis)
 Tx: Ibuprofen 10 mg/kg PO q6h, crutches, ortho f/u w/in 24hrs
 Difficult to distinguish synovitis vs septic, if suspect septic arthritis with
effusion, need to tap

4. Legg-Calve-Perthes Dz (Avascular necrosis of femoral head)

 2-12yo w/insidious limp & c/o groin/thigh/knee pain, hip pain worse w/↑activity,
no fever, no irritability, ↓ROM 2/2 pain (esp w/internal rotation and abduction of
thigh
 Most common in 4-8yo ♂
 XR (AP/frog-leg lateral)→most often neg in early dz; WBC/ESR WNL
 Tx: No wt bearing until ortho consult/urgent f/u, bone scan/MRI
 15% have bilateral dz

5. Slipped capital femoral epiphysis

 12-15yo♂/10-14yo♀, limp, groin/thigh/knee pain; externally rotated,
±shortened, pain w/flexing hip/internal rotation
 ↑Risk AA, obese, ♂
 Dx: XR with frog-leg diagnostic; no fever, wbc/esr/crp wnl
 Stable vs. unstable: if they can’t bear weight, consider not doing frog-leg
(concern for further slip) as unstable. can still do cross table lateral
 Earliest sign: widened physis, Klein’s lines
 Tx: No wt-bearing until urgent ortho f/u
 Differential: Growing pains – bilateral, pain at night only without limp

6. Osgood-Schlatter disease
 Pre-teen ♂ knee pain worse w/activity & better w/rest
 Tender anterior knee, enlarged/indurated tibial tuberosity, pain reproduced by
extension against resistance
238
  Dx: XR→soft-tissue swelling, no effusion
 Tx: Restricted activity X 3m, crutches, ibuprofen, RICE

7. Immunologic
 Rheumatic fever: School age children, 2-3wks s/p strep infection, joint
involvement early in dz w/mild arthralgia, migratory arthritis; tx→NSAIDs
w/rheum referral
 Juvenile rheumatoid arthritis: most common ♀ 4-10yo, acute vs insidious joint
pain, intermittent low-grade fever, ≥6 wks, morning stiffness/pain s/p rest that
improves
 Lupus: Arthralgia, myalgia, arthritis, ↑risk small joints of hands/wrists/knees
 Lyme dz: Most common 5-9yo, acute migratory polyarthritis that becomes
monoarticular of knee/ankle, sx ~1wk
 Tumor
o Rhabdomyosarcoma: Most common <10yo, painless soft tissue mass
o Osteosarcoma: Most common adolescents, pain/swelling, get alk phos & r/o
septic joint
o Ewing’s sarcoma: Most common 10-20yo, pain/swelling, get alk phos & r/o
septic joint

Trauma
1. FOOSH
 Distal radius fracture most common, also consider elbow and clavicle
 If XR shows no fx but clinically suspect a fx, splint & f/u XR 5-7d

2. Nursemaid’s elbow
 Subluxation of radial head under annular ligament
 Often via pulling/lifting toddler by outstretched hand
 Tx: Traction on distal forearm/pressure on radial head, flex at elbow while
supinating hand (may feel pop). Should start using again in ~30m if successful
 If no redux s/p 2-3 attempts get XR
 Recurrence is common

3. SCIWORA
 Spinal cord injury w/o radiographic (Xr or CT) abnormality
 Get MRI if high concern but CT neg

4. Concussion
 Prolonged HA, Δvision, Δbalance, Δconcentration, memory loss, sensitivity to
light, irritability, ringing in ears, Δsleep, ↓smell/taste, n/v, dizziness
 Can return to play if
o Grade I: No LOC, no amnesia>30m. Returns when no sx X 7d
o Grade II: LOC<5m or amnesia 30m-24hr. Returns when no sx X 7d, if repeat
concussion than must take off rest of season
o Grade III: LOC>5m or amnesia>24hr. Must take 1m off then may return
when no sx X 7d s/p 1m

5. Salter-Harris
 Type I/II: Often splint w/ortho f/u 7-10d

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  Type III-V: Ortho consult (surg fixation)
 If TTP over physis w/nl XR, tx as Salter I (but only 15% of Salter I are XR neg)
 75% are Salter II

6. Other peds fractures and elbow ossification centers (see Radiology

chapter)

7. CTH: Kupperman decision rule for imaging to r/o clinically important TBI
(see Radiology chapter for more details)
 ≤2yo: Get CTH if AMS*, GCS <15*, palpable skull fx*; consider obs vs. CT if
non-frontal scalp hematoma, LOC>5s, severe mech, not acting normally
 2-18yo: Get CTH if AMS*, GCS<15*, basilar skull fx*; consider obs vs. CT if
+LOC, vomiting, severe mech, severe HA
(*=sig predictor, otherwise single factor~1% risk of ciTBI)

8. Cervical spine (see Radiology chapter for imaging algorithm)

 ≥9 yo similar to adults and can apply NEXUS
 < 8 yo: 72% spine injuries in <8 yo in c-spine; 87-100% injuries in C3 or
higher, with higher morbidity/mortality
 Greater mobility of spine, laxity of ligaments, shallow and angled facet joints,
underdeveloped spinous process  less prone to fx
 Large head, thin muscle  higher risk of cord injury
 Consider MRI > CT or admit for obs to peds if high concern for injury to
minimize radiation

9. Abdominal Trauma
 Abd begins in kids @ level of nipple
 ↑Risk solid organs (spleen, liver, kidneys); ↑risk stomach perf if bicycle
handles/hit by car s/p meal, spearing mechanism in football player
 Small bowel most common injury in restrained MVC (±delayed px 24-48hrs)
 50% of +seat belt injuries also have retroperitoneal injuries (±spinal injuries)
 ↑Lipase not sensitive for pancreatic injury (handlebar)
 Most frequently missed injury is hollow viscous

Nausea/Vomiting
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1. Ddx
 Infection: GI, AOM, strep throat, PNA, UTI
 GI inflammation, GI obstruction
 CNS
 Metabolic

2. Necrotizing enterocolitis
 Preterm neonate w/bilious vomiting, abd distention, bloody stool; toxic-
appearing, lethargic, abd tenderness, distention, heme-positive stool
 Usually w/in 1 few days/10days of life but up to 1mo
st

 Dx: XR→pneumatosis intestinalis in 75%

 Tx: NPO, aggressive IVF, NGT for gastric decompression, ±definitive airway
b/c ↑risk apneic episodes, broad spectrum abx (amp/gent)

3. Pyloric stenosis
 2-8wo (up to 3mo, most common 5wo) w/nonbilious (vs volvulus) projectile
vomiting
 Olive-size mass RUQ from hypertrophied pylorus (60-80%)
 ↑Risk 1 born ♂/FHx/white
st

 ±HypoCl, hypoK metabolic alkalosis

 Dx: US
 Tx: Hydration, OR

4. GERD
 <2yo w/irritability/spitting up/vomiting during feeding
 Tx: Frequent small meals of thickened formula w/child sitting upright, PMD f/u

5. Pancreatitis
 Rare in kids
 Epigastric pain rad to back s/p abd trauma/mumps/steroids or if
cholelithiasis/hyperTG/congenital biliary/pancreatitic duct; epigastric TTP
 Dx: US for pseudocyst/abscess/severity if septic/toxic
 Tx: NGT, NPO, IVF
 ↑Risk w/cystic fibrosis/sickle cell

6. CNS
 N/v w/o generalized/GI sx
 Hydrocephalus & tumor±isolated GI sx

7. Acute gastroenteritis
 Dx of exclusion if <3mo
 For severe abd pain, should r/o appendicitis/other abd pathology
 Tx: Hydration
st
o For mild/mod: PO pedialyte 5-30cc q5-15min X 1hr w/goal 20cc/kg in 1 hr
then ↑ w/goal to replace deficit w/in 4 hrs
o Try Zofran 0.15mg/kg PO before starting IV
st
o Or rehydrate IV can do up to 40cc/kg NS over 1 1-2hrs then convert to PO

8. Diarrhea
241
  Blood or mucous in stool? Sick contacts?
 Viral enteritis: Typically non-bloody, <5PMN/hpf, lasts ~5d, most often late
winter/spring
 BRAT diet + yogurt, avoid juice/sugar
 Bacterial enteritis: Severe abd pain, tenesmus, bloody/mucoid stool, fever
 No antimotility rx in peds (esp no abx or antidiarrheal in bloody
diarrhea→↑HUS); No cipro/fluoroquinolones 2/2 cartilage damage
 Most common infectious causes of bloody diarrhea: shigella & E coli
 If severe diarrhea: Non-anion gap metabolic acidosis 2/2 HCO3 loss in stool

Pediatric Seizure
1. Ddx
 Neonatal: Hypoxia, drugs (lead, cocaine, ASA, CO), trauma, infection,
↑/↓glucose, pyridoxine deficiency, maternal drug w/d, inborn errors, ↑/↓Na
 0-6mo: Infection, ↓Ca, ↑PO4, ↓Na, developmental malformation, inborn error
 6mo-3yo: Febrile seizure (benign), child abuse, infection, toxin, trauma,
metabolic d/o
 ≥3yo: Idiopathic (epilepsy), infection, trauma, mass

2. Tx (see Resuscitation chapter for pediatric status epilepticus guideline)

 1 line: Benzodiazepines
st

o Lorazepam 0.1mg/kg IV (max 4mg/dose) q5m X 2 OR

o Midazolam 0.5mg/kg IV SOLN buccally, max 10mg OR 0.2mg/kg IM) OR
o ±Diazepam PR (0.5 mg/kg/dose if <5yo, 0.3 mg/kg/dose if 6-11 yo, 0.2
mg/kg/dose if >12 yo)
 2 line: Fosphenytoin 30mg/kg IV/IO/IM over 10m (max 150mg/m, can start
nd

@20mg/kg dose if concerned for hypoTN)

 Call Pediatric Neurology (443-9204)
 3 line
rd

o 1mo-2yo: Phenobarbital 20mg/kg IV over 10m X 2

o >2yo: Valproate 20mg/kg IV over 4m (if CI via inborn error or liver dz then
levetiracetam 30mg/kg IV max 3g over 6m)
 Unresponsive status: Prepare to intubate, midazolam 0.2mg/kg bolus (max
10mg) then 0.1mg/kg/hr (repeat bolus & ↑via 0.1 to max 2mg/kg/hr
q5min)→pentobarbital 10mg/kg bolus then 1mg/kg/hr (repeat 5mg/kg bolus
q30m & ↑via 1mg/kg/hr qhr)

3. Simple Febrile Sz
 Peaks 9mo-3yo, typically seen with onset of febrile illness
 “Simple” = 6mo-6yo w/single generalized sz<15m & no recurrence X 24hrs
 Tx: Antipyretic, obs until baseline/2-4hrs
 Recurrent febrile sz risk ~35% (majority w/in 1 yr), lifetime epilepsy risk ~2%
(vs 1% general pop)
 Ddx : Trauma, toxic ingestion, meningitis (↑risk doctor visit w/in 48hrs, sz in
ED, focal, abnl neuro), child abuse, epilepsy
 Simple febrile seizure workup = no different than for febrile illness in that age
group
 LP only if indicated: “Strongly consider” in <12mo; or if recent abx use

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 Acute Otitis Media – see Infectious Disease chapter

Endocrine
1. DKA
 Tx with same weight based dosing and precautions as adults EXCEPT
st
o Fluid rate of 10mL/kg 1 hr
 Another 10mL/kg bolus over next hr if hemodynamic instability then ≤1.5X
maintenance fluids
st
 Never>40mL/kg in 1 4 hrs
 NS first, switch to ½ NS after 1-4h
o Insulin: Regular 0.1 U/kg/hr gtt IV, start 1-2h after initial IVF. Expect
↓glucose 50-100 mg/dl/hr
 If glucose <250 before ketoacidosis resolves, add dextrose to IVF
 No insulin bolus in <18 yo 2/2 concerns for cerebral edema, controversial
 Watch potassium levels, add 40 meq/L K if normokalemic
 Cerebral edema/herniation: Usually 4-24hrs s/p tx
o 50% Δneuro before collapse
o HA, incontinence, Δbehavior/lethargy/AMS→obtundation, sz, posturing,
Cushing’s reflex
o ↑Risk w/new-onset DM, <2yo, pH<7.1 or PCO2<20, rate of
hydration>50cc/kg/hr
o Tx: Mannitol 0.2-1g/kg IV over 30min, hyperventilation (↑RR by 5-10 breaths
over baseline)

2. Hypoglycemia
 <30-40mg/dL 1 24hrs of life, <45-50mg/dL thereafter
st

 Draw extra heparinized tube & place on ice to be used for later testing by
endocrinologist
 Tx
o If taking PO give 5g glucose tablet or 240cc milk or 1 teaspoon granulated
sugar (~5g glucose)
o If IV, give 2.5cc/kg of D10 @2-3cc/min
o If no IV, give glucagon SC/IM 0.03mg/kg (max 1mg)
o If refractory give hydrocortisone 1-2mg/kg IV q6hrs
o Goal glucose 70-120mg/dL

3. Adrenal Crisis
 Hypoglycemia, hypoNa, hyperK, metabolic acidosis, shock, ambiguous
genitalia, often 2-5wks of age; poor feeding, no wt gain, lethargy, irritability,
vomiting
 Get chem, FSBS, ACTH/renin/cortisol/aldosterone, sepsis w/u as precip
 Tx: 20cc/kg NS; hydrocortisone IV 25mg if <3yo, 50mgif 3-12yo, 100mg (if
>12yo)

3. Congenital adrenal hyperplasia

 Ambiguous genitalia (♀ usually px 2/2 viralization)
 May present as gradual onset malaise/anorexia/wt loss
 HypoNa, hyperK, hypoglycemia
 Tx: NS, ±glucocorticoids e.g. hydrocortisone 1-2mg/kg IV q6hrs

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4. Metabolic disorder
 Irritability, lethargy, vomiting, poor feeding, sz, coma, FTT; hypotonia,
hepatomegaly, sz
 Chem-7, ABG, NH4, lactate, plasma amino acids, carnitine, UA, urine reducing
substances/organic acids (MMA/PPA/IVA)
o Draw labs before tx and put in heparinized tube & on ice

Immunologic/Hematologic
1. Acute Leukemia
 Most common childhood malignancy; peaks 3-7yo; ↑risk w/♂ & white
 Fatigue, malaise, wt loss, low fever, bone pain, anemia, petechiae, easy
bruising/bleeding, splenomegaly
 Leukocytosis in 50%, neutropenia, thrombocytopenia, anemia; smear
w/lymphoblast & other immature
 Tumor lysis syndrome: Triad of hyperuricemia, hyperK, hyperPO4; can cause
ARF

2. Hemolytic uremic syndrome

 Triad of microangiopathic hemolytic anemia, thrombocytopenia, ARF
 Most common cause of peds ARF
 Peak<10yo (majority<4yo), clusters can occur during summer; 90% p/w
diarrhea, also abd pain, bloody diarrhea, pallor w/petechial/purpura, CNS (15%
sz/coma)
 Tx: CAUTIOUS IVF (if oliguric), give to correct hypovolemia only, w/NS or LR
 Often need dialysis, pRBC for Hgb<6-7, plt only if life-threatening bleed
(↑intravascular coagulation), plasma exchange if CNS sx

3. Hemophilia
 X-linked ♂
 Bleeding from umbilicus/circumcision/lips/tongue, hemarthrosis, hematuria
 ↑PTT but nl INR
 Tx: Factor VIII (for hemo A), Factor IX (for hemo B)
o Hemarthrosis: Factor VIII 20-40 U/kg, factor IX 30-40U/kg
o Muscular bleed: Factor VIII 20-40U/kg, factor IX 40-60U/kg
o Epistaxis: Factor VIII 40-50U/kg, factor IX 80-100U/kg
o ICH: Factor VIII 50U/kg, factor IX 100 U/kg
o Desmopressin for mild/mod hemo A w/minor bleed (if ≥3mo, 0.3mcg/kg,
case reports of hypoNa sz so caution)

4. Henoch-Schö nlein Purpura

 Triad of palpable purpura (on dependent parts of body), arthralgias (most
often knees), abd pain (GIB, n/v/d)
 Peaks 4-15yo; get CT a/p
 Tx: Supportive (usually can be d/c home w/PMD f/u next day)

5. Idiopathic thrombocytopenia purpura

 Peaks 2-4yo; well-appearing, purpura, mucosal bleeding, hematuria
 Only lab finding is ↓plt

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  Tx: Admit for Plt <10; for life-threatening bleeding- plts, steroids, IVIG

6. Kawasaki’s Dz
 Clinical diagnosis via fever X 5d + 4/5 of “CRASH”
o Conjunctivitis (bilateral)
o Rash (on torso)
o Adenopathy (Cervical w/≥1 ≥1.5cm)
o Strawberry tongue/fissuring of lips/erythema of pharnynx
o ΔHand/feet (erythema→desquamation)
 May also have lab findings: ↑ESR/CRP, ↑plat, ↑ANC, ↑leuks,↓albumin
 Peaks 18-24mo, majority <4yo, ♂>♀
 Prolonged unexplained fever w/ no response to abx  consider Kawasaki
 Tx: Admit, IVIG, high-dose ASA (20-25 mg/kg q6h until no fever, then 1-5
mg/kg daily), echocardiogram (coronary aneurysms)
 Incomplete Kawasaki’s: still at risk for coronary aneurysms if F + 2-3 criteria.
Send esr/crp, need to check wbc, plt (2004 guidelines from pediatrics)
 Child < 6 mo with fever x5 days and incr esr/crp  echo

Urology
1. Pyelonephritis – see Infectious Disease chapter
 Febrile UTI in < 2yo = pyelo
 Can do outpt pyelonephritis tx if non-toxic, tol PO, > 2 mo of age
 Rx 10 days of cephalexin 10-25 mg/kg PO q6-8h (good coverage for E.Coli),
and adjust based on culture results
 Can give 1 dose ceftriaxone 50 mg/kg IV/IM or 1 dose cephalexin in ED
st st

 Must return for admission if persistent fever/vomiting s/p tx X 48h

 If <3 mo age or recurrent, FU with PMD to R/O reflux/anatomic abnormality

2. UTI – see Infectious Disease chapter

 Usually diagnosed in girls >3
 Simple cystitis in child > 3 can be treated with 5 days of abx
 Best treatment = cephalexin 10-25 mg/kg PO q6-8h
 If recurrent, consider voiding dysfunction

Miscellaneous
1. Abuse
 Always consider if injuries or MS change unexplained by history
 Infant ↑risk closed head (30% missed), toddler ↑risk abd (most have no
bruises)
 75% of fx<1yo, 30% of all fx; ↑risk metaphyseal/post rib/scapular/spinous
process/sternal
 Bruises if <6mo, esp if multiple on hands, buttocks, cheek, nose, neck,
forearms, lumbar, chest
 20% of burns (↑risk buttocks, BLE, sharply demarcated, symmetric)
 Sexual: <72hrs need full exam (ALWAYS call abuse consultant), >72hrs can
defer exam to outpatient FU,
 Prepubertal: No speculum exam, no ppx for asx prepubertal,
 Offer plan B, document using quotes, document tanner stage

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2. Cerumen impaction
 Try debrox (carbamide peroxide) or Colace in ED for cerumen impaction
 Home rx of cerumenex/baby oil/mineral oil/glycerin/hydrogen peroxide
(1:10) BID-TID X 3-5d & after 1-2d can try to squirt out w/syringe

3. Colic
 Rule of 3s→>3hrs/d >3X/wk >3 wks in otherwise healthy infant
 Stops crying to feed
 Onset 2-16wks old (peak 6 weeks); most often 10pm-3am
 Tx: Soothed by the 5 s’s (shushing/white noise, swaddling, swinging, side-
lying, sucking-breast/pacifier)

4. Inconsolably crying infant

 Nl paroxysm of crying ↑ @ 2-3wks old – should always stop to feed/consolable
 Presume all are sick- dangerous to d/c a child who is not consolable
 Ddx: “IT CRIES”
o Infection
 Head/ENT: Encephalitis/meningitis, AOM, bulging fontanelle
 Resp: URI, viral prodrome
 GI: Gastritis/AGE
 GU: UTI/pyelo
o Trauma: Skull fx/bleed, MSK fx
o Cardiac: SVT, CHF (sweating with feeding), coarctation of aorta, anomalous
origin of L coronary artery from pulmonary artery
o Reflux/reaction to meds
o Immunization/intussusception
o Eyes (corneal abrasions)
o Strangulation (hair tourniquet, torsion)/surgical causes
 Appendicitis, volvulus, incarcerated hernia
o Other: Behavioral (colic, parental anxiety)

5. 1 pill kills in a 1yo

 Fe: N/v/d, GIB→ recovery→@>24hrs metabolic acidosis, coma, sz
 βB/CCB: ↓HR, ↓BP, AV block, hypoglycemia in βB, hyperglycemia in CCB
 Clonidine: AMS, lethargy, hypoT, miosis, ↓RR, coma, tx w/narcan
 Glucophage: Hypoglycemia, lethargy, metabolic acidosis, tx w/octreotide 1-
2mcg/kg q6hr
 Methylsalicylate (via icy hot/oil of wintergreen): Coma, lethargy, sz, tinnitus,
electrolytes, pulmonary edema, tx if severe w/HD

6. Pinworms
 Passed via fomites & fecal-oral
 Anal/vulvar pruritus; scotch tape test (1 awakenings X 3d), ±direct
st

visualization of worm 2-3hrs s/p sleep

 Tx:>2yo get mebendazole single dose then repeat in 2 weeks & tx all
family/close contact empirically

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 Psychiatry
By Annemarie Sheets Res ed. M. Kennedy Hall Faculty ed. Eric Isaacs

General Information
1. Goals of evaluating the psychiatric patient
 Status: Are they on 5150? If not, do they need to be?
o (Code Section) 5150: May be written by police, SF Mobile Crisis, and
Psychiatry, it is valid for 72 hours and can only be removed by Psychiatry. ED
does not place 5150 at UCSF/SFGH
 Danger to self
 Danger to others
 Gravely disabled
o ED hold (at UCSF only): May be placed by attending (preferred), licensed
residents, or PA/NP and provide 24 hours to determine the need for psychiatric
treatment (based on same criteria as above)
o A patient on either type of hold must be accompanied by a security officer
when transported for scans or other tests
 Medical clearance: depends on patient presentation
o Evaluate other potential medical causes of agitation/psychosis
 Glucose: Hypoglycemia
 Oxygen: Hypoxia
 Trauma/Temperature/Tox: Head injury or bleed; hypothermia or
hyperthermia; drugs
 Infection: Meningitis or sepsis
 Vascular: Stroke or subarachnoid hemorrhage
 Seizure: Postictal or status epilepticus
*Adapted from Rossi et al, Emerg Med Clin N Am 28 (2010):235-256.
o Anticipate needs for labs/tests (esp. if at Moffit)
 Chem10 and LFTs if anticipating start of antipsychotics
 EKG to check for prolonged QTc
 If working up dementia, consider TSH/FT4, B12 levels, RPR (discuss with
psych)

2. Safety
 Always protect yourself!
o Stay between the door and the patient, never block the exit
o Maintain distance and do not turn your back on the patient
o Look for clues of impending agitation e.g. hands making a fist,
restlessness, pacing, intimidating physical behavior, flushing skin, dilated
pupils, shallow respirations, excessive perspiration
o Leave if you feel unsafe
o Be non-confrontational, avoid arguments, do not challenge patient or make
provocative comments
 Call security and get as many people involved as you can if the situation
escalates, i.e. code 100

Restraining the Agitated Patient

1. Physical restraint

247
  Use for violent or self-destructive behavior placing the patient or others in
danger of physical harm and non-physical interventions are not effective
 MD must sign the restraint order form
 Common restraints used: Soft ties (2 or 4 point), posey vest
o Need one person per limb when placing four limb restraint: Restrain legs
ABOVE the knee, arms are less powerful when elbows are straight
2. Chemical restraint
 Medication used to control the behavior of or restrict the patient's freedom of
movement. Use after failed physical restraint, usually need IM given agitation
o “HAC” or Haldol (5mg)/ Ativan (2mg)/ Cogentin (1mg)
 Effective for agitated / combative patient with known psychotic illness
 Beware QT prolongation with antipsychotics (esp. if QTc > 500), especially
if on methadone, cocaine, or other psych meds (Get EKG once sedated!)
 Variant: Benadryl 50 mg + Ativan 2 mg ± Haldol 5 mg (used in PES) or
replacing Midazolam for Ativan for faster onset
 May use Haldol alone (esp in elderly with delirium), but concern for akathisia
 If repeat dosing, consider haldol or ativan alone depending on etiology of
agitation (psych vs. tox)
o Consider Seroquel (25mg PO) for Parkinson's with psychosis
o Restrained patients should have pulse ox and cardiac monitoring
Med Dose Time of Onset Half-life CI
Midazolam 5-15 mg IM 15-20 min IM 2-6 hrs Pregnancy
(Versed) q15 min (up to 13 h *caution in
1-2 mg IV q2- 1-5 min IV in renal elderly
3 min failure)
*Midazolam: Works quickly, can be used for undifferentiated agitation, avoid in
the elderly due to delirium
Lorazepam 1-2 mg PO 16 h PO 14 h PO Sleep apnea
(Ativan) 0.5-2 mg IM 20-30 min IM Severe renal
<2 mg/min IV 5-20 min IV insufficiency
Pregnancy
Haloperidol 5-10 mg PO 2-6 h PO 12-18 h Mvmt disorder
(Haldol) 5-10 mg IM 30-60 min Severe liver
1-2 mg IV IM/IV disease
Breast Feeding
*Haloperidol: decrease dose in elderly, concern for EPS e.g. akathisia, NMS
Droperidol 2.5-5 mg IV 30 min IV 2-4 h Prolonged QTc,
(give slowly) caution in
5-10 mg IM alcoholics
*Droperidol: black box warning for prolonged QTc, but has more rapid onset,
shorter half-life, strong sedative, no long-term side-effects compared to haldol
Ziprasidone 10 mg IM 60 min IM 4-10 h IM Prolonged QTc,
(Geodon) q2h recent
20 mg IM myocardial
q4h infarction, DM
*caution in
elderly
*Ziprasidone: more calm with less sedative effects, used more at Moffit,
approved for acute agitation in schizophrenic and bipolar-manic patients

248
Ketamine 1 mg/kg IV 1 min IV 15 min IV Heart disease
4-5 mg/kg IM 4-5 min IM 30-60 min
*subdissoc IM
0.1 mg/kg IV
*Ketamine: intact airway reflexes, may consider using subdissociative doses to
help with procedures (e.g. CT), avoid in states with increased sympathetic surge
(e.g. cocaine intoxication)
*adapted from Rossi et al, Emerg Med Clin N Am 28 (2010):235-256.

The Suicidal/Homicidal Patient

1. General approach
 Rule out organic causes; is this delirium or dementia rather than psychosis?
 Patient should have all belongings and clothing removed if they are going to
be placed on hold (e.g. green gown at SFGH, psych rm placement at UCSF)
 NOTIFY SECURITY IMMEDIATELY IF PATIENT HAS WEAPON. Do not
attempt to confiscate weapon during interview

2. Evaluation
 History
o SI/HI
o Plan? Target?
o Access to weapons
o Past attempts
o Past psychiatric history including meds, hospitalizations
o Substance use and abuse including amount, change in habit
o Past medical history and non-psych meds
 Exam
o Evaluate level of consciousness, demeanor, and affect
o Assess for hallucinations and delusions
o Look for signs of injury (e.g. prior cutting scars) or abuse.
o Every patient needs VS (including temp), exam of heart, lungs, abdomen,
neuro, and back.
 Diagnostic considerations: Perform medical clearance as dictated by H&P

Medical Clearance
1. General approach
 Completion of medical work up to address all medical issues i.e. psychotic
patient with UTI has gotten dx and abx
 Exclude 'medical' causes of behavior or mental status, i.e. delirium from
infection, AMS from head injury, hypothermia, metabolic abnormality, etc.
 Labs to consider
o ASA/APAP levels: If any concern for ingestion
o Lithium level: Always if patient takes this medication, consider if access to
lithium and concern for ingestion
o Urine tox: Rarely useful in the ED, but psych will almost always want it. If
patient is likely to be admitted, try to get a urine sample in anticipation of this
request to speed up your dispo.
o Blood tests. Consider Chem7, LFTs, CBC, and alcohol level: rarely useful in
the ED, but psych will usually want it if question of EtOH intoxication.
o EKG: useful in ingestion and to assess QT interval, plus helps with dispo to
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 psych
o Often PES (and less likely LPPI) may take patients without labs. However, if
the patient needs transfer to other institutions, they are more “sellable” with
labs. Consider this upfront to save time and spare conflict with psychiatric
colleagues. Ultimately, it is up to you to determine how you will medically clear
your patient

Axis II patients
1. General approach
 Set firm limits on behavior
 Don't undermine the nurse by promising a demanding patient an exception to
policy
 Beware of splitting, secondary gain

Suggested reading
 Rossi J, Swan MC, Isaacs ED. Emerg Med Clin N Am 2010; 28:235-256

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 Pulmonary
By Neda Farzan Res ed. Marianne Juarez Faculty ed. Chris Fee

Asthma
1. History
 Previous ED visits, hospital admissions, steroid use, intubations
 Known triggers, how often using rescue inhalers
 Duration of current attack, degree of dyspnea, cough, wheezing

2. Dx
 Peak flow: Helpful in trending response to treatment. Highly effort dependent,
may not be reliable
 CXR: Not indicated in asthma unless new onset, or different symptoms (such
as r/o PTX with pleuritic chest pain or r/o PNA if fever)
 ABG/VBG: For patients suffering severe or prolonged attacks (i.e. whose O2
sat remains <90% with O2 therapy), or decreased MS (CO2 retaining)

3. Mgmt
 Oxygen
 Albuterol 2.5 mg/Atrovent 0.5 mg neb q20 min x3. Consider Albuterol 10-
20mg continuous inhaled if severe/requiring >3 nebs without improvement
 Steroids: Given for most asthma exacerbation in the ED. Prednisone 60 mg
PO OR Dexamethasone 0.6mg/kg PO/IM/IV (Peds, max 10 mg) or solumedrol
125 mg IV (2 mg/kg IV in peds)
 For severe exacerbation: Magnesium sulfate 2 g over 20 minutes, consider
heliox, bipap
 If intubating, ensure adequate vent settings: Low RR (8-10), low TV (6-8
cc/kg), high inspiratory flow time to allow longer expiration, monitor plateau
pressure

4. Dispo
 May consider d/c home if well appearing, no hypoxia, improved with ≤3 nebs
without prior history of severe exacerbations (e.g. intubations), and reliable;
Otherwise consider admission
 Consider measuring an ambulatory O2 sat prior to discharge – reassess if low
 Ensure pt has albuterol, and if given steroids, should provide rx (e.g.
Prednisone 60 mg PO daily x5 days). Consider slower taper if h/o frequent
exacerbations
 For pediatrics, see Pediatrics chapter

COPD
1. History
 Rapidity of onset, duration of symptoms, precipitating factors, medications,
character of sputum
 Course of previous exacerbations including h/o prior intubations,
hospitalizations, recent steroids/antibiotics
251
2. Dx
 CXR: Hyperinflation, flattened diaphragm
 ABG: ↓PaO2 + ↑PaCO2 and ↓pH (the latter 2 indicate acute ventilatory
failure; consider VBG instead of ABG)

3. Mgmt
 Oxygen titrate to SpO2 90-93%
 Albuterol 2.5 mg/Atrovent 0.5 mg neb q20 min x 3
 Prednisone 60 mg PO or solumedrol 125 mg IV
 Antibiotics if change in sputum or new consolidation on CXR: Doxycycline
100mg PO x 3-5 days
 Noninvasive positive pressure ventilation (NIPPV) if moderate-severe
exacerbation, but normal mental status (ie does not require immediate
intubation, will tolerate CPAP/BiPAP, no AMS or risk for aspiration)
o COPD pts have autopeep – so titrate up the pressure support (e.g. 10/5 
increase top number)
o Must be monitored closely; if no improvement within 30 minutes, intubate
 Intubated patients (similar to asthma): Ensure adequate vent settings with Low
RR (8-10), low TV (6-8 cc/kg), high inspiratory flow time to allow longer
expiration with permissive hypercapnea, monitor plateau pressure
o Beware autoPEEP-induced shock: Tachycardia + hypotension after
intubation, with decreased BS b/l. Progressive air-trapping with decreased
venous return. Disconnect from vent, allow expiration (?squeeze chest)

4. Dispo
 May consider d/c home if well appearing, no hypoxia, improved with ≤3 nebs
without prior history of severe exacerbations (e.g. intubations), and reliable;
Otherwise consider admission
 Consider measuring an ambulatory O2 sat prior to discharge – reassess if low
 Ensure pt has albuterol/atrovent, provide rx for steroids (Prednisone 60 mg
PO x5 days)/antibiotics (Doxycycline 100mg PO x 3-5 days). Consider slower
taper if h/o frequent exacerbations

Pneumonia – see Infectious Disease chapter

Pleural Effusions
1. History
 Shortness of breath
 Most common causes: CHF, PNA, malignancy, PE, viral disease, ascites
o Exudates: Infection (pna), malignancy, immunologic, inflammation (PE)
o Transudates: Hydrostatic/oncotic pressure imbalance e.g. heart failure,
hypoalbuminemia, nephritic syndrome, peritoneal dialysis

2. Dx
 CXR: Blunting of costophrenic angle or elevation of hemidiaphragm on upright
PA film

252
  Consider subpulmonic effusion if elevated diaphragm or increased distance
between gastric bubble and L hemidiaphragm
 Lateral decubitus films vs. ultrasound

3. Mgmt – see diagram below

 If a new effusion, perform thoracentesis to characterize fluid as transudate or
exudates
 Light’s criteria for exudates
o Pleural fluid protein/Serum protein >0.5
o Pleural fluid LDH/serum LDH >0.6
o Pleural fluid LDH >2/3 upper limits of normal serum LDH

4. Dispo
 Consider admitting new pleural effusions (not attributable to CHF/ascites),
those with hypoxia/significant distress

Pulmonary Embolism
1. History
 Keep a high index of suspicion in patients with pleuritic chest pain or
unexplained dyspnea, tachycardia or hypoxia
 Common symptoms: Dyspnea (73%), pleuritic chest pain (66%), cough (37%),
leg swelling/pain (27%) and hemoptysis (13%)
 Common signs: Tachypnea (70%), rales (51%), tachycardia (30%), loud P2
(23%)
 Strongest predictors for PE (OR >2): Prior PE/DVT, unilateral leg swelling,
SpO2 <95%, estrogen use, surgery w/ general anesthesia within 4 wks
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  Risk factors: Immobilization, surgery within last 3 months, malignancy (esp
lung cancer), prior DVT or PE, trauma, CHF, smoking, CVA, obesity,
pregnancy, OCP use or hormone replacement therapy, hypercoagulable states,
inflammatory bowel disease

2. Dx
 Gestalt risk assessment: Determine likelihood of PE based on risk factors,
presentation e.g. <15% vs. 15-40%, >40%
 PE rule out criteria (PERC): Kline JA et al, J thromb Haemost, 2008
o Use if low suspicion (<15% risk). No further testing needed if all criteria are
met and low risk for PE – only 1% VTE at 45 days
o Sens 97%, spec 21%
Age <50 yo No hospitalization/ surgery within 4 weeks HR <100
No prior VTE No hemoptysis SpO2 ≥95%
No estrogen No unilateral leg swelling

 Wells criteria: Wells PS et al, Ann Intern Med, 2001

o Use if fail PERC or moderate suspicion, usually used with d-dimer
Criteria Points Criteria Points
Clinical symptoms or signs of 3 Previous PE/DVT 1.5
DVT
PE more likely than other 3 Hemoptysis 1
diagnosis
HR >100 1.5 Malignancy with treatment 1
Immobilization >3 days or 1.5 within 6 mo or palliative
surgery within last 4 wks
o <2 : Low probability, PE risk in 3 mo 1.3%
o 2-5: Moderate probability, PE risk in 3 mo 16%
o 6: High probability, PE risk in 3 mo 40%
 D-dimer: Order only when prepared to go to next step (e.g. CT PE protocol),
and when pretest probability is low-moderate
o Sens 95% (ELISA), Spec 40-68%
 Lower extremity U/S if signs/symptoms of DVT
 If PE still suspected: CT PE protocol – see Radiology chapter
o Radiation: CXR 0.07 mSV vs. CT PE 5-10 mSV
o Sens 83%, Spec 96% (PIOPED II - Stein et al, N Engl J Med, 2006)
 PPV 96, 92, and 58% based on high, moderate, or low pretest probability
 V/Q: Normal V/Q excludes PE, but must of normal lungs, usually need to
admit, consider if high creatinine
 Other
o CXR: Rule out other causes. Usually normal in PE; however in late dz can
see Westermark sign (dilatation of pulmonary vessels and a sharp cutoff),
atelectasis, a small pleural effusion, and an elevated diaphragm, hampton’s
hump (wedge-shaped opacity in lung periphery)
o EKG: Nonspecific ST and T wave abnormalities. Classic S1Q3T3 (S wave in
lead 1, Q wave and flipped T in lead 3) is not sensitive or specific for PE

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3. Mgmt
 Enoxaprin 1 mg/kg SQ Q12 hours vs. unfractionated heparin gtt
o Choose unfractionated heparin if renal insufficiency, obese
 If hemodynamically unstable, consider alteplase 100 mg IV over 2 hrs
o If PEA arrest, consider alteplase 100mg IVP (over 10 min)
o See AHA guidelines below (Jaff MR et al, Circulation, 2011); keep in mind
alteplase in submassive PE (RV strain but no hypotension) is controversial, not
currently done at UCSF

4. Dispo
 Admit to medicine
 ICU admission if massive PE (SBP <90), respiratory distress, AMS

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 Hemoptysis
1. History
 Quantify amount of bleeding
o Massive: 600 ml within 24-48 hours or at a rate of >100ml/hour
 Rule out GI or ENT source
 Causes: Bronchitis, PNA, PE, lung abscess, TB, neoplasm, AVM, vasculitis,
Goodpasture's, trauma, coagulopathies, cocaine use, cardiovascular dz (mitral
stenosis, CHF)

2. Dx
 CXR
 Consider CT chest if concern for PE
 Consider CBC, UA to look for hematuria (vasculitis, Goodpastures), PT/PTT to
rule out coagulopathy

3. Mgmt
 Minor hemoptysis: Find source of bleeding and treat underlying cause
 Massive hemoptysis/unstable patient
o Intubate with a large ETT (8.0) to facilitate suctioning and passage of
fiberoptic laryngoscope
o Place patient in Trendelenburg
o 2 large bore (18ga or larger) IVs, Type and Cross, consider activation of
Massive Transfusion Protocol – see Hematology chapter
o If GI source, consider Blakemore tube (at Moffitt call the GI fellow on-call) –
see GI chapter
o Consider use of the Level 1 rapid infuser

4. Dispo
 Consider admission depending on underlying cause, need to r/o TB
 Admit to ICU for massive hemoptysis

Tuberculosis
1. History
 Risk factors: HIV, recent +PPD, travel or emigration from a TB endemic area,
homelessness, incarceration
 Classic symptoms: Cough, weight loss/anorexia, fever, night sweats,
hemoptysis, chest pain
 KEEP IN MIND that classic symptoms are often absent in the immune-
compromised and elderly and that up to 20% of patients with active TB may be
asymptomatic

2. Dx
 CXR
o Primary active TB: Nonspecific (ie infiltrative process in the middle or lower
lung regions) and sometimes normal
o Classic reactivation TB: Cavitary lesions in posterior segment of the RUL,
apicoposterior segment of LUL and apical segments of the lower lobes

256
 o HIV+ patients: Lesions often atypical (i.e. place HIV+ patients with CAP in
negative pressure isolation)
 Sputum samples for AFB smear and culture

3. Mgmt
 Can begin therapy in ED based on clinical suspicion, to be tailored once
cultures come back
 Standard 4 drug treatment
o Rifampin
o Isoniazid
o Pyrazinamide
o Ethambutol

4. Dispo
 Admit all patients suspected of TB, place in isolation

Suggested reading
 Jaff MR, Mcmurtry MS, Archer SL, et al. Management of Massive and
Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and
Chronic Thromboembolic Pulmonary Hypertension. Circulation. 2011;
123:1788-1830
 Kline JA et al. Prospective multicenter evaluation of the pulmonary embolism
rule-out criteria. J Thromb Haemost. 2008; 6(5):772-80
 Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed tomography
for acute pulmonary embolism. N Engl J Med 2006; 354 (22): 2317
 Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at
the bedside without diagnostic imaging: management of patients with suspected
pulmonary embolism presenting to the emergency department by using a
simple clinical model and d-dimer. Ann Intern Med. 2001; 135(2): 98-107

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 Radiology
By Eric Silman Res ed. Elizabeth Brown Faculty ed. Michelle Lin

General Information
1. Tips
 Read EVERY study you order. You’ll be surprised how much you learn/avoid
getting burned
 ALWAYS order 2 or more views of plain films
 Give the radiologist a history (more than “R/O fx”). This helps THEM, YOU,
and YOUR PATIENT
 If you have questions, CALL the radiologist, don’t be afraid to request an
attending read
 YOU are the steward of radiation. Use it only as needed, and stand up for
your patients!
o While CT use has >doubled since the 1990’s, the negative appy rate has not
changed!
o 20 year old has a 1/1000 chance of dying of radiation-induced cancer after
ONE abdominal CT
Study Radiation Dose CXR Equivalent Cancer Risk*
CXR (AP) 0.1 mSv --- Negligible
Head CT 2 mSv 20 Low
Chest CT 7 mSv 70 Moderate
Abd/Pelvis CT 15 mSv 150 Highest
*A pediatric head/neck CT carries a 1 in 1500 risk of fatal cancer
*In general, dose and risk increase as age and body mass decrease
 Contrast
o At Moffitt, rads will ONLY inject IV contrast into peripheral IV’s >22g (NOT EJ
or deep brachial) and pressure-injectable central lines (as of 2010, all of our
central lines are approved)
o When to use PO contrast: Rule out perforation/fistula ONLY! (use water-
soluble contrast)
o What can you see on a non-con CT? Kidney stones, SBO, appy,
diverticulitis.
o General summary of contrast data: It’s the radiologist, not the contrast, that
makes the difference

Abdominal Imaging
1. General tips
 ONLY order Abdominal XR to look for FB, (screen) for SBO/LBO, and in
children with abd pain or vomiting
 Don’t get a “KUB,” get an Acute Abdominal Series (supine and upright AXR,
upright CXR)
 Check bowel gas pattern, see air in rectum, look for air fluid levels
 General rule of bowel dilatation: 3-6-9 cm (small bowel, colon, cecum)
 Look for air in the rectum (absent in SBO), free air under diaphragms (perf),
and pneumatosis in bowel wall (necrotic bowel)
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2. Pediatric abdominal film signs
 Double bubble (distal stomach and proximal duodenum) for pyloric stenosis
 Distal decompression (no gas) with gastric distention for duodenal atresia

3. Abd CT (Trauma)
 Check lung bases for fluid (hemothorax)
 Scroll through liver and spleen to check for lacs, hematomas and free fluid
 Check kidneys for lacs/hematomas
 Evaluate splenorenal, hepatorenal, and pelvis for free fluid (dark gray)
 Use bone window to check vertebrae and pelvis for fractures

4. Abd CT (Non-Con R/O Kidney Stones)

 Find kidneys and scroll through looking for bright stones
 One-at-a-time, find collecting system of each kidney and follow ureter down
anterior to psoas muscle, into pelvis where the join bladder on its posteroinferior
wall
 Look at relative size of ureters and pelvis, asymmetry suggests hydro
 Look for perirenal stranding (wisps of hyperdense material in dark perirenal
fat) suggesting hydro/inflammation

5. Abd CT (R/o appy, diverticulitis, colitis, abscess)

 CT is 95% sensitive for appy, REGARDLESS of IV/PO contrast!
 Visualize appendix (find the ileocecal valve and scroll down”), colon
 Look for fat stranding (hyperattenuating “whisps” in hypoattenuating fat)
 Standard of care is IV contrast. SFGH “requires” PO contrast but if patient
cannot tolerate it, call radiology back and expedite scan without it

Chest Radiography
1. General tips
 If the patient can stand or does not require continuous monitoring, ALWAYS
order PA and lateral CXR as it provides more information

2. Medical CXR
 Aortic dissection: Mediastinum >10cm, indistinct borders or aortic knob
 Pleural effusion: Indistinct hemidiaphragm, meniscus, also generalized
haziness if supine. Best seen on lateral
 CHF: Cardiomegaly, cephalization, indistinct vessels, alveolar edema,
effusions
 Pneumonia: Infiltrate, silhouette, retrocardiac, can look NORMAL (consider
time course, hydration status)
 Asthma/COPD: Hyperinflation, barrel chest, flat hemidiaphragms, can look
NORMAL

3. Trauma CXR
 Hemothorax: Unclear diaphragmatic lines, unilateral haziness if supine

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  Pneumothorax (70% sens): Look for pleural line at apex and laterally, deep
sulcus sign if supine, subcutaneous air
 Rib fractures: Posterior most common, rotate film 90 degrees to trace chest
contour
 Infiltrates: Fluffy consolidations, silhouette signs= pulmonary contusion

4. Tubes on XR
 ETT and chest tube position: 2-4cm above carina, below clavicles
 Chest tube: Last hole in chest with tube pointed at medial apex

Chest CT for PE
1. Clinical diagnostic criteria for PE
 Dx of PE is about pretest probability. Scores are used to determine post-test
probability
 When to order a CT Angio chest for PE
o A high clinical suspicion (ie. good story, VS or ECG changes) OR
o A decision rule DOES NOT allow you to forgo the scan
o Note that clinician gestalt has been repeatedly shown to be as good or better
than a decision rule in determining PE risk
 Decision rules and diagnostics – see Pulmonary chapter
 CTA Chest (“CT Angio Chest r/o PE” = “CT PE Protocol” = “PE CT”)
o The test of choice. Sensitivity for LARGE =100%. Small = 60-90%
o Need 20g IV or larger, forearm or AC only unless pt has pressure-injectable
CVC
o Reading the scan
 Scroll to see the main (bifurcating) pulmonary artery
 Adjust windowing so it’s white but has SOME density in the lumen (Main PA
should be >200HU for proper opacification)
 Divide chest into 4 quadrants
 Follow PA branches to apex and base looking for “target” and “railroad”
signs
 Look at the heart: The RV should be smaller than the LV. If it’s not, think
strain

Neuroimaging
1. Head CT
 Imaging criteria
o Much controversy exists about imaging criteria. Rules developed 1) to not
miss clinically significant injuries and 2) to reduce scans in general
o If you think the adult patient needs a head CT, order it. Be more careful in
kids
 Adult CT Imaging Decision Rules
o Canadian CT Head Rule: GCS 13-15, age ≥16, no coagulopathy, no
obvious open skull fx AND
 High risk: GCS <15 2 hrs post-injury, suspected open/depressed skull fx, sx
of basal skull fx, Vomit ≥2, age ≥65
 Medium risk: retrograde amnesia ≥30 min, dangerous mech (PVA, any
occupant ejection from vehicle, fall ≥3 ft/5 stairs)

260
  Sensitivity 99%, specificity 47%
o New Orleans Criteria: CT if GCS <15, LOC, and any of the following - [HA,
vomiting, age >60, drugs/ETOH, short term memory deficit, visible trauma
above clavicles, seizure]
 Sensitivity 99%, specificity 33%
o Nexus II: CT if age ≥65, e/o skull fx, scalp hematoma, neuro deficit, AMS,
abnormal behavior, coagulopathy, recurrent/forceful vomiting
 Sensitivity 97%, specificity 47%
 Children imaging criteria: Best study by Kupperman et. al., Lancet 2009
o Children <2 years

o Children > 2 years

*ciTBI: Clinically important traumatic brain injury

o Death from TBI
o Requiring neurosurgical intervention e.g. ICP monitoring, elevation of
depressed skull fx, ventriculostomy, haematoma evacuation, lobectomy, tissue
debridement, dura repair, etc
o Intubation for >24 h for TBI
o Admission for ≥2 nights for persistent neuro sx or signs e.g. persistent
alteration in MS, recurrent emesis 2/2 head injury, persistent severe ha, or
ongoing sz mgmt

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§Depends on: Physician experience, multiple vs. isolated findings, worsening
during ED obs, age <3 months, parental preference
[Isolated findings: Isolated LOC, isolated headache, isolated vomiting, certain
types of isolated scalp hematoma (e.g. frontal) in infants <3 mo have <1% risk of
ciTBI]
†Other signs of AMS: Agitation, somnolence, repetitive questioning, slow
response to verbal communication
‡Severe mechanism of injury: MVC with patient ejection, death of another
passenger or rollover; pedestrian or bicyclist w/o helmet struck by motorized
vehicle; fall >3 ft (age < 2 yrs) or >5 ft (age ≥2 yrs), or head struck by high-impact
object
 How to read a head CT
o Quick scroll-through for HUGE bleeding (bright white)
o Use “Blood Can Be Very Bad” method
 BLOOD: BLOOD is white clot in extra-axial, subarachnoid space, ventricles,
parenchyma
 CAN: CISTERNS should be open, dark, and visible. Check around
brainstem (“Mickey Mouse” for room, if it’s tight, there may be impending
herniation, ie. NO LP!
 BE: BRAIN should be symmetric, with no hypodensity (ischemia or swelling)
or mass and with discernable gyri and sulci. Note kids gyri/sulci are packed
more tightly and elderly/alcoholics less so due to atrophy.
 VERY: VENTRICLES should be open EXCEPT temporal horns and free of
blood. Choroid plexus can calcify and mimic blood. Evaluate for midline shift
(septum between lat vents)
 BAD: BONE window and scroll through looking for fractures. Sutures are
irregular but symmetric. Use soft tissue swelling as your guide (coup and
contracoup)
 Ischemic Stroke
o At Moffitt and SFGH when you order “Stroke Protocol” you get three scans
 Noncon: look for indistinct basal ganglia (comma sign), blurring of gray-
white border
 CT Angio: look for clot/cutoff in cerebral arteries, paucity of ACA/MCA/PCA
branches
 Perfusion: look for prolonged mean transit time (ORANGE) in vascular
territory
o NOTE: CT/CTA are not sensitive enough for posterior fossa ischemia.
Consider MRI
 Extra-axial blood
o Epidural: Lenticular, usually parietal
o Subdural: Crescentic, variable size, crosses sutures
o SAH: Suprasellar cistern/starfish pattern (may be aneurismal) vs. along
cortex/sulci (may be traumatic)
 Intraparenchymal Hemorrhage: Basal ganglia > Thalamus > Cerebellum >
Brainstem. Evaluate for midline shift, sulcal effacement (swelling), and
herniation (basilar cisterns)

2. MRI in the ED

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  Indications for MRI in the Emergency Department
o Suspected spinal cord compression (ie. story and/or hard exam findings)
o Acute posterior circulation stroke
o Suspected spinal epidural abscess (back pain with fever, h/o IVDU, DM,
elevated ESR/CRP, etc)
 Any other indications require patient admission to appropriate service and MRI
ordered by them during daylight hours

Musculoskeletal
1. General tips
 In general, get at least 2 views for every MSK film
 For fractures, trace the entire cortex looking for disruption, then trabeculations
for disturbance
 Look for bone angulation or rotation
 For fractures, note the following
o Bone
o Fracture orientation
o Displacement
o Translation
o Shortening
o Comminution
o Articular involvement
 Ortho films: if reduction needed, image joint distal/proximal to fracture

2. Upper extremity: Shoulder, Elbow, Wrist and Hand

 Shoulder
o Always get 2 views: AP and either axillary (best) or Velpeau (patient must be
standing) or lastly scapular Y (can have false negatives). Axillary and Velpeau
r/o dislocation
o AC separation: Grade I may look normal, high grades have more widening
and superior displacement of clavicle next to acromion
o Proximal humerus fractures: Common in older women. Must rule out
concomitant dislocation. Usually surgical neck
o Anterior dislocation
 Hill-Sacks: Medial impaction of humeral head
 Bankart: Inferior glenoid avulsion
o Posterior dislocation can look normal on AP, MUST get axilary or Y view.
Can see “lightbulb” sign on AP as humerus externally rotates
o Clavicle fractures: Divided into medial, middle, lateral 1/3. May consider
getting clavicle views if needed
o Scapular fractures: Indicate high-force trauma, consider CT chest and watch
for pulmonary contusions

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 Scapular Y

Axillary Lateral

Velpeau

 Elbow
o Assess for “true lateral:” Hourglass sign of distal humerus
o Check for ANY posterior fat pad: Radiolucent area posterior to very distal
humerus. Always abnormal
o Check for ENLARGED anterior fat pad (“Sail Sign”)
o These are signs of joint effusion. In kids, think supracondylar humerus fx, in
adults radial head fx
o Draw anterior humeral line, should split capitellum into anterior 1/3, posterior
2/3. If not, think supracondylar humerus fracture
o Draw radiohumeral line, should split capitellum in HALF. If not, think radial
head dislocation
 Wrist
o Assess for distal radius fracture. Note volar or dorsal displacement,
comminution
o Check radial and ulnar styloids (fractures here indicate ligamentous injury)
o Colles’ Fracture Post-Reduction: restore radial length, volar tilt, and fix dorsal
displacement
 Hand
o Check proximal and distal “arches” of carpal bones as they line up
o Check all metacarpals and phalanges for cortical defects, angulation,
dislocation
o Fifth metacarpal neck fracture “Boxer’s Fracture” common, r/o open joint
“Fight Bite”
o Max allowable volar angulation at MC neck is 50-40-30-20 degrees from 5th-
>2nd digit.
o Can get scaphoid (“navicular”) view for increased sensitivity. If films
NEGATIVE but TENDER, place in thumb spica and f/u in 1 week for repeat XR

264
3. Lower extremity: Knee, ankle, foot
 Knee
o Order AP, Lateral and sunrise (patellar fracture) or oblique (tibial plateau)
o Check contours/cortex of distal femur, proximal tibia and fibula
o Check patella on all views (if fracture plane is oblique you may need a
sunrise view)
o Look for joint effusion, lipohemarthrosis (layering density on lateral) which
suggests intra-articular fracture
o If mechanism is severe or suspect tibial plateau and XR is read negative, get
obliques or a CT
o Avulsion of tibial spine or medial tibial plateau (“Segond Fragment”) suggests
major ligament tear
o Ottawa knee rules: Sensitivity 100%
 Age ≥55
 Isolated patellar ttp
 Head of fibular ttp
 Inability to flex knee 90 degrees
 Inability to walk 4 steps (immediately or in ED)
 Ankle
o Order AP, Lateral, and mortise views
o Assess medial, lateral, posterior malleoli for fractures
o Medial, lateral, superior clear space (space between talus and tib/fib) should
be <4mm on mortise view. Suspect ligament tear if more
o Syndesmosis (tibiofibular overlap 1cm above joint) should be >6mm in all
views, otherwise suspect interosseus membrane disruption (“High Ankle
Sprain”)
o Don’t forget to assess for fibular head tenderness and get knee films if
positive (medial malleolus injury + proximal fibula fracture = Maisonneuve
Fracture)
o Ottawa ankle rules (combined foot and ankle rules: Sensitivity 97.8%,
specificity 31.5%, neg LR 0.07; see foot for foot rules)
 Age >16
 Distal posterior 6 cm fibula ttp
 Distal posterior 6 cm tibia ttp
 Inability to walk 4 steps (immediately and in
ED)
 Foot (lines, angles, growth plates)
o There can be several accessory bones in the
foot. These are usually round/oval and
corticated
o Bohler’s angle (see pic): Angle formed by two
lines drawn at top of calcaneus. Should be 20-
40 degrees, if less suspect calcaneus fracture.
Get calcaneal views or CT
o Metatarsal fractures usually oblique, easily seen on XR
th
o Proximal 5 MT fractures
 Avulsion (“Dancer’s”) Fracture: Proximal to intermetatarsal joint
 Jones Fracture: Transverse fx <1.5 cm from proximal end. Fracture extends
medially onto intermetatarsal joint surface

265
 o The navicular is the “scaphoid” of the foot, ie. can have occult fracture, treat
as fracture if XR negative but point TTP
o Ottawa foot rules
th
 Ttp base of 5 metatarsal, ttp navicula, inability to walk 4 steps (immediately
and in ED)

4. Pelvis and Hips

 Screen trauma patients with HYPOTENSION,
proximal leg deformities
o Trace circles in pelvis: Pelvic brim, obturator
foramina, Shenton’s lines, femoral trabeculae
o Find a fracture, look for a second one
o Check SI joints and L5 transverse process
(many pelvic ligaments attach here)
o If you suspect a hip fracture and the films are
read negative but patient cannot bear weight? Get a CT to r/u occult fracture.
MRI and bone scan are inpatient options

5. Spine
 In general, CT more sensitive for spinal trauma
 If you suspect cervical spine injury, get a CT. Plain films are NOT sensitive
enough
 If a CT c-spine is negative and the patient is still altered or has severe
multiorgan trauma, DO NOT remove the collar. See Trauma chapter for
clearance guidelines
 Screen for thoracolumbar spine fractures with plain films, but if severe
mechanism or elderly, get CT
o T and L-spine fractures may be associated with concurrent intrathoracic or
abdominal injuries, consider CT chest with T-spine reformat or CT abd/pelvis
with L-spine reformat
 C-spine imaging decision rules (Helps decide who NOT to image)
o NEXUS: Sensitivity 99.6%, specificity 12.6% (91% sensitive for fracture seen
on plain film). “NSAID” mnemonic
 No Neurologic deficits
 No Spine tenderness (no midline tenderness)
 No Altered mental status
 Not Intoxicated
 No Distracting injury
 Distracting injury: long bone fx, visceral injury requiring surgery c/s, large
lac/degloving or crush injury, large burns, other injury assoc with functional
impairment or interfering with ability to appreciate other injuries
o CCR: Sensitivity 99.4%, specificity 45.1%
 Inclusion: age >16, GCS 15, VS normal (RR <30, SBP ≥90), injury w/in 48h,
blunt injury, no acute paralysis, no known verterbral dz, no prior evaluation for
same injury, not pregnant
 High risk (CT vs. XR if ≥1): Age ≥65, dangerous mech (fall ≥3ft or 5 stairs,
axial loading to head, MVC >62 mi/hr or with rollover/ejection, motorized
recreational vehicle crash, Bike crash), extremity paresthesias

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  Low risk (clinically clear if ≥1 low-risk + active ROM 45° left/right): Simple
rear-end MVC, sitting position in ED, ambulatory post trauma, delayed onset
of neck pain, absence of midline cervical-spine tenderness
 Moderate risk: If no high risk findings + no low risk findings. obtain XR
o Note the Canadian Rule is MORE SENSITIVE but more inconvenient than
NEXUS
 Stable C-Spine Fractures: Transverse process, extension teardrop, type I
odontoid, spinous process, lamina
 Pediatric C-spine evaluation (see SFGH algorithm below)
o XR: Lateral view diagnostic for 98% fractures, but need both AP and lateral,
odontoid (if ≥9 yo). <9 yo should not get open mouth view

*Significant mechanism: axial head load/hyperextension injury, high speed

MVA (>60 mph), fall onto head from height > body length
o CT: Good sens/spec for bony injury, but 10-90x more radiation than plain
films (<5 yo most sensitive to radiation)

267
 o MRI recommended over CT if suspicion of c-spine injury: better for soft
tissue/cord injuries, and less radiation

6. Ortho trauma associations

 Calcaneal fractures, lumbar compression fractures, acetabular fractures
 Proximal ulnar fractures, radial head dislocations (Monteggia Fx)
 Radial metaphyseal fractures, distal radioulnar joint dislocation (Galeazzi Fx)
 Sternal fractures, thoracic compression fractures

7. Peds MSK
 Bones tend to break before ligaments in children, and generally more
deformity tolerated in kids
o Greenstick Fractures: Disruption of only one cortex with bowing of long bone
o Torus Fractures: Soft bones collapse with little or no fractures lines, look for
cortical buckling
o Toddler Fractures: Spiral distal tibial fractures with minor or unknown
mechanism. Check for NAT. Very subtle on XR, may need obliques
o Nursemaid’s elbow: usually subtle if not normal on XR
o SCFE: Klein’s lines drawn along superior femoral neck should intersect
femoral head
o Femoral head AVN: deformity, sclerosis, lucency of femoral head and/or
narrowed joint space
 Salter-Harris fracture classification – see Pediatrics chapter
 Elbow Ossification Centers
Come Capitellum 1-2 years old
Rub Radial Head 3-4
My Medial Epicondyle 5-6
Tree Trochlea 7-8
Of Olecranon 9-10
Love Lateral Epicondyle 11-12

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 Renal, Urology, and Acid-Base
By Natalie Desouza, Res ed. Sarah Gertler Faculty ed. Charles Murphy
Benjamin Hippen

Renal Failure in Renal Transplant Patients

1. General
 Mild ARF: Decreased UOP, htn, increased Cr by 20%
 Severe ARF: Fever, leukocytosis, allograft ttp

2. Ddx
 Ddx considerations for infections and complications depend on timing since
transplant e.g. first month vs. first year
o Complications
 First wk: Vascular occlusion (acute renal artery occlusion/thrombosis),
urinary leak, bleeding at anastomosis/hematoma.
 <3 mo: Post-surgical lymphocele (5-15%), obstructive uropathy
 Other: Renal artery stenosis (CRF and proteinuria), bleeding post renal
biopsy
o Infection
 <1 mo: Pyelonephritis, assoc with gram pos and neg bactgeria; surgical
wound infection, pneumonia, line-sepsis
 1-6 mo: CMV which may be invasive with pulm, GI, CNS involvement; HCV,
other opportunistic infections (bacterial, mycobacterial, fungal, viral, parasitic)
 >6 mo: Community-acquired infections
o Rejection
 Acute: T lymphocytes attacking donor tissue Ag
 Chronic: Initimal proliferation  decreased renal vascular lumen size with
nephrosclerosis, htn; irreversible within few days. Progressive with increased
proteinuria
 Other
o Prerenal hypovolemia
o Disease recurrence
o Immunosuppressive toxicity
 Cyclosporine: Nephrotoxicity, hyperkalemia, hypomagnesemia,
hyperuricemia/gout, hemolytic-uremic syndrome, hyperlipidemia,
hepatotoxicity, gingival hyperplasia, neurotoxicity. Drug interactions with
amphotericin B and other antifungals, aminoglycosides, bactrim, ranitidine;
increased toxicity with CYP450 inhibitors e.g. diltiazem, nicardipine, verapamil;
increased metabolism with rifampin and phenytoin; caution with potassium-
sparing diuretics
 Tacrolimus: Similar to cyclosporine with more common neurotoxicity
(paresthesias, HA, sz); hair loss, diabetes, no gingival hyperplasia
 Azathioprine: BM suppression, hepatotoxicity, pancreatitis. Drug interactions
with ACE-inhibitors, allopurinol, warfarin
 Mycophenolate mofetil (Cellcept): Abd pain, anorexia, nausea/vomiting,
UGIB, diarrhea, anemia, leucopenia, thrombocytopenia
 Sirolimus: Thrombocytopenia, hyperlipidemia, buccal ulceration, diarrhea,
interstitial pneumonitis

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  Steroids: Weight gain, cataracts, thin skin, osteoporosis, avascular necrosis,
UGIB/ulcers, diabetes, psychosis, hyperlipidemia
 Antilymphocyte monoclonal antibody (OKT3, antithyroglobulin): Chills, fever,
hypotension, headache, pulmonary edema

3. Dx
 Labs: CBC, chemistries, ua/ucx/UNa/Ubun/Ucr, LFTs (to eval for
immunosuppressive toxicity)
o WBCs in UA may represent UTI vs. rejection
o Hematuria may be from native or transplant kidney, need to evaluate all
kidneys and bladder (e.g. cystoscopy)
o Cyclosporine/tacrolimus levels must be drawn within 1-3 hrs before
scheduled dose for true trough level to be useful
o Caution with low FeNa: May be 2/2 prerenal azotemia vs. acute cyclosporine
or tacrolimus nephrotoxicity or rejection
 Doppler ultrasound to assess vascular flow, presence of obstruction
(hydronephrosis), peritransplant fluid collections (abscess, leak)
 CT abd/pelvis if concern for post-transplant hematoma

4. Mgmt
 D/w KTU at UCSF or with pt’s nephrologist regarding mgmt, consider
admission if e/o infection, rejection, or graft complication
 If concern for rejection, consider high dose methylprednisolone 500-1000
mg daily x3 days in d/w KTU

Complications in Dialysis Patients

1. Complications of vascular access
 Thrombosis: Consult vascular surgery first, consider Alteplase 2.2mg at
access site (check nursing protocols)
 Infection: Send cultures from access site and a peripheral site, give empiric
Vancomycin 1gram IV, admit all febrile patients
 Hemorrhage: Apply direct pressure, consult vascular surgery

2. Complications during hemodialysis

 Hypotension
o Hypovolemia from excessive fluid removal most common; consider cardiac
dysfunction, pericardial disease, infection, GI bleeding
o Trial of small fluid bolus, w/u for other causes, consider admit for further
work-up if not clearly due to hypovolemia, d/w nephrologist
 Dialysis disequilibrium syndrome
o Decreased level of consciousness, focal neuro deficits during or shortly after
dialysis, probably due to cerebral edema; may include nausea, vomiting, and
hypertension with papilledema, could progress to seizure, coma or death.
Associated with aggressive dialysis
o Stop dialysis, consider mannitol
 Air embolism
o Abrupt neuro changes in a sitting patient, or chest pain, SOB in a recumbent
patient
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 o Immediately place patient in Trendelenburg, left lateral decubitus, and
give100% oxygen
 Electrolyte abnormalities: Just about any electrolyte may be involved, but
specifically consider, Ca, K, glucose, magnesium
 Bleeding: Pts receive boluses of heparin during dialysis! D/w KTU

3. Complications of peritoneal dialysis

 Peritonitis
o Abd pain, fever (>37.5 C), nausea, diarrhea, cloudy dialysate
o Often due to infection from skin bacteria, but consider secondary causes (e.g.
cholecystitis, appendicitis, bowel ischemia or perforation, etc)
o Send peritoneal fluid for cell count, gram stain and culture. Positive study
3
if >100 WBCs/mm and >50% neutrophils (assuming normal dwell times)
o Treat with Vancomycin 1 gram load IV then 30 mg/kg intraperitoneally per
2L exchange + ceftriaxone or gentamicin if gram neg rods
o Consider admission if ill or at least follow-up within 24-48hrs
 Infection at catheter site: Usually S. Aureus or Pseudomonas
o Mild infection w/o drainage: Clean site with povidone iodine or chlorhexidine
then dilute hydrogen peroxide bid. May consider topical gentamicin (use eye
gtts) if suspect gram negative infection, avoid occlusive dressing. F/u in 1 wk
o Infection + drainage: Culture drainage fluid, start empiric antibiotics e.g.
amoxicillin 500 mg bid, cephalexin 500 mg bid-tid, bactrim DS 1 tab daily
x2-3 wks, may add rifampin/vancomycin if no improvement in 7 days for
MRSA coverage. Consider ciprofloxacin 250 mg bid if suspicious for
pseudomonas
o If no improvement with antibiotics or e/o abscess, admit, may need catheter
removal (DO NOT REMOVE IN ED)

Urinary Tract Infections – see Infectious Disease chapter

Hematuria
1. General
 Not all red urine is blood
o Udip negative, RBC negative: Porphyria, food dyes, beets, Pyridium
o Udip positive, RBC negative: Myoglobinuria (rhabdomyolysis)
o Udip positive, RBC positive: True hematuria
 Approach to mgmt
o Determine source and consider large ddx: cancer, infection, trauma,
glomerular disease
o If gross hematuria with clots, place triple lumen Foley catheter for bladder
irrigation
o If stable/mild, may consider outpatient management unless significant
clotting and retention. Consider discussing with urology

2. Nephrolithiasis
 Number one dx in missed AAA!  imaging getting more common in elderly
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 esp >50
 Presentation: Acute onset of unilateral flank pain, may radiate to groin,
nausea/vomiting
o 10-30% with acute nephrolithiasis may present w/o hematuria
 Ddx: AAA, pyelonephritis, appendicitis, abdominal abscess, SBO, biliary
(biliary colic, cholecystitis), gyn etiologies (cyst, torsion, PID) or testicular
(torsion, epididymitis)
 Dx
o Labs: UA with RBCs, chem panel if decreased urine output or chronic renal
problem
o Bedside US to evaluate for hydronephrosis (difficult to see stone on US)
o Consider non-contrast abd/pelvis CT* for first-time presentation
*At UCSF, enroll in Ralph Wang’s STONE study for US vs. CT
 Mgmt
o NSAIDS: Ketorolac 30 mg IV/IM (onset 30-40 min) or
ibuprofen/indomethacin PO. Should be used as adjunct with opioids
o Opioids: Fentanyl, dilaudid, or morphine
 For pts who need to drive, pts may pass machinery test 4 hrs after
administration of fentanyl 1mcg/kg but not with other opioids
o Consider Tamsulosin 0.4 mg po daily until stone passage (1-2 wks) -
?improved pain control
o Phenazopyridine (Pyridium) 200 mg PO TID x 2 days if significant dysuria
(avoid longer therapy 2/2 methemoglobinemia)
o Anti-emetics, ±IVF (no e/o increased stone passage with fluids)
o Admit patients with single kidney or post-transplant, ARF, intractable pain, or
evidence of infection or obstruction
o If imaging reveals stone >5mm, need outpt Urology follow-up 2/2 low
spontaneous passage rate (>7 mm stones have 10% chance of spontaneous
passage), but all pts get trial of spontaneous passage
o All other stones should f/u with PMD, need recheck in 3-5 days for pain,

2. Rhabdomyolysis
 Breakdown of skeletal muscle  release of myoglobin, cellular potassium,
phosphate/sulfate; retained fluid within injured myocytes  hypovolemia,
hyperkalemia, metabolic acidosis, acute renal failure
 Association with viral syndrome: thigh pain in kids with influenza may have
elevated ck due to myositis (“benign acute childhood myositis”), but rarely lead
to kidney failure
 Presentation
o History of crush injury, immobility, muscle overuse, drug or alcohol use
o Myalgias, stiffness, weakness, malaise, low grade fever
o May have brown urine, but normal color urine does not r/o!
 Ddx: Compartment syndrome, electrolyte abnormality
 Dx
o Labs: Chem, serum CK, UA
 Five-fold increase above upper limit of normal of serum CK in the absence
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 of cardiac or brain injury suggests rhabdomyolysis
 CK rises 2-12 hours after onset of muscle injury and peaks in 24-72 hours
 Brown heme-positive urine with negative RBC on UA micro
o Get an EKG immediately – may get fatal hyperkalemia even if K under 6!
Release of intracellular phosphate  decreased calcium, very sensitive to any
rise in K. Give calcium if ekg changes past peaked t waves (e.g. qrs widening)
 Mgmt
o Aggressive hydration with NS (200-1000 ml/hr), titrate to goal UOP of 2-3
mL/kg/hr
o May consider alkalinizing urine with D5W + 100 meq (=2 amps) bicarb/L,
though no clear evidence this is better than NS
o May consider use of mannitol 1 g/kg IV over 30 min, but may cause osmotic
nephrosis
o Loop diuretics are controversial (acidification of urine, worsened clearance)
o Monitor for electrolyte abnormalities, especially hyperkalemia
o Avoid nephrotoxins
o May consider dialysis for severe hyperkalemia, volume overload, or acidosis
o Exertional rhabdo in healthy patients may be rehydrated and sent home if
mild, but most require aggressive IV hydration and admission
o Patients with comorbidities should be admitted to telemetry bed
o Patients with severe metabolic abnormalities should be admitted to ICU

Urinary Retention
1. General
 Presentation: History of urgency, frequency, nocturia, incontinence, cancer,
trauma, neurologic spx, med changes (especially anti-cholinergics)
 Mgmt
o Bedside ultrasound for post-void residual
o Foley catheter
o U/A, UCx, chem panel
o Further maging depends on etiology
o Patients with BPH-related retention may d/c home with Foley, leg bag,
Flomax, Urology follow-up. If ill, or complicated, admit

Urology in the ED
1. Urologic devices
 Ureteral stents
o Infection may be difficult to diagnose due to constant presence of WBCs/LE
on UA, need culture to confirm. Dx should be based on symptoms
o UTI: Treat as complicated outpatient UTI if not ill
o Pyelonephritis: Image to confirm stent position, IV antibiotics, consult
Urology
 Urinary diversion and orthotopic bladder substitution: Usually colonized. A
4
positive culture in these patients is >10 CFU/mL of a pathologic organism

2. Testicular torsion
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  Presentation: Acute severe pain in lower abdomen/testis/inguinal canal that
can be constant or intermittent
 Ddx: Epididymitis, hernia, testicular mass
 Dx
o Clinical: Tender testicle with cephalad elevation, abnormal lie in scrotum.
Classically absent cremasteric reflex, neg Prehn’s sign (no pain relief with
elevation), but in practice limited utility
o Color doppler ultrasound if diagnosis unclear
 Mgmt
o Minimize ischemic time: Emergent manual detorsion. Place patient in frogleg
position with adequate analgesia/sedation. Rotate affected testis medial-to-
lateral (“open book”) until pain is relieved. Consult Urology early!

3. Priapism
 Most cases are low-flow (ischemic) secondary to decreased venous outflow,
2/2 vasoactive drugs  engorgement of the corpora cavernosa
 High-flow (non-ischemic) is uncommon and usually secondary to trauma
 Sickle cell disease most common risk factor
 Presentation: Prolonged, painful penile erection, usually in the absence of
sexual stimulation
 Dx: Low-flow priapism is diagnosed by history and physical. If suspect high-
flow priapism, consider doppler U/S and corporal blood gas analysis (for arterial
vs venous blood) does it look arterial-ish?
 Mgmt
o Trial of terbutaline 5mg PO x2 doses q15 mins or 0.5 mL SQ x2 doses q20
mins
o Aspiration: anesthetize penis (dorsal penile block), aspirate from a single
corporal body at 10 or 2 o'clock. Do not aspirate from glans. Bilateral aspiration
is not necessary because the corpora communicate freely
o If priapism persists, dilute phenylephrine 1mg in 9mL sterile saline (final
concentration 0.1mg/mL) and inject as 0.2mL aliquots into punctured corpus
cavernosum until flaccid. Patient must be placed on cardiac monitor

4. Paraphimosis
 Presentation: Inability to replace the foreskin distally over the glans penis
 Mgmt
o Sedation or penile block
o Place fingers of both hands behind the paraphimotic foreskin and apply
gentle pressure on the glans with both thumbs. (Gauze may improve traction)
o Application of sugar may reduce glans edema and facilitate reduction
o Surgical release of the paraphimosis necessary if mechanical reduction fails

5. Phimosis
 Associated with scarring from previous injuries, poor hygiene, or infection
 Presentation: Inability to retract the foreskin proximally over the glans penis
 Mgmt: Asymptomatic phimosis is non-emergent, urology follow-up

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 6. Acute prostatitis
 Most commonly 2/2 E. coli. Also, Pseudomonas, Klebsiella, Enterobacter,
Serratia, and Staph
 Presentation: Low back pain, perineal, suprapubic or genital discomfort,
obstructive lower urinary tract voiding symptoms, frequency, dysuria, perineal
pain with ejaculation, fever, chills
 Dx: Clinical
o Perineal tenderness, rectal spincter spasm and prostatic tenderness or
bogginess
o UA/UCx are frequently negative and prostatic massage is no longer
recommended (induces bacteremia)
o Send Gonorrhea and Chlamydia
 Mgmt
o Non-STD prostatitis: Treat for 30 days with Ciprofloxacin 500mg PO BID
x28 days or TMP/SMX DS 2 tabs PO BID x 28 days
o Appropriate STI treatment as indicated
o Follow up with Urology

7. Balanoposthitis
 Associated with inadequate hygiene or irritation. Most commonly 2/2
colonization w/ Candida, consider Gardnerella, Group B Strep, or anaerobes if
warmth, erythema, edema are present
 Diabetes is a risk factor
 Presentation
o Balanitis: Inflammation of the glans penis
o Posthitis: Inflammation of the foreskin
o Balanoposthitis: Inflammation of the glans and foreskin
 Dx: clinical. Exclude STIs
 Mgmt
o Cleanse w/ mild soap, sitz baths
o And topical antifungals plus fluconazole 150mg PO x1 if Candida

8. Urethral stricture
 Typically 2/2 scarring from STI or trauma
 Presentation: Urinary retention or difficulty voiding
 Dx: Failure of 14/16F Coudé catheter to pass. Retrograde urethrogram
required for definitive diagnosis, but not required
 Mgmt: Try to gently pass a 12/14F Coudé catheter. If fails to pass, discontinue
attempts and consult Urology since continued attempts could create a false
passage and bacteremia. Urgent bladder decompression can be performed
using suprapubic cystotomy (consult urology first)

9. Epididymitis/Epido-orchitis
 Most commonly bacterial infection. Men < 40 usually STIs. Men > 40 usually
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 enteric bacteria
 Presentation: Lower abdominal/inguinal canal/scrotal or testicular pain, usually
gradual onset
 Dx
o U/A (pyuria in 50%), UCx; physical exam may show relief w/ elevation
(Prehn’s sign), epididymal tenderness
o Chlamydia and gonorrhea tests
o Need to distinguish from torsion! Esp when present within first 24 hrs
 Mgmt
o Scrotal elevation with ice q 10-15 mins q 6hrs
o Ceftriaxone 250mg IM x1 in ED; doxycycline 100mg po bid x 10-14 days or
other organism-directed ATBs.
o NSAIDS
o Stool softeners to avoid Valsalva/strain
o Usually managed as outpatient. Admit for fever or systemic signs

10. Orchitis
 Isolated orchitis (without epididymitis) is rare; think of mumps. In
immunosuppressed patients it is usually due to secondary seeding from
epididymitis

Acid/Base: Blood Gas Interpretation

1. Determine the primary disorder: Look at pH, HCO3, PCO2

2. Determine compensation
Disorder Compensation
Metabolic ↓pCO2 1.2 mmHg per 1 mmol/L ↓HCO3
acidosis *pCO2 = last 2 digits of pH
Winter’s: pCO2 (exp) = (1.5 x HCO3) + 8 ±2
*if pCO2 (serum) >pCO2 (exp) there is an additional respiratory
acidosis
Metabolic ↑pCO2 0.6 mm Hg per 1 mmol/L ↑HCO3
alkalosis

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Respiratory Acute: ↑HCO3 0.1 mmol/L per 1 mmHg ↑pCO2
acidosis Chronic: ↑HCO3 0.35 mmol/L per 1 mmHg ↑pCO2
Respiratory Acute: ↓HCO3 0.22 mmol/L per 1 mmHg ↓pCO2
alkalosis Chronic: ↓HCO3 0.5 mmol/L per 1 mmHg ↓pCO2

3. Calculate anion gap to differentiate metabolic acidosis

 AG = Na – (Cl + HCO3)
 Gap acidosis: AG >12. Normal gap = non-gap acidosis

4. Calculate the excess anion gap (∆AG) to reveal additional metabolic

disorders
 ∆AG = AG -12
 HCO3 exp =HCO3 + ∆AG
o >30: Co-existing metabolic alkalosis
o <23: Co-existing non-gap metabolic acidosis
 Delta-delta = ∆AG/(24- HCO3)
o >2: Co-existing metabolic alkalosis
o <1: Co-existing non-gap metabolic acidosis

5. Differential diagnosis
 Primary respiratory alkalosis: Ex) 7.49/28/80/22
o Stimulation of pulmonary receptors: Asthma, pneumonia, PE, pulmonary
edema, hypoxia
o Anxiety
o Meds e.g. salicylates
o Sepsis, hepatic encephalopathy, hyperthyroid
o CNS disease
o Pregnancy
 Primary respiratory acidosis: Ex) 7.2/60/80/24 (acute) vs. 7.35/60/80/33
(chronic)
o Neuromuscular disorder: Guillain-Barré, myasthenia gravis
o CNS depression: opiates, CO2 retention
o Airway obstruction
o Chest wall: Flail chest and rib fractures
o Lung disease: PTX, OSA, COPD
 Primary metabolic alkalosis: Ex) 7.5/45/80/35
o Urine Cl <10 meq/L: Hypovolemia with vomiting, diuretics, NG drainage,
post-hypercapnia. Responsive to volume
o Urine Cl >20 meq/L: Hypokalemia, excess corticoid or mineralocorticoid
activity (Cushing’s, Conn’s), 2° hyperaldosteronism (CHF, cirrhosis),
 Primary metabolic acidosis: Ex) 7.2/25/80/10
o Non-gap acidosis
 Renal: Renal tubular acidosis, kidney disease
 Non-renal
 GI: Diarrhea, fistula, ileus
 Urinary tract diversion
 Chloride, TPN, cholestyramine
o Anion gap acidosis: MUDPILES
 Methanol

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  Uremia
 DKA
 Paraldehyde
 INH, Iron toxicity
 Lactic acidosis
 Ethanol
 Salicylates

Suggested Reading
 Venkat KK, Venkat A. Care of the renal transplant recipient in the emergency
department. Ann Emerg Med 2004; 44(4): 330-41.

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 Toxicology
By Hangyul Chung-Esaki Res ed. Joseph Freeman Faculty ed. Craig Smollin

General approach
1. Contacts
 Poison Control 1 800 222 1222/1800 411 8080

2. Considerations
 ABCs, IV access, O2, monitors, FSG, EKG (QRS, QTc; aVR R>S, R>3mm
e.g. TCA O.D.)
o D= DON’T forget in coma = D50/Decontaminate, O2, Narcan, Thiamine
o E=Enhanced elimination (i.e. Dialysis)
 Hx: How much? when? check bottles/Rxs/drugs, check belongings, collateral
info from family/chart
 Px: VS, identify toxidromes

3. Decontamination
 Activated charcoal (AC):10:1 ratio drug:AC or 50 G (1 G/kg) in slurry
o Some need repeat: sustained-dose, salicylate, carbamazepine, phenobarb
o PHAILS to bind: Pesticides, Hydrocarbons (benzene, toluene, turpentine,
kerosene, mineral spirits), Alcohols/Acids/Alkali, Iron, Lithium/Lead, Solvents
o SE: N/V, aspiration risk!
 Whole-bowel irrigation: Polyethylene glycol 1.5-2 L/hr (peds 0.5 L/hr),
OGT/NGT; Used for controlled-release drugs, body packers, iron, lead, arsenic
 Gastric lavage: 36-40 F tube, 200-300 mL (peds 10 mL/kg)
o Not common, consider in TCA, CaB, BB, severely ill within 1 hour
o Aspiration risk. CI in large pills, caustics, hydrocarbons

4. Lab considerations
 Anion gap: Na - (Cl + HCO3 ).
+ - -

o MUDPILES: Methanol, Uremia, DKA/AKA, Paraldehyde or

Phenformin/metformin, INH/iron, Lactic acid*, Ethylene glycol, Salicylates.
*Ddx of lactic acidosis: CN, CO, Antiretroviral drugs, Hydrogen sulfide,
Seizures, shock or hypoxia, Sodium azide
o Alternative: KULT (Ketones, Uremia, Lactate, Toxic alcohols)
 Osmolar gap = measured Sosm - (2Na + glucose/18 + BUN/2.8 + ethanol/4.6)
o If >10-20, consider alcohols (methanol, ethylene glycol, isopropranolol),
mannitol, propylene glycol, glycerol, ethyl ether
o Other causes: hyperlipidemia, hyperproteinemia, DKA, AKA, multiorgan
system failure, chronic renal failure
 Tox screen
o Utox: amphetamines/MDMA, benzo, cocaine, opiates, MJ (no PCP @
SFGH), though caution in interpretation
o Amphetamine is non-specific, methadone is neg on opiates (but SFGH has
separate methadone assay)
o Comprehensive plasma and urine drug screening available at SFGH if
needed with rapid turn-around, but need to contact poison control
o Serum levels: ETOH, Salicylate, tylenol, valproic acid, digoxin, phenytoin, etc
o Carboxyhemoglobin: need to specify on ABG/VBG (CO-oximeter @ UCSF)
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Anticholinergic
S/sx "Blind as a bat (vision changes, dilated pupils), Dry as a bone (dry skin,
dry mouth, eyes, ↓urine), Red as a beet (flushing), Mad as a hatter
(AMS/agitation), Hot as a hare (fever)"; "can't see, can't pee, can't sh*t"
↑HR, ↓bowel sounds, myoclonus. Sz, dysrhythmias if severe.
*hyperthermia - hepatic necrosis, rhabdo, cerebral edema, DIC
Cause Antihistamines, antipsychotics, antiparkinsonians, antidepressants,
antispasmodics/muscle relaxants, amantadine, atropine, disopyramide,
scopolamine, TCA; Plants (Jimson weed, Amanita muscaria)
Mgmt Physostigmine 1-2 mg IV q10min (peds 0.02 mg/kg over 3-5 min) for
severe delirium/agitation. AVOID in TCA, abnml EKG;
IV benzos for agitation/shivering/sz; sodium bicarb for wide complex
dysrhythmias; evaporative cooling, hydration
Cholinergic
S/sx DUMBELS: Diarrhea, Urination, Miosis, Bradycardia, bronchorrhea,
bronchospasm, Emesis, Lacrimation, Salivation
Weakness, AMS, seizures, spasms/fasciculations
Cause Organophosphates/nerve agents, physostigmine, nicotine, pilocarpine,
bethanechol, mushrooms
Mgmt Airway/ventilation; atropine 1-2 mg IV (peds 0.03 mg/kg), titrate to
secretions; pralidoxime (2-PAM) 1-2 G IV q4-6h (peds 25-50 mg/kg)
Extrapyramidal
S/sx parkinsonism e.g. oculogyric crisis, rigidity, torticollis, trismus, dysphagia,
dystonia, akathisia, tardive dyskinesia
*NMS: F, labile BP, lead pipe rigidity, AMS, dyskinesia, rhabdo, dysrhythmia
Cause Haldol, phenothiazines, metoclopramide (removal of dopamine agonists)
Mgmt Benadryl 1-2 mg/kg IV q6h PRN; benztropine 0.05 mg/kg IV q12h prn;
*NMS: Supportive care, aggressive management of hyperthermia, benzos
Opioid
S/sx Small pupils, AMS, resp depression, ↓HR, ↓reflexes, ↓bowel sounds, Nl/↓BP
*withdrawal: diarrhea, abd cramps, piloerection, yawning
Cause Heroin, morphine, fentanyl, etc
Mgmt Naloxone 0.05-0.1 mg IV, titrate RR ≥12
Sedative/hypnotic
S/sx AMS (drowsy, coma), ataxia, respiratory depression
Cause Benzos, barbiturates, ɣ-hydroxybutyrate (GHB)
Mgmt Airway; flumazenil (0.2 mg -> 0.3 mg -> 0.5 mg, max 5 mg) acute OD only
Serotonin syndrome
S/sx AMS, fever, agitation, tremor/myoclonus, ataxia, hyperreflexia,
incoordination, diaphoresis, shivering
Cause Drug interaction b/w SSRIs, SRIs (venlafaxine), trazodone with MAOIs,
tryptophan, sympathomimietcs, TCA, Li, etc
Mgmt Supportive care and aggressive management of hyperthermia.
Cyproheptadine 4 mg po prn (watch for anticholinergic sx)
Sympathomimetic
S/sx ↑HR (↓HR if pure α agonist), ↑BP, diaphoresis, dilated pupils, agitation,
AMS, hyperthermia, piloerection, hyperreflexia, aggression, diaphoresis (vs.
dry skin in anticholingeric). Sz, dysrhythmias, hypotension if severe.
Cause Cocaine, meth/amphetamines (PCP→nystagmus), theophylline,
decongestants, caffeine. *mimics: hypoglycemia, etoh/benzo withdrawal
Mgmt Benzos, hydration, cooling

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 Analgesics
1. Acetaminophen: NAPQI toxic metabolite
 Toxic dose: >150 mg/kg
o Rumack-Matthew nomogram based on time of ingestion
(e.g. toxic if >150 mcg/mL @ 4hrs)
 Phases of toxicity
o I (<24 hrs): Anorexia, N/V, diaphoresis, pallor, malaise
o II (24-48h): RUQ abd pain, ↑bili, ↑PT, transaminitis, oliguria
o III (72-96 h): LFTs peak; encephalopathy, coagulopathy, hypoglycemia,
ARF, (N/V/malaise)
o IV (>4 days): Resolution or hepatic failure/death
 Mgmt: Consider AC; NAC best within 8 hours, given until APAP undetectable
and AST/ALT start trending down, at least <1000s
o PO: 140 mg/kg load then 70 mg/kg q4h (limited by "rotten eggs" odor)
o IV: 150 mg/kg over 30 min then 50 mg/kg over 4h, then 100 mg/kg over 16h

2. NSAIDS: Inhibition of COX

 Toxic dose: Variable, at least >100 mg/kg, should evaluate if >300 mg/kg
 Sx: Most with mild GI/CNS sx within 4 hrs, resolves in 24 hrs
o Reversible ARF with massive overdose, can resolve with supportive care
o Indomethacin: Headache, tinnitus (even in therapeutic levels)
o Oxyphenbutazone, phenylbutazone, mefenmic acid, piroxicam: Sz, coma,
renal failure, cardiopulmonary arrest
 Mgmt: Consider AC. antacids for GI upset. obs for 4-6 hours until sx resolve

3. Salicylates: ASA, methyl salicylate (wintergreen oil), bismuth salicylate

 Toxic dose (ASA): 150-200 mg/kg; 500 mg/kg potentially lethal (acute); >100
mg/kg/day for >2 more days (chronic)
 Respiratory alkalosis, AG metabolic acidosis
 Acute sx: N/V, tinnitus, hearing loss, abd pain, ataxia, dizzy, agitation,
lethargy, hyperventilation w/ respiratory alkalosis, metabolic acidosis, cardiac
irritability, tetany, sz, cerebral/pulmonary edema, ARF
 Chronic: More toxic at similar levels. hypoglycemia, sz, coma, pulm edema
 Dx: Serum level, vbg, chem-10, lfts, lactate, u/a, ekg
o Serum level q2-4h: >30 mg/dL (300 mcg/mL) toxic;>100 mg/dL can be fatal
o VBG/ABG for pH (late/severe if pH <7.4, Urine pH <6)
 Mgmt
o Consider AC (may need multiple doses to reach 10:1), whole bowel irrigation
o Sodium bicarbonate150 mEq (3amps) in 1 L D5W with 20-40 mEq KCl @
2-4 mg/kg/h (150-200 mL/hr). 1 amp increases serum pH by 0.1
o Urine alkalinization to pH >7.5 ("ion trapping")
o K supplementation to correct loss and aid alkalinzation
o CNS complications: CNS hypoglycemia (even if normal glucose), Sz,
cerebral edema
o HD: Mostly depends on clinical scenario – e.g. elderly may not tolerate fluids
required for alkalinization. Renal failure, pulmonary edema, coma/AMS/Sz,
severe cardiac toxicity, severe acidosis, rising salicylate levels despite
alkalinization, salicylate >100 mg/dL (acute) or >60 mg/dL (chronic)
o Be very cautious if need to intubate because very difficult to match pt’s
needed respiratory alkalosis (e.g. will need to hyperventilate)
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4. Opioids
 S/sx: AMS, miosis, respiratory depression; N/V, abdominal distention, ↓BS
o Methadone and propoxyphene: hypotension, ↓HR 2/2 ca channel block
o Tramadol, meperidine: serotonin syndrome, seizures
o Methadone: can prolong QTc
o MPTP (meperidine analogue): severe parkinsonian symptoms
 Miosis: consider pontine hemorrhage! (tachypnea, hypertension)
 Mgmt: respiratory support. Naloxone 0.1-2mg IV/IM/SCq2-3 min (0.01 mg/kg)
for respiratory depression, seizures. Lasts 30-100 min consider gtt for
methadone OD (start at ½ dose, titrate to RR)
*CAUTION: even 0.1mg can put a chronic opioid abuser into withdrawal.
Consider even lower dosage (ie. 0.01 mg), titrate up rapidly as needed.
 Withdrawal: restlessness, mydriasis, tachypnea, N/V/diarrhea, abdominal
cramps, myalgia, piloerection, rhinorrhea, diaphoresis
o Clonidine 0.1-0.2 mg PO – monitor for hypotension
o Methadone 5-25 mg IM/PO

Alcohols
1. Ethanol
 Intoxication (>100 mg/dL): Euphoria, disinhibition, flushing, tachycardia,
diaphoresis, hypothermia, ataxia, dysarthria; coma, respiratory depression
 Withdrawal: Hypertension, tachycardia, diaphoresis, hyperthermia, tremulous,
hallucination (visual, formication), seizures
o DTs: AMS, autonomic instability, hyperthermia, within 24-96 hrs
o Ativan 2mg IV q5-15 min prn; Librium 25-50mg PO bid once stable
 Disulfiram rxn: flushing, vomiting, HA, tachycardia, urticaria, pruritus
o Flagyl, sulfonylureas, bactrim, cephalosporins, mushrooms (Copirinus)
 Wernicke's encephalopathy (thiamine): AMS, ophthalmoplegia (CN VI), ataxia
 Korsakoff's psychosis: Anterograde/retrograde amnesia, confabulation
 Co-morbidities/related illnesses: AKA, pancreatitis, hypoglycemia,
hypothermia, gastritis, hepatitis, fall with ICH, PNA
 BAC falls 10-30 mg/dL/h; >300-350 mg/dL in naive pts may be comatose
 Thiamine 100 mg PO/IV, folic acid 1 mg PO/IV, FSG/dextrose, fluids, mg

2. Ethylene Glycol (antifreeze)  glycolic acid, oxalic acid  Ca oxalate

 Sx: Slurred speech, ataxia, nystagmus, lethargy. N/V, abd P--> CN abnl,
hyperreflexia, tremor, tetany, sz; ↑HR, dysrhythmia, pulmonary edema, oliguria,
proteinuria, ATN (EG >8 mmol/L, AG >20, pH <7.30 predictive of RF),
hyperchloremia, hypotension, resp depression, hemolysis, hepatic dysfnc, DIC
 Anion gap metabolic acidosis, Osmolar gap. No Ketones
 Dx: U/a, quantitative serum EG, chem10, serum osm, abg, utox, ekg
*estimate EG level: osmolal gapx6.2
 Urine may have fluorescence with wood's lamp (dye in antifreeze)
 Mgmt: Start empiric fomepizol based on hx, AG acidosis, or EG >20 mg/dL.
give cofactors
o Fomepizol (4-MP) 15 mg/kg IV load then 10 mg/kg q12hx48h
o ETOH goal >100 mg/dL:10% ETOH 10 mL/kg IV load then 1.5 mg/kg/h IV
o Folic acid 50 mg IV q4h x6 doses (peds 1mg/kg)

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 o Pyridoxine 50 mg IV/IM q6H
o Thiamine 100 mg IV/IM q8H
-
o Sodium bicarb 1 mEq/kg for metabolic acidosis, goal HCO3 >24
o Ca 7-14 mEq (peds 1-7 mEq) for symptomatic hypocalcemia
o HD if EG >50 mg/dL with renal insufficiency, severe acidosis

3. Isopropyl alcohol --> acetone

 No AG (mild metab acidosis); positive osmolar gap, +Ketones
 Sx: Abd pain/V/gastritis, CNS depression, hypotension, similar sx as ethanol
 Dx: FSG, ethanol level, abg, serum/urine ketones, osm
 Mgmt: Supportive care, HD if refractory hypotension, levels >400-500 mg/dL

4. Methanol: Wood solvents, windshield washer fluid  formic acid

 Toxic dose: >100mg/kg (fatal: 30-240 mL, 20-150g)
 AG metabolic acidosis, +Osmol gap, No ketones
 Sx: N/V, abd pain/gastritis, anorexia, HA, vision changes ("snowfields"),
photophobia. coma, resp/circ failure, ARF with myoglobinuria. Symptoms may
be significantly delayed from time of ingestion
 Dx: Abg, chem7, methanol or formic acid levels. Toxic level >200 mg/L
*estimate level: osmolal gap x 2.6
 Mgmt: Fomepizole, ethanol, cofactors, bicarb, HD as in ethylene glycol
o Folinic acid 1 mg/kg IV or folic acid 50 mg IV q6h
 HD for renal insufficiency, >25 mg/dL, severe acidosis, visual sx

Anion Gap (AG) Osmolar gap Ketones

Ethylene glycol + + -
Methanol + + -
Isopropyl alcohol - + +
*Late presentation of severe EG or Methanol may have AG acidosis but no
osmolar gap because all the alcohol has been converted to acid.

Anesthetics
1. General info
 Esters (benzocaine, cocaine, procaine, tetracine) – rapidly hydrolyzed by
plasma cholinesterase
 Amides (bupivacaine, lidocaine) – hepatic metabolization
 Toxicity 2/2 sodium channel blockade
o Local: Prolonged anesthesia
o Systemic
 Neuro: HA, confusion, perioral paresthesias, tremors, convulsions,
dysarthria, coma, resp arrest
 Cardiac: AV block, reentrant arrhythmia, vt/fib, hypotn, arrest
o Methemoglobinemia assoc with benzocaine, lidocaine
 Allergic rxn: Assoc mostly with esters or preservatives (methylparaben)
o In cases of true lidocaine allergy, may infiltrate benadryl sq

2. Local anesthetics
 Bupivacaine: Usually 0.25%, max dose 1-2 mg/kg, t½ 1.5-2h (500 mg, t½ 2h
with epi)

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  Lidocaine: 1% for SQ (10 mg/mL), max dose 4 mg/kg (300 mg), t½ 1.5-2h (7
mg/kg or 500 mg, t½ 2h with epi)
 Tx of overdose: Intralipid 1 ml/kg IV

Anticoagulants
1. Overall Mgmt
 Consider activated charcoal for warfarin, evaluate for bleeding, AMS
 Superwarfarins e.g. brodifacoum have long onset/duration – may need to
check coags in 48h
o Beware Dabigatron: Direct thrombin inhibitor. No real known antidote, toxicity
with renal dysfunction, need dialysis for overdose
 Protamine sulfate for life-threatening hemorrhage with heparin
o Half life of heparin 60-90 min
o IV over 1-3 min, 1 mg for 100 U heparin (if <1/2 hr), 0.5 mg/100 U (30-120
min), 0.25/100 U (if >2hr)
o 1 mg/mg lovenox (if <8 hr) or 0.5 mg/mg lovenox (if >8hr)
o Beware anaphylaxis in 0.2% pts (caution if fish allergy as protamine is derived
from salmon sperm)
 Vitamin K/FFP for warfarin based on INR or significant bleeding
o 10-20 mg acute warfarin ingestion usually benign
o Vit K (see Hematology chapter for more on reversal)

Antidepressants
1. TCA
 Toxic dose: Usually >10 mg/kg (1000 mg)
 S/sx: Tachycardic, htn, anticholinergic sx --> bradycardic, hypotension,
dysrhythmia,cardiogenic shock. sz, coma, RAPID instability.
o QRS >100ms associated with sz, >160 ms ventricular dysrhythmias
o Wide S in I and aVL, R wave in aVR
 Mgmt: EKG, labs prn. treat sz, hypotension, hyperthermia, coma
o Activated charcoal
o Sodium bicarb 1-2 mEq/kg IV bolus for dysrhythmia, wide qrs
o AVOID physostigmine in prolonged QRS 2/2 asystole
o AVOID β-blockers, calcium channel blockers, flumazenil

2. MAOIs e.g.selegiline, phenelzine

 Usually associated w/ drug interactions (SSRI, SNRI), tyramine (aged cheese/
meat, wine)
 S/sx: Hyperadrenergic, hyperdopaminergic, hyperserotonergic; htn, delirium,
hyperthermia, dysrhythmias, seizures, obtundation, nystagmus, hallucination,
tachypnea, orthostatic hypotension
 Management: Treat hyperthermia (cooling, NM block), sz (benzos). NO Beta
blockers. Cyproheptadine 4 mg po prn for serotonin syndrome

3. SSRIs
 Fluoxetine, sertaline, citalopram, escitalopram with active metabolites
 S/sx: Depends on agent. sedation, QTc prolongation, agitation, tremor,
hyperreflexia, tachycardia, bradycardia, N/V, abdominal pain, facial flushing,
dizziness. may cause SIADH sx, priapism (trazodone, mirtazapine)

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 o Venlafaxine: Sz in >3G, conduction delays and VT in >8G
 Mgmt: EKG, FSG,
o Treat sz, bicarb for QRS prolongation, cooling and benzo for hyperthermia
 Serotonin syndrome: Acute autonomic, NM, MS changes.
o Meperedine, MAOIs, dextromethorphan, SSRI, TCAs
o Autonomic: Hyper/hypotension, tachycardia, flushing, hyperthermia,
rhabdo
o NM: Agitation, akathisia, ataxia, clonus, coma, delirium, dysarthria, HA,
hyperreflexia, myoclonus, mydriasis, nystagmus, seizures, tremors
o GI: Abdominal cramps, diarrhea, salivation
o Mgmt: Symptomatic and supportive care (airway, cooling)
o Cyproheptadine 4 mg PO x3 doses
o Chlorpromazine 50-100 mg IV/IM, watch for dystonic rxn, sedation.
 SSRI discontinuation: HA, dizzy, N, irritable, paresthesia, insomnia, <1-2 wks
Serotonin syndrome NMS
Cause Serotonin excess DA blockade/depletion
Onset of sx ≤24 h Days to weeks
NM sx Hyperreflexia, clonus, "lead pipe" muscle rigidity,
hypertonicity (esp LE) bradyreflexia
Length of sx Days Days to weeks
*Adapted from Harwood-Nuss Clinical Practice of Emergency Medicine, 5th ed
Chapter 327
Antiepileptics
1. Carbamazepine (Tegretol)
 Toxic dose: >20-30 mg/kg, >140 mg/kg potentially lethal
 >10-20 mg/L toxic level, >40 mg/L associated with coma, hypotension,
dysrhythmia, sz
 S/sx: Dizziness, ataxia, tremors, hemiballismus, nystagmus, ophthalmoplegia,
tachycardia; coma, sz, dysrhythmias, myoclonus, hyperthermia, hypotension.
cyclical coma may result due to GI absorption
 Mgmt: Treat sz, coma, hyperthermia, hyponatremia, dystonia, arrhythmia
o Multiple dose activated charcoal

2. Gabapentin (Neurontin)
 Sx: Drowsy, dizzy, nausea/vomiting, tachycardia, hypotension. coma,
respiratory depression, peripheral edema
 Hydrocodone, morphine, renal failure can decrease clearance!
 If severe overdose consider HD

3. Lamotrigine (Lamictal)
 Sx: Nystagmus, somnolence, ataxia, lethargy; coma, seizures, hypokalemia,
encephalopathy, abnml conduction (↑PR, ↑QRS), organ failure, Stevens-
Johnson, TEN

4. Levetiracetam (Keppra)
 Sx: Drowsy, coma, respiratory depression, somnolence, agitation, aggression
 Mgmt: Consider HD if severe

5. Phenobarbital

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  Toxic dose: Depends on tolerance. usually 6-9 g (8 mg/kg)
 >30 mg/L minimal toxic level. 60-80 mg/L assoc with coma
 S/sx: Cutaneous bullae ("barb blisters"), lethargy, slurred speech, nystagmus,
ataxia. Hypothermia
 Mostly supportive. Multi-dose AC, alkalinize urine. May be dialyzed if severe
 Primidone metabolized to phenobarbital and phenylethylmalonamide

6. Phenytoin (Dilantin)
 Toxic dose: >20 mg/kg. Increased toxicity w/RF, hypoalbuminemia
 Toxic level usually >20 mg/L
*Corrected level= Measured phenytoin level /[(albumin x 0.2) + 0.1]
or if CrCL < 20= Measured phenytoin level /[(albumin x 0.1) + 0.1]
 May be increased 2/2 drug interactions (SSRI, amiodarone, INH, tamoxifen,
disulfiram), decreased protein binding (uremia, hepatitis, low albumin, valproic
acid, NSAIDs)
 S/sx: Ataxia, nystagmus, dysarthria, tremor--> stupor, coma, resp arrest;
profound hypotension, bradycardia, cardiac arrest 2/2 rapid IV (glycol).
extravasation may cause tissue necrosis, gangrene, compartment syndrome,
hypersensitivity syndrome, Stevens-Johnson, TEN, drug-induced lupus
 Mgmt: AC, supportive care

7. Pregabalin (Lyrica)
 Sx: dizziness, somnolence, ataxia, myoclonus, confusion, peripheral edema,
mild ↑PR, decreased platelets, transaminitis, rhabdomyolysis

8. Topiramate (Topamax)
 Sx: coma, generalized seizures, nonanion gap metabolic acidosis
 Mgmt: consider HD if severe

9. Valproic acid (Depakote)

 Toxic dose: >200 mg/kg. overall poor correlation b/t level and outcome
 Serum level >450 mg/L assoc with drowsiness/obtundation, >850 mg/L coma,
resp depression, metabolic abnml
 Sx: GI upset (N/V), CNS depression, cerebral edema, hypotension with
tachycardia, hemorrhagic pancreatitis, hepatic failure (chronic); ↑QT, paradoxic
sz, hypernatremia, hypocalcemia, AG acidosis, lactic acidosis; optic nerve
atrophy, pulmonary edema, thrombocytopenia, neutropenia, alopecia.
 Mgmt: AC, ?WBI
o L-carnitine 100 mg/kg IV (up to 6 G) over 2-3 min then 15 mg/kg q4h for
hyperammonemia and hepatotoxicity
o HD if >850 mg/L, renal insufficiency, hemodynamic instability, severe
metabolic acidosis

*Serum drug levels

Drugs Therapeutic Toxic
Carbamazepine (Tegretol) 4-12 mg/L >10 mg/L
Phenobarbital 15-35 mg/L >30 mg/L
Phenytoin (Dilantin) 10-20 mg/L >20 mg/L
Valproic acid (Depakote) 50-150 mg/L >100-450 mg/L

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 Antihistamines
1. General approach
 Toxic dose: Diphenhydramine 20-40 mg/kg PO
 Sx: Anticholinergic syndrome, convulsions, rhabdo, hyperthermia if severe.
Massive OD: QRS widening, myocardial depression
 Mgmt: treat coma, seizures, hyperthermia, atypical VT
o Physostigmine used ONLY if pure antimuscarinic OD due to risk of seizures;
consider only in consultation with poison control
o Sodium bicarbonate 1-2 mEq/kg IV for myocardial depression/↑QRS

Antipsychotic/Neuroleptics/Lithium
1. Haldol
 Extrapyramidal symptoms (EPS)
o Dystonic: Torticollis, trismus, oculogyric crisis
o Akathisia: Anxiety and restlessness
o Tardive dyskinesia: Choreoathetoid mvmts of face/tongue
o NMS: Hyperthermia, muscle rigidity, autonomic dysfunction
 Mgmt
o Benadryl 1-2 mg/kg IV q6h PRN; benztropine 0.05 mg/kg IV q12h prn,
benzodiazepines
o NMS: Treat hyperthermia (cooling), benzos, dantrolene

2. Lithium
 Therapeutic dose 0.6-1.2mEq/L, toxic >1.5mEq/L; toxicity very common (most
common 2/2 renal dysfxn). Usually get a 4-6 hour level after acute ingestion
 S/sx: N/V/diarrhea, tremor, ataxia, hyperreflexia, dehydration (DI),
encephalopathy, sx
 Renal excretion  decreased with ARF 2/2 dehydration, DI
 Mgmt: IVF, HD
o HD: Renal failure, inability to hydrate (CHF, pulmonary edema), AMS, coma,
sz, symptomatic acute ingestion >4mEq/L (depends on the time of ingestion,;
need to consult with poison control)

Benzodiazepines
1. General approach
 Increase GABA activity  inhibition
 Flunitrazepam (Rohypnol): Not detected in usual benzo utox, can request
specific test if suspected. >8 hrs effects, elimination half life 20-30 hrs
 Sx: Lethargy, slurred speech, ataxia, coma (hyporeflexia and
midposition/small pupils) respiratory arrest (short-acting e.g. triazolam,
alprazolam, midazolam, zolpidem), cardiopulmonary arrest
 Mgmt: Airway, treat coma, hypotension, hypothermia.
o Flumazenil 0.2 mg IV over 30 s (peds 0.01 mg/kg) 0.3 mg  0.5 mg, max
3mg). Only lasts 1-5hrs. rarely used as half life shorter than most benzos,
concern for seizures!
*CI: Risk of seizures in TCA, INH, MAOI, bupropion, cocaine, lithium, or other
drugs which lower seizure threshold or h/o seizures. induction of acute
withdrawal may also cause refractory seizures in chronic user

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 Cardiovascular drugs
1. Digitalis: inhibition of sodium-potassium ATPase pump
 S/sx: N/V, visual color changes (yellow-green), dysrhythmias
o PVCs most common; paroxysmal atrial tachycardia w/ block, bidirectional
VT, slow afib, junctional tachycardia, VF, AV block, etc
 Potassium >5 mEq/L in acute ingestions = poor prognosis
 Mgmt
o ACLS for bradycardia/VF/VT: atropine, pacemaker
o Calcium: controversial, concern for “stone heart” and dysrhythmia but not
supported by evidence (Levine et al, JEM 2009)
o Digoxin Fab (see below and package insert for dosing): Indicated for
elevated levels with significant sx (hyperkalemia, ventricular arrhythmias,
bradyarrhythmias, hypotension)
*Empiric dosing (if unknown digoxin level)
o Acute ingestions: 10 vials over 30 minute
o Chronic toxicity: 5 vials *cardiac arrest: 20 vials by IV bolus
*Calculated dosing (if known digoxin level):
# of digoxin-Fab vials = (serum digoxin level (ng/mL) x body weight (kg))/ 100

2. Antiarrhythmics
Type I Fast sodium channel Examples Toxic effects
inhibition
Ia Slow depol and Quinidine Sinus bradycardia,
conduction in normal Procainamide arrest/asystole,
tissue, prolong action anticholinergic
potential (quinidine),
↑PR/QT/QRS,
n/v/diarrhea
Ib Slow conduction in Lidocaine, Dizzy, confusion,
ischemic tissue; Phenytoin, agitation, seizures;
shorten action potential Mexiletine bradycardia, arrest,
hypotension, AV block
Usually nml QRS/QT
Ic Also blocks K channel. Propafenone cholestatic hepatitis
slow depol and flecainide Dizzy, blurred vision, HA,
conduction GI upset, ventricular
arrhythmias,
hypotension,
bradycardia, AV block,
prolonged QRS/QT
Type II Beta blockers Propranolol, Heart block, hypotension,
atenolol bradycardia, cardiogenic
Sotalol* (both II shock; ↑PR; convulsions,
and III) coma, resp arrest,
bronchospasm,
hypoglycemia,
hyperkalemia
Type III Potassium channel Amiodarone Acute: Bradyarrhythmia,
blockade Sotalol* (both II acute hepatitis (IV load)
and III) Chronic: VT or arrest, AV
block, pneumonitis, pulm

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 fibrosis, photosensitivity
dermatitis, corneal
deposits, abnml
hypothyroid, tremor,
ataxia, peripheral
neuropathy
Type IV Calcium channel Verapamil Hypotension,
blockers Amlodipine bradycardia. Nml QRS.
Diltiazem N/V, AMS, metabolic
acidosis, hyperglycemia
 Quinidine
o Toxic dose 1 gram
o Sx: Anticholinergic effects, seizures/coma, bradycardia, ventricular
tachycardia, hypotension. prolonged PR/QRS/QT
o Treat wide QRS intervals and hypotension with sodium bicarbonate 1-2
mEq/kg q5-10 min
 Procainamide
o Toxic dose 5 grams
o Sx: Prolonged PR/QRS/QT. bradycardia, ventricular tachycardia,
hypotension, GI upset, sz/coma, lupus-like syndrome (chronic)
o Treat wide QRS intervals and hypotension with sodium bicarbonate 1-2
mEq/kg q5-10 min
o Active metabolite: N-acetylprocainamide (NAPA), can cause hypotension
 Lidocaine
o Toxicity usually assoc with IV injection or accumulation with repeat doses in
liver dz or chf. Level >6-10 mg/L considered toxic
o Hypotension, av block, asystole, cns sx (perioral paresthesias, tremors,
convulsions) – see Anesthetics
 Propafenone
o Toxic levels >1mg/L
o Sx: Dizzy, blurred vision, HA, GI upset, ventricular arrhythmia, seizures,
bradycardia, hypotension. cholestatic hepatitis.
 Amiodarone
o Usual dose 200-600 mg, toxic level >2.5 mg/L
o Sx: (acute) bradyarrhythmia (during load), acute hepatitis; (chronic)
ventricular arrhythmia or bradyarrhythmia, pneumonitis, pulmonary fibrosis,
hepatitis, photosensitivity dermatitis, corneal deposits,
hypo/hyperthyroidism, tremor, ataxia, peripheral neuropathy

3. β-blockers
 S/sx: Bradycardia, hypotension, hypoglycemia, AMS. AV block. Refractory
anaphylaxis, bronchospasm. May have wide QRS with severe propranolol OD
(2/2 Na channel blocking properties)
 Mgmt
o Fluids, ACLS bradycardia: Atropine 0.5-1 mg up to 3 mg (0.02 mg/kg peds),
pacemaker, pressors (e.g. epinephrine – start at 1 mcg/min, dopamine,
isoproterenol) prn
o Glucagon 5-10 mg IV then 2-5 mg/h gtt (peds 0.05-0.1 mg/kg IV boluses
q3min then 0.05-0.1 mg/kg/h gtt) (*give with antiemetic 2/2 side effect of n/v)
o Sodium bicarbonate for wide QRS 1-2 mEq/kg (e.g. propranolol overdose)

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 o Consider Hyperinsulinemia/euglycemia therapy (HIE): Insulin 1 U/kg IV then
0.5-1 U/kg/h gtt (titrate to SBP >90, HR >50), keep glucose >200 (D50 prn,
D10 ½ NS at 80% maintenance)
o IABP for refractory severe hypotension

4. Calcium channel blockers

 S/sx: Bradycardia, hypotension. N/V, AV block, hyperglycemia. BEWARE
VERAPAMIL given longer duration, higher mortality in OD
 Mgmt: Consider AC
o Fluids, ACLS bradycardia: atropine 0.5-1 mg up to 3 mg (0.02 mg/kg peds),
pacemaker, pressors (e.g. epinephrine – start at 1 mcg/min)
o Calcium chloride 5-10 mL IV q5-10 min (0.1-0.2 mL/kg) through central line
for faster onset or calcium gluconate 10-20 mL (peds 0.2-0.3 mL/kg).
*if responsive, consider gtt (CaCl 0.2-0.4 mL/kg/h or CaGluc 0.6-1.2 mL/kg/h)
o Glucagon 5-10 mg IV then 2-5 mg/h gtt (peds 0.05-0.1 mg/kg IV boluses
q3min then 0.05-0.1 mg/kg/h gtt)
*controversial but often still tried if un-responsive to calcium tx
o Hyperinsulinemia/euglycemia therapy (HIE): Insulin 1 U/kg IV then 0.5-1
U/kg/h gtt (titrate to SBP >90, HR >50), keep glucose >200 (D50 prn, D10 ½
NS at 80% maintenance).
o Consider inamrinone 0.75 mg/kg IV over 2-3 min then 5-10 mcg/kg/min
o Consider intravenous lipid emulsion (20% IFE 100 mL over 20 minutes then
0.5 mL/kg/h similar to TPN) – case reports (Resuscitation 80: 591–593)
o IABP/bypass as last resort
o Effects peak 90min to 6 hrs, but caution with extended release

5. Clonidine: central α2 agonist

 AMS, hypotension, miosis, bradycardia, respiratory depression (similar to
opioid overdose)
 Mgmt
o Naloxone for AMS (0.1 mg/kg IV). *controversial, ?concomitant opiate use.
o Pressors prn (NE or phenylephrine)

Drugs Therapeutic Toxic

Digoxin (Lanoxin) 0.8-2.0 ng/mL >2.0 ng/mL
Lidocaine (Xylocaine) 1.5-6 mcg/mL >6 mcg/mL
N-acetyl procainamide 15-25 mcg/mL >40 mcg/mL
Procainamide 4-10 mcg/mL >10 mcg/mL
Quinidine 2-4 mcg/mL >5 mcg/mL

Chemicals and Gases

1. Caustic agents
 S/sx: Severe GI injuries with necrosis, hypovolemic shock, dysphagia,
drooling, vomiting, tachypnea, pneumonitis; ocular splash injuries, skin injuries
 Acid : Cause coagulation necrosis (gastric>esophageal burns)
 Alkali: Cause liquefactive necrosis (oral, proximal esophageal burns)
 Mgmt: ABCs, immediate irrigation (mouth, eye, skin – at least 20 min),
antiemetics, prophylactic intubation if oral injury, NO AC/lavage/inducing
emesis, consider small glass of water to dilute if recent ingestion

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 o Eye irrigation: Connect NC to IV tubing, irrigate with NS at least 20 min (~1L)
until pH neutral, wait 5-10min then retest pH to see if need more irrigation
o Corneal injuries: Topical abx, steroids, cycloplegics, mydriatrics
o Endoscopy if ingestion, surgery for perf/peritonitis
o DO NOT irrigate if alkali metal exposure (sodium, potassium, Li, Cesium,
rubidium) as they can react to form hydroxides

2. Carbon monoxide: Binds to Hgb to form carboxyhemoglobin (COHb)

 S/sx: 2/2 hypoxia and decoupling of ox-phos. HA, dizziness, n/v, diarrhea;
confusion, syncope, dyspnea, chest pain, sz, coma, dysrhythmia, hypotension,
pallor (rarely “cherry-red” skin)
 SpO2 falsely high - need to obtain COHb levels on ABG/VBG (positive if >10-
15% smokers or >3% non-smokers). Can screen with Rad-57 oximeter (Sn
48%, Sp 99%)
 Fetus at higher risk (higher affinity of CO for fetal hgb)
 Mgmt: Decontamination, O2, fluids prn
o COHb half life: RA 5 hours, 100 % O2 45-90 min, HBO <20 min
o Hyperbaric oxygen (HBO): Need to consult with poison control for indiciation,
location of chambers. Generally, consider if COHb >25%, Neuro sx (Sz, Coma,
AMS, LOC, abnormal cerebellar sx), severe acidosis, cardiac sx (dysrhythmia,
ischemia, syncope, hypotension), pregnancy with COHb >20% or fetal distress

3. Cyanide: Bitter almond smell. ox-phos decoupling

 Nitroprusside gtt, burnt plastic, amygdalin (apricot pits), jewelry makers.
Consider with smoke inhalation + severe lactic acidosis (lactate >10)
 S/sx: Cellular hypoxia  lactic acidosis. LOC, coma, sz, dysrhythmia,
hypotn/CV collapse
 Mgmt: ABC, O2, address acidosis
o Hydroxyocobalamin 5 g in 100 mL NS IV over 15 min (peds 70 mg/kg),
may repeat over 15 min to 2 hr if severe. Preferred over nitrites 2/2 lack of
hypotension, SE of red skin/secretions, N/V
o Previous kits with amyl nitrite, sodium nitrite to induce methemoglobinemia,
but causes hypotension, further decreased oxygen carrying capacity. (Amyl
nitrite pearls 1-2 ampules crushed under nose q30 seconds, sodium nitrite
IV 300 mg (10 mL of 3%) over 3-5 min (peds 0.15-0.33 mL/kg, max 10 mL).
usually combined with sodium thiosulfate
o May give sodium thiosulfate alone, IV 12.5 G (50 mL of 25%) at 2.5-5
mL/min (peds 400 mg/kg or 1.6 mL/kg of 25% up to 50 mL), may repeat half
initial dose prn

4. Hydrocarbons
 S/sx: Euphoria, hallucination, agitation, CNS depression, syncope, coma
 Aspiration pneumonitis after ingestion or inhalation, worse if less viscous
o Absence of tachypnea has high NPV for aspiration
 Mgmt: Decontamination, O2, bronchodilators/ventilator support, treat sz
o Indications for gastric emptying: lavage if Camphor, Halogenated
hydrocarbons, Aromatic hydrocarbons, Metal-containing hydrocarbons,
Pesticide-containing hydrocarbons
o If no sx and CXR neg at 6 hrs, medically clear

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  Sudden death associated with sniffing 2/2 cardiac sensitization to endogenous
catecholamines
 Lindane: Chlorinated hydrocarbon, s/sx include AMS and sz, toxicity 2/2 large
exposure (scabies rx in kids)

5. Hydrogen fluoride: jewelers, metal cleaning, glass etching

 Ca/Mg binding, result of skin exposure/ingestion
 Toxic dose: 30 ppm (gas) – 5 min exposure ~50-250 ppm; 50-70% toxic (soln)
but lower concentrations can still cause delayed injury
 S/sx: Severe pain without apparent burn --> hypocalcemia, hypomagnesemia,
arrhythmias, hyperkalemia
 Mgmt: Irrigation, consider adding Epsom salts/calcium (if skin)
o If severe pain or delayed presentation, mix 10% calcium chloride with
methylcellulose or lubricant and apply to skin for at least 30 min
2
o 10% CaGluc intradermal (0.5 mL/cm ), or IA or IV with Bier block (10-20
mL, peds 0.2-0.3 mL/kg)

Heavy metals
1. Arsenic: Tasteless, odorless, GI absorption. Impair cellular respiration
 Acute s/sx: N/V, abdominal pain, “rice water” diarrhea  shock, pulm edema,
rhabdo, seizures, coma, death
 Urine level most reliable (24 hr urine, or spot). Nml: <50 mcg/L or 50 mcg/g Cr
 Mgmt: Supportive, fluids, monitor K, Mg, Ca and replete, avoid QT prolonging
meds
 Consider dimercaprol or BAL 3-5 mg/kg IM q4-6h if severe (may shift to
brain)

2. Iron
 Toxic dose: >20 mg/kg elemental iron (Fe), >60 mg/kg severe
o Fe: Ferrous sulfate - 20%, Ferrous fumarate 33%, ferrous gluconate 12%
 S/sx: Abdominal pain, diarrhea, vomiting, GI bleed, hypotension, shock, lactic
acidosis, coagulopathy, hepatic injury, renal failure, pyloric scarring
 KUB shows pills, follow serum Fe levels (TIBC not useful in acute ingestion)
 Mgmt: Whole bowel irrigation, deferoxamine 1(SE: “Vin rose” (red wine)
urine), 1000 mg IM/IV then may repeat 500 mg q4h x2. blood products for
severe hemorrhagic gastritis

3. Lead
 S/sx: HA, fatigue, malaise, abd pain, constipation, v, neuro sx (paresthesia,
wrist/ankle drop)
 Serum level >40 mcg/dL (peds >10 mcg/dL) suggest increased exposure
*Venous sample preferred as capillary samples can be falsely elevated if finger
not cleaned appropriately.
 FEP (free erythrocyte protoporphyrin) >35 mcg/dL suggest poisoning (but lab
result takes several days so won’t affect initial management). FEP lags from
lead level  high lead level with normal FEP suggest acute exposure
 Mgmt: treat cerebral edema, sz. Goal lead <40 mcg/dL (peds <20 mcg/dL).
o Stop ongoing absorption: KUB to look for paint chips in kids. If present, must
decontaminate first with WBI prior or in conjunction with chelation.

292
 o Dimercaprol IM 3-5 mg/kg q4-6h (painful, foul-smell, Fever common)
o EDTA 50 mg/kg/d IV gtt or IM (phlebitis, may increase brain levels/sx)
o Dimercaptosuccinic acid (combo dimercaprol and EDTA, use in peds >45
mcg/dL) PO 10 mg/kg q8h x5 days then 10 mg/kg q12h x14days.
o D-penicillamine (adults) PO 30 mg/kg/d (1-1.5 g/d), less effective

4. Mercury: Elemental absorbed via inhalation

 Acute s/sx: Cough, fever/chills, nausea/vomiting, pneumonitis, bronchitis
 Normal serum level: <10 mcg/dL. Treat only if >25 mcg/dL
 Normal 24hr urine: <20 mcg/dL. Treat only if >150 mcg/dL
 Mgmt: Supportive. UGI endoscopy if corrosive lesions with ingestion
 DMSA 10 mg/kg TID x5 days then BID x14 days if able to PO, nml renal fnc
 Consider BAL 5 mg/kg q4h IMx48h then 2.5 mg/kg q6hx48h then 2.5 mg/kg
q12hx7days

Hypoglycemic Agents
1. Overview of Hypoglycemia
 S/sx
o Autonomic: Tachycardia, diaphoresis, anxiety, tremor
o Neuroglycopenic: Agitation, confusion, coma, sz, dizziness, blurry vision
 Mgmt
o Dextrose 1-2amps (50-100mL) D50W IV at 3 mL/min (adults), 2-4 ml/kg
D25W (peds), then D5 or D10 gtt @ 0.5 g/kg/h to maintain glucose 60-110
o Octreotide 50-100mcg SQ/IV q6-12 h (4-5 mcg/kg/day div q6h peds) for
sulfonylurea and meglitinides.
o Check FSG q1-2 h until stable
o If able to take PO, give food for longer maintenance

2. Insulin: ↑Cell uptake and metabolism

 Toxic dose: Severe hypoglycemia and neuro sequelae >800-3200 Units
 C-peptide: Distinguish endogenous (elevated) vs. exogenous
 Supportive care: Fluids, fsg, dextrose prn

3. Glitazones [rosiglitazone (Avandia), pioglitazone (Actos)]: ↓Glucose

production, increase cell sensitivity
 Overall benign. Rosiglitazone associated with cardiac adverse outcomes

4. Meglitinides (nateglinide, repaglinide): ↑Insulin release. Similar to

sulfonylurea with shorter onset/duration
 Mgmt: Dextrose. Consider IV octreotide 50-100mcg SQ/IV q6-12 h (4-5
mcg/kg/day div q6h peds)

5. Metformin: ↓Glucose production and intestinal absorption, ↑peripheral uptake

 Lactic acidosis: Consider in renal insufficiency, alcoholism, advanced age
o S/sx: Malaise, vomiting, myalgias, respiratory distress. Up to 50% mortality!
 Consider bicarb for lactic acidosis, but may worsen intracellular acidosis
 Consider HD for severe lactic acidosis

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6. Sulfonylurea: E.g. glipizide, glyburide. Block potassium outflow, stimulate
pancreatic insulin secretion, ↑receptor sensitivity, ↓glycogenolysis.
 Toxic dose: Depends on amount/agent. Increased if drug interaction with other
hypoglycemics, sulfonamides, propranolol, salicylates, clofibrates, probenecid,
pentamidine, valproic acid, dicumarol, cimetidine, MAOI, alcohol; hepatic/renal
insufficiency
 *Glyburide: looks similar to Valium
 Mgmt: Dextrose. Consider IV octreotide 50-100mcg SQ/IV q6-12 h (4-5
mcg/kg/day div q6h peds)
 Concern for prolonged hypoglycemia, require observation for 24 hrs
regardless of symptoms

Organophosphates and carbamates

1. Overview
 Pesticides, chemical warfare (soman, sarin, tabun); pyridostigmine, donepezil
 Acute: DUMBELS: Diarrhea, Urination, Miosis, Bradycardia/ Bronchorrhea/
Bronchospasm, Emesis, Lacrimation, Salivation; weakness, sz, spasms, htn,
AMS, tachycardia, pancreatitis, rhabdomyolysis
 Intermediate syndrome (CN palsy, truncal/prox weakness) and delayed
polyneuropathy (“Jamaican ginger paralysis” with distal flaccid paresis)
 Mgmt: ABC, decontamination of skin/GI
o Atropine 1-4 mg IV (0.02-0.05 mg/kg peds) for bronchorrhea or bradycardia,
may repeat q5-15 min
o Pralidoxime (2-PAM) 1-2 g in saline over 30 min (20-40 mg/kg to max 2g in
peds), repeat q1-2h if fasciculations, then q 6-12h x24-48h
o Observe for 6 h, may discharge if asymptomatic

Sedative-hypnotics (non-benzodiazepine, non-barbiturate)

1. Baclofen: GABA
 Toxic dose: Usually >3-5x therapeutic dose
 Sx: Profound CNS depression, respiratory depression, autonomic
disturbances (hypotension, bradycardia), paradoxic sz/dysrhythmia
 Withdrawal: Spasticity, tachycardia, bp changes, severe hyperthermia,
rhabdomyolysis, hallucinations, seizures, multiorgan system failure
 Mgmt: Supportive e.g. treat coma, hypothermia, hypotension. *slow
elimination

2. Carisoprodol (aka SOMA = coma)

 Sx: CNS depression, tremor, myoclonus, tachycardia, hyperreflexia,
opisthotonus, increased muscle tone
 May also have withdrawal syndrome
 Mgmt: Supportive

3. Chloral hydrate
 Sx: Coma, miosis, hypotension, nausea/vomiting. hemorrhagic gastritis/gastric
necrosis, hepatic injury/renal failure/cardiotoxicity, ventricular dysrhythmia
 Mgmt: Treat dysrhythmia (lidocaine, mg, BB, overdrive pacing)
o HD if profound hypotension, unstable dysrhythmia

294
4. Cyclobenzaprine (aka flexeril)
 Sx: CNS depression, anticholinergic sx
 Mgmt: AC, supportive

Street drugs
1. Amphetamines
 Sympathomimetic s/sx: Tachycardia, hypertension, diaphoresis, mydriasis,
agitation/aggression, CNS excitation (euphoria, talkativeness, anxiety,
seizures), muscle rigidity, hyperthermia, ventricular arrhythmia, ICH, coma
 Mgmt: Sedation (benzo, ?haldol), cooling if hyperthermic.
o Tachyarrhytmias: Esmolol/propranolol
o Vasospasm: NTG 0.4 mg SL or 5-20 mcg/min IV (coronary); nitroprusside
1-2 mcg/kg/min or phentolamine 0.5 mg/min until improved (peripheral/htn)
 Hallucinogenic: MDMA (Ecstasy - assoc with hypoNa, serotonin syndrome),
MDA, MDEA

2. Cocaine
 S/sx: Sympathomimetic
 Complications: Cocaine chest pain, dissection, ICH, hypertensive crisis
(unopposed α)
 Mgmt: Benzos

3. Hallucinogens: LSD, psilocyubin mushrooms, mescaline

 Serotonin-like
 S/sx: Anxiety, paranoia, agitation, hallucination, psychosis
 Mgmt: Quiet environment, sedation with benzos prn agitation, haldol

4. ɣ-hydroxybutyric acid (GHB): GABA antagonist, "date rape drug"

 Usual recreational dose 2-3 grams, >60 mg/kg dose may cause coma
 S/sx: Hallucinations, disorientation, amnesia, nystagmus, CNS depression
(lethargy, stupor, coma, hypoventilation)  violent awakening, self extubation
(emergence delirium); death from cardiopulmonary arrest, asphyxia, aspiration
 Not on routine tox screen, not detectable in blood/urine after 4-6hrs
 Mgmt: ABCs, supportive care, treat coma, seizures, bradycardia
 Withdrawal: Anxiety, tremor, agitation, autonomic abnml, hallucinations,
delirium. Treat with benzos, consider phenobarb/propofol if severe

5. Opioids (see Analgesics)

6. PCP: similar to ketamine

 S/sx: Dissociative state, rotary nystagmus, agitation, violence, seizure,
hyperthermia, elevated CK. emergence phenomenon
 Mgmt: Sedation (benzo), haldol
 AVOID acidifying urine, may precipitate myoglobin

Miscellaneous
1. INH
 GABA inhibition via vit B6 depletion
 Sx, coma, acidosis (MUDPILES), consider in refractory sz
295
  Mgmt: Pyridoxine (vit B6)
2+ 3+
2. Methemoglobinemia: due to decreased oxygen binding 2/2 Fe  Fe
 Nitrites, nitrates, dapsone, phenazopyridine, benzocaine
 Cyanosis 2/2 blue color, chocolate brown blood
 "85%" on SpO2  need cooximetry methemoglobin level
 Mgmt: Methylene blue (caution in G6PD)

3. Mushrooms
 Earlier onset sx (<2hrs) tend to be benign
 Send gastric contents for evaluation
 Mushrooms with delayed onset of sx
o Orellanine (Cortinarius): Delayed renal toxicity, may need HD/kidney txp
o Gyromitra (looks like brain): Hepatic toxicity and refractory sz (similar to
INH), treated with benzos and pyridoxine
o Amatoxin (cyclopeptides) e.g. Amanita phylloides: hepatotoxicity with
coagulopathy, encephalopathy, treat w/ activated charcoal, penicillin G IV,
NAC

4. Strychnine: glycine antagonist

 Muscle twitching, extensor muscle spasms, opisthotonos, trismus, facial
grimacing
 Mgmt: Muscle relaxation (benzo, paralytics), supportive care, eval for rhabdo

7. Theophylline
 Sympathomimetic toxidrome
 Therapeutic 10-20mcg/mL, toxic >20mcg/mL
 S/sx: N/V, tachycardia, sz, dysrhythmia (MAT, PAC, AF, PVC, VT),
hypokalemia
 Mgmt: Antiemetics (metoclopramide, zofran), activated charcoal, HD
 Hemoperfusion/HD: Malignant dysrhythmia, sz, >100 mcg/mL acute OD or
>60 mcg/mL chronic OD

Pediatric pearls
1. 1 pill can kill (in a 1yo): See Pediatrics chapter
 Fe, βB, CCB, clonidine, glucophage, theophylline, methylsalicylate (icy hot, oil
of wintergreen)
o Ask family to bring all pills that child could have had access to (e.g. all rx in
house) into ED
o Consider delayed metabolism and prolonged sx
o ‘Pincer grasp’ (to pick up pills) rare before 8mo (?abuse)

2. Carbamazepine (Tegretol): Common peds OD

296

By Hangyul Chung-Esaki Res ed. Eric Silman
SFGH Trauma Activation Criteria
911
Mechanism
 Fall ≥20 ft (2 stories); peds ≥10
ft (1 story or 2-3x ht of child)
 High risk mvc: ejection, death
of passenger, intrusion >18” (or
>12” occupant site), abd seat
belt sign (ecchymosis/abrasion)
 2-3 wheeled vehicle crash >20
mph
 PVA or BVA: thrown, run over,
or significant (≥20 mph) impact
 Serious burns <15% to hands,
face, perineum
Physiologic
 GCS 9-11 2/2 trauma
 SBP <110 in age >65 w/ major
Criteria
mechanism
Anatomic
 Limb ischemia or compartment
syndrome
Other
 Blunt abd trauma in ≥24 wks
pregnant
 Anticoagulation (Coumadin,
plavix, prasugrel, NOT asa) w/
intracranial or serious injury
 ED attending or charge RN
discretion
297
Trauma
Faculty ed. Alan Gelb
900
Physiologic
 SBP≤90 at any time (including
arrest)
*Peds: neonate<60,1mo-2yo <80,
2-8yo <85
 Severe shock with no peripheral
pulse
 Requires blood transfusion
 GCS≤8 (2/2 trauma)
 Intubated 2/2 resp compromise
due to burns, major trauma
Anatomic
 GSW/SW to torso, head, neck
(if significant penetration,
evisceration, sucking chest
wounds, or other criteria)
 Penetrating trauma to extremity
w/ active bleed, expanding
hematoma, absent/asymmetric
pulses
 Traumatic amputations (proximal
to wrist/ankle)
 Mangled, crushed, or degloving
injury
 Open/depressed skull fx
 Traumatic para/quadriplegia
 ≥2 long LE bone fx (femur/tibia)
 Pelvic fx (open or unstable fx)
 Flail chest or major pulm
contusion
 Major burns (>15%)
Other
 ED attending discretion
 General Approach to Trauma Resuscitation
1. Crowd control: Only those caring for patient allowed in the room

2. Each trauma should be run systematically

 EMS report: Mechanism, ABCD, VS, interventions.
 Primary Survey + FAST (fix problems ie. ETT, Chest Tube, IVF)
 Secondary Survey and CXR/PXR if indicated
 Imaging and DISPO (CT, OR, IR, ICU- determined by stability)

3. Sample simplified algorithm

What to call out Interventions/notes
Primary Survey
A – Airway
Pt phonating Open airway-jaw thrust
Blood/debris in airway OPA/NPA, suction
Prehospital airway/integrity O2 (preoxygenate), Intubation
B – Breathing
Chest excursion, rate, effort Supplemental O2
Crepitus/ptx/tenderness Needle thoracostomy
Breath sounds, O2 Sat Chest Tube
[Optional: JVD, Tracheal deviation]
C – Circulation
Pulse Two 18 or larger gauge IV’s or IO
Palpated BP, Cordis (9 French)
Perfusion (cap refill, color) Cutdown
IV Access Direct pressure on bleeding
Labs (including POC hgb, blood gas) FAST – where’s the blood?
D – Disability
Pupils Check corneal reflexes if intubating
GCS
Motor (moves all extremities)
E – Exposure
Expose patient then COVER Check axillae, gluteal folds for
Log roll and spine exam (+/- rectal) penetrating trauma
BSA for burns
Whenever the patient status changes, reassess and go back to the ABC’s
Adjuncts: CXR, Pelvis XR, repeat FAST
Secondary Survey
Head - tenderness, hematoma, posterior ears for battle sx, TMs for
hemotympanum, facial tenderness/sensation, nose for bleeding/CSF
Neck/shoulder - midline tenderness w/ C-spine collar off, replace collar; check for
shoulder tenderness
Chest – palpate/compress for tenderness, bruising/abrasions, seat belt sx
Abdomen - tenderness, bruising/abrasions
Pelvis - bruising, stability, tenderness, hip ROM if possible
Extremities - deformities, abrasions, knee instability
Neuro - strength, sensation

298
 th
4. Mechanism and associated injuries (from Rosen’s Emergency Med 7 ed)
 MVC
o Head-on collision: Face, LE, and
aortic injuries Glasgow Coma Score (GCS)
o Rear-end: C-spine
hyperextension/fractures, central cord Spontaneous 4
syndrome
To speech 3
o Lateral (T-bone): Thoracic, Eyes
abdominal (spleen, liver), pelvic To pain only 2
injuries; clavicle, humerus, rib fractures No response 1
o Rollover: High risk, ejection; crush
injuries, spine compression fx Oriented, appropriate 5
o Ejection: Usually unrestrained, spinal Confused 4
injuries, significant mortality Verbal Inappropriate words 3
o Windshield damage: TBI, face
Incomprehensible words 2
injuries, c-spine fx
o Steering wheel: Sternal/rib fx, flail No response 1
chest, cardiac contusion, aortic
injuries, hemo/pneumothoraces Obeys commands 6
o Dashboard: Pelvic and acetabular Localizes pain 5
injuries, hip dislocation Withdraws to pain 4
o 3-point seatbelt: Sternal/rib fx, pulm Motor
Flexion to pain 3
contusions, chance fx, abd/head/face
Extension to pain 2
injuries, c-spine injuries
o Airbag: More severe injuries in kids; No response 1
less thoracic/head injuries; assoc with
limb soft tissue injuries/fractures, corneal abrasions, hyphema
 PVA
o Low speed: Tib/fib fx, knee injuries
o High speed: Waddle’s triad (tib/fib or femur fx, truncal injuries, craniofacial
injuries). “Thrown” multisystem injuries
 Bike: Closed head injuries, “handlebar” spleen/liver lac, other intra-
abdominal (pancreas), pelvic fx, penetrating injuries, extremity injuries
 Fall: LD50 = 30-60 ft.
o Vertical: Calcaneal/LE fx, pelvic fx, TBI, c-spine fx, renal injury, spine
compression fx (10-15% with calcaneal fx with spine compression fx!)
o Horizontal: Craniofacial fx, hand/wrist fx, abd/thoracic visceral injuries, aorta

5. Trauma airway
 Call for difficult airway cart, think about backup in advance (boogie,
glidescope)
 Preoxygenate as soon as pt moved onto bed; 100%, 30 sec (4 breaths)
 If intubated in field, check position, replace combitube/King tubes if possible
 C-spine precautions: Manual immobilization; trial of miller blade
 Med considerations
o Consider lidocaine (1.5-2 mg/kg IV 2-3 min before intubation), fentanyl (2-4
mcg/kg IV) pretreatment for ICP only if time allows
o Induction agents: Etomidate preferred; ketamine controversial in head
injury. midazolam, thiopental, and propofol assoc with hypotension

299
  Succinylcholine NOT assoc with hyperkalemia in ACUTE burn/crush; caution
in IOP/ICP
 Crichothrotomy: Can’t intubate, can’t ventilate; facial/nasal trauma, upper
airway bleed
o CI: Tracheal transaction
o Relative CI: Anterior neck trauma, unclear landmarks

6. Traumatic shock
 Field hypotension and transient hypotension is real and incr mortality
 Ddx in trauma – hemorrhagic vs. neurogenic (cord injury)
 Major bleeding sources: Abdomen, thorax, pelvis, legs(femur), retroperitoneal;
external (EBL!). Consider intracranial in children.
 Try to control external bleed, pelvic binder for open book pelvic fx
 Transfusion: Give blood for shock ASAP, minimize crystalloid; goal SBP 90-
100, caution with over-resuscitation especially with ongoing internal bleeding
 Massive transfusion: 4pRBC:2FFP or 8 pRBC:4FFP:1plt. Attending activates
protocol at SFGH. Suggest PRN
 Damage control resus (>10 pRBC, thoraco-abdominal): 1pRBC:1FFP:1plt.
Greater 30 day survival, may target dilutional coagulopathy (J Trauma 2010;
69(1):46)
 Classification of hemorrhagic shock (note 30% loss before hypotension)
Blood Vol UOP
Class HR SBP RR MS
Loss (ml/hr)
15% (~750 14-
I <100 NL >30 Slightly anxious
cc) 20
15-30%
100- 20-
II (~750-1500 NL/↓ 20-30 Mildly anxious
120 30
cc)
30-40%
120- 30- Anxious,
III (1500-2000 ↓ 5-15
140 40 confused
cc)
>40% (>2000 Confused,
IV >140 ↓↓ >35 minimal
cc) lethargic

7. Traumatic Arrest
 ED thoracotomy
o Indications: Penetrating torso trauma with signs of life in the field and loss of
VS in transport or in the ED
o Overall poor outcomes (<5% survival)
o Best in anterior thoracic stab wounds with tamponade
o Make sure R sided chest tube and intubation is being done concurrently/first

Abdominal/Pelvic Trauma
1. Penetrating
 Need to know number of wounds, mechanism, EBL
 SW: Liver, spleen injuries. Peritoneum violated in 70% (anterior), 44% (flank),
15% (back)
th
o Consider intraabdominal injury in all SW below 4 intercostals space
o Organs injured: Liver > small bowel > diaphragm > colon
300
 o Shock or peritonitis, eviscerationOR
o Unreliable exam  laparotomy (unstable) vs. imaging (stable)
o Stable + reliable exam  consider triple-contrast CT A/P vs. local wound
exploration (by Trauma)
o Neg FAST does not replace CT in stable pt, neg CT does not r/o bowel injury
 GSW: Unpredictable trajectory
o Organs injured: Small bowel > colon > liver > vessels
o Most go to OR unless wound is clearly not intraperitoneal
o GSW anywhere without an exit wound may have intraabdominal or chest
injury unless bullet found on Xray

2. Blunt
 Injuries to spleen>liver, intestine; (kids: liver, spleen, kidney)
 Ask: MVA - airbag? Seat belt? Position in car, mechanism, intrusion; BVA –
handlebars? Position/mechanism? Extent of damage to car?
 Seat belt injuries: mesenteric lac  hemoperitoneum, jejunal injuries,
pancreatic injuries, diaphragmatic rupture, lumar spine injuries. “seat belt sx” in
1/3 pts, highly assoc intraperitoneal lesions
 Imaging
o FAST: Detects 100-500 mL with 60-95% Sn; serial FAST increases
sensitivity. Can’t see retroperitoneum, diaphragmatic defects,
parenchymal/bowel injury. High false negative for hemoperitoneum in pelvic fx
 Positive FAST in pelvic fx suggests associated liver/spleen injury
o CT: May detect organ/visceral injury, see retroperitoneum, urinary tract,
vascular hemorrhage
 Laparotomy indications: Persistent hypotension/unstable w/ hemoperitoneum,
peritonitis, viscus rupture or diaphragmatic rupture, persistent GIB in NGT/vomit

3. Pelvic trauma
 Consider PXR if suspect pelvic fx
 Apply binder if exam suggests instability, XR with open book fx
 Anterior fx: Associated with bladder injury
 Posterior fx: Associated with neurological injury
 Best treated in IR, not OR

Chest Trauma
1. Chest wall injuries
 Rib fx: Assoc penetrating injury to adj organ (liver, spleen, ptx), risk for
pna/atelectasis.. 50% rib fx not seen on CXR, heal in 3-6 wks
o ≥3 usually admit for obs for analgesia, pulm toilet
o Need adequate analgesia (at least 1-2 wk course). May consider intercostal
nerve block if severe
o Displaced rib fx may be assoc with delayed bleeding (intercostal artery tear)
o Flail chest: ≥3 adj rib fx at 2 points with free chest wall segment. Assoc pulm
contusion, paradoxical chest wall motion, splinting. Clinical dx.
 Mgmt: O2, analgesia, pulm toilet; intubate if e/o respiratory decompensation
 Sternal fx: Assoc w/ seat belt
o Dx with lateral CXR or CT. Most are transverse
o Isolated fx are benign

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 o Cardiac issues (contusion) in 1.5 – 6%, eval should r/o other mediastinal
injuries
o Some may need fixation (displaced, bone fragments  risk for nonunion)
o Most require admission for pain control or for associated injuries

2. Pulmonary
 Pulmonary contusion: Bruising  edema + hemorrhage. Assoc dyspnea/
tachypnea, cyanosis, tachycardia, hypoTN, may see infiltrates on CXR/CT
o Early infiltrates on imaging suggest severe contusion and need admission
o Mgmt: O2, consider CPAP, analgesia, restrict IVF; pt frequently dev PNA
 Pneumothorax: Simple vs. communicating (“sucking”) vs. tension
o Immediate needle decompression w/ 14 G if suspect tension
o Simple: May observe <25%, isolated, asymptomatic, apical, not intubated.
o/w need to place chest-tube
o Communicating: Cover on 3 sides with xeroform, no packing
o Chest tube: Mod-large ptx, symptoms, increasing size, recur ptx post chest
tube removal, hemothorax, tension ptx, b/l ptx, anticipate positive pressure
ventilation/general anesthesia
 Trauma: Use 36-40 F in adults, 16-32 F for kids esp for hemothorax
 Complications: Hemothorax, pulm edema, bronchopleural fistula, pleural
leaks, empyema, subQ emphysema, infx, contralateral ptx
 Hemothorax: Usually need chest tube
o Massive: >1500 mL(>20 ml/kg) or 200 ml/hr (7 ml/kg/hr) x3 hrs, persistent
hypotension, decompensation, increasing hemothorax OR for thoracotomy

3. Tracheobronchial injury
 Assoc with penetrating >blunt. Persistent air leak (despite tube), subQ
emphysema, pneumomediastinum, hemoptysis. ?Hamman’s crunch. Complete
transection w/o cnxn to pleural space may p/w atelectasis/pna
 Dx: CT vs. bronchoscopy (fiberoptic)
 Tx: Operative repair. May need to intubate w/ fiberoptic to pass beyond site

4. Cardiovascular
 Myocardial contusion: 2/2 compression b/w sternum + vertebrae or diaphragm.
Assoc pericardial effusions >50%. Sinus tachycardia in 70% (most sn). CK-MB
may be falsely elevated, troponin lower sn for contusion. Consider echo if high
risk/strong suspicion
 Myocardial rupture: P/w tamponade/severe hemorr. Harsh murmur,
hypotension unresponsive to fluids, massive hemothorax, pericardial effusion,
RBBB on EKG
o US to dx; pericardiocentesis to temporize, may need ED thoracotomy and
pericardiotomy
 Penetrating cardiac trauma: RV most common, p/w exsanguinating hemorr vs.
tamponade, likely will require ED thoracotomy (if pulses in field, severe shock
with e/o tamponade, BP <50 systolic post fluids)
 Pericardial tamponade: Usually 2/2 penetrating. If high suspicion, hypotension/
tachycardia, positive FAST (pericardial effusion)  OR. Arrest  thoracotomy
o EDUS 98.1% Sn, 99.9% Sp for pericardial effusion
o Pericardiocentesis? May consider with pigtail catheter for repeated aspiration
only in community ED awaiting txf to trauma center, o/w to OR
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 o Avoid intubation and positive pressure ventilation in tamponade unless doing
planning ED thoracotomy
 Blunt aortic injury – most at desc aorta @ isthmus. Suspect with 1 rib or
st

scapular fx. Interscapular/ retrosternal pain in 25%, htn 2/2 sympathetic afferent
nerve stimulation @ isthmus, normal mediastinum (<6cm on PA, <8 cm on AP
CXR) may have false neg 0-45%
o Tx: Manage bp (SBP 100-120) with esmolol, nitroprusside, to OR

5. Other
 Diaphragmatic rupture: L>R (in blunt). risk of viscera strangulation. Need OR
 Esophageal perforation
o Causes: Iatrogenic, FB, caustic burns, blunt/penetrating trauma,
spontaneous (Boerhaave), postop/anastomosis failure
o Pleuritic pain along esophagus course, worse with swallowing/neck flexion;
CXR with mediastinal air, L sided pleural effusion, ptx, wide mediastinum.
Need CT/endoscopy
o Tx: Broad spec abx, emergent surgery c/s, NPO. Avoid NGT

Burns
1. Severity
 1 degree: “Sunburn.” superficial, epidermis only. Painful
st

 2 degree: “Partial thickness”

nd

o Superficial: Epidermis + shallow dermis with blisters, blanching skin, painful

o Deep: Epidermis + deep dermis, may need skin graft
 3 degree: “Full thickness.” dark brown, charred, no blanching, insensate.
rd

need skin graft

2. General resuscitation
 Rule of 9’s; patient’s palm = 1% TBSA
 Parkland: 4 mL/kg/%TBSA over 24 hrs (half in 8hrs) if >20% TBSA
 Titrate to UOP (30-50 cc/hr adults, 1 cc/kg/hr kids <30 kg, 1-2 cc/kg/hr <2 yo,
0.5-1 cc/kg/hr >2 yo)

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3. Wound care
 Minor: Tdap, pain meds, debride, ±unroof blisters >2 cm, bactrim + dressing,
24 hr f/u
 Large: Silver sulfadiazine or mafenide for gram negative coverage
 Circumferential 3 degree: Early escharotomy
rd

4. Burn center referral (St. Francis, unless a Trauma activation)

 Partial thickness >10% TBSA
 3 degree burn
rd

 Face, hands, feet, genitalia, perineum, major joints

 Electrical/chemical burn
 Inhalational injury
 Significant co-morbidities
 Other: Social, emotional, long-term rehab considerations

5. Other
 Electrical burns

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 o High voltage (>1000 volts): admit, obs
o Household current: may d/c
o Perioral burns via electrical cord – evaluate airway, systemic injury. close
obs, ENT/plastics consult. ?concern for delayed labial artery bleed
 Chemical
o Exothermic rxn vs. acidic (coagulative necrosis) vs. alkali (liquefaction)
o General mgmt: Decontamination, remove clothing, gentle low-pressure, large
volume irrigation with water x15-30 min

Facial/HEENT Trauma
1. General
 Early eval/mgmt of airway
 Usually no abx for facial wounds unless wounds are thru&thru buccal mucosa,
in cartilage of ear/nose, have extensive contamination
 XR vs. CT: Panorex for isolated mandibular fx, dental fx, alveolar ridge fx, o/w
CT (better imaging of condylar fx, more sensitive)
 Nose fx: Don’t need to image if straight nose, no septal hematoma, controlled
epistaxis, able to breathe thru nare. clinical dx of fx (ttp bridge of nose)
o Refer to plastics/OMFS if deformity present as soon as swelling resolves

2. Wounds
 Consider facial nerve blocks for wound repair to avoid anatomy distortion
 Multiple layer closure if involving muscle; chromic gut on mucosa/lip
 Nose lac repair in layers if involve cartilage; risk of stitch abscess due to large
pores, consider subcuticular sutures, irrigate copiously
 Ear hematoma: Risk of cauliflower ear, need to drain + compressive dressing;
 Ear lacs involve cartilage – use absorbable for cartilage; use field blocks
 Fix tongue lacs if: Likely to collect food, form thick scar, deep/gaping
 Consult if involvement of: Parotid/submandibular duct, facial nerve, eyelid
margin/duct or deep wounds, loss of tissue for eye lacs,
 Abx prophy: Only with bite wounds, thru and thru buccal mucoa, involving
cartilage of nose/ears, extensive contamination (poop, barnyard)

3. Dental trauma – see Ear/Nose/Throat and Dental chapter

4. Fractures and assoc injuries

 “Open fx”: abx only if thru sinus (clindamycin 300 mg PO qid or augmentin
875/125 mg PO bid x7 days)
 Frontal sinus/forehead fx: Cosmesis. r/o csf leak if thru posterior frontal sinus
 Blowout fx: Orbital floor fx into maxillary sinus; diplopia on up gaze (inferior
rectus entrapment), anteromedial cheek/upper lip anesthesia (infraorbital
nerve); sx may resolve with edema, need f/u with max/face
 Orbital compartment syndrome: Retro-orbital hematoma  exophthalmos,
decreased visual acuity (neurapraxia of retinal nerve/stretch on retinal artery 
lateral canthotomy w/ cantholysis
*Note: orbital blowouts greatly reduce the incidence of concomitant orbital
compartment syndrome (“pop-off valve”)
 Ruptured globe (blunt) /open globe laceration (penetrating)

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 o Sx: Acute decr visual acuity, relative APD, eccentric/teardrop pupil or corneal
tenting, vitreous extraction, uveal prolapsed; Seidel sx (fluorescein streaming),
monocular diplopia
o Avoid removing FB or stain if obvious, avoid pressure, no IOP checks
o Avoid increasing IOP (avoid ketamine/sux meds; treat nausea)
o Mgmt: Eye shield, zofran, analgesics/sedation prn, ophtho c/s, CT orbit with
fine cuts to r/o fb/fx. Tdap, abx (vanco15 mg/kg, max 1.5 G + ceftazidime 50
mg/kg, max 2 grams)
 TMJ injuries: Meniscus, collateral ligaments, dislocation
o For first time dislocation, r/o fx with xr/panorex. o/w soft diet x2wks,
analgesia, f/u with oral surgeon for most injuries (esp for peds)
 Mandibular fx: Need inter-dental fixation (wiring, arch bars) if involves
symphysis, body, angle, or rami
o If open fx, requires abx and usually admit
o Caution in 4-11 yo: assoc w/ facial growth disturbance
 Tripod fx: Lateral orbit, zygoma, maxilla, usually need op mgmt to stabilize fx
 General facial fx: If assoc CSF leak, elevated HOB 40-60°, ?abx prophy

GU Trauma
1. General
 Examine lower abdomen, pelvis, genitalia, rectum for urethral injury, Gross UA
for gross hematuria (higher assoc with urologic injury)
 Females: Examine vaginal introitus for blood, esp in pelvic fx

2. Urethral injury
 Most posterior urethral injuries assoc with pelvic fx, esp straddle fx and
Malgaigne
 Sx: Blood at meatus, high riding prostate, penile/scrotal/perineal hematoma.
 Dx
o If no external e/o injury and unable to void, trial of foley passage (14-16 Fr).
If successful, unlikely to have complete urethral disruption, can’t r/o partial
o If unable to pass foley or if suspect urologic injury, consider retrograde
urethrogram. Extrav + bladder filling suggest partial tear
 Mgmt
o Partial tear: Urology c/s. Trial of 12-14 Fr foley or coudet catheter passage.
o Complete tear: May require suprapubic catheter
o Definitive mgmt depends on location, extent, mechanism, hemodynamic
stability. Stent vs. open/endoscopic repair
 Females w/ proximal urethral injuries usually require OR repair for
exploration (↑risk of urethrovaginal fistulas or obliterative urethral strictures)

3. Bladder
 Contusions, intraperitoneal ruptures (in blunt trauma w/ distended bladder),
extraperitoneal ruptures (assoc with pelvic fx)
 Gross hematuria present in 95%  need imaging to r/o bladder injury
 Dx: Retrograde CT cystography, retrograde cystography
 Mgmt
o Contusions: If no e/o extrav, conservative ±foley.

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 o Extraperitoneal ruptures: Usually heal w/ foley drainage. OR repair if vaginal
or rectal injury, bladder neck injury, or other laparatomy indications
o Intraperitoneal ruptures: Require OR repair (concern for lower urinary tract
infection  peritonitis)

4. Renal injury
 Mostly 2/2 blunt (90%), assoc with rapid deceleration
 Renal vein injuries >renal artery avulsions/intimal tears, but can’t visualize
renal vein injuries with CTA directly (suspect if large hematoma around kidney)
 Hematuria correlates poorly with severity of renal injury, but consider imaging
if gross hematuria, microscopic hematura + shock, or h/o sudden decal w/o
hematuria/shock
 Peds: Kidney commonly injured, microhematuria can be assoc with major
blunt renal injuries (50 rbc/hpf)
 Imaging
o CT A/P with contrast first choice: detects renal contusions, lacs, pedicle
injuries, urinary extrav, devitalized segments; allows grading, detects other
injuries
o IVP: Less accurate than CT, time and labor intensive, only sees urinary tract
o US: not sensitive for renal trauma (may miss up to 78%)
 Mgmt
o Most renal injuries requiring OR have associated liver/spleen injuries
requiring operative intervention
o Blunt: Obs and bed rest for grade I/II; higher grade, more likely to require op
mgmt. OR if persistent life-threatening renal bleed, main renal artery injury
o Penetrating: Most need OR; absence of hematuria does not r/o injury

5. Ureteral injury
 Most iatrogenic (abd/pelvic surgery). When assoc w/ trauma, usually avulsion
 Most w/ hematuria, but absent in <25%!
 Imaging: CT a/p with contrast (slightly less sensitive than retrograde
pyelography but faster and practical)
 Most need operative repair
 Complications: Urinoma, sepsis, loss of renal function, death

6. Genitalia
 Penis
o Mechanism, state of penis (erect vs. flaccid)
o Strangulation injuries of shaft, lacerations, contusions, degloving, amputation,
traumatic rupture of corpus cavernosum (aka fx; tearing of tunica albuginea)
o Penile fx need immediate operative repair
 Testicles
o Testicular rupture, scrotal hematoma, hematocele, intratesticular hematoma,
traumatic testicular torsion, testicular avulsion, epididymal injury
o Scrotal trauma: need exploration if testicular rupture, large hematocele,
traumatic torsion, testicular dislocation
 Labia: Hematomas, lacerations

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 Head Trauma
1. Traumatic brain Injury
 Categorization
o Primary: Irreversible brain injury 2/2 initial impact
o Secondary: Related to sequelae (hypoxia, hypotension, reperfusion injuries,
infection)
 Severity: Mild (GCS 14-15), moderate (GCS 8-13). severe (GCS <8)
 TBI 2-5% if GCS 15, >90% if GCS 3
 Herniation
o Supratentorial
 Uncal (1) aka transtentorial: Sx progress from
anisocoria (III compression, parasymp) 
down&out pupil (III motor)  blown pupil 
contralateral hemiparesis (peduncle) 
decerebrate  LOC, abnml resp/CV  death;
may compress PCA
*Kernohan’s notch: Contralateral peduncle
compression w/ ipsilateral hemiparesis
 Central (2): Compressed suprasellar cistern;
stretch basilar artery (Duret hemorrhage). rostrocaudal progression. AMS 
pinpt pupils  brady or tachypnea  incr tones  decorticate  decerebrate
 Cheyne-Stokes  arrest
 Cingulate (3): AKA subfalcine. compresses ACA  ischemia
 Transcalvarial (4): Squeeze thru fx/crani
o Infratentorial
 Upward (5): Compressed quadrigeminal cistern; usually posterior fossa
bleed, may cause 2/2 downward or tonsillar; pinpt pupils, downward
conjugate gaze w/o vertical eye mvmt
 Tonsillar (6): Cerebellar; resp/CV collapse (compress medulla), pinpt pupils,
flaccid quadriplegia (corticospinal tracts); chronic = Chiari malform.
 Imaging rules: See Radiology chapter
 General mgmt: Maximize CPP (=MAP – ICP), avoid hypotension/ischemia
o Elevate head of bed (reverse Trendelenberg) if T+L spine not cleared
o Mannitol 0.25-1.0 g/kg IV bolus if s/o herniation/progressive decline (decr
edema w/in 30 min, lasts 90 min-6 hrs); caution with hypotension
o Hyperventilation: only as final effort, could be harmful – ischemia, hypoxia
o Target ETCO2 = 35
 Posttraumatic seizures: Prophy with fosphenytoin 20 PE/kg within first 24hrs
in “significant TBI” requiring admission, usually in significant bleeds; d/w NSU

2. Blunt head trauma

 Epidural: 2/2 epidural artery bleed r/t fx (e.g. middle meningeal; also assoc w/
middle meningeal vein, venous sinuses). LOC lucidAMS. Convex on CT.
3
Immediate surgical evacuation esp if >30 cm volume, anisocoria + coma
 Subdural: 2/2 bridging veins, assoc w/ alcoholics/elderly. Concave. May
present later. Evacuate if: acute, >10 mm thick, midline shift >5 mm, ↓condition
*subdural hygroma: xanthochromic blood-tinged fluid in dural space, assoc w/
AMS or focal deficit, ha/n/v 2/2 ↑ICP, crescent in extra-axial. obs if asymp,
surgical evacuation if symptomatic. 12-55% mortality

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  Subarachnoid: 2 most common. usually no mass effect, common vasospasm
nd

2-3 days post risk of ischemia, treat with ca blockers (nimodipine/nicardipine)

 Parenchymal contusion: Most common. usually frontal, temporal, occipital,
assoc with depressed skull fx. countrecoup if opposite side of impact
 Intracranial hematoma: Deep, 85% frontal/temporal. >50% with LOC upon
impact, 45% mortality with LOC. assoc ↑ICP, often need intervention, especially
cerebellar
 Intraventricular hemorrhage: Rare. if isolated, may observe
 Diffuse axonal injury: Immediate onset, prolonged traumatic coma w/o mass
lesions, ischemia; deceleration/shearing of axons  loss of gray-white, edema;
MRI preferred, usually supportive care. 1/3 with posturing. mortality 15-25% for
mild-moderate, severe with persistent brainstem and autonomic dysfnc,
disability/veg state/death
 Concussion: S/sx of TBI with normal CT. sx – traumatic amnesia, HA, nausea,
blurry vision, vertigo, sleep disturbances, emotional lability, diff conc
Grade Symptoms Return to play
I Transient confusion, no Return to sports if no sx x15 min
LOC, <15 min sx
II Transient confusion, no Can’t return to play; may later return if
LOC, sx >15 min no sx x1wk
III LOC  needs ED eval LOC <1 min may return if no sx x1 wk;
>1 min must wait until no sx x2 wks
 Skull fractures
o Types
 Linear: Hard to distinguish from sutures, usu >3 mm, often in
temporoparietal, frontal, and occipital. conservative mgmt
 Depressed: 2/2 blunt impact with object, parietal/temporal, assoc infx, sz. if
depression deeper than inner table of skull, likely operative
 Basilar: Assoc w/ blood in sinus, CSF leak via nose/ears, battle sx, raccoon
eyes. Need to r/o carotid injury get CTAngio. CSF leak may develop
meningitis, but no routine abx prophy temporal bone thinnest part of skull,
most common fx. ENT c/s
 Diastatic: Thru skull suture, usually in kids; adults w/ coronal or lamboid
o Basilar fx: Assoc with blood in sinuse, CSF leak via nose/ears, battle sx,
raccoon eyes  r/o carotid injury. get CTAngio. CSF leak may develop
meningitis, but no routine abx prophy

3. Penetrating head injuries

 GSW: 90% mortality; 75% if GCS >8 and reactive pupils
 Impalement: Get XR, don’t remove object (must be done at OR)
 Mgmt: Intubate, IV abx, NSU, sz prophy
 Sequelae: 30-50% with sz, physiologic derangement (broken BBB, edema/
↑ICP, loss of cerebral autoregulation); abscess , cranial osteomyelitis

4. Scalp lacerations/avulsions: See Procedures chapter

Spinal Injuries
1. General exam
 Palpate midline for stepoffs/pain, motor, sensory; find level of lesion
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 C4 Spontaneous breathing L1-L2 Hip flexion
C5 Shoulder shrugging L3 Hip ADDuction
C6 Elbow flexion L4 Hip ABduction
C7 Elbow extension L5 Foot dorsiflexion
C8-T1 Finger flexion S1-S2 Foot plantar flexion
T1-T12 Intercostal/abd muscles S2-S4 Rectal sphincter tone
 DTRs: C6 biceps, C7 triceps, L4 patellar, S1 Achilles

2. Spinal cord lesions

 Complete: Total motor/sensation loss distal to lesion
 Partial: Presence of any functional sparing in addition to lesion suggests
incomplete lesion e.g. sacral sparing, toe flexion
 Cord Syndromes
o Central cord: 2/2 buckling of ligamentum flavum into cord with
hyperextension of c-spine in DJD. contusion of central gray matter (pyramidal
and spinothalamic tracts)  UE>LE motor deficit, variable sensory deficit, with
sacral sparing
o Brown Sequard: Usually penetrating injury cord “hemisection.” Ipsilateral
motor deficit and contralateral hypesthesia distal to level
o Anterior cord: Preservation of posterior column (position, touch, vibratory)
with paralysis and numbness below level of injury. Usually need emergent OR
o Cauda equina (actually a radiculopathy): perineal/b/l leg pain, bowel/bladder
dysfunction, perinanal anesthesia, ↓rectal tone, LE weakness
 Spinal shock: Acute weakness with hyporeflexia, lasts days to weeks
 Neurogenic shock: Hypotension and bradycardia 2/2 sympathectomy (high
cord lesion)

310
311
312
  Spinal cord injury without radiographic abnormality (SCIWORA): SCI in kids
without BONY abnormality (most have pos MRI. 2/2 flexible ligaments. Brief
UE weakness/paresthesias  show deficits hrs to days

3. Imaging: See Radiology chapter for more details

4. Fractures (stable vs. unstable)

 Unstable: Atlanto-occipital dislocation, anterior atlantoaxial dislocation,
jefferson fx (C1 burst fx), hangman’s fx (C2 spondylolisthesis), extension or
flexion teardrop fx, bilateral facet dislocation, anterior subluxation. Admit, place
in hard collar
 Stable: C1 posterior arch fx (unless assoc with C2 fx), C2 dense fx (except if
fx at base of dens), articular mass fx, burst fx, spinous process fx, unilateral
facet dislocation, transverse process fx, wedge fx. Discuss mgmt/dispo with
Ortho/Spine

5. Clearing the c-collar

 Clinical without imaging: Apply NEXUS criteria, and if no indication for
imaging, have pt range neck laterally and vertically. If successful, remove color
 With imaging: If pt has negative imaging (e.g. plain film or CT) and is neuro
intact, not intoxicated, not distracted, and without significant pain, allow pt to
actively range neck as above. If unable to range or has significant pain, place
in Aspen collar and f/u with PMD in 1 wk for flex-ex XR
 If concern for neurological symptoms despite negative CT, consider spine cs
and MRI

Neck Trauma
1. Penetrating neck trauma
 Zones: Zone I and III difficult to control
bleeding 2/2 difficult surgical access
o Zone I: Sternal notch/clavicles to cricoid
cartilage
o Zone II: Cricoids cartilage to angle of
mandible
o Zone III: Angle of mandible to base of skull
 Platysma: Superficial but if violated, suspect injury to deeper structures.
 Signs of vascular injury
o Hard: Expanding hematoma, severe active bleeding, shock unresponsive to
fluids, decreased/absent radial pulse, vascular bruit/thrill, focal CNS findings,
airway obstruction  To OR for exploration
o Soft: Hemoptysis/hematemesis, bloody oropharynx, dyspnea,
dysphonia/dysphagia, SQ or mediastinal air, chest tube air leak, nonexpanding
hematoma, focal neuro deficits  consider CT angio
o Zone Mnemonic: zones go up: 1,2,3 just like the floors of a building.

2. Laryngotracheal injuries
 Sx: Bubbling/air leakage from neck wound, SQ air, bony crepitus, etc
 CT detects hematoma, fx (hypoid bone, laryngeal/trach cartilage)

3. Esophageal injury: Rigid scope + contrast esophagography = 100% Sn

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4. Vascular: Carotid, subclavian, vertebral arteries, IJ/EJ. Carotid dissection
 Angio: “Gold standard” with 100% Sn
 CTA: Rapid and easily available, but may miss pseudoaneurysm
 Duplex angio: May miss ZI and ZIII injuries, not easily available
 Consider heparin, possible antiplatelet agents for dissection
 Venous air embolism: Air in neck vein with inspiration  distal occlusion and
infarct. Place in trendelenburg, consider RV aspiration if PEA

5. Near hanging/strangulation
 Assoc with high c-spine fx, cord transaction, death
 Venous congestion w/ cerebral blood flow occlusion  LOC  further
tightnening, vagal reflexes
 Pulmonary sequelae: 2/2 neurogenic vs. postobstructive. edema, broncho-
pna, ARDS

Obstetric Trauma
1. Key pearls
 Airway/Breathing: Supplemental oxygen
o Severe hypoxia may decrease uterine blood flow by 30%
o Decrease in FRC 2/2 elevated diaphragm hypocapnea at baseline (PaCO2
30, bicarb 21), beware “normal” PaCO2, adjust for vent (↑TV, ↑RR)
th
o Chest tubes: Place in 3-4 interspace to allow for higher diaphragm
o If intubating, caution re: aspiration risk, decreased reserve
 Circulation
o Displace gravid uterus off IVC in >20 wk to avoid supine hypotension (can
↓28% CO): Left lateral decubitus, 15° tilt with backboard or manual
displacement
o Beware “normal” BP or HR: Increase blood volume may delay maternal
hypotension with bleed, but still have decreased placental perfusion
o Hyperdynamic flow to uterus, venous congestion in pelvis/LE  ↑risk hemorr
th
o Changes in hemodynamics (from Rosen’s Emergency Medicine, 7 ed)
st nd rd
Normal 1 tri 2 tri 3 tri
HR 70 78 82 85
SBP 115 112 112 114
DBP 70 60 63 70
CVP 9 7.5 4.0 3.8
Hct 40 36 33-34 34-36
WBC 7.2 9.1 9.7 9.8
Blood vol 4L 4.2 L 5L 5.6 L
o Perimortem c-section: Maternal arrest, start within 4 minutes from loss of
pulse if suspect no ROSC by 5 min; unlikely to survive >20 min. 2 vertical cuts
 Viscera displacement and abd wall stretching higher risk for bowel injury,
less likely to have usual guarding/peritoneal sx with intra-abdominal injury
 Radiation: <5-10 rads usually ok, fetus more sensitive in first tri (2-9 wk), but
15 rad assoc 6% chance of MR, 15% microencephaly. normal fetus receives
th
50-100 mrad during 9mo (from Rosen’s Emergency Medicine, 7 ed)

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 Study Uterine radiation Study Uterine radiation
(mrad) – unshielded (mrad) - unshielded
C-spine XR Undetectable Pelvis 140-2200
T-spine XR <1 KUB 200-503
L-spine XR 31-400
Chest (PA) <1 Head CT <50
Chest (AP) <5 Chest CT 10-590
Femur XR <50 Abd CT 2800-4600
Hip 10-210 Pelvis CT 1940-5000
*Actual radiation exposure depends on pt, scanner, technique; shield if possible

2. Abruptio placentae: 50-70% all fetal losses 2/2 trauma

 Due to deceleration force/shear  may occur w/o significant sx abd injury
 Fetal distress 2/2 limited oxygen delivery via placenta; may be exacerbated
with uterine contractions further limiting blood flow
 Sx: Vaginal bleeding (63% w/o bleed!), abdominal cramps, uterine tenderness,
maternal hypovolemia, change in fetal heart rate
 Dx: Limited value of ultrasound (<50% accurate), Kleihauer-Betke; need to
have high suspicion, observe on toco for fetal distress (most sensitive); check
CBC, T&C, DIC labs
 Complications: Assoc with 8.9x risk stillbirth, 3.9x preterm delivery;
coagulopathies/DIC (release of thromboplastic)

3. Uterine rupture: Rare, 2/2 injury to uterus via pelvic fx, penetrating trauma
 Sx: Abdominal pain, palpable fetal anatomy, fetal demise
 Mgmt: Stat OB c/s – OR for repair vs. hysterectomy

4. Fetal injuries/concerns:
o Common injuries: Intracranial hemorrhage, skull fractures usually assoc with
maternal pelvic fx. 38% fetal mortality with pelvic/acetabular fx
o Viability: 24-26 wks (uterus beyond umbilicus, +FHT)
o Normal FHR: 120-160s; beware late decelerations
o Fetomaternal hemorrhage (FMH): 8-30% incidence post trauma; K-B screen
>5mL only empiric rhogam if Rh- within 72 h (50 mcg 1 tri; 300 mcg 2 and
st nd
rd
3 ). D/w with OB if >30 mL FMH
o Even minor trauma has 1-3% fetal loss (usually abruption) 4hrs monitoring.
o >3 contractions, persistent uterine tenderness, vag bleed, abnml strip,
membrane rupture, serious maternal injury at least 24 hr monitoring
o If d/c’ed: return if <4 fetal mvmt/hr, vag bleed, ROM, labor, uterine pain
o Emergent c-section: Fetal distress in viable fetus, uterine rupture, placental
rupture with significant vag bleed, fetal malpresentation during premature
labor, uterus mechanically limiting maternal injury repair

5. Uterine contractions: Most common problem post trauma.

 Due to prostaglandins; progression to labor depends on amount of damage.
 Persistent contractions concerning for pathology e.g. abruption

315
 Pediatric Trauma
1. Key pearls
 Airway/Breathing
o Vagal bradycardia with intubation: consider atropine/glycopyrrolate in infants
o Big head, large tongue, floppy epiglottis, anterior larynx – miller blade,
improve head positioning
o ETT (age/4)+4, depth 3x (ETTsize) at lip
o VT 10-12cc/kg (8-10cc/kg asthma), RR (age appropriate, infant~20-30, ped
16-20)), FiO2 100%, PEEP 3-5, Ppeak 20-30
o Crich CI in age <5-7 yo; use transtracheal jet vent (needle crich with 14 G)
 Circulation
o Check skin signs for shock (pallor, mottling, cyanosis), even with normal BP.
Kids compensate for shock very well, until the end  high suspicion for shock.
o Fluids: 20 cc/kg boluses, up to 60 cc/kg
o Blood products: pRBC 10-20cc/kg (↑2-3 hgb), FFP 10-15cc/kg (↑10-20%
clotting factors); Platelet dosing depends on wt/availability - 1 adult unit (250
mL, single donor apheresis) if >20-25 kg, 1 pedi unit (half adult or 125 mL) if
10-15 kg, 1 quad pack (50-75 mL) if <10 kg (↑50-100,000 plt)
 Disability: see Resuscitation chapter for pediatric GCS
o Big head, thin bones = greater risk of significant head injury
o Pediatric TBI imaging algorithm – see Radiology chapter
 Exposure: Large surface area = greater heat loss!
 Other
o Wt estimate (kg): 1 yo ~10 kg; 8+ (2x age)
o Small size = risk for multisystem trauma.
o Elastic chest = pulmonary contusion/PTX without rib fx
o Anterior liver/spleen, thin muscles = higher risk for liver/spleen injury
o GU: Mobile/protected kidney  hematuria post-trauma more likely to be
congenital (50% with congenital abnormalities)

Vascular Trauma
1. General
 Due to penetrating (stab, shotgun wounds), blunt (crush injury, soft tissue
avulsion, severe burns, compartment syndromes). Concern for ischemia
 Irreversible nerve/muscle injury after 6 hours of warm ischemia
 Hard sx: Pulsatile bleed, distal pulse loss, bruit/palpable thrill, expanding/
pulsatile hematoma, pallor/cyanosis/cool extremity, superficial vein distension.
Assoc w/ >90% incidence of arterial injury  CT angio then OR vs. IR
 Soft sx: Decreased pulses, isolated peripheral nerve injury, severe bleed in
field, unexplained hypotension, large nonpulsatile hematoma. 35% w/ +angio
 Suspect with knee dislocations
 Dx options: XR to r/o fx/FB; pulse ox/Doppler on limb, ABI/API (<0.9 = abnml).
Doppler US, CT angio.
 General mgmt: Control active bleed (direct pressure, foley in wound), avoid
tourniquets/blind clamping. Surgical c/s

2. Occlusive injury
 Transection: Often retract and undergo spasm to minimize blood loss, but may
have exsanguinations with longitudinal lacerations

316
  Thrombosis: Intraluminal thrombosis 2/2 compression of artery or intimal
disruption
 Reversible spasm: Response to trauma with segmental narrowing. May
reverse with warm saline, nitropaste; sometimes require other vasodilators

3. Nonocclusive injury
 Intimal flap/dissection: Intimal break 2/2 extreme stretch, does not change flow
but can form clot. Most heal on their own, can be treated conservatively
 AV fistula: Arterial flow into vein 2/2 injury, may result in steal syndrome, high-
output CHF. May have bruit/thrill
 Pseudoaneurysm: Tear in vessel, hemorrhage contained by fascia /fibrous
tissue. At risk for rupture 2/2 thin wall, may form mural clots with distal emboli

4. Compartment syndrome
 Assoc with crush injury, long bone fx, reperfusion of ischemic limb. Initially
nonocclusive, but progr edema limits arterial perfusion
o Displaced fx: Forearm fx, supracondylar fx, tibial plateau fx, tib/fib fx
o Knee dislocations
 Palpable pulses does not r/o: larger vessels may be patent despite incr in P
 Earliest sx: Pain with passive stretch, loss of sensation (fine touch,
proprioception) 2/2 injury to hypoxia-susceptible fast conducting fibers
 Other sx: Severe pain out of proportion, tight compartment, weakness,
hypesthesia/paresthesia
 If cast: Split cast, bivalve, remove constrictive bandaging
 If suspect, call Ortho ASAP. Need immediate fasciotomy if high suspicion,
pressures >30 mm Hg (w/in 4 hrs)
o Release leg compartments: superficial and deep posterior, lateral, anterior
 Caution in pressure interpretation – “normal” is 30-35 but stryker may not be
dependable; degree of perfusion depends on MAP (= MAP – Pcompartment)

317
 Procedures
By Jillian Mongelluzzo, Res ed. Benjamin Hippen Faculty ed. Jeanne Noble
Brooke Hensley

Nerve Blocks
1. General tips
 Reduce pain by using 27-30g needle, slow injection, and warming lidocaine

2. Digital nerve block: block of volar and dorsal nerves at the base of the finger
 Draw up lidocaine 1% with or without epinephrine into a syringe (Epinephrine
may be used safely in digits, despite traditional teaching)
 Position the patient’s hand with the palm down. Insert a 27 gauge needle in
the dorsolateral aspect of the base of the finger and raise a small wheal
 Advance the needle toward the base of the phalanx until it contacts bone.
Slowly infiltrate1 mL of anesthetic while withdrawing the needle 1 to 2 mm from
the bone. Infiltrate another 1 mL while withdrawing the needle to the skin
 Infiltrate bilaterally (on the radial and ulnar sides of the base of the finger) to
block the entire finger

2. Wrist block
 Full hand anesthesia involves blocking the median, ulnar, and radial nerves
 May need to block only 1 or 2 of these nerves depending on the location of lac

318
 Wrist block landmarks: see www.nysora.com for full pictures and descriptions
o Flexor carpi ulnaris tendon: Flex wrist, ulnar-most palpable tendon
o Palmaris longus tendon/ Flexor carpi radialis tendon: Flex wrist, palpate
middle of wrist for 2 tendons  the tendon on the radial side is the palmaris
longus, tendon on the ulnar side is the flexor carpi radialis
o Radial styloid: Palpable along radial aspect of wrist, ~1 cm from crease
 Ulnar nerve block
Ulnar nerve block

o Insert the needle under the tendon of the flexor carpi ulnaris muscle close to
its distal attachment just above the styloid process of the ulna.
o Advance the needle 5-10 mm to just past the tendon of the flexor carpi
ulnaris and infiltrate 3-5 mL of local anesthetic solution

319
 o May also inject 2-3 ml of local anesthesia subcutaneously just above the
tendon of the flexor carpi ulnaris to block the cutaneous branches of the ulnar
nerve extending into the hypothenar area
 Median nerve block
o Insert the needle between the tendons of the palmaris longus and flexor
carpi radialis
o Advance until the needle pierces the deep fascia (you may feel a fascial
“click” or insert the needle until it contacts the bone)
o Withdraw 2-3 mm and infiltrate 3-5 mL of anesthetic

Median nerve block

 Radial nerve block – mostly local infiltration due to less predictable anatomic
location and division into multiple, smaller cutaneous branches

Radial nerve block

o Insert the needle just above the radial styloid, aiming medially, and inject 5
mL of local anesthetic
o Extend infiltration laterally using an additional 5 mL of local anesthetic

3. Ankle block: Anesthesia to foot

 Innervation of the foot
320
 o Two deep nerves: Posterior tibial (PTN), deep peroneal (DPN). Anesthetized
by deep injection.
o Three superficial nerves: superficial peroneal (SPN), sural, saphenous
(saph). Anesthetized by subcutaneous injection
 General principles
o First clean entire foot with disinfectant (e.g. betadine or chlorhexidine)
o Block DPN and PTN first to avoid deforming anatomy

Foot innervation

*Calcaneal and Plantar nerves are branches of the PTN

 Deep peroneal nerve (1 web space)
st

o While dorsiflexing the big toe, palpate the extensor hallucis longus (EHL)
tendon. The deep peroneal nerve lies lateral to the tendon and the dorsalis
pedis artery
o Insert needle 2cm distal to the intermalleolar line, just lateral to dorsalis pedis
artery. After raising a skin wheal, advance perpendicularly until you hit bone.
Withdraw slightly, redirect 30° laterally, advance to bone, inject 2 ml of
anaesthetic; repeat again with medial redirection of needle
 Posterior tibial nerve (Heel/plantar surface)
o Insert needle in groove behind the medial malleolus, 1cm superior to pulse of
posterior tibial artery. Advance toward posterior tibia at 45 degree angle until
you hit bone. Withdraw slightly, then inject 5 mL of local anesthetic while
withdrawing needle to surface.
 Superficial blocks: Block the superficial peroneal, sural, an saphenous nerves
with subcutaneous circumferential injection of anesthetic

321
 Deep peroneal
nerve block

4. Dental blocks*
Landmarks
Block Area Picture
/procedure
Individual tooth Insert needle 3-4
and associated mm into
Supra-periosteal

soft tissue mucobuccal fold,

toward maxilla.
(local)

Withdraw 1mm
from maxilla and
inject 1-2mL of
anesthetic

Three most Above canine,

anterior teeth insert needle 1cm
Anterior Superior

from midline, into mucobuccal

Alveolar (ASA)

and associated fold at 45 degree

mucosa angle. Inject 2mL
of anesthetic

322
 Upper molars Insert needle into
and mucosa mucobuccal fold
st
(incomplete for between 1 and
Posterior Superior
Alveolar (PSA)

st nd
1 molar) 2 molar. Direct
45 degrees
superiorly and
medially. Insert 2
cms, then inject
2mL of anesthetic.
Redirect laterally if
hit bone
Midline to Place index finger
premolars (plus on infraorbital
upper lip, lateral foramen and
nose, cheek, retract upper lip
and lower with thumb. Insert
Infra-orbital

eyelid) needle into

mucobuccal fold
st
over 1 premolar
Advance needle
toward index
finger 1.5-2cm.
Inject 1-2mL of
anesthetic
Ipsilateral lower Insert needle
lip, skin, lateral to buccal
nd
mucosa (not surface of 2
teeth) premolar .
Advance to
mandible, retract
Mental

slightly, and inject

1-2mL anesthetic

Cheek mucosa Retract cheek w/

thumb and insert
needle 1mm
Buccal nerve

lateral to last
molar at level of
occlusal plane,
advancing to
anterior ramus.
Inject 2mL of
anesthetic

323
 All ipsilateral
Place index finger
teeth, lip and
behind ramus,
chin
with thumb in
coronoid notch.
With barrel of
Inferior Alveolar (lingual)

syringe resting on
opposite
premolars, insert
needle towards
index finger, lining
up needle w/
midline of
thumbnail.
Advance 2.5 cm
until hitting bone.
Withdraw slightly
and inject 2-4mL
of anesthetic
*Pre-treat injection site with lidocaine 5% solution for 3 minutes or benzocaine 20%
(hurricaine spray). Inject slowly with 27g needle to reduce pain.

Lacerations and Suturing

1. General principles
 Always document neurovascular assessment distal to the laceration (pulses,
motor, sensation), presence/absence of foreign body, laceration size
 Hemostasis – when direct pressure fails, try blood pressure cuff, occlusive
dressings, or lidocaine with epinephrine for persistent bleeding.

2. Wound anesthesia
 Administer prior to irrigation. Consider nerve blocks in specific anatomic
locations (i.e. digits, lips)
 Use small needle (27g) and inject slowly to minimize pain
Concentration* Max Dose Onset Duration
Lidocaine 0.5 - 2.0% 4.5 mg/kg 2 - 5 min 1 - 2 hours
with epi 7 mg/kg 2 - 4 hours
Bupivacaine 0.125 - 0.25 % 2 mg/kg 2 - 5 min 4 - 8 hours
with epi 3 mg/kg 8 - 16 hours
*% solution = grams/100mL. 2% lido = 20mg/mL
 Topical anesthesia: useful in kids, but need 45 min-1 hour for full effect
o LET (lidocaine, epinephrine, tetracaine) – epinephrine limits excessive
absorption
o LMX cream sometimes used, but may get excessive absorption
o Viscous lidocaine
 Always irrigate wounds with high pressure irrigation (normal saline or tap
water)

324
  Consider alternatives to suturing: Staples, hair-tie + skin adhesive (dermabond)
steri-strips, tissue adhesive
o Frail skin: Use steri-strips + adhesive alone or to reinforce skin for sutures

3. Suture materials
 Absorbable sutures – for deep layers, peds, poor follow-up pts
Effective
Complete
Wound Comments
Absorption
Support
Gut treated with chromium to
Chromic decrease tissue reactivity and
10-21 days >90 days
Gut slow absorption, may use for
lip/tongue, extremities

Fast Gut treated with heat to speed

Absorbing 5-7 days 14-28 days absorption, may use in face for
Gut peds, poor follow-up pts

Less reactive than gut; synthetic,

Vicryl 21 days 90 days
use for deep multi-layer closure
 Non-absorbable sutures
Tensile Tissue
Comments
strength reactivity

Silk Low High Use for securing lines/tubes

Nylon
High Low Use for skin closure
(Ethilon)
Use for skin closure, slippery
Prolene Moderate Very low
(extra throw in knot)

4. Suture size and removal: Depends on location and wound tension

Location Size # Days until Removal
Face 6-0 3–5
Oral Mucosa 4-0 or 5-0 3–5
Scalp 5-0 5–7
Chest/Back 3-0 or 4-0 7 – 10
Extremities/Hands/
4-0 or 5-0 9 – 10
Feet/Digits

5. Suturing techniques
 Simple Interrupted: commonly used, use for simple linear lacs
 Vertical Mattress: “Far, far, near, near.” Allows eversion, less tension but
more scarring. Consider for deep gaping wounds
 Horizontal Mattress: Everting stitch, used more frequently in fascia than in
skin, or on palms and soles.

325
  Fixing scalp lacs
o SCALP layers: Skin, Connective tissue, Aponeurosis (aka “galea”), Loose
areolar connective tissue, Periosteum
o aponeurosis – contains occipitofrontalis and temporoparietalis (elevates
eyebrows, wrinkle forehead – must repair if disrupted and gaping)
o bleeding – apply pressure, lido with epi, staples, temporizing sutures
o lac repair options
 stapling – if superficial, galea not involved
 suture – 3-0 nylon or propylene; consider deep buried vicryl for galea
 tricks: apply bacitracin to hair if interfering with wound exam/repair, or use
hair for hair-ties (clump 5 strands per side, twist together once, apply
dermabond to knot; hair must be at least 3cm in length)
o need to irrigate thoroughly (scalp vessels drain into diploe veins venous
sinus; risk for intracranial infx

Procedural Sedation
1. Pre-sedation assessment
Difficult Airway (LEMON) Difficult Ventilation (MOANS)

Look externally Mask seal

(syndromic, obese, gestalt) (beard, trauma, prone)
Evaluate 3-3-2 rule Obesity
(mouth opening, thyromental, (redundant upper airway, OSA, poor
hyomental) reserve)
Mallampatti Score
I: uvula, ,tonsils, palate
Age >55
II: upper uvula, tonsils
(loss of airway tone)
III: base of uvula
IV: hard palate only
Obstruction
No teeth
(OSA, PTA, epiglotitis, mass, etc.)
Neck mobility
Stiffness
(rheumatoid arthritis, c-collar
(asthma, COPD, pregnant)
placement)

2. Preparation
 Last meal/liquids
 Basic airway equipment (with consideration of appropriate sizing)
 Airway adjuncts (Bougie, LMA, Glidescope)
 Good positioning
 ASA class documented
 Allergies to medications and foods
 15L NRB mask and BMV setup identified
 Difficult airway analysis (see above)

326
  EtC02 monitor (specific nasal cannula device)
 2 consent forms (1 for procedure, 1 for sedation)

3. ASA class
 I: Normal healthy patient
 II: Patient with mild systemic disease
 III: Patient with severe systemic disease
 IV: Patient with severe systemic disease that is constant threat to life
 V: Moribund patient not expected to survive without operation
 E: Emergent procedure

4. NPO requirements
>2 years < 2 years
Clear Liquids 4 hours 2 hours
Solids 6 hours 6 hours

5. Medications
Midazolam Etomidate Propofol Brevital*
Med

Ketamine **
(versed) (Amidate) (Diprivan) (Methohexital)
IV:
0.01-0.05 IV:
IV:
Adult dose

mg/kg (2- IV: 1-1.5 mg/kg

IV: 1-2 mg/kg
5mg w/ 0.5-1 mg/kg (~100mg)
0.15 mg/kg IM:
fentanyl) ~30mg then Pretreat
~10mg 10 mg/kg
IM: 10mg pushes w/ zofran (+/-
0.1-0.15 versed)
mg/kg
IV:
IV:
Re-dosing

IV: IV: 0.5mg/kg

0.5-1 mg/kg
Max total 0.1-0.2 mg/kg q 2-3 min
IM:
dose 10mg q30 sec PR*:
2-4 mg/kg
1/3 initial dose
IV: IV:
0.05-0.1 1 mg/kg IV:
Peds dose

mg/kg, IV: IV: IM: 1.5-2 mg/kg

max 6 mg 0.15 0.5-1.0 10 mg/kg IM:
IN: mg/kg mg/kg PR: 4-5 mg/kg
0.2-0.5 25 mg/kg Pretreat w/zofran
mg/kg (max 500 mg)

327
 Onset IV: IV: IV:
1-5 min IV: 30 sec 30 sec
<1min
IM: <1 min PR: IM:
10-15 min 10 min 3-4 min
IV:
IV/IM: 5-10 min IV:
Duration

IV:
1-2 h (peak IM: 15 min
3-5min 1-3 min
effect 30-60 30-60 min IM:
min) PR: 30-120 min
45-60 min
Short
Short duration, Pedi
Good for

Longer sedation,
Long duration, deep CT scans
awake intubation,
procedures No sedation, (Short
st unfasted state
hypotension 1 choice in duration)
pregnancy
Respiratory ↑HR/BP,
depression, emergence reaction
Side Effects

Desats, hiccups, (6%),

especially Myoclonus Hypotension cough, ↑salivation (rare),
w/ fentanyl salivation, laryngospasm
broncho- (0.3%),
spasm myoclonus
<3 mos,
↓ dose by +/- sepsis
Contras

severe HTN, CAD,

Soy, milk, Seizure d/o,
50% if use (adrenal schizophrenia,
egg allergy asthma
w/ opioid suppression) globe injury,
hydrocephalus
*PR Brevital: no recommendations on redosing, may consider 1/3 initial dose. When placing
dose, need to squeeze buttocks to limit medication leakage, may need to tape together. Use
8 Fr NGT with tip cut off for easier administration, and ensure brevital is reconstituted to
10% (100 mg/mL) to decrease total PR dose volume.

** Ketamine is the only sedative with significant analgesic properties. It is also the only
sedative which leaves airway reflexes intact, therefore it is often the preferred agent for
emergent sedations in the unfasted state.

§Ketamine/Propofol or Ketofol: Administer separately, or mix 50%/50% in 20cc syringe:

100mg propofol and 100mg ketamine and give 0.1 mL/kg (3-7 ml). Combo balances the
side effects of propofol and ketamine, i.e. CV stable, though the same contraindications
apply. CAUTION: ketamine comes in varied concentrations! Also, by Policy 50/50 mixture
not allowed at SFGH because of concern for mixture compatibility

328
 Ultrasound
By Patrick Lenaghan Res ed. Kristin Berona Faculty ed. Ralph Wang

Abdominal Aorta
1. Indications
 Undifferentiated hypotension, flank/abdominal pain, syncope
 EP’s can diagnose AAA’s with good accuracy, as high as 100% in one study,
with only 2 indeterminate studies out of 68 patients

2. Technique
 Curvilinear or phased array probe, probe indicator to patient’s right
 Scan from subxiphoid area to bifurcation above umbilicus
 Scan both transverse and sagittal planes
 Transverse view: aorta will be anterior to vertebral body. IVC lies to right of
aorta, and is compressible. Optimize depth
 Views
o Sagittal: Probe indicator to patient’s head. Aorta will run deep-superficial as
you scan distally. Try to identify SMA taking off of aorta
o Transverse: Visualize the entire length of the aorta from the celiac plexus
down to bifurcation (95% of AAA’s are infrarenal), and save supra- and infra-
renal images of aorta (ideally to the level of the SMA)
o Seagull sign: Takeoff of celiac trunk in subxiphoid region

3. Troubleshooting
 Use gentle firm pressure to displace bowel gas (can be up to 30 seconds of
pressure)
 Adjust depth so that vertebral body and aorta are primary visualized structures

4. Interpretation
 Positive study if aorta>3 cm
 If positive, perform FAST and get CT/ consult surgery as clinical situation
dictates

5. Pitfalls
 Aorta is not visualized in 20% of cases
 Free fluid from rupture usually cannot be detected unless it is intraperitoneal
 Beware irregular margin of aorta, as this can be a sign of intramural thrombus
 Oblique cuts will falsely elevate true aortic diameter. Scan at right angles to
main axis of vessel

Cardiac
1. Indications
 R/o pericardial effusion
 Assess global function
 Volume status assessment
 Identification of significant left and right ventricular enlargement
 Procedural guidance: Pericardiocentesis, pacemaker wire placement
confirmation
329
2. Technique
 Micro-convex or phased array probe
 4 basic views
o Parasternal long: Left costochondral junction at nipple level, probe marker to
patient’s right shoulder
o Parasternal short: Same as parasternal long view, but probe marker to
patient’s right hip. goal is to see a donut shape of the LV contracting. Best view
to assess global function
o Apical four chamber: Near PMI, looking up towards the right shoulder
o Subxiphoid: Probe inferior to xiphoid process, often have to flatten out probe,
place hand on top of probe (coronal plane), and increase the depth of the view
in order to obtain a good image
o Extended views
 Suprasternal notch for aortic dissection
 Subxiphoid sagittal view for IVC and volume status determination

3. Troubleshooting
 Move patient onto left lateral decubitus position to improve image quality, as
this brings heart closer to chest
 Be sure that machine is on cardiac mode. You likely will not obtain high quality
images in all four views

4. Interpretation
 Contractility: Comment on hyperdynamic, normal, or depressed systolic
function, based on how well the walls of the LV come together during systole
(they should nearly completely touch in the parasternal short view)
 RV strain: Look for bowing of the interventricular septum into the LV
 RV enlargement: RV : LV ≥ 1
 Volume status: IVC collapse during inspiration (“sniff test”) suggest
hypovolemia. No change in IVC diameter with inspiration = plethora
 Pericardial effusion: Presence of anechoic fluid in the pericardium
o If pericardial fluid is present, also evaluate IVC
o Echocardiographic signs of tamponade: RV or RA diastolic collapse in
presence of pericardial effusion (more sensitive than specific, but often present
in absence of hemodynamic compromise), IVC plethora
o Must be combined with clinical signs of shock: Beck’s triad (hypotension,
muffled heart sounds, jugular vein distension), tachycardia , pulsus paradoxus

5. Pitfalls
 Effusion vs. pericardial fat: Effusion should be circumferential and seen on
more than one view. You should not see effusion behind LA (LA tethered to
pericardium)
 Pleural vs. pericardial effusion: Differentiate by looking at effusion location with
respect to aorta

DVT
1. Indications
 Rule out DVT

330
  ED US up to 95% (87-99) sensitivity and 96% (95% CI 87-99) specificity
(Burnside PR et al, Acad Emerg Med 2008)

2. Technique
 Linear probe
 Scan in femoral and popliteal region for 2 point scan
o Positioning: Bend knee and externally rotate hip
o General compression technique: Apply firm pressure perpendicular to
vessel, until the vein lumen is fully collapsed. Inability to collapse the lumen
despite applying enough pressure to begin to efface the artery suggests clot
o Femoral: Identify femoral artery and vein. Start at the proximal common
femoral vein where the great saphenous vein joins it medially. Repeat
compression to interrogate multiple points along the vein down to bifurcation
o Popliteal: Look for vascular bundle in the popliteal fossa. POP ON TOP =
vein on top of the artery. Examine for full compression at multiple points

3. Troubleshooting
 Improve sensitivity by scanning proximally and distally in femoral region to
visualize more of the vein
 Scan in the center of the leg when looking for the popliteal vein
 In obese patients, lie them prone and scan the posterior knee with knee bent

4. Interpretation
 Positive study if artery is effaced, but vein is not completely compressed
 If high pretest probability but negative bedside scan, need formal study
 If scan is negative, and concern for isolated calf/distal DVT, arrange for repeat
follow up formal scan in 7 days

5. Pitfalls
 ED US cannot detect calf or segmental DVT
 Difficult to interpret study in patient with prior DVT
 False negative study is likely if you are not pressing hard enough to efface
artery

FAST
1. Indications
 Blunt trauma, r/o 3H’s – hemoperitoneum, hemopericardium, hemothorax
 Beware limited utility of FAST in blunt trauma with normal vital signs

2. Technique
 Phased array probe
 Four views
o RUQ: Probe sagittal, indicator to patient’s head, mid-axillary line at T11.
Look for free fluid in Morrison’s pouch, potential space between liver and
kidney
o LUQ: Same as RUQ, but start more posteriorly. Remember, place “knuckles
to the bed” to achieve adequate visualization. Fluid here often is in
splenodiaphragmatic recess

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 o Pelvic: Visualize bladder, look posteriorly for anechoic fluid, scan in two
planes
o Cardiac: Use subxiphoid technique as above, evaluate for pericardial fluid

3. Troubleshooting
 Turn probe parallel to ribs for LUQ and RUQ, repeat study if clinical condition
changes
 In bladder view, decrease far gain to maximize image quality.

4. Interpretation
 Positive: Presence of fluid (black)
 FAST is nearly 100% sensitive for significant hemoperitoneum causing shock
or requiring emergent laparotomy in blunt trauma

5. Pitfalls
 May miss up to 200-500 mL of free peritoneal fluid
 Only 50% sensitive at detecting need for laparatomy in penetrating trauma
(misses bowel injury)
 Pediatrics: Role of FAST not as clearly defined, as non-operative mgmt of
intraabdominal injuries is much more common

Pelvic
1. Indications
 Rule out ectopic pregnancy by visualizing intrauterine pregnancy (IUP) for
st
symptomatic 1 trimester patients (vaginal bleeding, abdominal pain)

2. Technique
 Transabdominal: Phased array or curvilinear probe.
o Use a full bladder for optimal sonographic window. Start in transverse view,
just above pubic bone, probe indicator to patient’s right, scan DOWN into
pelvis to visualize uterus, look for yolk sac/fetal pole. Scan in trans and sagittal
view
 Transvaginal (TVS): Endocavitary probe
o Perform if no IUP visualized
o Ask patient to empty bladder
o Place probe in sagittal plane with probe indicator towards patient’s head.
Bladder will be in left near field with uterus in long axis. Fan from ovary-ovary,
then turn probe 90 degrees to coronal plane and scan uterus fully again
 Always perform a FAST for a r/o ectopic pelvic U/S

3. Troubleshooting
 Radiology often uses GS with double decidual sign as positive study, but
currently our ED standard is to require GS + YS or fetal pole to call IUP
 Measure thinnest amount of myometrium around GS. should be >8 mm, to
ensure that you are not visualizing an interstitial ectopic
 Beware pseudogestational sac: Stimulated area of myometrium from ectopic
pregnancy, differentiate this from true GS because no double decidual sign
(double border of sac), can have echogenic material, irregular border, no yolk
sac

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4. Interpretation
 IUP: Yolk sac in gestational sac surrounded by adequate myometrium
 Findings: IUP or no IUP. Presence of free fluid
 Discriminatory zone: βHCG level above which you should expect to see IUP
o TVS: 1500 for radiology-obtained TVS. Ralph’s data suggests this could be
much higher in EPPUS, depending on sonographer’s experience
 Gestational sac (GS) visualized at 5 weeks TVS, 6 weeks TAS, fetal pole 6
weeks TVS, 7 weeks TAS.
o If GS is >10 mm, should see a yolk sac (YS) or fetal parts within it. If not,
consider embryonic demise

Renal
1. Indications
 Flank pain, rule out hydronephrosis
 Sensitivity and specificity of 82 and 86% compared to CT, in ruling out
hydronephrosis

2. Technique
 Curvilinear abdominal probe
 Kidneys
o On right side, place probe in midaxillary line, indicator to patient’s head
o On left, probe in posterior axillary line, probe indicator to patient’s head.
Obtain transverse and longitudinal views of kidneys
 Bladder: Ureteral jets
o Place color flow on ureterovesicular junction (little humps on floor of bladder
in transverse view), and wait several seconds to see if you see ureteral jets
filling bladder. Presence of jets suggest decrease the likelihood of having an
obstructing stone on the affected side

3. Troubleshooting
 Turn probe parallel to ribs
 Do not be confused by renal medullary pyramids, as these can appear
hypoechoic
 Pyramids are oriented further from hilum of kidney than the renal pelvis.

4. Interpretation
 Positive: Anechoic shadows within the renal pelvis suggest hydronephrosis
o Graded mild, mod, or severe
 A normal renal pelvis appears hyperechoic

RUQ/biliary
1. Indications
 RUQ/epigastric pain, rule out acute cholecystitis
 ED US sensitivity 87% (95% CI 66-97) and specificity 82% (95% CI 74-88) vs.
radiology US sensitivity 83% (95% CI 61-95), specificity 86% (95% CI 77-92)
(Summers SM et al, Ann Emerg Med 2010)

2. Technique

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  Curvilinear or phased array probe
 Start transversely below nipple at the level of the subxiphoid, which will usually
show the portal triad
 Gallbladder (GB): Fan probe down towards feet from portal triad. It is the most
anterior fluid filled structure in RUQ
 If you are having trouble visualizing GB, may also sweep probe from FAST
RUQ position towards midline along the costal margin in long axis
 Identify GB, scan through in transverse and longitudinal planes
o Stones: Casts a shadow, hyperechoic, obeys gravity. Must have stones to
further assess for cholecystitis
 Wall thickening: Measure GB wall in anterior field (>3 mm is considered
thick)
 Pericholecystic fluid
 Sonographic Murphy’s sign: Pain with compression of GB viewed on US.
Ballot all 4 quadrants starting with left lower, sono Murphy sign is positive only
if pain is specific to ballotment of GB
 Identify portal triad (PT): Superior to GB (GB hangs off the portal triad
anatomically). If GB is visualized, fan up towards head in transverse
o Measure CBD (>4-5 mm is dilated measured outside wall to inside wall).
Rule of thumb: 4-5 mm + 1 mm for every decade of life over 50 as normal CBD
size, although this is controversial

3. Troubleshooting
 Unable to visualize GB
o Scan in epigastrium with pt in left lateral decubitus view (this brings GB more
anteriorly)
o Sweep from Morrison’s pouch view in the lateral costal margin (helps to
maximize the acoustic window of the liver)
 Stones
o Scan in two planes, interrogate the neck closely, look at every shadow
o Consider the wall echo sign (WES) when multiple stones obliterate the
lumen of the GB (all you may see is anterior wall, hyperechoic stones, and
shadow from the GS)
 CBD measurement
o Use color flow to differentiate hepatic artery from CBD. CBD is always a
tubular structure anterior to the portal vein, but hepatic artery is an adjacent
fakeout. CBD is more lateral than artery in transverse view

4. Interpretation
 Ultrasound signs of cholecystitis: +GS and +Sono Murphy’s detects
cholecystitis in the ED (>90% PPV), and requires formal study or surgical
consultation. Additional data points are only supportive of the diagnosis

5. Pitfalls
 Do not rule out stones unless you can see the GB neck – interrogate the entire
GB in 2 planes
 The quality of shadowing can differentiate stone from bowel gas
 Do not over-rely on secondary signs of cholecystitis. Cholecystitis is a clinical
diagnosis, and any patient diagnosed with gallstones is at risk for cholecystitis.

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 In general, a patient with gallstone and RUQ pain should be considered to have
cholecystitis

Procedures
1. IV Access
 U/S guided femoral or internal jugular CVC placement
o Always be sure to know the orientation of your probe and its relationship to
the anatomic structures
 Peripheral or deep brachial IV placement
o Look in antecubital area for peripheral vein. Move medially and proximally up
the bicep to scan through the deep brachial space to find an adequate target
o Transverse or longitudinal methods can both be successful in cannulating
the vein under direct visualization. Use a longer angiocath (at least 1.5 inches,
on u/s machine at SFGH, in Pyxxis at Moffitt) to increase success rate

2. Nerve blocks
 Helpful for complicated lacerations, or painful fracture/dislocations
 Caution if concern for compartment syndrome and frequent neuro checks
 Types: Forearm nerve blocks, either median, radial or ulnar, femoral nerve,
and brachial plexus
 Technique: Nerves appear hyperechoic with honeycomb appearance. Center
nerve in field of view, and use sagittal image to visualize needle under real time
guidance to deposit local anesthetic to bathe the nerve. Avoid direct nerve
puncture

3. Abscess drainage
 Technique: Use linear probe, identify largest area of pus.
 Particularly useful in draining peritonsillar abscesses: use intracavitary probe
for access to this area (use nebulized lidocaine for anesthesia)

4. Paracentesis/thoracentesis
 Paracentesis: Use abdominal probe
 Thoracentesis: Either linear or abdominal probe
 May perform indirectly: Mark the location of the pocket of fluid immediately
prior to procedure, as long as patient can remain still

Miscellaneous
1. Thorax - eFAST
 Indications: R/o pneumothorax, evaluate for pulmonary edema
 Greater sensitivity than supine CXR for pneumothorax (48.8% vs. 20.9%).
Both eFAST and CXR have very high specificity (99.6% and 98.7%)
 Technique: Linear probe, sagittal plane
o Visualize pleura in between two ribs, scan in at least three intercostal spaces
on either side
 Interpretation
o Negative: Presence of BOTH pleural sliding and comet tail artifact coming off
the pleural space, “sandy beach” on m-mode

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 o Positive (PTX): Lack of pleural sliding, parallel lines on m-mode. May be
PTX, or an unventilated lung (i.e. left lung in a right mainstem intubation, dense
lung consolidation).
o Positive (pulmonary edema): Presence of B-lines or large, fat, and numerous
comet tail artifacts extending down to the edge of the screen from pleural line

2. Ocular
 Useful for posterior segment pathology
 Interpretation: Generally findings are more specific than sensitive
o Retinal detachment: Hyperechoic linear object in the vitreous
o Vitreous detachment: Hazy hyperechoic object anterior to the retina
o Papilledema: Outpouching of the optic disc into the vitreous

3. Foreign Body
 Good for localizing (shallow) objects
 Useful if the object is not visualized on radiography (i.e. wood)
 Tips
o Scan through water or jelly filled glove (“a bump”) to improve the resolution
of objects that are just below the skin surface
o Scan in two planes in order to improve object localization
 FB removal most successful under real time ultrasound guidance

Suggested Reading
 ACEP Policy Statement: Emergency Ultrasound Imaging Criteria
Compendium. http://www.acep.org/workarea/downloadasset.aspx?id=32886
 Barkin A, Rosen CL. Ultrasound detection of abdominal aortic
aneurysm. Emerg Med Clin N Am 2004; 22(3): 675-82
 Burnside PR, Brown MD, Kline JA. Systematic review of emergency
physician-performed ultrasonography for lower-extremity deep vein thrombosis.
Acad Emerg Med 2008; 15(6):493-8
 Ciccone TJ, Grossman SA. Cardiac Ultrasound. Emerg Med Clin N Am 2004;
22 (3): 621-40
 Moore C, Promes SB. Ultrasound in Pregnancy. Emerg Med Clin N Am 2004;
22(3): 697-722
 Gaspari RJ, Horst K. Emergency Ultrasound and Urinalysis in the Evaluation
of Flank Pain. Acad Emerg Med 2005; 12(12): 1180-4
 Horangic N, Malet PF, Schwartz JS, et al. Revised estimates of diagnostic test
sensitivity and specificity in suspected biliary tract disease. Arch Intern Med
1994; 154(22):2573-8
 Kirkpatrick AW, Sirois M, Laupland KB, et al. Hand-held thoracic sonography
for detecting post-traumatic pneumothoraces: the Extended Focused
Assessment with Sonography for Trauma (EFAST). J Trauma 2004; 57 (2):
288-95.
 Kuhn M, Bonnin RL, Davey MJ, et al. Emergency Department Ultrasound
Scanning for Abdominal Aortic Aneurysm: Accessible, Accurate, and
Advantageous. Ann Emerg Med 2000; 36(3): 219-23
 Rose SJ. Ultrasound in Abdominal Trauma. Emerg Med Clin N Am 2004;
22(3): 581-99

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 Shah K, Wolfe RE. Hepatobiliary Ultrasound. Emerg Med Clin N Am 2004;
22(3):661-73
 Soffer D, McKenney MG, Cohn S, et al. Prospective evaluation of
ultrasonography for the diagnosis of penetrating torso injury. J Trauma
2004;56:953-7
 Summers S, Scruggs W, Menchine MD, et al. A Prospective Evaluation of
Emergency Department Bedside Ultrasonography for the Detection of Acute
Cholecystitis. Ann Emerg Med 2010; 56: 114-122
 Wang R and Sargent M. UCSF-SFGH Ultrasound Handbook

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 Resident as Teacher
By Caitlin Bilotti Res ed. Kendall Allred Faculty ed. Susan Promes

Bedside Teaching in the ED

1. Getting started
 Identify learner’s needs
o Probe learner’s experience prior to patient encounter
“Have you seen a patient with aspirin ingestion before?”
o Ask questions after presentation
“What do you think we should do?”
 Discuss expectations

2. Tools for time-limited teaching

 One Minute Preceptor: the five microskills
o 1) Get a commitment
“What do you think is going on?” or “What do you want to do?
o 2) Probe for supporting evidence/reasoning
“What factors did you consider in making that decision?” or “Were there other
options you considered and discarded?”
o 3) Teach general rules
For back pain, teaching about “red flags” of back pain or different classes of
therapeutic agents
o 4) Reinforce what was done well
“I really liked your brief description of your general physical exam, but give me
a more complete neurologic exam in that patient with back pain”
o 5) Correct mistakes and discuss next steps
“Next time I would like you to consider a broader differential for back pain,
rather than just thinking about musculoskeletal problems”
 Aunt Minnie: rapid pattern recognition
o Learner evaluates patient independently based on chief complaint
o Presents only chief complaint and presumptive diagnosis
o Instructor discusses case and management plan with learner after s/he
evaluates patient independently
 SNAPPS: encourage self learning
o Summarize
o Narrow down
o Analyze
o Probe
o Plan
o Select
 “Activated” Demonstrations
o Learner observes instructor at task
o Provide learner with a specific assignment/goal
o “Activate” learner by asking what they have learned
 Case Presentations at the Bedside: engages patient and learner. Allows both
learner and patient to engage is discussion about missing data

3. Tips on giving feedback

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 Goals
o Describe objective observations about the learner
o Improve performance to help the learner achieve their goals
 When formulating your feedback
o Start with positive aspects of the situation
o Identify specific behaviors that need improvement
o Offer constructive suggestions for improvement
o Be brief, clear, and concise
o End on a positive note with a plan
o Ex) “Keeping a to-do list of your patients might help you stay organized at
signout” is better than “you seem disorganized at signout”
 Effective feedback
o Recipient is voluntarily receiving it
o Involves recipient (i.e., when the recipient gives feedback on him/herself as
well as receiving it from others)
o Timely (avoids the recipient from becoming detached from the situation, and
thinking “that was a long time ago—I wouldn’t make a mistake like that
anymore”)
o Concrete: use objective data/examples
o Focus on the behavior (“it was difficult for anyone else to get in a word
edgewise” is better than “you are a loudmouth”), and address its
consequences
o Descriptive rather than evaluative to reduce defensiveness (“some important
things to add to your differential diagnosis of chest pain are X, Y, and Z” is
better than “your differential diagnosis of chest pain is not very thorough”)
o Positive feedback is more effective when given in the second person (“you
did a great job at X, Y and Z today”)
o Negative feedback is more effective when given in the first or third person (“I
didn’t understand your…” or “people were concerned when you…” OR when
phrased as a question (“were you distracted during…?”)
o Feedback is a process; it takes repeated rounds of feedback to change
someone’s self-perceptions and behaviors
 The effectiveness of feedback depends on the recipient’s degree of self-
esteem
o Those with high self-esteem do not perceive negative information as clearly
as they perceive positive information, and might benefit more from video
feedback (harder to ignore the feedback when watching oneself on videotape!)
o Those with low self-esteem respond more to negative information

Suggested Reading
 Brinko KT. The practice of giving feedback to improve teaching. J Higher Educ
1993; 64(5): 574-93
 Ende J. Feedback in clinical medical education. JAMA 1983; 250(6): 777-81
 Flynn, Mark J. Feedback and Evaluation: Comparison and Contrast
 Irby DM and Wilkerson L. Teaching when time is limited. BMJ 2008;336:384-
387
 Neher and Stevens. The One-minute Preceptor: Shaping the Teaching
Conversation. Fam Med 2003;35(6):391-3

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