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DR. HAMID SHAALAN. FRCS Ed.


Consultant G. Surgery And Emergency Medicine.



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INTRODUCTION

The emergency department (ED) is an integral unit of a hospital and the
experience of patients attending the ED significantly influences the public
image of the hospital offering medical service.

Thousands of people attend ED every year or more come into contact with
one or any other hospital service .Some of them are acutely ill or injured and
need immediate, sometimes life-saving treatment. Many of whose condition
are not so serious, require urgent assessment and treatment for their injury or
sickness.

Non-urgent visits comprise a significant proportion of total pts., attending ED
, but still their medical conditions have to be evaluated and managed.

The ED also providers for reception and management of disaster plan in the
region. For these reasons EDs have a high public profile and are viewed by
many as essential local service.

To achieve our goal towards offering best service according to accepted
standards, this proposed plan for developing and evolution EDs. is created.

This plan suggests :

I ) Structure and Manpower Standards .
II ) Policies and Procedures.
III ) Protocols for management of critical cases commonly
encountered in ED.
IV) Algorithms.
V) Procedural skills.

The purpose of these standards is to establish an organized, safe, efficient
and customer service focused utilization of the Emergency Depatment..

Here are the 2nd updated revised edition of third part , that I think they are
very important pillars in ED protocol implementation's success.

WA[t|w f{ttt
Vt|? WxvA ECDF

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PART III




PROTOCOLS FOR MANAGEMENT OF CRITICAL
CASES COMMONLY ENCOUNTERED
IN ED





















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Initial Assessment And Management Of
Polytrauma

Objectives :

1. To identify the correct sequence of assessing the polytrauma patient.
2. To apply the Guidelines of priorities for the primary and secondary
survey.
3. To resuscitate and manage life threatening injuries.

General principles

1) Follow ( A, B, C and D )
2) Maintain spinal stabilization at all times.
3) Evaluate and treat simultaneously
4) Do not add further harm
5) The primary and secondary survey should be repeated at
the time and adverse change is identified.
6) In actual clinical situation, may of these activities occur in
parallel or simultaneously.

What's Initial Assessment?
A systematic approach to a seriously injured patient that can be
easily reviewed, practiced and it includes:

I. Rapid primary survey and resuscitation.
II. Adjuncts to primary survey.
III. Detailed secondary survey.
IV. Adjuncts to secondary survey.
V. Re-evaluation
VI. Definitive care.
"There is a Golden hour between life and death. If you are critically injured
you have less than 60 minutes to survive. You might not die right then; it may
be three days or two weeks later -- but something has happened in your body
that is irreparable." Dr. R. Adams Cowley, Shock Trauma Center section of the University of
Maryland Medical Center




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1 Primary Survey And Resuscitation
- Primary survey and resuscitation of vital functions are done
simultaneously.
If a life threatening problem is identified during the primary survey,
manage it immediately, NOT Later.
- Adult/ pediatric/ pregnant women priorities are the same.
A. Airway with C-spine protection.
B. Breathing and ventilation.
C. Circulation with hemorrhage control.
D. Disability (NEUROLOGICAL EXAM.).
E. Exposure/Environmental control.
Primary survey :

1.1 Airway with C-Spine protection
- Initial assessment should be done without moving the neck.
(if possible)
It must be assumed that the casualty (especially if they are unconscious
or has any significant injury above the clavicles) has a cervical spine
injury, until can be excluded.
Check the patient's responsiveness by gentle shaking them by the
shoulder or giving a command.
If the patient is able to communicate verbally, the airway is not likely to
be obstructed.

- NOTE :
Maxillofacial fractures.
Tracheal deviation.
Engorged neck veins.
Swelling and deformity.
Lacerations.
Surgical emphysema.
- Establish a patient airway

Chin left or jaw thrust maneuver: clear the airway of foreign bodies.
Insert an oropharyngeal or nasopharyngeal airway.
Establish a definitive airway.
- Orotracheal or nasotracheal intubation.
- Surgical cricothyroidotomy.
- Apply a rigid cervical collar and only remove it to examine the neck
further while maintaining full spinal immobilization.


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Soft collar - In general, this decreased rotation by 8 degrees but
insignificantly protected against flexion and extension.
Hard collars - A variety of collars available . They all allowed about
8% flexion, 18% lateral movement, and 2% rotation. The
Philadelphia collar allowed the least extension.
Sandbags and tape - Surprisingly, this was the best. It allowed no
flexion and only a few percent movement in any other direction.

1.2 Breathing With O
2
Supplementation
- A) Assessment
Expose the neck and the chest.
Determine the rate and depth of respiration.
Look for tracheal deviation, chest movement, asymmetry, use of
accessory muscles and signs of injury
Listen for movement of air on both sides of the chest.
Percussing for dullness or hyper-resonance.
- B) Management
Administer high flow O2 (10L/min.)
Ventilate with ambu-bag (a bag valuemask device) if
respiration is absent, impaired or inadequate
Chest decompression if tension pneumothorax is suspected.
Seal open pneumothorax.
Monitor the patient's arterial O2 saturation with a pulse oximeter.
And maintain saturation greater than 95%
Sizing and fitting Cervical Collar



a) From angle of the mandible to b) From lower edge to black nail or level c) pushing strip side from Rt. side
the clavicle the chin bridge

d) fitting anterior part e) stretching the strip and fix to anterior f) put head suppot or sand bags on both sides
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Tension pneumothorax is a clinical diagnosis
History of penetrating trauma, positive pressure ventilation or airways
disease
Air hunger
Hypotension
+/- distended neck veins
+/- hyperresonant on tension pneumothorax side
Do NOT x-ray - this is a clinical diagnosis
Immediate needle decompression.
Confirm side clinically.
Inform patient.
14G cannula .
2nd intercostal space
Insert vertically while aspirating
Note air bubbling.
Protect with gaue.
!ape and leave in situ.
Preare chest drain for insertion.
1.3 Circulation With Control Of Hemorrhage :
Assessment :
- Check the patient's
Skin colour
Pulse
Bp
Identify source of external major hemorrhage.
Identify any evidence of hypovolemic shock.
Management :
- Basic and advanced cardiac life support if needed.
- Apply direct pressure to external bleeding site.
- Vascular access by inserting 2 large bore peripheral IV cannulae
(14-16gauge). The desirable sites in adult are the forearm or
antecubital veins >
- Central venous(femoral, subclavian, jugular) if not in profound
hypovokemia to avoid complications > Cutdown for saphenous
vein.
- In pedia, forearm > intraosseous > femoral > cutdown age less
than 6 years.
- Obtain blood sample for CBC, Bio-Chemistry type & cross match,
blood gases.

a! "ocate #
nd
$CS midclvicular line %! &hile asiratin' insert vertically a
Sterile usin' (etadine )*+ cannula a,ached to a syrin'e with -S


c" Protect and tae
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- Fluid therapy with warm Ringer's Lactate, normal Saline, (Initially 1-
2 liters for an adult, and 20 ml/kg for pediatric patient in first 10
minutes.) and blood replacement.
- Splint any long bone fracture.
- Consider using pneumatic anti-shock garment (PSAG).
- Operative intervention.
** Prevent hypothermia during assessment and
management
1.4 Disability
- Rapidly assess the patient's central (brain)
and peripheral (spinal cord) neurological status.

- CNS :
AVPU scale( Alert ,responds to Verbal command,respnds to Pain
,Unresponsive)
The pupils : size, equality and reactivity.
- Peripheral nervous system
Ask the patient if he can feel : Fingers, toes.
Ask the patient to squeeze your hand with his fingers.

1.5 Exposure/Environment Control :
- The patient should be completely undressed.
Prevent hypothermia ******
II Adjuncts to Primary Survey :
Vital sign
ABGs
Pulse oximeter and exhaled CO2
Urinary & gastric catheters unless contraindicated.
Urine output hourly.
ECG
X-ray (chest, pelvis &lat. Cervical spine( C7-T1 should be visualised)
Ultrasound or DPL
Consider early transfer
- Referring doctor receiving communication is essential.
- Don't delay transfer for diagnostic tests.
- Use time before transfer for resuscitation.




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Re-evaluate the patient :
Before beginning secondary survey be sure that :
- The primary survey is completed.
- The ABCD are reassessed.
- Vital functions are normal

Remember : Life saving SHOULD BE initiated when the
problem is identified, rather than after the primary survey.



Airway Adjuncts:
1- Oropharyngeal Airway



A correctly positioned O/P Airway O/P Airway showing flange , body ,and tip Sizing O/P Airway .Measured from
incisors to angle of the jaw

Step by- step guide



A) Inserting O/P Airway upside down B) Rotation of Airway180 when reaching C) Final position of airway, Ensure
after opening the mouth ( if assistant the back of the tongue so the tip faces downwards tongue/lips are not caught bet .airway &
available let him do jaw thrust) incisors








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2-Naso-pharyngeal Airway



N/P Airway & Lubricant Sizing the N/P tube using pt's little finger



Inserting the lubricated tube with bevel towards medial Direct upwards while rolling gently
Bag-Valve Mask



Holding B/V Mask E/C Technique








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Needle Cricothyrotomy


Papate Cricothyroid membrane Puncture midsagitally with a 12-14 canula attached to a syringe
.Direct caudally at angle 45

while aspirating


Aspirating air signifies entery into trachea, remove stylet with syringe and fix O2 tube .
Secure in place , Apply intermittened ventilation


III Secondary Survey :

Components :
- History
- Physical examination : Head-to-toe
- Special diagnostic procedures.
- Re-evaluation of the patient.
Secondary survey can be summarized as tubes and fingers in every
orifice.
History :
A- Allergies
M- Medications currently used.
P- Post illness/frequency
L- Last meal
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E- Events ( mechanism of injury)/Environment related to the injury.
Blunt trauma
Penetrating injury
Burns
Chemicals, toxins, radiation



Physical examination :
1. Head :
GCS
Monitor the level of consciousness at regular intervals
Look for
- Any obvious injury
- Mastoid staining/bruising
- CSF leakage : Rhinorrhea, otorrhea
- Eye : injury, Hge, foreign body
Palpate for lacerations, swellings, depression, fractures at the base
of lacerations.
Hemorrhage from the scalp should be stopped with pressure dressing.

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2. Maxillo-facial :

Palpate the face for deformities and tenderness.
- If there is facial injury :
Check for loose or lost teeth.
Grasp the upper incisor and check for the maxilla (suggesting a
middle third fracture).

- If Maxillofacial injury or fracture compromises the airway :
Pull the relevant fracture facial segment forward.
Pull the tongue forward.
Consider intubation

Cervical Spine & Neck :

Patients with maxillofacial or head trauma should be presumed to
have cervical spine fracture/or ligamentous injury .
Stabilize the neck in a semi-rigid cervical collar and a rigid spine board
until the patient reaches the hospital.
Repeat the neurological examination to assess motor power,
sensation and reflexes.
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3. Chest :
- Inspect the anterior, lateral and posterior chest wall for:
Tracheal deviation ( a late sign)
Signs of resp. obstruction : stridor, intercostal recession
Asymmetrical chest movement.
Wounds
Bruising
- Palpate for :
Tenderness & crepitus over the ribs & sternum, clavicle.
Subcutaneous emphysema.
Blunt & penetrating injury
- Percussion for hyperresonance or dullness.
- Auscultation : breath & heart sounds
Management :
o Tension pneumothorax : needle decompression, chest tube
o Flail chest : Intubation and ventilation
o Open chest wound : Cover with an occlusive dressing and
tape down on three edges.
o Cardiac tamponade : Pericadiocentesis


4 . Abdomen :
- Inspect: the anterior and posterior abdomen for : Brusing,
movement and open wounds and distension.
- Palpate for : Tenderness, involuntary muscle guarding, rebound
tenderness
- Auscultate: for bowel sounds
- Investigations :
X-ray pelvis
DPL or FAST if haemodynamically unstable.
CT IF the patient haemodynamically stable.
- Put 2 IV infusion with large bore cannulae.
- Transfer the patient to the operating room if indicated.
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5 . Perineum/Rectum/Vagina :
Perineum : Laceration, contusion, hematomas, urethral
bleeding
Rectum : Rectal blood, anal sphincter tone, bowel wall
integrity, pelvic fracture, prostate position
Vagina : Vaginal laceration, blood in vaginal vault
6. Musculoskeletal :
- Extremities :
Inspect for laceration, contusion, deformity, burns.
Palpate for : tenderness, crepitations, abnormal movement,
peripheral pulses (presence, absence, equality)
Apply appropriate splinting for extremity fractures.
- Pelvis fracture :
Suspected by ecchymosis over iliac wings, pubis, labia or
scrotum
Palpable for : tenderness, mobility, leg length uneven
X-ray pelvis
Apply the pneumatic antishock garment for control of Hge
associated with pelvic fracture.
- Back :
Log roll the patient, if a spinal injury is suspected.
Inspect for : laceration, contusion deformity
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Palpate for : tenderness, Bogginess, irregularity of the contour
of spinous process
Auscultate the back of the chest.
Immobilization of the back.

7. neurological Examination :
- Re-evaluate the patient level of consciousness, papillary size and
response.
- Re-determine GCS.
- Evaluate the upper & lower extremities for motor & sensory
functions.
- Early neurological consultation if needed.
- Adequate oxygenation ventilation and perfusion.
- Immobilization of the entire patient
- Document any neurological deficits when identified.

IV Adjuncts to the secondary survey :
Further diagnostic procedures, if needed, should only be performed after the
patient life threatening injuries have been identified and managed and the
patient hemodynamic and ventilation status returned to normal.

Spinal, extremity x-rays
C.T. of the head, chest, abdomen.
Contrast x-ray studies
Endoscopy

V . Re-evaluation :
- Revaluate the patient constantly to minimize missed injures and
to discover any deterioration.
- Continuous monitoring of vital sings, urine output, cardiac
monitoring, pulse oximeter
- Relief sever pains by I.V. opiates or anxiolytics





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VI. Definitive Care :
- Rational for patient transfer.
- Direct doctor-to-doctor communication
- Transfer procedures.
- Patients needs during transfer

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20







Management of Multiple Trauma
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2- Rapid Sequence Intubation (RSI)

RSI refers to technique of simultaneous administration of a sedative
agent (induction) and neuromuscular blocker along with cricoid
pressure designed to facilitate intubation and reduce the risk of gastric
aspiration.

RSI should only performed if emergent intubation is necessary
(respiratory failure, acute intracranial lesion, some overdose, status
epilepticus, combative trauma patient where behavior threatens life,
possible cervical spine fracture and immobilization is not possible
because delirium ), the patient may have a full stomach, the
intubation is predicted to be successful.

Patients for whom intubation is likely to be difficult should
not have RSI

Features of possible difficult intubation: obesity, short neck ,
short or long chin, airway deformity, limited oral opening, and limited
neck mobility.
Steps:
1. Preparations:
Ensure that all needed items are available (IV line,O2,monitor,
suction, different sizes endotracheal tube, laryngoscope, assess
airway, draw medications.
2. Pre-oxygenation: 100%O2 for 3 minutes by mask, if ventilatory
assistance is necessary, ventilate gently to avoid stomach inflation
and possible regurgitation.
3. Pre-medication: depending on the underlying condition of the
patient.
Fentanyl: 2-3 mcg/kg IV for analgesia in a wake patient.
Midazolam (sedation, amnesia, hypnosis, NO analgesia) 0.1-
0.3mg/kg IV, onset 30 seconds, last 15-20 minutes.
Atropine: 0.01 mg/kg IV for children or adolescent if there is
bradycardia.
Lidocaine: 1-2 mg/kg IV, to suppress response in HTN, IHD
ICP.
Morphine: 0.1mg/kg in pulmonary edema.



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4. IV induction agent
Thiopental (provides sedation, amnesia, hypnosis)
- A short acting highly lipid soluble barbiturate.
- Dose 1-4mg/kg, Onset: 60 seconds, duration 5-50 min.

- Side effects:
Respiratory depression, apnea myocardial depression,
hypotension anaphylactoid reaction
- Advantage: ICP and cerebral 02 consumption, rapid onset &
short duration, consider an alternative drug in pregnancy.
- Effect antagonized by aminophylline.
Propofol
Ketamine
Etomidate

5. Cricoid pressure (Sellick's maneuver): is applied by an assistant
till the ETT is in place and cuff is inflated and proper position is
confirmed.

6. paralysis (neuromuscular blocking agent):
Succinylcholine (Scoline): dose: 1-1.5 mg/kg in adults, 1.5-2
mg/kg in children, depolarizing neuromuscular blocker, rapid
onset < 60 see, short duration (6min).
Side effects:
Fasciculation (pre treat with small dose(1-2mg) of
Pancuronium or vecuronium), hyperkalaemia (e.g. in renal failure,
crush injury, burns, mitral stenosis) trismus, malignant
hyperthermia, bardycardia (pretreat with atropine in children),
hypotension, ICP , intraocular pressure, Histamine release
may cause bronchospasm or anaphylactoid reaction.
Contraindications:
Risk factors for hpyerkalaemia
Hereditary pseudocholinesterase deficiency
Penetrating ocular trauma or glaucoma.

Recuronium: (esmeron)
- A rapid onset, short acting a nondepolarising neuromuscular
blocking agent (NDNMB).
- Dose: 0.6 mg/kg, 1-2 minutes, duration 30 minutes
- Excellent choice for NDNMB, good alternative for use when
succinylcholine is contraindicated.

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7. Immediately intubate upon onset of apnea: Place ETT under direct
visualization and confirm placement by primary and secondary
confirmation.

8. Post-intubation management: secure tube, provide long-term
paralysis and sedation as indication mechanical ventilation.

N.B
1. To calculate approximate tube size:
For children: (age in years/4)+4
For adults (> 12 years): 7-8 cuffed.
2. Long term paralysis
Pancuronium (pavulon)
- A longer-acting NDNMB.
- Dose: 0.05-0.2 mg/kg onset 1-3 minutes. Duration dose
dependant, averaging 60-90 minutes.
- Main use is prolonged blockade after intubation is complete
- No elevated intracranial pressure or fasciculation
- Contraindication: hypersensitivity to Pancuronium, IHD,
HTN.
Atracurium (Tracurim)
- Dose : 0.4 mg/kg, onset 3-5 minutes, duration 20-25
minutes
- Contraindications: Hypotension Bronchial asthma
- Advantage: best in renal failure liver failure.


















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3
3
-
-
S
S
H
H
O
O
C
C
K
K


I Definition:

Shock is inadequate organ perfusion and tissue oxygenation.
In adults, a systolic90 mmHg, a mean arterial BP 60mmHg or a
decrease in systolic BP of 40 mmHg from the patient's baseline
pressure and a pulse pressure20 mmHg constitutes significant
hypotension .In children, if a child's BP 2 times the child age, pulse
70, hypotension is present.
Evidence of hypoperfusion includes
Mental status change .
Cyanosis, cold limbs.
Oliguria or lactic acidosis.
Hypoperfusion may lead to organ dysfunction or death.
Management should be directed towards correcting
hypoperfusion, NOT HYPOTENSION, as a primary endpoint.

II Pathophysiology

In most cases, tachycardia is the first sign of shock.
Progressive vasoconstriction of cutaneous and visceral
circulation.
The release of catecholamines increases peripheral vascular
resistance.
This increases diastolic blood pressure and decreases pulse
pressure. Increase aldosterone secretions, which retain sodium
and water to expand blood volume.
Aerobic metabolism will be shifted to anaerobic one with
development of metabolic acidosis.

III Types & common causes of shock:

1. Hypovolemic shock

Loss of blood( Haemorrhagic shock )

o Trauma
o Hematoma
o Hemothorax or hemoperitoneum



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Loss of plasma

o Burns
o Exfolutive dermatitis

Loss of fluids and electrolytes

o Vomiting
o Diarrhea
o Excessive sweating
o Ac. Pancreatitis
o Ascitis
o bowel obstruction
2.Cardiogenic shock
o Dysrhythmia

- Tacharrhythmia
- Bradyarrhythmia

o Pump failure

- MI
- Cardiomyopathy

o Acute valvular dysfunction

3.Obstrutive shock
Tension pneumothorax
Pericardial disease( tamponad,constriction)
Disease of pulmonary vasculature
- Massive pulmonary embolism
-Pulmonary hypertension
0bstructive valvular disease
- Aortic stenosis
- Mitral stenosis

4.Distributive shock
Septic shock
Anaphylactic shock
Neurogenic shock
Acute adrenal insufficiency


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I. Stages of shock

3 Main stages:

STAGE I : Compensation stage:

The body is able to compensate for loss in the circulation.
Reflex sympathetic activation leads to tachycardia and
peripheral vasoconstriction, so maintaining BP and cardiac
output.
Signs and symptoms of shock may be minimal as the
compensation is effective
( Volume loss up to 15% of COP. Pulse < 100, urine output > 30ml/hr,BP
normal, CNS normal or anxious).
STAGE II : Decompensation stage:

The body's compensation functions are working at full
stretch but are unable to compensate adequately, the vital
organs are not getting sufficient O2, signs and symptoms of
shock appear, as tachycardia, tachypnea. Agitation,
confusion obtundation, metabolic acidosis, oliguria or anuria.
Urgent intervention is needed to slow down shock.

STAGE III : Irreversible stage

When prolonged shock has produced irreversible cellular
damage involving major organs including encephalopathy of
brain, coagulative necrosis of the heart, acute tubular necrosis
of the kidney, and diffuse alveolar damage of the lungs, The
aim of the first aider is to prevent the casualty reaching this
stage.

IV Symptoms and signs of shock:

General symptoms
Anxiety & nervousness.
Dizziness.
Weakness.
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Confusion.
Fainting.
Nausea &vomiting.
Decreased or no urine output.
Excessive thirst.
Symptoms associated with specific cause
Symptoms associated with hypovolemia.
External (bleeding) or internal Hge .
Pain of burn.
Pain of Pancreatitis.
Chest pain-{cardiogenic}.
Fever, rigors,{ septic shock}.

Signs :
Rapid pulse.
Cool, clammy skin.
Profuse sweating.
Rapid shallow breathing.
Pallor, bluish lips and finger nails.
Drowsiness ,agitation or altered consciousness.
Hypotension.


Type

Pathophysiology

Clinical manifestation

Mild( 20%of
Bl. Volume lost)
Decrease peripheral of
organs able to withstand
prolonged ischaemia
(skin, fat, muscles and
bone)
Ph is normal.
Patient complains of feeling
cold, postural hypotension,
tachycardia.
Cool, pale, moist skin.
Collapsed neck veins,
Concentrated urine.

Moderate(20%-
40% of Bl
volume lost)
Decrease central
perfusion of organs able
to tolerate only brief
ischaemia (liver, kidney,
gut).
Ph : metabolic acidosis.
Thirst, supine hypotension,
tachycardia,
oliguria or anuria.

Severe ( 40%
of Bl .volume
lost.)
Decrease perfusion of
heart and brain.
Metabolic acidosis is
severe.
Respiratory acidosis may
also be present.
Agitation,confusion,obtundation.
Supine hypotension and
tachycardia,
Rapid, deep respiration.

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* These clinical findings are most consistently observed in
hemorrhagic shock but apply to other types of shock as well.




V. Management of shock:

A.General management of shock ( all types )
i. Airway
ii. Breathing
iii. Circulation
iv. Disability
( See INITIAL ASSESSMENT & MANAGEMENT )

B.Specific treatment:

1- Hypo-volaemic shock
Treatment of hypovolaemic shock should be aggressive and
directed by response to therapy than by initial classification of
Hge.
Crystalloids (e.g. 0.9% NaCl & LR ) and colloids ( e.g. 5%
Albumin and hetastarch ) are equally effective if given in
sufficient amount for restoration of intravascular volume .
An initial fluid bolus is given as rapidly as possible. The usual
dose is 1-2 Liters for an adult and 20ml/kg for a pediatric patient.
A rough guideline for total amount of crystalloid volume acutely
required to replace each ml of blood with 3ml of crystalloid fluid
( 3 for 1 rule ).
Dextrose 5% should not be used to treat hypovolemic shock
as it is rapidly distributed throughout body fluid compartment.

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Indices of successful resuscitation
o Improved blood pressure
o Falling lactate
o Increase O2 saturation
o Urine output >0.5 ml/kg/h (adult), 1ml/kg/h (child)
and 2ml/kg/h ( infant ).
o Peripheral perfusion improving
o Level of consciousness improvement
o Normalizing Ph
o Tachycardia

Blood : Whale blood or packed red blood cells is
indicated in patients with moderate to severe Hge. To
restore the oxygen-carrying capacity of the intra
vascular volume. Fully cross matched blood is
preferable but requires about 45 minutes, type specific
blood can be prepared within 10 minutes. For life
threatening blood loss, use of unmatched, type specific
blood is preferable over type O blood. Fresh frozen
plasma should be used only for correction of
coagulopathy and not for volume replacement.








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1. Cardiogenic shock

Diagnosis
ECG may reveal arrhythmia, MI, ischemia,
electrolyte abnormalities.
CXR can show signs of CHF (vascular
congestion, Kerley B lines), wide mediastinum in
aortic dissection.
Cardiac enzymes for MI as troponin & CPK-
MB., and Troponin I
ECHO to identify pericardial tamponade of
effusion
Pulmonary artery catheterization reveals
decreased cardiac output index (< 2.2 L/min./m2),
wedge pressure (> 18 mmHg), systemic
vascular resistance, peripheral O2 extraction.
CBC,
Coagulation profile
Bl. chemistries.

Treatment
Airway control with intubation or CPAP as necessary
IV access, pulse oximetry, cardiac monitoring
Rhythm disturbances, hypoxia,hypovolemia, and electrolyte
abnormalities should be identified and treated immediately.
Monitor urine output hourly.
Patient should chew and swallow Aspirin 160-325 mg, unless
contraindicated.
Morphine IV in 2mg, repeated if needed. Hemodynamic
parameters should be monitored.
IV Inotrope administration:
-Dopamine(2.5-20mcg/kg/min.)for hypotensive patients
to cause inotropy and vasoconstriction.
-Dobutamine(2.5-20mcg/kg/min)for normotensivepatient
to cause inotropy.
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Nitroglycerine (5-100mcg/min) to preload
COP.
Na nitroprusside (0.5-10mcg/kg/min) to improve
COP by of after load.
Norepinephrine may be used if is no or poor
response to other pressors infusion. It should
be started at 2mcg/min and titrated to desired
effect.
PTCA( Percutaneous Transluminal Angiopathy
) is preferred method for reperfusion in cases of
cardiogenic shock following MI, Thromblytics
are much less effective in shock state.
Intra-aortic balloon pump placement may be
used as temporizing measure to decrease after
load,so improving perfusion and cardiac arrest.

NB:
- Drugs causing preload reduction :loop diuretics( furosemide
or bumetanide) and vasodilators (nitroglycerine and morphine).
- Drugs causing afterload reduction ACE inhibitors,nitroprusside.
3- Distributive shock
Hypotension.
Wide pulse pressure.
Mental status changes.
Warm extremities.
Urine output.
Septic shock ( Temperature 38C or 36C, tachycardia,
tachypnea, evidence of underlying infection).
Neurogenic shock ( Bradycardia, hypothermia, HX. Of
trauma, focal neurological deficit ).


TREATMENT
o ABC of resuscitation should be addressed.
o Hemodynamic stabilization : rapid infusion of NS or RL
( 500ml every10 minutes,(20ml/kg in children), often
6L(60ml/kg in children) is necessary.
o BP, mental status, pulse, capillary refill, urine output should
be monitored.
o If no response to fluid administration,
- Systolic BP < 70mmHg infuse norepinephrine 0.5-30ug/min.
34


- Systolic BP 70 90 mmHg Dopamin 5-20 ug/kg/min, Then
Dopamine can be combined with Dobutamine in dose of 5-20ug/kg/min

o SEPTIC SHOCK
- Remove source of infection e.g. catheter, I&D abscess.
- Blood, urine and sputum for culture.
-Empiric antibiotic therapy IV against gram-positive and gram-
negative organisms. Anaerobic organisms may be considered in
some cases.
- acidosis is treated : O2, ventilation and fluid replacement,
NaHCO
3
1mEq/kg IV in metabolic acidosis.
-DIC should be treated with fresh-frozen plasma: 15-20ml/kg
initially to keep PT at 1.5-2 times normal, platelet infusion of 6U,
to maintain serum conc. of at least 50,000/ml.
- If adrenal insufficiency suspected, glucocorticoid
(hydrocortisone100mgIV) should be given.

o NEUROGENIC SHOCK

- Maintain C-Spine protection
- Rapid IV fluids usually successful in the absence of other
interventions
-Bradycardia may be treated with atropine 0.5-1 mg/5min for
total 3mg. A pacemaker may be used.
- Methylpredisolone (high dose) should be instituted within 8
hours of injury, 30mg/kg bolus over 15 min. followed by an
infusion 5.4mg/kg/h for 24 hours.

o ANAPHYLACTIC SHOCK
(See Anaphylaxis Algorithm following pages)


o OBSTRUCTIVE SHOCK

Tension pneumothorax must be treated promptly
by needle decompression then chest tube.

CARDIAC TAMPONADE by pericardiocentesis Fluid
resuscitation may improve cardiac output.







35


























36














































Figure 2 Anaphylactic Reactions: Treatment Algorithm for Children by First
Medical Responders














































1 An inhaled beta2-agonist such as salbutamol may be used as an adjunctive measure if bronchospasm
is severe and does not respond rapidly to other treatment.
2. If profound shock judged immediately life threatening give CPR/ALS if necessary. Consider slow
intravenous (IV) adrenaline (epinephrine) 1:10,000 solution. This is hazardous and is recommended
only for an experienced practitioner who can also obtain IV access without delay. Note the different
strength of adrenaline (epinephrine) that may be required for IV use.
3. For children who have been prescribed an adrenaline auto-injector, 150 micrograms can be given
instead of 120 micrograms, and 300 micrograms can be given instead of 250 micrograms or 500
micrograms.
4. Absolute accuracy of the small dose is not essential.
5. A crystalloid may be safer than a colloid.
37














































38















































Anaphylactic Reactions: Treatment Algorithm for Adults


Consider when compatible history of severe allergic-type
reaction with respiratory difficulty and/or hypotension
especially if skin changes present



Oxygen treatment
when available



Stridor, wheeze,
respiratory distress or
clinical signs of shock1



Adrenaline (epinephrine)2,3
1:1000 solution
0.5 mL (500 micrograms) IM


Repeat in 5 minutes if no clinical
improvement



Antihistamine (chlorphenamine)
10-20 mg IM/or slow IV



IN ADDITION
If clinical manifestations of shock
For all severe or recurrent do not respond treatment
drug reactions and patients give 1-2 litres IV fluid.4
Hydrocortisone Rapid infusion or one repeatdose
100-500 mg IM/or slowly IV may be necessary




1. An inhaled beta2-agonist such as salbutamol may be used as an adjunctive measure
if bronchospasm is severe and does not respond rapidly to other treatment.
2. If profound shock judged immediately life threatening give CPR/ALS if necessary. Consider
slow IV adrenaline (epinephrine) 1:10,000 solution. This is hazardous and is recommended
only for an experienced practitioner who can also obtain IV access without delay.
Note the different strength of adrenaline (epinephrine) that may be required for IV use.
3. If adults are treated with an adrenaline auto-injector, the 300 micrograms will usually be sufficient.
A second dose may be required. Half doses of adrenaline (epinephrine) may be safer for patients on
amitriptyline, imipramine, or beta blocker.
4. A crystalloid may be safer than a colloid.





39


T Tr ra au um ma a T Te ea am m

The trauma team is ideally made up of a group of doctors, nurses, operating
department assistants, radiographers and other support personnel who have
no other commitment that day than to receive and treat trauma patients.

This is a very expensive arrangement. If the doctors involved are residents,
senior consulting staff should be immediately available if necessary. Many
centers now have their trauma teams led by consultants.

Core Trauma Team is group of professionals that receives and treats
the patient:

Team Leader
Anaesthetist
Anaesthetic Assistant
General Surgeon
Orthopaedic Surgeon
Emergency Room Physician
2Nurses (Three if no anaesthetic assistant)
Radiographer
Scribe (Nurse or doctor)






40


Additional staff need to be mobilized to provide ancillary services:

Porters - to run samples to the lab, collect blood
Haematologist and Biochemist to receive and process samples.
Blood Bank

Other staff, while not involved in every trauma call, need to be available
to the trauma team immediately :

Neurosurgeon
Thoracic Surgeon
Plastic Surgeon
Radiologist

Certain areas need early notification of the trauma victim.

CT Scanner
Intensive Care
Theatres
The core trauma team comprises 10 people working around a single
patient.
everyone must know their place and their tasks, and has the skills,
equipment and support to accomplish these.
The trauma room should be quiet so that the voice of the team leader
can be heard and assessments from team members can be relayed
back to him.
Vital signs should be called out every five minutes and these must be
heard by everyone.

Trauma Team Tasks

The Team Leader Responsibilities
Obtain history from paramedics.
Direct team members in their actions.
Establish priorities for investigation and management.
Order or authorize investigations and procedures.
Keep track of whole state of the patient.
Receive and interpret all results of investigations
Order fluid or blood administration.
Supervise spinal manoeuvres.
Consult with other specialities.
Decide on appropriate disposition.
Talk to relatives.
Write in the notes.
41


Record audit information.
Dismiss and debrief team members.
Educate trauma team.


The trauma team leader should be the most experienced team member
present before the patient arrives in hospital.
The leader's role should not be superseded by late arriving members
or passing senior staff.
This avoids confusion for team members of who to take direction from
and who to report to.

Anaesthetist Responsibilities

Airway Control
Cervical Spine Control
Ventilation
Monitoring of vital signs.
Monitoring of fluid and drug administration.
Analgesia
Provide anaesthesia for surgical procedures

General Surgeon Responsibilities
Pimary Survey
Assessment of thorax and abdomen, head and facial injuries, Log roll.
Thoracostomy or thoracotomy.
Diagnostic peritoneal lavage.
Urinary Catheter

Orthopaedic Surgeon
Assessment of spine, pelvis.
Application of external fixator.
Assessment of limb injury.
Dressing of wounds and stabilization of fractures

Emergency Room Physician
Intravenous access.
Venous and arterial blood samples.
Thoracostomy.
Urinary Catheter.
Assist with diagnostic peritoneal lavage
Some overlap is necessary between the general surgeon, orthopaedic
surgeon and emergency department physician to ensure that tasks continue
simultaneously and no time is lost and no hands wasted.


42



Nursing staff
If their is no anaesthetic assistant , one nurse should be solely
dedicated to the anaesthetist.
Nurses should attach themselves to each hands-on surgeon or ED
physician and assist in their tasks
Nurses should not have to leave the resuscitation room to fetch
equipment or run samples to the labs.
Ancillary staff should be outside the main resus. area to provide this.

Radiographer
Radiographer should immediately start with the trauma series of
X-rays,
I. Cervical Spine,
II. Chest,
III. Pelvis
unless directed otherwise by the team leader.
Once these have been processed, other views may be required by
evidence of other injuries.
The radiographer should also act as liaison to the CT scanning
department.

Scribe
The scribe is responsible for the full record of the trauma call.
A separate doctor or nurse should be allocated to the roll.
They should be situated near the team leader so that all information
passing through the leader is then passed to the scribe

Records
Time of arrival.
Mechanism of injury.
Personnel present at call
Physical findings
Vital signs; Urine output, Glasgow Coma Scale. Results of X-rays and
other investigations.
Fluids administered.
Drugs administered.
Previous Medical History.
Summary of injuries.
Disposal of patient


43



THE GOLDEN HOUR

starts at the time of injury. So most trauma teams will have
about 30 minutes to accomplish this aim and should work towards
achieving this goal (saving life).






























44



A An ng gi io oe ed de em ma a

Angioedema is is clinically characterized by :
Acute onset of well demarcated cutaneous swelling of the face and tongue,
edema of the mucous membranes of the mouth, throat, or abdominal viscera,
or nonpitting edema of the hands and feet ( often asymmetric ).


Severe Angioedema mandates urgent cricothyrotomy (ACE) inhibitor-induced angioedema

It is either hereditary, allergic, or idiopathic.

Hereditary angioedema is an autosomal dominant trait associated with a
deficiency of serum inhibitor of the activated first component (C1).

Allergic angeoedema can result from medications or contrast agents,
environmental antiagens such as hymenoptera, or local trauma.

Complications range from dysphagia and dysphonia to respiratory distress,
airway obstruction, and death.
Angiotensin converting enzyme (ACE) inhibitor-induced angioedema has a
predilection for involvementof the lips, tongue, and glottis and like hereditary
angioedema, is often refractory to medical the



(ACE) inhibitor-induced angioedema Hereditary angioedema


45


Emergency department treatment and disposition

Airway protection remains the primary focus of emergency treatment.

Frequent reassessment and early airway management is mandatory as
deterioration due to edema formation can be rapid.

Medical therapy includes steroids, H
1
and H
2
histamine blockers, and s/c or
i/m epinephrine.

Chronic angioedema responds better to corticosteroids and H
2
blockers .

Disposition depends on the severity and resolution of symptoms.
I) Patients with symptomatic improvement or showing no worsening after 4
hours of observation may be discharged home. Discontinue suspected
medications.
II) Airway involvement requires admission to a monitored environment with
surgical airway equipments at bedside.

ADVICE:

1- Do not underestimate the degree of airway involvement, act early to
preserve airway patency.

2- Angioedema can also cause gastrointestinal and neurologic involvement.

3- Early response to medical intervention does not preclude rebound of
symptoms to a greater extent than at presentation.

4- Patients who have been using ACE inhibitors for months or years can still
develop angioedema from these agents.















46



E Ey ye e i in nj ju ur ri ie es s


An injury to the eye or its surrounding tissues is the most common cause for
attendance at an eye hospital emergency department.

History
The history of how the injury was sustained is crucial, as it gives clues as to
what to look for during the examination. If there is a history of any high
velocity injury (particularly a hammer and chisel injury) or if glass was
involved in the injury, then a penetrating injury must be strongly
suspected and excluded.
If there has been a forceful blunt injury (such as a punch), signs of a
blowout fracture should be sought. The
circumstances of the injury must be elicited and carefully recorded, as these
may have important medicolegal implications. It may not be possible to get
an accurate and reliable history from children if an injury is not witnessed by
an adult. Such injuries should be treated with a high index of suspicion, as a
penetrating eye injury may be present.

Common types of eye injury
Corneal abrasions
Foreign bodies
Radiation damage
Chemical damage
Blunt injuries with hyphaema
Penetrating injuries

Examination
A good examination is vital if there is a history of eye injury.
Specific signs must be looked for or they will be missed. It is
vital to test the visual acuity, both to establish a baseline value
and to alert the examiner to the possibility of further problems.
However, an acuity of 6/6 does not necessarily exclude serious
problemseven a penetrating injury. The visual acuity may also
have considerable medicolegal implications. Local anaesthetic
may need to be used to obtain a good view, and fluorescein
must be used to ensure no abrasions are missed.



47



Corneal abrasions
Corneal abrasions are the most common result of blunt injury. They may
follow injuries with foreign bodies, fingernails, or twigs. Abrasions will be
missed if fluorescein is not instilled.
Treatment
The aims of treatment are to ensure healing of the defect, prevent infection,
and relieve pain.
Small abrasions can be treated with chloramphenicol ointment twice a day
or eye drops four times a day until the eye has healed and symptoms are
gone. Ointment blurs the vision more but provides longer lasting lubrication
compared with eye drops. This will help prevent infection, lubricate the eye
surface, and reduce discomfort.
Larger or more uncomfortable abrasions a double eye pad can be used
with chloramphenicol ointment for a day or so until symptoms improve. If the
eye becomes uncomfortable with the pad, it can be removed and the eye
treated as per a small abrasion. The pad must be firm enough to keep the
eyelid shut. Ointment or drops can then continue. If there is significant pain
cycloplegic eye drops (cyclopentolate 1% or homatropine 2%) may help,
although this will further blur the vision. Oral analgesia such as paracetamol
or stronger non-steroidal anti-inflammatory drugs can also be used. Patients
should be told to seek futher ophthalmological help if the eye continues to be
painful, vision is blurred, or the eye develops a purulent discharge.
Recurrent abrasionsOccasionally the corneal epithelium may repeatedly
break down where there has been a previous injury or there is an inherently
weak adhesion between the epithelial cells and the basement membrane.
These recurrences usually occur at night when there is little secretionof tears
and the epithelium may be torn off. Treatment is long term and entails drops
during the day and ointment at night to lubricate the eye. Occasionally, a
surgical procedure (such as epithelial debridement or corneal stromal
puncture) may be carried out to enhance the adhesion between the
epithelium and the underlying basement membrane.

Foreign bodies
It is important to identify and remove conjunctival and
cornealforeign bodies. A patient may not recall a foreign
body having entered the eye, so it is essential to be
on the lookout for a foreign body if a patient has an
uncomfortable red eye. It maybe necessary to use
local anaesthetic both to examine the eye and to
remove the foreign body. Although patients often
request them, local anaesthetics should never be
given to patients to use themselves, because they
48


impede healing and further injury may occur to an
anaesthetized eye. Small loose conjunctival foreign bodies can be removed
with the edge of a tissue or a cotton wool bud or they can be washed out with
water. The upper lid must be everted to exclude a subtarsal foreign body,
particularly if there are corneal scratches or a continuing feeling that a
foreign body is present. However, this should not be done if a penetrating
injury is suspected. Corneal foreign bodies are often more difficult to remove
if they are metallic, because they are often rusted on. They must be
removed as they will prevent healing and rust may permanently stain the
cornea. A cotton wool bud or the edge of a piece of cardboard can be used. If
this does not work, a needle tip (or special rotary drill) can be used, but great
care must be taken when using these as the eye may easily be damaged. If
there is any doubt, these patients should be referred to an ophthalmologist.
When the foreign body has been removed any remaining epithelial defect can
be treated as an abrasion.
Removal of a foreign body
Use local anaesthetic
If the foreign body is loose, irrigate the eye
If the foreign body is adherent, use a cotton wool bud or the
edge of a piece of cardboard

Radiation damage
The most common form of radiation damage occurs when welding has been
carried out without adequate shielding of the eye. The corneal epithelium is
damaged by the ultraviolet rays and the patient typically presents with painful,
weeping eyes some hours after welding. (This condition is commonly known
as arc eye.) Radiation damage can also occur after exposure to large
amounts of reflected sunlight (for example, snow blindness) or after
ultraviolet light exposure in tanning machines. Treatment is as for a corneal
abrasion.

Chemical damage
All chemical eye injuries are potentially blinding injuries. If
chemicals are splashed into the eye, the eye and the conjunctival sacs
(fornices) should be washed out immediately
with copious amounts of water. Acute management should consist of the
three Is: Irrigate, Irrigate, Irrigate. Alkalis are
particularly damaging, and any loose bits such as
lime should be removed from the conjunctival sac,
with the aid of local anaesthetic if necessary.
The patient should then be referre immediately to
an ophthalmic department. If there is any doubt,
irrigation should be continued for as long as
possible with several litres of fluid.

49



Dealing with chemical damage to the eye
Immediately wash out eye with water
Remove loose particles
Refer patient to ophthalmic department
Beware alkalis
Blunt injuries
If a large object (such as a football) hits the eye most of the impact is usually
taken by the orbital margin. If a smaller object (such as a squash ball) hits
the area the eye itself may take most of the impact. Haemorrhage may
occur and a collection of blood may be plainly visible in the anterior
chamber of the eye (hyphaema). Patients who sustain such injuries need to
be reviewed at an eye unit as the pressure in the eye may rise, and further
haemorrhages may require surgical intervention. Haemorrhage may also
occur into the vitreous or in the retina, and this may be accompanied by a
retinal detachment. All patients with visual impairment after blunt injury
should be seen in an ophthalmic department
. The iris may also be damaged and the pupil may react poorly to light.
This is particularly important in a patient with an associated head injury, as
this may be interpreted as (or mask) the dilated pupil that is suggestive of
an acute extradural haematoma. The lens may be damaged or dislocated
and acataract may develop.
Damage to the drainage angle of the eye (which cannot be seen without a
Mirror contact lens and a slit lamp microscope) increases the chances of
glaucoma developing in later life. If the force of impact is transmitted to the
orbit, an orbital fracture may occur (usually in the floor, which is thin and has
little support). Clues to the presence of an inferior blowout fracture include
diplopia, a recessed eye, defective eye movements (especially vertical), an
ipsilateral nose bleed, and diminished sensation over the distribution of the
infraorbital nerve. These patients need to be seen in an ophthalmic
department for assessment and treatment of eye damage, and a maxillofacial
department for repair of the orbital floor.

Penetrating injuries and eyelid lacerations
Lacerations of the eyelids need specialist attention if:
The lid margins have been tornthese must be sewn together accurately
The lacrimal ducts have been damagedthe laceration may involve the
medial ends of the eyelids and it is likely that the lacrimal canaliculi will have
been damaged, and these may need to be reapposed under the operating
microscope
There is any suspicion of a foreign body or penetrating eyelid injury
objects may easily penetrate the orbit and even the cranial cavity through the
orbit.
50


Penetrating injuries of the eye can be missed because they may seal
themselves, and the signs of abnormality are
subtle. Any history of a high velocity injury (particularly a hammer and chisel
injury) should lead one strongly to suspect a penetrating injury. In that case,
the eye should be examined very gently and no pressure should be brought
to bear on the globe. It is possible to cause prolapse of intraocular
contents and irreversible damage if the eye and orbit are not examined
with great care.
Signs to look for include a distorted pupil, cataract, prolapsed black uveal
tissue on the ocular surface, and vitreous haemorrhage. The pupil should be
dilated (if there is no head injury) and a thorough search made for an
intraocular foreign body. If there is a suspicion of an intraocular or orbital
foreign body then orbital x ray photographs, with the eye in up and down
gaze, should be taken. If the eye is clearly perforated it should be protected
from any pressure by placing a shield over the eye, and the patient should be
sent immediately to the nearest eye department.
Sympathetic ophthalmia, in which chronic inflammation develops in the
normal fellow eye, is a potentially serious complication of any severe
penetrating eye injury. The risk of this increases if a penetrating eye injury is
left untreated. All penetrating eye injuries should receive immediate
specialist ophthalmic management without delay.


R
R
e
e
d
d
e
e
y
y
e
e

The red eye is one of the most common ophthalmic
problems presenting to the general practitioner.
An accurate history is important and should pay
particular attention to vision, degree, and type of
discomfort and the presence of a discharge. The
history, and a good examination, will usually permit
the diagnosis to be made without specialist ophthalmic
equipment.
Symptoms and signs
The most important symptoms are pain and visual loss;
these suggest serious conditions such as
corneal ulceration, iritis,and acute glaucoma.
A purulent discharge suggests bacterial
conjunctivitis; a clear discharge suggests a
viral or allergic cause. A gritty sensation is
common in conjunctivitis, but a foreign body
must be excluded, particularly if only one
eye is affected. Itching is a common symptom
in allergic eye disease, blepharitis, and topical drop hypersensitivity.
51



Corneal abrasions will be missed if fluorescein is not used

Equipment for an eye examination
Snellen eye chart
Bright torch or ophthalmoscope with blue filter
Magnifying aidfor example, loupe
Paper clip to help lid eversion
Fluorescein impregnated strips or eye drops
Conjunctivitis
Conjunctivitis is one of the most common causes of an
uncomfortable red eye. Conjunctivitis itself has many causes,
including bacteria, viruses, Chlamydia, and allergies.
Bacterial conjunctivitis
HistoryThe patient usually has discomfort and a purulent
discharge in one eye that characteristically
spreads to the other eye. The eye may be
difficult to open in the morning because the
discharge sticks the lashes together. There
may be a history of contact with a person
with similar symptoms.
ExaminationThe vision should be normal after
The discharge has been blinked clear of the
cornea. The discharge usually is mucopurulent and there is uniform
engorgement of all the conjunctival blood vessels. When fluorescein drops
are instilled in the eye there is no staining of the cornea.
ManagementTopical antibiotic eye drops (for example,
chloramphenicol) should be instilled every two hours for the
first 24 hours to hasten recovery, decreasing to four times a day
for one week. Chloramphenicol ointment applied at night may
also increase comfort and reduce the stickiness of the eyelids in
the morning. Patients should be advised about general hygiene
measures; for example, not sharing face towels.
Viral conjunctivitis
Viral conjunctivitis commonly is associated with upper
respiratory tract infections and is usually caused by an
adenovirus. This is the type of conjunctivitis
that occurs in epidemics of pink eye.
HistoryThe patient normally complains
of both eyes being gritty and uncomfortable,
although symptoms may begin in one eye.
There may be associated symptoms of
a cold and a cough. The discharge is usually
watery. Viral conjunctivitis usually lasts longer
52


than bacterial conjunctivitis and may go on for many weeks; patients need
to be informed of this. Photophobia and discomfort may be
severe if the patient goes on to develop discrete corneal
opacities.
ExaminationBoth eyes are red with diffuse conjunctival injection
(engorged conjunctival vessels) and there may be a clear discharge. Small
white lymphoid aggregations may be present on the conjunctiva (follicles).
Small focal areas of corneal inflammation with erosions and associated
opacities may give rise to pronounced symptoms, but these are difficult to
see without high magnification. There may be associated head and neck
lymphadenopathy with marked pre-auricular lymphadenopathy.
ManagementViral conjunctivitis is
generally a self Limiting condition, but
antibiotic eye drops (for example,
chloramphenicol) provide symptomatic
relief and help prevent secondary bacterial
infection. Viral conjunctivitis is extremely
contagious, and strict hygiene measures
are important for both the patient and the
doctor; for example, washing of hands and
sterilising of instruments. The period of
infection is often longer than with bacterial pathogens and patients should be
warned that symptoms may be present for several weeks. In some patients
the infection may have a chronic, protracted course and steroid eye drops
may be indicated if the corneal lesions and symptoms are persistent.
Steroids must only be prescribed with ophthalmological supervision, because
of the real danger of causing cataract or irreversible glaucomatous damage.
Furthermore, if long term steroids are required, patients should remain under
continuous ophthalmological supervision.

Topical steroids should not be prescribed or continued without continuous
ophthalmological supervision potentially blinding complications may occur

Chlamydial conjunctivitis
HistoryPatients usually are young with a
history of a chronicbilateral conjunctivitis with a
mucopurulent discharge. There may be
associated symptoms of venereal disease.
Patients generally do not volunteer genitourinary
symptoms when presenting with conjunctivitis; these need to be elicited
through questioning.
ExaminationThere is bilateral diffuse conjunctival injection with a
mucopurulent discharge. There are many lymphoid aggregates in the
53


conjunctiva (follicles). The cornea usually is involved (keratitis) and an
infiltrate of the upper cornea (pannus) may be seen.
ManagementThe diagnosis is often difficult and special bacteriological
tests may be necessary to confirm the clinical suspicions. Treatment with oral
tetracycline or a derivative for at least one month can eradicate the problem,
but poor compliance can lead to a recurrence of symptoms. Systemic
tetracycline can affect developing teeth and bones and should not be used in
children or pregnant women. Associated venereal disease should also be
treated, and it is important to check the partner for symptoms or signs of
venereal disease (affected females may be asymptomatic). It often is helpful
to discuss cases with a genitourinary specialistbefore commencing treatment,
so that all relevant microbiological tests can be performed at an early stage.
In developing countries, infection by Chlamydia trachomatis results in severe
scarring of the conjunctiva and the underlying tarsal plate. These cicatricial
changes cause the upper eyelidsto turn in (entropion) and permanently scar
the already damaged cornea. Worldwide, trachoma is still one of the major
causes of blindness.

Conjunctivitis in infants
Conjunctivitis in young children is extremely importantbecause the eye
defences are immature and a severe conjunctivitis with membrane formation
and bleeding may occur. Serious corneal disease and blindness may result.
Conjunctivitis in an infant less than one month old (ophthalmia
neonatorum) is a notifiable disease. Such babies must be seen in an eye
department so that special cultures can be taken and appropriate treatment
given. Venereal disease in the parents must be excluded.

Allergic conjunctivitis
HistoryThe main feature of allergic conjunctivitis is itching. Both eyes
usually are affected and there may be a clear discharge. There may be a
family history of atopy or recent contact with chemicals or eye drops. Similar
symptoms may have occurred in the same season in previous years. It is
important to differentiate between an acute allergic reaction and a more long
term chronic allergic eye disease.
ExaminationThe conjunctivae are diffusely injected and may be
oedematous (chemosis). The discharge is clear and stringy. Because of the
fibrous septa that tether the eyelid (tarsal) conjunctivae, oedema results in
round swellings (papillae). When these are large they are referred to as
cobblestones.
ManagementTopical antihistamine and vasoconstrictor eye drops provide
short term relief. Eye drops that prevent degranulation of mast cells also are
useful, but they may need to be used for several weeks or months to achieve
maximal effect. Oral antihistamines may also be used, particularly the newer
compounds that cause less sedation. Topical steroids are effective but
54


should not be used without regular ophthalmological supervision because of
the risk of steroid induced cataracts and glaucoma, which may irreversibly
damage vision.
Cases of allergic eye disease in association with severe eczema will often
need careful combined ophthalmological and dermatological management.

Corneal ulceration
Corneal ulcers may be caused by bacterial, viral, or fungal infections; these
may occur as primary events or may be secondary to an event that has
compromised the eyefor example, abrasion, wearing contact lenses, or use
of topical steroids.
HistoryPain usually is a prominent feature as the cornea is an exquisitely
sensitive structure, although this is not so when corneal sensation is
impaired; for example, after herpes zoster ophthalmicus. Indeed, this lack of
sensory innervation may be the cause of the ulceration. There may be clues
such as similar past attacks, facial cold sores, a recent abrasion, or the
wearing of contact lenses.
ExaminationVisual acuity depends on the location and size of the ulcer,
and normal visual acuity does not exclude an ulcer. There may be a watery
discharge due to reflex lacrimation or a mucopurulent discharge in bacterial
ulcers. Conjunctival injection may be generalised or localised if the ulcer is
peripheral,giving a clue to its presence. Fluorescein must be used or an ulcer
easily may be missed. Certain types of corneal ulceration are characteristic;
for example, dendritic lesions of the corneal epithelium usually are caused by
infection with the herpes simplex virus. If there is inflammation in the anterior
chamber there may be a collection of pus present (hypopyon). The upper
eyelid must be everted or a subtarsal foreign body causing corneal
ulceration may be missed. Patients with subtarsal foreign bodies sometimes
do not recollect anything entering the eye.
ManagementPatients with corneal ulceration should be referred urgently to
an eye department or the eye may be lost. Management depends on the
cause of the ulceration. The diagnosis usually will be made on the clinical
appearance. The appropriate swabs and cultures should be arranged to try
to identify the causative organism. Intensive treatment then is started with
drops and ointment of broad spectrum antibiotics until the organisms and
their sensitivities to various antibiotics are known. Injections of antibiotics into
the subconjunctival space may be given to increase local concentrations of
the drugs.

Topical antiviral therapy should be used for herpetic infections of the cornea.
Cycloplegic drops are used to relieve pain resulting from spasm of the ciliary
muscle, and as they are also mydriatics they prevent adhesion of the iris to
the lens (posterior synechiae).
55


Topical steroids may be used to reduce local inflammatory damage not
caused by direct infection, but the indications for their use are specific and
they should not be used without ophthalmological supervision.

Acute angle closure glaucoma
Acute angle closure glaucoma always should be considered in a patient over
the age of 50 with a painful red eye. The diagnosis must not be missed or the
eye will be damaged permanently.
HistoryThe attack usually comes on quite quickly, characteristically in the
evening, when the pupil becomes semidilated. There is pain in one eye,
which can be extremely severe and may be accompanied by vomiting. The
patient complains of impaired vision and haloes around lights due to oedema
of the cornea. The patient may have had similar attacks in the past which
were relieved by going to sleep (the pupil constricts during sleep, so relieving
the attack). The patient may have needed reading glasses earlier in life. A
patient with acute angle closure glaucoma may be systemically unwell, with
severe headache, nausea, and vomiting, and can be misdiagnosed as an
acute abdominal or neurosurgical emergency. Acute angle closure glaucoma
also may present in patients immediately postoperatively after general
anaesthesia, and in patients receiving nebulised drugs (salbutamol and
ipratropium bromide) for pulmonary disease.
ExaminationThe eye is inflamed and tender. The cornea is hazy and the
pupil is semidilated and fixed. Vision is impaired according to the state of the
cornea. On gentle palpation the eye feels harder than the other eye. The
anterior chamber seems shallower than usual, with the iris being close to the
cornea. If the patient is seen after the resolution of an attack the signs may
have disappeared, hence the importance of the history.

Features of acute angle closure glaucoma
Pain Hazy cornea
Haloes around lights Age more than 50
Impaired vision Eye feels hard
Fixed semidilated pupil Unilateral

ManagementUrgent referral to hospital is required.
Emergency treatment is needed if the sight of the eye is to be preserved. If it
is not possible to get the patient to hospital straight away, intravenous
acetazolamide 500 mg should be given, and pilocarpine 4% should be
instilled in the eye to constrict the pupil.
First the pressure must be brought down medically and then a hole made in
the iris with a laser (iridotomy) or surgically (iridectomy) to restore normal
aqueous flow. The other eye should be treated prophylactically in a similar
way. If treatment is delayed, adhesions may form between the iris and the
56


cornea (peripheral anterior synechiae) or the trabecular meshwork may be
irreversibly damaged necessitating a full surgical drainage procedure.

Subconjunctival haemorrhage
HistoryThe patient usually presents with a
red eye which is comfortable and without any
visual disturbance. It is usually the appearance
of the eye that has made the patient seek attention.
If there is a history of trauma, or a red eye after hammering or chiselling, then
ocular injury and an intraocular foreign body must be excluded.
Subconjunctival haemorrhages are often seen on the labour ward post
partum.
ExaminationThere is a localised area of
Subconjunctival blood that is usually relatively
well demarcated. There is no discharge or
conjunctival reaction. Look for skin bruising
and evidence of a blood dyscrasia.
ManagementIt is worth checking the blood
pressure to exclude hypertension. If there are
no other abnormalities the patient should be
reassured and told the redness may take
several weeks to fade. If patients are anticoagulated with warfarin then
the coagulation profile (international normalised ratio, INR) should be
checked. If abnormal bruising of the skin is present then consider checking
the full blood count and platelets












57



H Hy yp pe er rt te en ns si io on n & &h hy yp pe er rt te en ns si iv ve e e em me er rg ge en nc ci ie es s

Definition
Systolic Blood Pressure > 140 mmHg, Diastolic Blood Pressure >
90mmHg.
Hypertensive emergencies: SBP > 200mmHg & DBP > 120
mmHg,with new or progressive end-organ damage(CNS, CVS or
Renal)
Hypertensive Urgency: Severe hypertension without end-organ
damage.

Symptoms & signs:
Mild to moderate hypertension is asymptomatic until end organ
damage occurs.

Neurologic symptoms
o Headache.
o Nausea & vomiting.
o Blurring of vision.
o Confusion.
o Seizures.
o Papilledema.

Cardiovascular

o Chest pain ( ischemic )
o Acute aortic dissection
- Severe tearing chest pain
- Pulse deficit
- New aortic regurgitation murmur
o Lt. Ventricular failure
- Shortness of breath with orthopnia
- Third heart sound
- Tachycardia
- End-respiratory crackles wheezes

Renal
- Lower limb odema
- Oliguria
- High JVP
- Weakness
- Nausea & vomiting
58


Diagnosis
Measure BP in both arms at least twice,5 min. apart.
Examine pt. carefully to rule out end-organ damage (
i.e.Encephaopathy, Heart failure, Chest pain, Fundal Hge
and or Ppilledema etc.)
ECG if cardiac symptoms are present.
CBC if BP is very high to check for microangiopathic hemolytic
of malignant hypertension
Urea, creatinine and electrolytes to check for renal impairment (
as sign for end-organ damage or as a cause of hypertension)
Urine analysis to investigate for secondary causes of
hypertension specially if patient has renal impairment
CXR: Cardiomegaly, pulmonary edema or aortic dissection

Treatment:
I. Hypertensive emergency
(very high BP with end-organ damage )

1) Sodium nitroprusside
- patient needs continuous monitoring
- solution and bottle should be covered by foil and should be
changed every 6h
- start with 0.25 /kg/min and titrate up to of 1 /kg/min and reduce
the dose if BP is acceptable
- do not allow BP to fall more than 25% of pre-treatment BP
- CONTRA-IDICATED IN PRESENCE OF RENAL FAILURE
2)Hydralazine IV infusion
- Used if nitroprusside is contra-indicated (i.e., renal failure)
- May give 5-10 mg iv, slowly over 10 min. or im
- Do not allow BP to drop more than 25% of the pre-treatment BP
- DOSE MAY BE REPEATED IF NO EFFECT FROM FIRST DOSE
- If BP drops to reasonable level start infusion at 1-10 mg/hour and
measure BP every 5-10 min, titrate dose up and down (do not
allow BP to drop to less than150/100 )
- May start oral and discontinue IV if reasonable BP is attained.

3)Nitroglycerine infusion
- Used if nitroglycerine or hydralazine are contra-indicated
- Drug of choice if cardiac symptoms or shortness of breath are
present ( CHF or IHD )
- Start infusion at 5g/min. and titrate up until adequate control is
achieved ( maximum dose is 100 g/min.)

59


II. Hypertensive urgency
( Very high BP with no end-organ damage )

No urgency to lower BP to near normal in emergency
department, BP can be normalized in 24-48hs
Ask patient if he (she) missed his (her) medication, if yes
resume their medication with possibility of increasing the
dose.
Always aim for monothrapy, add other drug if no response
with maximum dose of one drug or if side effect of the drug
arises
The following are available option:

Nifedipine ( Adalat ) should not be given
sublingually
May give Nifedipine retard 20mg BID ( maximum
dose 40 mg TID ), if unavailable give Nifedipine
10mg TID ( maximum dose 20mg TID )
If no contra-indicated to beta blocker (renal failure,
bradycardia, or bronchial asthma ) may give
Atenolol( Cardol,Hypoten,or Tenormin) 50 -100mg
OD
If no contra-indication to ACEI (Renal artery
stenosis, hyperkalemia), may give Captopril(
Capoten) 12.5mg-50mg TID
Indipamide (Natrilix) 205mg is good add on drug to
Captopril
Furosimide (Lasix) is good diuretic if edema is
present (use initially small dose 20mg OD to BID














60



A Ac cu ut te e P Pu ul lm mo on na ar ry y E Ed de em ma a

o It is one of the most common medical emergencies and very life
threatening.
o Signs and symptoms represent the transference of fluids from the
pulmonary capillaries into the pulmonary interstitial and alveolar air
spaces.
o Causes:
Cardiac:
MI / Ischaemia.
Valvular disease (miteral, aortic stenosis).
Cardiomyopathy.
Pericardial effusion.
Constrictive pericarditis.
Hypertensive emergencies.

Non- cardiac:
Sepsis. Trauma.
Inhalation injuries. Near drowning.
Drug (e.g. opioids,
salicylates).
Inhaled toxins.
Renal failure. DIC.
High altitudes. Airway obstruction (croup,
FB).
Aspiration pneumonia. Lung re-expansion.
ARDS.

Presentation:
Dyspnea, weakness, anxiety and sweating.
Tachypnea, orthopnea, tachycardia and thoracic oppression.
Cold extremities with cyanosis or not.
Cough with a frothy or pink sputum.
Excessive use of accessory muscles of respiration.
Crackles and wheezing.
Cardiogenic causes may result in cough, jugular venous distension,
peripheral oedema and cardiac murmur or rub.

Differential diagnosis:

COPD. Pulmonary embolism.
Asthma. ARDS.
Pneumonia. MI.
Cardiac Tamponade. Restrictive lung disease.

61


Diagnosis:
Pulse oximeter: may reveal hypoxemia.
Chest x-ray:
Mild congestion may result in cephalization of pulmonary vessels,
pleural effusion.
Interstitial oedema (Kerley B lines) i.e. horizontal lines seen laterally in
the lower zones, 2cm long at least, that, on the contrary of blood
vessels reach the lung edge.
Alveolar oedema (can be observed with its butterfly pattern)
characterized by the central predominance of shadows with a clear
zone at periphery lobes.
Enlarged cardiac, silhouette may be present in chronic CHF.
ABG:
May reveal hypoxemia ( PO
2
) and respiratory alkalosis (PCO
2
)
due to Tachypnea.
Respiratory acidosis ( PCO
2
) is an ominous sign of tiring and
impending respiratory failure.
P02 values <50 mmHg and Pco2>50 mmHg denotes severity and the
need of mechanical ventilation.

ECG: vent, hypertrophy, conduction abnormalities and Ischaemia /
infarction.

Blood studies: CBC, Electrolytes, BUN and Creatinine.

Treatment:
(O2, preload reducers, diuretics, after load reducers and in tropic
agents).
1. Put the patient in sitting position with legs dangling over the side of the
bed in order to make perspiration easier and to reduce venous return.
2. Administer 100% O2 by mask:
If hypoxia persist despite O2 therapy, continuous positive
airway pressure (CPAP) or biphasic airway pressure should
be applied.
Immediate intubation is indicated for unconscious or visibly
tiring patients.
3. Nitroglycerine:
o Decrease hydrostatic pressure by
venodilatation.
o 0.4 mg SL (can be repeated twice every 5
minutes as long as there is no important
decrease in BP
62


o If there is no response or ECG show ischaemia
or infraction given IV drips (10 mcg / min.) and
titrated.


4. Furosemide (40-80 mg IV bolus) causes venodilatation, decrease
after load by volume reduction.
5. Morphine (2-3 mg IV) and repeat as needed reduce anxiety,
sympathetic activity, venodilatation, its use is controversial, may
cause respiratory depression and add little to O2, diuretics and
nitrates.
6. In tropes( congestion by cardiac output).
Dopamine (5-10 mcg / kg / min.) and titrate to a systolic BP 90-100
mmHg.
Dobutamine (provided the patient is not in server Cardiogenic shock)
start 3 mcg / kg / min. and titrate to desired response.
7. Inhaled B2 agonist or aminophylline IV to treat bronchospam that may
occur in response to pul. Oedema. (Aminophylline renal blood flow,
excretion of Na, cardiac contraction, venodilatation side effects:
Tachycardia and supraventricular arrhythmia).
8. Digoxin ( 0.25 mg in a slow IV push) can be given if AF and rapid
vent. reasons is a contributory factor. The total dose 1-1.5 mg IV in
the first 24 hours.

N.B. : Non-Cardiogenic oedema : treat the underlying cause and
maintain respiratory function (diuretics are minimally helpful and
steroids have no benefit).

















63



B Ba as si ic c L Li if fe e S Su up pp po or rt t

o It is the simple procedures which prevent circulatory or respiratory
arrest or insufficiency prompt
Basic knowledge
o BLS at this level can be considered primarily a public community
responsibility.
o Our heart position is behind lower two third of the sternum with its apex to
the left in the 5
th
intercostals space mid clavicular line.
o External cardiac compression give 25% of original Cardiac Output.
o It contract around 70 times/min, every contraction ejects 70 ml of blood, so
minute Cardiac Output is around 5 L/min.
o Respiratory center is located in the brain which is stimulated by the level
of the arterial carbon dioxide.
o Adult respiratory rate is about 12-15 times/min.
Room air contain 21%O2 our expiration contain 16% O2
Definitions of death
1. Clinical death means that the heartbeat and breathing have stopped.
This process is reversible.
2. Biological death is permanent, cellular damage due to lack of
oxygen, the brain cells are the most sensitive to the lack of oxygen.
o Brain damage occurs after 4 minute of cardio-respiratory
arrest.



64


To start CPR
The patient is
- Unresponsive
- Breathlessness
- Pulselessness
Once life threatening condition recognized Chain Of Survival
( Sequences of action linked together too tightly with no gap )
should be followed


The links include the following:

Immediate recognition of cardiac arrest and activation of the
emergency response system.
Early CPR with an emphasis on chest compressions
Rapid defibrillation
Effective advanced life support
Integrated postcardiac arrest care
65




Check the following algorithm, and keep it in your mind all the time

66






67













68



69







70







71




















72




















73


N Ne ea ar r D Dr ro ow wn ni in ng g ( (S Su ub bm me er rs si io on n) )
General consideration
Drowning: Death from suffocation following submersion.
Near drowning: Survival after suffocation following submersion
Secondary drowning: Death due to complication > 24h after submersion
Wet drowning: Consists of aspiration of water into lungs causing washout of
surfactant, which results in diminished alveolar gas transfer, atelectasis and
ventilation perfusion mismatch. Non-cardiogenic pulmonary edema results from
moderate to severe aspiration.
Dry drowning : results from laryngospasm causing hypoxemia and different degree
of neurologic insult and represents up to 20% of submersion injuries.
The rapid sequence events after submersion (hypoxia, laryngospasm, fluid
aspiration, ineffective circulation, brain injury and brain death) may occur within 5-
10 minutes.
The difference in the pathophysiology of fresh water ( hypotonic ) and sea water (
hypertonic ) usually have little clinical significance in humans ,because the amount
of fluid aspirated in most patients is small. The primary effect in both instances is
disruption of vascular endothelium and dilution of pulmonary surfactant, with
resulting atelctasis and perfusion of poorly ventilated alveoli.
Hypoxia, acidosis and hypo-perfusion of vital organs are common factors accounting
for high incidence of illness and death associated with drowning.
Resuscitation can extend longer time than other cases of arrest due to hypothermia.
Clinical findings:
The victim of near-drowning may present with wide range of clinical manifestations:
Spontaneous return of consciousness often occurs in healthy individuals when
submersion is brief. Others may respond promptly to immediate artificial ventilation.
Patient with more severe near-drowning may experience frank pulmonary failure,
pulmonary edema, shock, anoxic encephalopathy, cerebral edema or cardiac arrest.
74


A few patients may be asymptomatic during the recovery period, only deteriorate as a
result of respiratory failure in the ensuing 6-24h.
SYMPTOMS & SIGNS
Patient may be unconscious, semiconscious, or awake and apprehensive.
Cyanosis.
Trismus.
Apnea,or Tachypnea
Pink froth from the mouth indicates pulmonary edema.
Tachycardia, Arrhythmia, shock and cardiac arrest.
Patient are at risk of hypothermia even in " warm water " submersion
Investigations:
CBC Leucocytosis.
Urine analysis Proteinuria, hemoglobinuria, ketonuria
ABG Hypoxemia,or combined metabolic& respiratory
acidosis.
CXR Pneumonitis or pulmonary edema.
C-spine X ray To exclude spine injury specially in diving injury
TREATMENT
Take the patient from the water to dry area, remove all wet clothes and avoid
hypothermia (cover him with blanket, warm atmosphere).
Immobilize him on long spinal board with cervical collar assuming he has spinal
injury
Resuscitation must start at scene rapidly. Do not waste time to drain water from the
victim's lungs or stomach as there is only a minimal volume of water in the lungs.(
however, if a tense, water-filled stomach prevents adequate lung expansion, place
the victim supine, perform Hemlich Maneuver ) clear the victim's mouth with finger
sweep.
Start rapid CPR, Rescue Breathing. Do not press over the abdomen or thrust as
these will make complications.
Intubate for hypoxia, poor respiratory effort, decline respiratory status.
If pulse can't be detected, start chest compression according to ACLS protocols.
Core temperature should be monitored, warmed IV. NS. and warming adjuncts
should be used if the patient is hypothermic.
Hypothermic victims in Cardiac Arrest should undergo prolonged, aggressive
resuscitation until they are normothermic or considered nonviable.
Antibiotics, steroids are not indicated for prophylactic pulmonary protection
75


Effort at " brain resuscitation" including the use of Mannitol, loop diuretics,
hypertonic saline, fluid restriction, mechanical hyperventilation,barbiturate coma,
have not shown benefit.
Prognosis:
Alert or responsive to pain at presentation will survive without neurological
deficit.
Even patient who requires CPR may have good prognosis( 25% of children with
GCS 3 survive with full neurological recovery ).
Poor prognostic indicators include fixed dilated pupils, need for cardiac
medications and GCS less than 5.
Long term sequelae include ischemic encephalopathy, aspiration pneumonia,
ARDS and chronic lung disease.





















76


M Ma an na ag ge em me en nt t O Of f C Co on nv vu ul ls si io on n
I In n E Em me er rg ge en nc cy y D De ep pa ar rt tm me en nt t

The most common cause of convulsion is Epilepsy.
Epilepsy is idiopathic in 75% of cases and secondary in 25% of cases.
Secondary causes are:
Intoxication,
Uraemia,
Cholaemia,
Eclampsia,
Alcohol.
Physiological:
Hypoxia,
Alkalosis,
Water retention,
Hypoglycaemia,
Hypocalcemia
Investigations:
CBC
ABG
Liver function
Electrolytes especially Ca
Blood sugar
History of drug addiction.
Brain activity increases so it consumes more O
2
and glucose.
All body muscle tone increased leading to respiratory insufficiency or
aspiration, which is the brain anoxia.
Sudden diaphragmatic contraction lead to vomiting and possible
aspiration, which is the main cause of death after epileptic fit.
Secondary trauma due to convulsive movement and fall down.
Muscular pain, exhaustion then sleep (post-ectal stage).


77


T Tr re ea am me en nt t O Of f T Th he e F Fi it t
Protect the patient form injury during resuscitation.
1. Airway:
Open airway, suction, protect from aspiration and put in recovery position
2. Breathing:
Supply O2 through face mask or endotracheal intubation as needed, guided by pulse
oximeter to ensure O2 saturation > 94%.
3. Circulation:
Insert peripheral line and take blood sample for the above-mentioned investigation
4. Drugs.
1. Diazepam (Valium)
o Adult: 5-10 mg/dose - repeat 5 min as needed for 3 times
o Paedia: 0.3 mg/kg/dose repeat twice every 5 minutes
In paedia, if no IV line, give valium rectally
If Diazepam fail to control the fit or after controlling the fit start
2. Phenytoin sodium
Adult: 15-20 mg/kg bolus over 20 min - repeat 10mg/kg if not controlled
Paedia: loading dose 10 mg/kg/ repeat after 2 hours 5mg/kg, infuse
1mg/kg/min
If seizures persist may need intubation
3. Phenobarbital
Adult:l15-20 mg/kg over 30 min. if persist, second dose 7mg/kg
Paedia: 2-5 mg/kg over 15 min
If seizures persist need intubation
4. Thiopentone sodium
2-3 mg/kg/dose, maintenance 1 mg/kg as needed
78


M Ma an ng ge em me en nt t O Of f
S Se ev ve er re e B Br ro on nc ch hi ia al l A As st th hm ma a
Clinical picture:
Severe shortness of breath.
Usual precipitating factors
Non-compliance with medications.
Exposure to allergens or medications.
Sinus infection(URTI)
Stress.
History
Should include prior HX, of intubation, hypoxic seizure or ICU admission.
On Examination:
1. Cannot complete one sentence
2. Respiratory rate > 25/min
3. Heart rate > 110/min
4. On auscultation, bilateral wheezes with respiratory distress
5. Arterial blood gas respiratory alkalosis, then in prolonged severe attack it
becomes acidosis
6. Treatment:
o Start -agonist ( Ventolin ) by nebulization 2.5mg every 15*20 minutes delivered
by O2, if nebulizer is not available then 4-8 puffs of ventolin is equivalent to 2.5
mg nebulized ventolin.
o Contiuous nebulization ( back to back ) is more effective than intermittent dosing.
o In young patients with severe airflow limitation (life threatening ),
subcutaneous epinephrine may be considered.
o Ipratropium bromide ( Atrovent ) 500g might be added to ventolin
nebulizer.
o Those who fail to respond to initial -agonist therapy should be given
IV or oral corticosteroids, start with methylprednisolone 125mg IV
79


then prednisone 60 mg orally q 12h, the anti-inflammatory effect
needs 6h to be manifested, it is used mainly to prevent relapse.
o Those patient on oral theophylline should be continued on oral
theophylline after checking serum level !
o Do not start IV aminophylline or oral theophylline if patient was not
taking it or he (she ) is planned for discharge.
o PO theophylline might be added if the patient is admitted to decrease
the requirement for -agonist.
o If patient fail to improve 4h after initiation of treatment, they should be
admitted.
o Those with severe hypoxia, increasing PCO2, worsen mental status or
hypoxic seizure should be intubated and mechanically ventilated.
o Treat any documented exacerbating factor, (antibiotic for sinusitis or
chest infection( Augmentine 250-500mg 12h) ,H2-blocker( ranitidine
for GERD)

Treatment of more stable patient
Intermittent Asthma
Symptoms < once/week
Night symptoms < twice/month
Normal PEF between exacerbations.
TX. Ventolin 2 puffs qid & prn. Oral steroids may be added for severe
exacerbation.
Mild persistent
Symptoms > once/week < once/day.
Night symptoms < twice/month.
PEF > 80% of predicted.
TX. Long acting -agonist (Serevent) or steroid inhaler+ PRN
( Ventolin).
Moderate persistent
Daily symptoms.
Exacerbation affects activity and sleep.
Night symptoms > once/week.
PEF 60-80% of predicted.
80


TX. Inhaled long acting -agonist+ inhaled corticosteroids.

Severe persistent
Continuous symptoms and frequent exacerbations.
Frequent nighttimes symptoms
Physical activity limited by symptoms.
PEF< 60% of predicted.
TX. Long acting -agonist ( Serevent ) + PRN ( Ventolin ) + Steroid
inhale (Fluticasone or Budesonide) + or oral steroid
SPECIAL CONSIDERATIONS
Exercise Induced Asthma
Advise patient to use Salbutamole or Cromolyn before
initiating the exercise.
Inhaled steroid should be considered with more severe and
frequent symptoms.
Asthma in pregnancy
o One third of patients worsen during pregnancy.
o -agonist have strong tocolytic effects.
o Avoid leuktrien modulator.
o Treat just like non-pregnant subjects in severe cases.
o The harmful effects of acute asthma to the mother and
the fetus seem to outweigh the potential drug adverse
effects.






81








82


H Ho ow w t to o r re ea ad d E EC CG G
P Wave : Atrial depolarization.
QRS Complex: Ventricular depolarization.
PR Interval: Conduction time from atrium to ventricles.
T Wave: Ventricular repolarization
ECG. Interpretatiion ( For arrhythmia & ischemia )
o Rhythm Regular R-R equal distance.
Irregular R-R unequal distance.
Rate If regular rhythm use 300 .
Number of big square bet.R-R
If irregular a) Count 30 big square
b) Count number of R Waves inside 30
big square
c) Number of R X 10 = HR/MIN




R Wave present or no, width must be less than 3 small
squares otherwise it is wide.




Normal Absent R (VF)
wide
83



P Wave : present or no, If no, means atrial fibrillation, junction
beat or rhythm and premature ventricular beat or rhythm.
P-R Interval: normal length 3-5 small squares.
If more than5 means heart block.
S-T Segment: It must be iso-electric. If raised or
depressed means ischemia. To say there is S-T
Segment changes,it must be raised 1mm in limb leads
or 2 mm in chest leads(v1-v6)



T Wave : increase magnitude of T (hyperacute T ) OR flat T or
inverted T all are signs of ischemia









CRITERIA FOR NORMAL ECG
Regular rhythm- Rate for adult (60-100), R & P Waves are
present with normal P-R interval (3-5 small square) , S-T segment
isoelectric and T wave upright of double size P Wave.









84


C Ca ar rd di ia ac c I Is sc ch he em mi ia a

Definition of the terms:
o Arteriosclerosis means thickening and lost elasticity.
o Atherosclerosis means arteriosclerosis plus irregular inner wall
due to fat deposits. So blood flow is reduced.
o Coronary heart disease means coronary atherosclerosis plus
angina or history of acute MI.
o Ischemic heart disease is a more general term (poor oxygen
supply to the myocardium).

RISK FACTORS:
Non-Changeable Risk factors
Heredity sex race age.
Changeable & controlable risk factors
SMOKING HYPERLIPIDEMIA DIABETES - HIGH BP.
Contributing risk factors
STRESS OBISITY - LACK OF EXERCISE.

Clinical syndromes of coronary heart disease

Variable presentation, presumptive diagnosis. Exam. May be
normal and nonspecific.
Coronary artery lesion may rapidly evolve through plaque
disruption and vessel occlusion.
Hypoxemia, shock, anemia, etc. may reduce Myocardial
oxygen supply.
Increased myocardial demandial O2 .Demand may exceed
supply capability.
Angina pectoris is transient retrosternal (crushing, pressing,
constricting or heaviness) may radiate to lt. shoulder or both,
inner of lt. arm, neck and jaw, epigastrium and back. Pain is
induced by effort or stress and lasts 2-15 min. Pain relieved by rest and/or
nitroglycerine
85


Acute myocardial infarction due to severe narrowing or complete blockage
of a diseased coronary artery. It leads to injury to myocardium then death of
the muscle. Pain is severe MAY OCCURE AT REST OR DURING
SLEEPING and may be associated with nausea and sweating. Chest pain
may be atypical not relieved by rest or nitroglycerine. Usually lasts for more
than 15 min.
It may show signs of complications ( hypotension, bradycardia, arrhythmia,
heart failure ).
Sudden cardiac death (cardiac arrest), in 80% is due to ventricular
fibrillation, 15% asystole and 5% pulseless electrical activity.
Cardiac enzymes : CK rises4-6 hours after infarction, CK-MB more
specific. SGOT and LDH will rise later on.
Echocardiogram.
ECG FINDINGS



















86



































87



































88
















Arrhythmia

















89

































90



M Ma an na ag ge em me en nt t o of f I Is sc ch he em mi ic c A At tt ta ac ck k

o Complete bed rest , ECG, CBC, Chemistry ( Cardiac enzymes),
Chest X-rays.
o O2 supply 2-5 L/min through nasal cannula or face mask.
o Aspirin 300mg.chewed.
o Isordil 5mg. sublingual 3x 3-5 min apart.
o Nitroglycerin infusion start by0.5mg/h.if SBP above 90mmHg.
o Consider Morphine 3-5mg. IV if pain still severe.
o Thrombolytic drugs in absence of contra-indications. Infuse
Streptokinase 1.5 million units over 30 min.
o Treat complications( Arrhythmia, Heart Failure, Bradycardia)
o Transfer to coronary care unit.











91


92
















































93


A Ap pp pr ro oa ac ch h T To o S Su ur rg gi ic ca al l C Ca au us se es s O Of f A Ab bd do om mi in na al l P Pa ai in n


Although abdominal pain is common and often trivial, acute and severe
pain nearly always is a symptom of intra-abdominal disease.
Abdominal pain is one of the most common presentations in
emergency department. The most important concern is to decide if
the condition requires surgical intervention or can be managed
medically
Common causes of abdominal pain are listed in the following
illustrations.

Initial Evaluation
History
Physical exam
Investigations
Sound interpretation
Diagnosis can be made most of the time by a good history and a proper
physical examination.

Investigations are usually carried out :
To confirm the diagnosis.
To exclude other diagnosis.
To asses surgical fitness for operation.
For medico-legal documentation

History (AMPLEHF)
Allergy to drug or asthma.
Medication or History of drugs taken .
Previous surgery , blood transfusion & past Medical history
Last meal & last menses in female.
Event that could have led to the problem ( in patient opinion.)
History of Present illness
Family History
Pain
The Most Important Symptom
History of pain should include:
Location ( site , radiation & reference )
Quality (character & severity )
Time (onset , Duration, course & Change in nature of Pain)
Aggravating or alleviating factors
Associated symptoms.
Other relevant symptoms of same affected system.

94


Abdominal pain ( The Dilemma )
1) Abdominal causes
2) Extra-abdominal causes
3) Metabolic & blood diseases

1) Extra-abdominal causes e.g.
Otitis media & upper respiratory tract infection specially in children.
Sudden raised intracranial pressure & intraocular pressure.
Pneumonia specially basal and in children.
Hip arthritis .

2) Metabolic & blood diseases e.g.
Diabetic keto-acidosis
Hypercalcemia
Lead poisoning
Porphyria
Sickle cell crises
Uremia & acidosis.
Is it truly difficult ?
The history and physical examination are crucial to determine the most
likely causes of an acute abdomen.
The precise location of abdominal pain and tenderness helps the
practitioner to make a differential diagnosis. Although there are many
acute abdominal conditions, only a few causes are common

3) Abdominal pain ( the key )
The location of referred abdominal pain is based on the embryological
origin of the affected organ.
The location of peritoneal irritation (somatic pain ) depends on the
anatomical position of the diseased organ.
In cases where the diagnosis is not clear, repeated physical
examination at frequent intervals will often clarify the diagnosis

Peritoneal irritation
Peritoneal irritation can be localized or generalized. Findings that are
important indications for surgery, are:
Abdominal tenderness, suggesting inflammation of an underlying
organ ::Rebound abdominal tenderness elicited by percussion, which
confirms peritoneal irritation ::Involuntary contraction of the abdominal
wall, a sign of peritoneal irritation, which presents as local guarding or
generalized rigidity.



95


Referred abdominal pain
Fore gut pain (stomach, duodenum, gall bladder) is referred to the
upper abdomen
Mid gut pain (small intestine, appendix, right colon is referred to the mid
abdomen
Hind gut pain (mid transverse, descending, sigmoid colon and rectum)
occurs in lower abdomen
Diseased retroperitoneal organs (kidney, pancreas) may present with
back pain
Ureteric pain radiates to the testicle or labia
Diaphragmatic irritation presents as shoulder tip pain.

Onset of Pain
Sudden onset pain which wakes up the patient from sleep
e.g.. perforation or strangulation of bowel
Slow insidious Onset
e.g.. Inflammation of visceral peritoneum.
Crampy or colicky pain
Biliary colic, Ureteric colic or Intestinal colic

Progression of Pain
Progression from:
Dull, aching, poorly localized character To:
Sharp, constant & better localized pain indicates involvement of Parietal
peritoneum

Associated Bowel Symptoms

CONSTIPATION
a. Progressive intestinal obstruction
from a neoplasm or inflammatory
bowel disease
b. Paralytic Ileus
c. Post Operative
d. Obstructed groin hernia

DIARRHOEA
Diarrhea with pain is mainly medical.
The following are the exceptions:
a. Obstructed Richter's Hernia
b. Gall Stone ileus
c. Superior mesenteric vascular occlusion
d. pelvic abscess
e. Spurious diarrhea in chronic faecal impaction
f. Pelvic appendicitis

96


Nausea & vomiting
Frequency of vomiting
Character of vomiting:
projectile, non-projectile or self-induced
Nature of vomiting:
a. Bilious vomiting of small bowel obstruction
b. Non-bilious vomiting in obstruction proximal to ampulla of Vater
c. Feculent vomiting in distal small gut obstruction, large bowel
obstruction , strangulation
Vomiting is very prominent in.
1. Acute gastritis,
2. Acute pancreatitis.
3. High intestinal obstruction.
4. Biliary colic & acute cholecystitis.
5. Ureteric colic.
6. Acute appendicitis. (Anorexia with pain is usually seen or infrequent
vomiting )

Relevant items in history
Past Surgical history: previous operations- leading to adhesions
Past Medical history: Sickle cell disease, Diabetes or Cancer or Renal
failure
Menstrual History in females
(i) Missed period- ectopic pregnancy
(ii) Mid of period-ovulation pain (Mittel- schmetz)
(iii) With heavy periods- endometriosis
Family history of colon cancer, any other malignancy or inflammatory
bowel disease

Physical examination

Look , Feel , Listen

When doing a physical examination:
Determine the vital signs
Rapid respiration may indicate pneumonia
Tachycardia and hypotension indicate patient decompensation
Irregular pulse (AF, POSSIBLE MESENTERIC ISCHEMIA)
Temperature is elevated in gastrointestinal perforation and
normal in gastrointestinal obstruction
Look for abdominal distension
Percuss to differentiate gas from liquid

97


Palpate the abdomen
Start away from the site of tenderness
Check for masses or tumors
Determine the site of maximum tenderness
Check for abdominal rigidity
Guarding- involuntary spasm of muscles during palpation
Rigidity- when abdominal muscles are tense & board-like. Indicates
usually surgical cause.
Listen for bowel sounds
Absence is a sign of peritonitis or ileus
High pitched tinkling indicates obstruction
Always examine:
Groin for incarcerated hernia
Rectum for signs of trauma, abscess, obstruction
Vagina for pelvic abscess, ectopic pregnancy, distended pouch of
Douglas.
Abdominal examination is never complete without
back ,PR & hernial orifices exam.

Helping examples
a. Anxious Patient lying motionless:
(i) Acute appendicitis
(ii) Peritonitis
b. Rolling in bed & restless:
(i) Ureteric Colic
(ii) Intestinal colic
c. Writhing in Pain:
Mesenteric Ischemia
d. Bending Forward: stooping
Pancreatitis
e. Jaundiced:
CBD obstruction
f. Dehydrated
(i) Peritonitis
(ii) Small Bowel obstruction
Ruptured AAA or ectopic pregnancy can lead to
-Pallor
-Hypotension
-Tachycardia
-Tachypnea

Low grade temp. is seen with
- Appendicitis
- Acute cholecystitis

98


High grade temp. is seen with
- Salpingitis
- Abscess , pyelonephritis

Very High Grade Temp .with increasing lethargy seen in
- Imminent septic shock
- Peritonitis
- Acute cholangitis
- Pyonephrosis

Systemic Examination

Cardiopulmonary examination
Check for:
- Possible MI
- Basal Pneumonia
- Pleural Effusion

Abdominal examination
-Scaphoid or flat in peptic ulcer
- Distended in ascitis or intestinal obstruction
-Visible peristalsis in a thin or malnourished patient (with obstruction)
-Erythema or discoloration
a. Peri-umbilical - Cullen sign
b. Inguinal Fox sign
c. Flanks - Grey Turner sign
Seen in Hemorrhagic pancreatitis
or any other cause of haemoperitoneum



Peri-umbilical - Cullen sign and Flanks - Grey Turner sign



99



TENDERNESS
Local Right Iliac Fossa tenderness:
a. Acute appendicitis
b. Acute Salpingitis in females
c. Amoebiasis of Caecum

Low grade, poorly localized tenderness:
Intestinal Obstruction
Tenderness out of proportion to examination:
a. Mesenteric Ischemia
b. Acute Pancreatitis
Flank Tenderness:
a. Perinephric Abscess
b. Retrocaecal Appendicitis
Rovsings Sign in Acute Appendicitis
Obturator Sign in Pelvic Appendicitis

Psoas Sign
- Retrocaecal appendicitis
- Crohns Disease
- Perinephric Abscess

Murphy's sign in Acute Cholecystitis

Thumping tenderness over lower ribs in inflammation of
-Diaphragm
- liver or spleen

.Pulsatile Abdominal Mass with Hypotension
Leaking AAA

.Cutaneous Hyperesthesia
Indicates involvement of Parietal Peritoneum

Per Rectal Examination:
- tenderness
- indurations
- mass.
- frank blood

Per Vaginal Examination
- Bleeding
- Discharge
- Cervical motion tenderness
- Adnexial masses or tenderness
- Uterine Size or Contour
100



Non-specific abdominal pain
It is the most common cause of abdominal pain in late childhood and
early adolescence. It is a colicky pain with some localization that
becomes worse after meals. Bowel sounds may be increased and a
palpable mass of feces may be present in right or left iliac fossa. The
causes commonly are constipation, irritable bowel and chronic spasm.
The treatment consists of antispasmodics

INVESTIGATIONS
Laboratory
Complete Blood Count with differential
Blood sugar.
Electrolyte ,Blood Urea , Creatinine
Urine dipstick
Amylase or Lipase
Liver Function Test

Radiology
1) Upright X ray chest for
- Basal Pneumonia
- Ruptured Esophagus
- Elevated Hemi- diaphragm
- Free Gas under diaphragm

2) Abdominal X ray film
Air-Fluid Levels
- Stones
- Ascites
- Eggshell calcification in AAA
- Air in Biliary tree.
- Obliteration of Psoas Shadow in retro- peritoneal disease
- Right lower quadrant sentinel loop in acute appendicitis
Other Investigations
- USG
- CT abdomen for AAA, Pancreatic disease, or ureteric colic (non-
Contrast)
- IVU
- Mesenteric Angiography for Ischemia, Hemorrhage



101


D Di ia ab be et ti ic c K Ke et to oa ac ci id do os si is s

Precipitating factors
Intercurrent medical illness (60%)
Omission of treatment
Emotional factors and stress
FEATURES:
Nausea, vomiting and abdominal pain.( mainly in children)
Unexplained tachycardia
Dehydration
Kaussmul respiratory pattern
Pain, coma and shock.

LABORATORY FINDING
Blood Sugar 500-600 mg/dl
15% could be less than 350 mg/dl
Anion gap is high.
Metabolic acidosis,
Na could be low
K could be high,
Mg is low, and low pH
S. creatinin is elevated
Positive ketones in urine
TREATMENT
Insulin
0.1 unit/kg IV (10 UNITS) Regular insulin
0.1 unit/kg 1hour after
Then follow the insulin infusion protocol
1- Standard insulin conc. 1 unit Regular insulin/10ml NS ( 25units
mixed with 250 ml NS )
2- Capillary glucose measured hourly for the first 6-8 hours while
receiving insulin infusion.
If Bl S. is stable, less frequent monitoring (every 2 hours) is acceptable.

3- Algorithm:

Capillary BS Action
> 350
6 units/hour
301-350 5units/hour
251-300 4 units/hour
201-250 3 units/hour
151-200 2 units/hour
100-150 1 unit/hour
102



If the blood sugar is still very high, not responding to the above
mentioned dose, its dose can be doubled.
If blood sugar reduction is more than 100-150 mg/hour, the dose of
infused insulin should be reduced.

Fluid replacement:

Normal saline
1 liter fast
3 liters over 3 hour
500 ml/hour for 4-8 hours

When plasma glucose reaches 250-300mg/dl change to 5%dextrose.

The range of K administration depends on serum K level
> 6 mEq no K required
5-6mEq 10mEq/hour
4-5mEq 20 mEq/hour
3-4mEq 30 mEq/hour

Give 10-30 mEq of potassium in each litre fluid to maintain serum
potassium at 4-5 mEq/L
IF SERUM POTASSIUM 1S> 3.3 mEq/L, insulin treatment should be
delayed till serum K is restored by IV potassium infusion

HCO3, Mg, Ph.Replacement
HCO3, is not indicated in routine management of DKA

IF pH< 7.0 ( 100ml of sod bicarb. Over 20-30min to
maintain
PCO2 =10-12 mmHg serum HCO3 10-12 mEq/L)
HCO3 < 5mEq/L

IV Mg is not necessary in most cases only if Ph replacement produces K
Ca & tetany

Complication of DKA

INFECTION
VASCULAR THROMBOSIS
CEREBRAL EDEMA
ARDS




103




H Hy yp po og gl ly yc ca ae em mi ia a

Biochemically, Hypoglycemia is defined as decrease of blood glucose level
below 40mg/dl(2.2mmol/dl).

Insuline or oral hypoglycaemic drugs(Sulphonylurea,Repaglinide,nateglinide)
therapy for diabetes accounts for the vast majority of cases of severe
hypoglycaemia encountered in ED due to:

Delay in eating meals.
Unusual physical exertion.
Excessive dose of exogenous insulin.
Unusual fluctuation in insulin absorption from varying
injection sites.
Impaired counterregulatory mechanisms due to autonomic
neuropathy.

Oral hypoglycaemic drugs which don't cause hypoglycaemia:
Metformine.
Thiazolidinediones: (Rosiglitazone &Pioglitazone).
Glucosidase inhibitors (Acarbose &Miglitol).
Diagnosis:

* Whipples triad is the basis of clinical diagnosis of:
Hypoglycaemic symptoms.
Associated blood glucose of 40mg/dl or less
Glucose relieves the symptoms.
* Typical symptoms of hypoglycaemia include:
sweating,shakiness,anxiety,nausea,headache,confusion,bizarre behaviour,
slurred speech,blurred vision&coma.

* Neurologic manifestations are cranial nerve palcies,hemiplegia,seizure.
* Breathing is normal or depressed (lack of Kussmaul breathing).
* Mild hypothermia (32.5
O
C-35
o
C) is common.

Treatment:
1. I.V glucose : 50ml, 50% dextrose at 10ml/min to comatosed patient.
A contininuous infusion of a 10% dextrose may be required to maintain
the blood sugar above 100mg/dl.

104


2. If there any concern of malnutrition,thiamine100mg iv should be given
before giving glucose to prevent precipitation of Wernicke
encephalopathy.

3. If iv glucose is not available or there is difficulty gaining iv access,
Glucagone 1mg can administered im or sc.

4. If there is not a prompt response to glucose infusion or if adrenal
insufficiency is suspected, hydrocortisone 100-200mg should be given.

5. Refractory hypoglycaemia 2ry to the sulfonylureas may respond to the
Somatostatin analog Octreotide 50-125 g .

6. Oral feeding of fruit juice should be given as soon as the patient regain
consciousness.

Disposition:
Factors considered in determining disposition include: the patient
response to treatment, cause of hypoglycaemia,comorbid
conditions and social situation.

Most diabetics with uncomplicated insulin reaction respond
rapidly.They can be discharged with instructions to continue oral
intake of carbohydrates and closely monitor their finger stick
glucose.

All patient with sulfonylurea induced hypglycaemia should be
admitted due to the prolonged half-life.













105









106


C Co om ma a
Definitions:
Coma has been defined as unarousable and unresponsiveness to
stimulation, although reflex movements and posturing may be present.
Other terms used to decreased level of consciousness:
Stupor: severely impaired arousal with some response to vigorous
stimuli.
Lethargy: a state in which arousal, though diminished, is
spontaneously maintained or requires only light stimulation.
Obtundation: a lesser state of decreased arousal with some
response to touch or voice.

Etiology:
Based on the anatomic location of the lesion and the mecahanisms by
which neurologic diseases produce coma, the causes of coma can be
classified into four major groups:

1. Metabolic and diffuse cerebral disorders.
Hypoxia, ischaemia, hypoglycaemia, endogenous and
exogenouns toxins, meningitis, concussion, post-ictal
state, metabolic and electrolyte disorders.
2. Supratentorial lesions.
Epidural haematoms, subdural haematoma, cerebral Hge,
cerebral infraction, tumour and abscess.
3. Infratentorial lesions.
Brain stem or cerebellar infraction, Hge, tumour and
abscess.
4. Psychogenic coma.
Up to 75% of patients in a comatose state, without obvious
cause, will likely have a diffuse systemic disorder.
Structural lesions make up the remaining causes of coma;
supratentorial lesions are more common than subtentorial
lesions.

Clinical features:

1. Metabolic encephalopathy:
Hypoventilation, abnormal respiratory pattern.
Reactive pupils (a midbrain function) in the presence of impaired
function of the lower brain stem (e.g. hypoventilation, loss of
extraocular movements)
Symmetric neurologic findings.
No focal hemispheric lesions (hemiparesis, hemisensory loss,
aphasia) before loss of consciousness.
Random eye movements, but not persistant ocular deviations.
Tremors, asterixis, multifocal myoclonic jerks and seizures.
107



2. Supratentorial lesions:
Premonitory symptoms as headache or seizure.

Symptoms and signs of hemispherical dysfunction are usually
present (sensory or motor disturbances, aphasia, visual field
defects) before onset of coma.

Signs of bilateral hemispheric dysfunction (e.g.decorticate
posturing).

When progressive, signs of transtentorial herniation.

Uncal herniation (herniation of the medial portion of the
temporal lobe i.e. the uncus across the cerebellar
tentorium produces midbrain signs)
Ipsilateral (unilateral) pupil dilatation and
oculomotor nerve paralysis.

Progressive impairment of the level of consciousness.

Central herniation.
Loss of consciousness.
Marked unilateral papillary dilatation, loss of light
reactivity and oculocephalogyric reflex.
Decerebrate posturing.

3. Infratentorial lesions:
Coma (sudden onset)
Conjugate gaze toward lesion i.e. the eyes are directed away
from the side of the lesion and towards the hemisphere.
Disconjugate eye movements with dolls eye or caloric testing
strongly suggest a subtentorial lesion.
Pinpoint pupils, non reactive, are often present in pontine or
cerebellar Hge or infarction.

inhibitors and opiates also produce pinpoint pupils. holinesterase C N.B:

4. Psychogenic coma:
Patient is unresponsive.
Normal physical examination.
Flaccid symmetric decreased muscle tone.
Normal and symmetric reflexes.
Normal Babinski (down response).
The pupils are normal in size (2-3mm).
Voluntary muscle tone of the eyelids during passive examination.
Ice water caloric test.




108


Approaches to Coma patient.

1. Evaluation of the comatose patient should progress as for any
patient in the ED.
2. Priorities include the initial ABCs monitorming, venous access
and high flow O2.
3. Maintain cervical spine stabilization if trauma cannot be role
out.
4. Examine pupils or reactivity to light and evaluate movement of
extremities for rapid determination of the cause i.e. diffuse
versus structural.
5. The coma cocktail
It is empiric treatment for common conditions presenting
as coma.
It consists of:
Thiamine 100mg IV.
Glucose: 50ml D 50% W (in children 2ml / kg of D25W) IV.
Naloxone: 0.4-2mg IV.
N.B: Flumazenil is not included in the coma cocktail because of its ability to
induce seizures and cardiac arrhythmias. It should be used only if coma is
definitively caused by benzodiazepine use

5. The history is vital and should include:
Onset (sudden or gradual).
The evaluation of the clinical picture.
The state of the patient health prior to the onset of coma.
The patient accessibility to drugs or poisons.
Inquiry concerning condition, that commonly cause coma (trauma,
epilepsy, drug abuse, CV diseases, pulmonary disease,
cerebravascular disease, metabolic disorders, infections,
neoplasm).
History of psychiatric illness.
Occupational or environmental exposures e.g. CO. cyanide,
organic solvents, lead
Past medical history: DM, HTN, epilepsy, liver, renal, respiratory
failure, endocrine disorder.

6. Physical Examination:
A. Vital Signs.
1. Temperature:
Fever may suggest: infection, thyroid storm, heat
stroke, anticholinergic toxicity.
Hypothermia suggests: myxoedema, cold exposure,
intoxication with ethanol or barbiturates
.
109


2. Heart rate:
Bradycardia, hypertension and bradypnea may indicate
ICP (Cushings triad).
Tachycardia ( > 140 / m) in ectopic paroxysmal
tachyarrhythmias.

3. Blood Pressure:
Hypotension: ethanol or barbiturates intoxication, Hge,
shock, MI.
Hypertension: Hypertensive encephalopathy, cerebral
or brain stem infraction, subarachnoid hemorrhage.

4. Respiratory rate:
Bradypnea: ethanol, narcotic or barbiturates intoxication.
Tachypnea: hypoxia,sepsis.
Hyperpnea: metabolic acidosis.

5. Respiratory pattern:
A normal breathing pattern suggests the absence of brain stem
damage.
Cheyne-stokes respiration (periods of waxing and waning
hyperpnea alternating with shorter periods of apnea) implies
bilateral hemispheric dysfunction with the brain stem intact. It may
occur in metabolic disorders and congestive heart failure.
Kussmaul respiration: metabolic acidosis.
A pneustic respiration (prolonged inspiration followed by an
expiratory pause) signifies a pontine lesion.
Ataxic (irregular) breathing signifies a medullary lesion.
Central neurogenic hyperventilation (deep rapid breathing)
indicates involvement of the brain stem between the midbrain and
pons.
B. Skin.
Jaundice, spider angiomata, palmar erythema point to hepatic
encephalopathy.
Petechiae and ecchymoses suggest a coagulation abnormality
or thrombocytopenia.
A maculohemorrhagic rash suggests meningococcal infection,
staphylococcal endocarditis.
Cherry-red skin suggests carbon monoxide poisoning.
Needle marks on extremities indicate possible drug abuse.
Check skin turgor.
C. Odor of the breath:
A fruity odor suggests diabetic keto-acidosis.
A uriniferous odor is found in uremia.

110


Fetor hepaticus points to hepatic encephalopathy.
The odor of alcohol is characteristic.
A burnt almond odor is found with cyanide toxicity.
A garlic scent maybe seen in arsenic poisoning.

D. Body orifices:
Bleeding from the ears or nose suggests cranial trauma.
Bleeding from other orifices suggests a bleeding disorder or
haemorrhage as the cause of coma.

E. Central nervous system:
Posture in bed:
Decorticate rigidity characterized by flexion of arms and elbows
with hyperextension of the legs, signifies bilateral hemispheric
dysfunction with the brain stem intact.
Decerebrate rigidity in which the arms and legs are in an extended
position, it reflects damage to the midbrain and upper pons.

Meningeal signs:
Resistance to passive flexion of the neck without resistance to
other neck movements is evidence of meningities or subarachnoid
Hge.
Restriction of movement of the neck in all directions may occur in
generalized rigidity or disease of the cervical spine.
Positive brudzinkis sign i.e. flexion of the hips on passive flexion of
the neck.
Positive Kernigs sign i.e. pain or resistance of the hamstrings
when the knees are extended with the hips flexed at 90 degree.

Eye movements:
When eyelids are opened, if the eyes flutter upwards,
exposing only the scalera, suspect psychogenic coma.
In comatose patients without involvement of the neural
pathways influencing ocular movements, the eyes
usually directed straight ahead or display slow roving
(spontaneous eye) movements.
Sustained, involuntary conjugate deviation of the eyes
toward the unaffected side suggests a hemispheric
lesion; towards the paralyzed side, a pontine lesion.
Absence of oculocephalic (dolls eye movement) and
corneal reflexes indicates pontine dysfunction.
Oculovestibular reflexes (cold calorics) may be lost in
brain stem lesion.



111


Pupils:
Equal, round, reactive pupils exclude midbrain damage as a cause
and suggest metabolic abnormality.
Reactive pupils in association with absent oculocephalic and
corneal reflexes generally signify a metabolic encephalopathy or
drug overdose.
Pinpoint pupils (<1mm) may indicate opiate, pilocarine or pontine
lesion.
A unilateral, fixed and dilated pupil suggests ipsilateral temporal
lobe herniation.
Bilateral, fixed and dilated pupil suggest anticholinergic poisoning,
anoxia, severe midbrain lesion or brain death. Also in response to
some drugs as atropine or glutethimide.

Motor system:
Hemiplegia, hyperreflexia and an extensor plantar response
indicate a structural lesion of the brain as the cause of coma.
Hyporeflexia without paralysis and with preservation of normal
planter response suggests a metabolic cause or drug ingestion.

Sensory system:
Sensory loss may be suspected if the patient exhibits variations in
responsiveness to noxious stimuli.

7. Investigations:

CBC.
Biochemistry: glucose, urea, Creatinine, bilirubin, alkaline
phophatase, transaminases, Ca, magnesium, (serum glucose can
be rapidly checked with a glucometer).
Platelets and coagulation profile.
Blood and urine culture if infection is suspected.
ABG.
Toxicology screening.
Chest films.
ECG.
CT Scan of the head specially in the presence of focal neurologic
signs, papilledema or in the absence of any other etiology.







112


COMA In summary
Assessment & Complications
Coma is commonly associated with ingestion of large doses of
antihistamines, barbiturates, benzodiazepines and other sedative
hypnotic drugs, -hydroxybutyrate (GHB), ethanol, opioids,
phenothiazines, or antidepressants.

The most common cause of death in comatose patients is respiratory
failure, which may occur abruptly.

Aspiration of gastric contents may also occur, especially in victims
who are deeply obtunded or convulsing.

Hypoxia and hypoventilation may cause or aggravate hypotension,
arrhythmias, and seizures.

Thus, protection of the airway and assisted ventilation are the most
important treatment measures for any poisoned patient.

EMERGENCY MANAGEMENT
The initial emergency management of coma can be remembered by the
mnemonic ABCD, for Airway, Breathing, Circulation, and Drugs (dextrose,
thiamine, and naloxone or flumazenil), respectively .


Initial Management Of Coma (A , B , C , D.)

A Airway control
B Breathing
C Circulation

D

Drugs (give all three):
Dextrose 50%, 50100 mL IV (unless bedside glucose
is normal).
Thiamine, 100 mg IM or IV.
Naloxone, 0.452 mg IV
1
.
And consider flumazenil, 0.20.5 mg IV
2
.

1
Repeated doses, up to 510 mg, may be required.
2
Do not give if patient has coingested a tricyclic antidepressant
or other convulsant drug or has a seizure disorder.



113


1. Airway
Establish a patent airway by positioning, suction, or insertion of an artificial
nasal or oropharyngeal airway. If the patient is deeply comatose or if there is
no gag or cough reflex, perform endotracheal intubation. These airway
interventions may not be necessary if the patient is intoxicated by an
opioid or a benzodiazepine and responds rapidly to intravenous naloxone or
flumazenil (see below).

2. Breathing
Clinically assess the quality and depth of respiration, and provide
assistance if necessary with a bag-valve-mask device or
mechanical ventilator. Provide supplemental oxygen.

The arterial blood CO
2
tension is useful in determining the adequacy
of ventilation. The arterial blood PO2 determination may reveal
hypoxemia, which may be caused by respiratory arrest,
bronchospasm, pulmonary aspiration, or noncardiogenic
pulmonary edema.

Pulse oximetry provides an assessment of oxygenation but is not
reliable in patients with methemoglobinemia or carbon monoxide
poisoning.

3. Circulation
Measure the pulse and blood pressure, and estimate tissue
perfusion (eg, by measurement of urinary output, skin signs,
arterial blood pH).

Place the patient on continuous electrocardiographic monitoring.

Insert an intravenous line, and draw blood for complete blood count,
glucose, electrolytes, serum creatinine and liver tests, and possible
quantitative toxicologic testing.

4. Drugs
A. Dextrose and thiamine
Unless promptly treated, severe hypoglycemia can cause
irreversible brain damage.
Therefore, in all comatose or convulsing patients, give 50%
dextrose, 50100 mL by intravenous bolus, unless a rapid
bedside blood sugar test is available and rules out
hypoglycemia.
In alcoholic or very malnourished patients who may have
marginal thiamin stores, give thiamine, 100 mg
intramuscularly or over 23 minutes intravenously.



114


B. Narcotic antagonists
Naloxone, 0.42 mg intravenously, may reverse opioid-induced
respiratory depression and coma.

If opioid overdose is strongly suspected, give additional doses of naloxone
(up to 510 mg may be required to reverse potent opioids).

Caution:
Naloxone has a much shorter duration of action (23 hours) than most
common opioids; repeated doses may be required, and continuous
observation for at least 34 hours after the last dose is mandatory.
Nalmefene, a newer opioid antagonist, has a duration of effect longer than
that of naloxone but still shorter than that of the opioid methadone.

C. Flumazenil
Flumazenil, 0.20.5 mg intravenously, repeated every 30 seconds as
needed up to a maximum of 3 mg, may reverse benzodiazepine-induced
coma.
Caution:
Flumazenil has a short duration of effect (23 hours), and resedation
requiring additional doses is common. Furthermore, flumazenil should not be
given if the patient has coingested a tricyclic antidepressant, is a user of high-
dose benzodiazepines, or has a seizure disorderbecause its use in these
circumstances may precipitate seizures. In most circumstances, flumazenil is
not advised as the potential risks outweigh its benefits.















115



A An ni im ma al l B Bi it te e

Rabies is a fatal disease, due to infection of CNS by a rhabdo virus.

Transmitted by inoculation with infectious saliva or by salivary contact
with a break in the skin or mucus membrane.

Foxes, cats, dogs, horses, camels, raccoons are more likely to be
infected.

Rats, mice, rabbits, guinea pigs rarely transmit the virus to humans.

Clinical picture
Initial manifestations: fever, headache, sore throat, pain and
parasthesia at the wound site.
CNS symptoms develop 1-2 weeks after the prodrome
Encephalitic form: bulbar and peripheral muscle spasms,
opisthotonus, agitation, and hydrophobia.
Paralytic form: symmetric, ascending flaccid paralysis.
Coma, apnea, death usually 4-7 days after the onset of CNS
symptoms.

Differential diagnosis: Guillain-Barre syndrome, tetanus, meningitis,
encephalitis, polio, and brain abscess.

Treatment:

1. Thorough cleaning, debridement, and repeated flushing of
wounds with soap and water. Wounds caused by animal bites
should not be sutured because this promotes rabies virus
replication.

2. Vaccination of non-immunized patients.
a) Passive immunization
- Human rabies immunoglobulin: 20 IU/Kg half of the
dose infiltrated locally at the exposure site and the
remaining should be injected IM distant from the
wound.
- Equine rabies antiserum 40 I.U/Kg can be used after
skin test of horse serum sensitivity, if human rabies
immunoglobulin is not available.
b) Active immunization:
- Human diploid cell vaccine (HDCV), given as 5
injections of 0.5 ml IM in the deltoid muscle
(anterolateral region of the thigh muscle in children).
116


Dont inject in the gluteal region. Vaccine is given on
days 0,3,7,14,28 after exposure.

3. Vaccination of subjects already immunized:
- Vaccination administered less than 5 years previously give
2 injections: days 0,3.
- Vaccination administered over 5 years previously or
incomplete give 5 injections: days 0,3,4,14,28 with
administration of immunoglobulin if required.
4. Prevention or pre-exposure vaccination (HDCV)
Primary vaccination: 3 injections: days(0, 7,21, or 28)
Booster injection: 1 year later
Booster injection every 5 years.
NB:
Schedule of vaccination is the same for adults and for children.
Rabies immunoglobulin and rabies vaccine should never be given in
the same syringe or the same site.



















117


M Ma an na ag ge em me en nt t o of f S Sc co or rp pi io on n s st ti in ng g


black scorpion yellow scorpion

Androctonus Crassicaude (black scorpion) and Leiurus quinquestriatus
(yellow scorpion) have been found the two most dangerous scorpions
and two of the most toxic in the world.

The toxins causes local pain, tenderness and swelling and rarely
systemic manifestations like vomiting, Dyspnea, hyperthermia,
hypertension, convulsion, acidosis and shock.

Investigations
CBC: lecucocytosis
Biochemistry: blood glucose, CPK, LDH, amylase:
Electrolytes: Na, Ca: K
ABG: Acidosis
ECG
X-ray chest

Management
Give scorpion antivenom to all patients confirmed to have
scorpion sting after a skin test. (This is done by injecting 0.1 ml of
antivenom intrademally).
5 x 1 ml ampules polyvalent scorpion antivenom diluted in a 20-
50 ml NaCl given IV over a period of 20 minutes. NaCl is to
be used for infants and children up to 6 years.
If systemic manifestations will exists, the same dose is to be
repeated every 2 hours up to 4 doses.
Children must be given the same dose of antivenom as adults.
Keep under observation for at least 24 h, after recovery.
Adjunctive therapy to support vital functions.

- Severe local pain
0.5 ml (maximum) of 1% xylocaine, infiltrated at the site of
sting.

118


- Vomiting
Chlorpromazine 0.5-1 mg/kg I.M repeated if necessary.
- Convulsion: Diazepam IV slowly.

- Pulmonary Oedema: O2, furosemide, fluid restriction.

- Hypertension: Hydralazine or Nifedipine.

- Shock:
CVP line with 0.5 N saline to keep value at 8-12 cm H2O
and maintains blood pressure at a level to perfuse vital
organs. (Systolic BP 60-70 mmHg in children).

Contraindicated Drugs:
- Barbiturates
- Morphine
- Pethedine
- Beta blockers




























119


Management of Snake Bite

There are 2 main types of poisonous snakes:


Rattlesnake Copra Snake

Crotalids or pit vipers (hemotoxic venom): causing haemolysis,
necrosis, DIC e.g. rattlesnakes.
Elapids (Neurotoxic venom): disrupt neuromuscular activity e.g. coral
snakes, cobras.
Presentation
Crotalids
Puncture marks (may have 1-4).
Local symptoms (pain, swelling, erythema, necrosis,
oedema, ecchymoses).
Systemic symptoms (weakness, nausea, vomiting, numbness,
tingling, perioral parasthesia, bruising, tachycardia, shock,
death.
Coral snakes
Multiple, painless small wounds.
Local symptoms of numbness & fasciculations.
Systemic symptoms: slurred speech, weakness cranial
never palsies, dysphagia, ptosis, diplopia, diaphoresis,
impaired consciousness, respiratory failure & death.

Do not handle dead snakes as reflex biting may occur.

Diagnosis
Identify the type of snake if possible.
Determine seriousness of envenomation.
None: puncture with no to minimal pain/tenderness.
Mild: local swelling, pain, perioral parasthesia, no systemic
symptoms.
Moderate: local symptoms, systemic symptoms, mild
coagulopathy.
Severe: severe symptoms of the entire extremity, severe
systemic symptoms and coagulopathy.
120



Lab. Investigations may be abnormal in crotalid bites (but usually
normal with neurotoxic venom).
CBC: haemolysis
PT/PTT, DIC Screen: Coagulation abnormalities.
Renal function: May reveal acute renal failure.
Electrolytes & LFTs: may be abnormal.

Treatment:
1. Immobilize the bitten part as if it were a facture and hold it below the
level of the heart.

2. Avoid incision, suction, and tourniquet, applying ice.

3. Monitor vital sign, IV access, blood samples for investigation,
resuscitation according to ACLS protocol.

4. Local wound care and tetanus immunization should be given. Limb
circumference at several sites above and below the wound should be
checked every 30 minutes and the border of advancing oedema should
be marked.

5. Patients with no evidence of envenomation after 8-12 hours may be
discharged.

6. Any patient with progressive local swelling, systemic effects or
coagulopathy should receive immediately antivenom therapy in
accordance with the following principles:

a. Perform a skin test as following: 0.1 ml of antivenom is
injected s.c. followed by 15 minutes watch then 0.25 ml of
antivenom is injected followed by another 15 minutes watch.
Erythema and a wheal reaction constitute a positive
reaction. In case of positive skin test a Goat antivenom may
be given. A negative reaction is no guarantee against
anaphylaxis.

b. 50 ml (5 x 10 ml ampules) antivenom to be diluted in 250 ml
N saline given by slow IV drip only, the infusion should
proceed at a slow rate for the first 10 minutes, if the patient
is stable the infusion can be increased to the rate 250 ml/h.

c. More antivenom should be given if severe signs persist after
1-2 hours, dose can be repeated every 4-6 hours until the
arrest of progressive symptoms and coagulopathy.

d. Children must be given the same dose as adults.
121


- NB: Polyvalent Crotalidae Immune Fab (CroFab), a new
sheep-derived antivenom has generally replaced
Antivenom polyvalent, an equine-derived product.
- Antivenom is the only specific antidote available at
present time for the treatment of venomous snake bite.

e. In case of anaphylaxis: see management of anaphylaxis.

f. Once initial control has been achieved, the protocol is completed
by administering additional 2vials doses /6hs for18 hours (3 more
doses).

7. Serum sickness reactions (late reactions) are common after antivenom
use, usually occur 5-10 days after antivenom, treated by prednisolone
45-60 mg daily with tapering doses over 1-2 weeks. An antihistamine
e.g. chlorpheniramine malleate, 2 mg/6h for adults (0.25 mg/kg day in
divided dose for children) may be added.





























Ingestion of an unknown
drug
Unconscious pt.
Conscious pt.
Patient
Stabilization
Airway Breathing Circulation Altered mental status
Stomach
Evacuation
Physical exam.
Baseline Lab
Investigations
Coma Cocktail: ***
Naloxone Glucose + thiamine
Ipecac* or
Gastric
Lavage
Activated
Charcoal +
MgSo4**
Symptomatic
Management
* Ipecac dosing:
Adults: 15-30 ml, Child> 1yr: 15 ml, Child < 1yr: 10 ml
** Activated charcoal
Adults: 60-100 mg
Child: 1-2 mg/kg
MgSo4:
Adult: 16 gm
Child: 250 mg/kg
*** Coma cocktail:
Naloxone: opioid antagonist
Adult/Child: 0.2-2 mg IV; repeat at 2-3 minutes intervals until desired effect or a total dose of 10-15 mg. Careful in opioids-dependent patient.
Flumazenil: Benzodiazepine antagonist.
Adult: 0.2 mg IV over 30 seconds, then 0.3 mg, then 0.5 mg (every 30 seconds) up to 3 mg.
Child: 0.01 mg/kg, titrate up to 1 mg
Careful use in case of mixed ingestion, may precipitate seizures or arrhythmias
Glucose:
Adults: 50-100 ml of 50%
Child: 2-4 ml/kg of 25%
Thiamine 100 mg is indicated concomitantly for alcoholic or malnourished patients.


Insecticide Exposure




Pyrethroids Caramate Organophophate


Carbamate










No Yes











- Dermal,Eye, Inhalation
Dermal + Eye
1. Removal of clothes
2. Local Irrigation of the
exposed are
Inhalation:
1. Remove to fresh air.
2. Give oxygen if required
If any symptomaticManifestations refer to oral
Exposure management
Oral
No Antidote
Symptomatic
Treatment only
LD: 10-100 mg
Suction of secretions until
Full atropinization
Establish an
airway
Is the patient
1. Comatosed
2. Convulsing
3. Without a gag reflex
1. Endotracheal
Intubation
2. Gastric Lavage
Induction of Emesis
Activated Charcoal + MgSo4*
Mild Symptoms
Severe Symptoms with/or
without
1. Weakness
2. Respiratory Depression
Atropine Therapy
alone
Atropine + Pralidoxime (for Carbamate give
atropine only) Atropinization should be
performed adequately & rapidly**
* Refer for dosing to the section: management of unknown ingestion
** Treatment Guidelines:
Atropine: for treatment of muscrinic effects.
1. Diagnostic dose: IV/IM adult: 1 mg; child: 02! mg "002 mg/#g$
If patient exhibit toxic effects of atropine (dry mouth, dilated pupil, and
rapid pulse) then probably not seriously poisoned.
2. Dosage: IM/IV Mild symptomology, initially 2-4 mg (child 0.05 mg/kg)
further 2 mg doses may be given every 10 minutes to maintain full
atropinization.
Severe symtomatology, initially 4-6 mg (child 0.05 mg/kg), followed by 2 mg
every 5-10 minutes to maintain full atropinization (not to exceed 50 mg/24
hours for adults).
3. Therapeutic endpoint: Administer until full atropinization (dry mouth,
pulse) (130-140/minute, and dilated pupil, clearing of rales). Maintain
some degree of atropinization fpr 48 hours.
Pralidoxime: for treatment of nicotinic manifestations, use as
adjunct and not a substitute to atropine.
Adult: 1-2 GM/IV in 100 ml NS 0.9% at 15-30 minutes.
1. Child: 20-40 mg/kg IV.
Alternatively doses may be administered IM or SC.
2. Administration may be repeated x 3 or as needed at an interval of 8-12
hours if muscle weakness has not been relieved.

11#



















































Management of acute burn

Burn injury is a common cause of morbidity and mortality.
Proper evaluation and management,coupled with appropriate
early referral to a specialist, greatly help in minimizing suffering
and optimizing results.
INITIAL EVALUATION AND RESUSCITATION
Before management of the burn wound can begin, the patient
should be properly and completely evaluated
Evaluation of the burn patient is organized into
primary survey and secondary survey.

Primary survey
A Airway .
B Breathing .
C Circulation.
D Disability.
E Expose patient.
F Fluid resuscitation
1- First evaluate the airway; early recognition of impending
airway compromise, followed by prompt intubation, can be
lifesaving.
2- Obtain appropriate vascular access .
3- Place monitoring devices.
4-Complete a systematic trauma survey, including indicated
radiographs and laboratory studies.
Secondary survey
Burn patients should then undergo a burn-specific secondary
survey,which should include:
Determination of the mechanism of injury.
Evaluation for the presence or absence of inhalation injury and
carbon monoxide intoxication.
Examination for corneal burns.
Detailed assessment of the burn wound.
The consideration of the possibility of abuse
Carbon monoxide intoxication is probable in persons
injured in structural fires, particularly if they are
obtunded.
Carboxyhemoglobin levels can be misleading in those
ventilated with oxygen
Patients trapped in buildings or those caught in an explosion are at
higher risk for inhalation injury. These patients may have facial burns,


singeing of the eyebrows and nasal hair, pharyngeal burns, carbonaceous
sputum, or impaired mentation. A change in voice quality, stridorous respirations,
or wheezing may be noted
The upper airway may be visualized by laryngoscopy, and the
tracheobronchial tree should be evaluated by bronchoscopy. Chest
radiography is not sensitive for detecting inhalation injury.

Patients who have suffered an inhalation injury are also at risk for carbon
monoxide (CO) poisoning. The pulse oximeter is not accurate in patients
with CO poisoning because only oxyhemoglobin and deoxyhemoglobin are
detected

Co-oximetry measurements are necessary to confirm the diagnosis of CO
poisoning. Patients exposed to CO should receive 100% oxygen using a
nonrebreather face mask.

Hyperbaric oxygen (HBO) therapy reduces the half-life of CO to 23 minutes.

HBO is recommended for patients with:
1. COHb levels greater than 25%.
2. Myocardial ischemia, cardiac arrhythmia.
3. Neuropsychiatric abnormalities.
4. Pregnant women and young children with COHb levels of 15% or greater.

After evaluation of the burn wound, begin fluid resuscitation and
make decisions concerning outpatient or inpatient management or
transfer to a burn center
Pathology tests: full blood count, urea, electrolytes, proteins (at time
of canula insertion)
Analgesia, preferably IV
Routine medication: Tetanus toxoid, Cimetidine ?
After evaluation of the burn wound, begin fluid resuscitation and
make decisions concerning outpatient or inpatient management or
transfer to a burn center
Pathology tests: full blood count, urea, electrolytes, proteins (at time
of canula insertion)
Analgesia, preferably IV
Routine medication: Tetanus toxoid, Cimetidine ?

Burn center transfer criteria
1. Second- or third-degree burns greater than 10% total body surface area
(TBSA) in patients younger than 10 years or older than 50 years. greater
than 20% in persons of other age groups
2. Second- or third-degree burns that involve the face, hands, feet, genitalia,
perineum, or major joints .
3. Third-degree burns greater than 5% TBSA .
4. Electrical burns, Chemical burns .
5. Inhalational injury .
6. Burn injury with preexisting medical disorder.
7. Any patients with burns and concomitant trauma.
8. A lack of qualified personnel (care taker ).


Burn injuries can be classified on the basis of the extent and the depth of the
injury.

Depth is classified as partial or full thickness into four degrees
Extent is expressed as a percentage of the total body surface area.

Extent of burn
An accurate estimate of burn size is important for treatment and transfer
decisions. Burn size or extent can be estimated in a number of ways.
The rule of nines. in adults is easy but less accurate in children because
their body proportions are different from those of adults.
For areas of irregular or nonconfluent burns, the palmar surface of the
patient's hand can be used.
For a wide age range, the area of the palm without the fingers represents
0.5% of the body surface.


% BSA .OF BODY PARTS ADULT CHILD

Head & Neck 9 18
Arms 9 9
Front & Back 18 18
Legs 18 13.5
Genitalia 1 1


Burn depth
Burn depths are routinely underestimated during the initial examination.
Devitalized tissue may appear viable for some time after injury, and often,
some degree of progressive microvascular thrombosis is observed on the
wound periphery. Consequently, the wound appearance changes over the
days following injury. Serial examination of burn wounds can be very
useful.

First-degree burns are usually red, dry, and painful. (e.g. sun burn)
Burns initially termed first-degree are often
actually superficial second-degree burns,
with sloughing occurring the next day.
Second-degree burns are often red, wet, and very painful.Their depth,
ability to heal, and propensity to form hypertrophic scars vary enormously
Third-degree burns are generally leathery in consistency, dry, insensate,
and waxy. These wounds will not heal, except by contraction and limited
epithelial migration, with resulting hypertrophic and unstable cover
Burn blisters can overlie both second- and third-degree burns.
Fourth-degree burns involve underlying subcutaneous tissue, tendon, or
bone.




Severity
Severity determines if the burn is critical, moderate or minor.

Classification of Burns
Critical burns - adults
Full - thickness of hands, feet, face or genitalia
Burns associated with respiratory injury - smoke inhalation
Full - thickness of more than 10% of body surface
Partial thickness of more than 30% of body surface
Burns complicated by painful swollen, & deformed extremity
Moderate burns in patients under 5 and over 55

Moderate burns - adults
A. Full - thickness burns of 2% to 10% of the body surface area,
excluding critical areas
B. Partial - thickness burns of 15% to 30% of the body surface area
C. Superficial burns of greater than 50% of the body surface area

Minor Burns - adults
a. Full - thickness burns of less than 2% of the body surface area
b. Partial - thickness burns of less than 15% of the body surface area

Critical burns - infant and children
a. Full - thickness or partial thickness burns covering more than 20 %
of the bodys total surface area
b. Burns involving the hands, feet, face, airway or genitalia

Emergency Medical Care
Adult Patients
Stop the burning process and prevent further injury
Use body substance isolation techniques
Monitor the airway - give Oxygen
Prevent further contamination
Cover burned area with dry, sterile dressing
Never use ointments, lotion, or antiseptic
Do not break blisters

Pediatric patients
Greater surface area in relationship to the total body size
Greater fluid and heat loss
Higher risk of shock, airway and hypothermia
Consider child abuse





Fluid resuscitation
Burn patients demonstrate a graded capillary leak, which increases with
injury size
Because the changes are different in every patient, fluid resuscitation can
only be loosely guided by formulas.
The inherent inaccuracy of formulas requires continuous reevaluation and
adjustment of infusions based on resuscitation targets
The modified Brooke or Parkland formulas are reasonable and are used to
help determine the initial volume of infusion.
Half of the total calculated 24-hour volume is administered in the first 8
hours post injury. Should the resuscitation be delayed, this volume is
administered so that infusion is completed by the end of the eighth hour
post injury.
After 18-24 hours, capillary integrity generally returns and fluid
administration should be decreased.


Volume = weight x percent burn area x 4ml




First 8 hrs - give half of total
next 16 hrs - give half of total
next 24 hrs - give half of total
Type of fluid is Hartmann's solution
Adjust volume for each patient according to urine output ( 30-35ml per hour
minimum).
Pigmented urine is commonly seen in the setting of high-voltage or very
deep thermal injury. This pigment should be cleared promptly to avoid
renal failure.
This can usually be achieved through the administration of additional
crystalloid. The administration of bicarbonate may facilitate clearance of
myoglobin by preventing its entry into the tubular cells.
Serum sodium, potassium, ionized calcium, phosphorous, and magnesium
levels should be monitored and kept within physiologic range.
Ideally, begin enteral feedings during resuscitation, except in patients with
massive injuries or those who are underresuscitated and less likely to
tolerate tube feedings because of ileus secondary to splanchnic
underperfusion

Cerebral edema and seizures can occur with severe
hyponatremia, and rapid correction of hyponatremia
may result in pontine demyelinating lesions.


C Ch he em mi ic ca al l b bu ur rn ns s

May occur from any toxic substance that comes in contact with
the skin
Mostly caused by Alkaline (alkali) and acid
Protect yourself from exposure or injury

Emergency Care

Stop the burning process

) 1 ) Immediately flush with large amounts of water
) 2 ) Do not contaminate uninjured areas
) 3 ) Continue flushing while enroute to hospital








Dry chemicals

Reaction with water can worsen burn
) 1 Brush - then flush
2) Remove victims clothing (shoes & socks
3) Cover with dry sterile dressing or clean sheet
Special care of the eyes
Gently /continuously flush
For direct eye injury hold lids open and irrigate the eye
Dry lime victim
Industrial shower for chemical removal

Electrical Burns

May be more serious than it seems
Entry wound is usually a small burn area
Look for an extensive exit wound
Possible tissue damage underneath (current spreads out as it travels
through the body)
Possible Cardiac arrest(VF or VT)
Possible Respiratory arrest
Treat any major complications first
Splint possible fractures
Treat wounds with a dry, sterile dressing (Entry wound on hand ,Exit
wound on foot)

Infection Control
Hand-washing BEFORE and AFTER touching each patient
Aseptic techniques for dressing and procedures
Environmental controls, such as air filtration and balanced ventilation
Microbiological screening of wounds, nose, throat, perineum and axillae
Isolation of infected patients
Early nutritional support
Early excision of deep burns
Use of topical antimicrobials, where applicable, to reduce wound
colonization
Conclusions
Proper early management of burns is crucial
A systematic approach to burn management is vital
Superficial burns heal by regeneration within weeks
Deep burns require surgery




B Bl la as st t I In nj ju ur ry y

1. Classification of Explosives
Explosives are categorized as
1- High-order explosives That produce a defining supersonic over-
pressurization shock wave.
Examples of HE include
TNT, C-4, Semtex, nitroglycerin, dynamite, and ammonium nitrate fuel oil.

2- Low- order create a subsonic explosion and lack HEs over-
pressurization wave
$%amples of &$ include
pipe bombs' gunpowder' (olotov coc)tails or aircraft improvised as
guided missiles.

Types of Blast Injuries:

Primary
(Direct effects of pressure of the blast wave , either overpressurization
and such as

Rupture of tympanic membranes,
Pulmonary damage,
Rupture of hollow viscera
Rupture eye globe
Traumatic Brain Injury

Secondary effects of projectiles ( objects strike persons),
causing penetrating trauma and fragmentation injuries .

Tertiary effects of structural collapse and of persons being
thrown by the blast wind ( persons strike objects)
causing crush injuries and blunt trauma, penetrating trauma,
fractures and traumatic amputations, open or closed brain injuries

Quaternary (burns, asphyxia, and exposure to toxic inhalants


infections, crush injuries, delayed collapse ).




Primary Blast Injuries





Unique to high explosives
Due to impact of over-pressurization wave with body surfaces
Most commonly involve air-filled organs and air-fluid interfaces
Middle ear
Lungs
Gastrointestinal tract
Types of injuries
Tympanic Membrane (TM) rupture
Blast lung
Intestinal hemorrhage and perforation
Globe rupture
Traumatic brain injury (TBI) without physical signs of head injury
Middle Ear Injury
TM - structure most frequently injured by blast
Most sensitive organ in barotrauma
As little as 5 psi above atmospheric pressure
Temporary neuropraxia is common




INJURIES:
TM rupture ( spontaneous healing in 50 % - 80 % )
Ossicle dislocation
Disruption of oval or round window (Permanent hearing loss can
occur with disruption of the oval or round windows in the cochlea )
Symptoms may include
Hearing loss, tinnitus, vertigo, bleeding from external canal, mucopurulent
otorrhea
Otologic exam and audiometry for all is essential .
TM rupture is sensitive marker, but absence does not exclude other organ
injury as blst lung injury may occurs in absence of TM rupture

Blast Lung Injury ( B L I )
Second most susceptible organ
Direct consequence of blast wave on the body
Overpressure needed is about 40 psi
At 80 psi- 50 % have severe pulmonary damage (at 200 psi-fatal)
Most common CRITICAL Injury in victims close to bomb
Can be life threatening
May not have obvious external injury to the chest
Can be associated with pneumothorax, haemothorax
Air embolism from pulmonary disruption (fatal)
Results in tearing, haemorrhage, contusion and oedema
Microhaemorrhages in alveoli
Disruption and weakening of alveolar walls
Disruption of perivascular and peribronchial tissue
Resultant Ventilation-Perfusion mismatch
Pulmonary contusions multifocal hemorrhages
Pulmonary C-fiber receptor injury causes vagal nerve-mediated cardiogenic
shock, pulmonary edema
Other injuries: traumatic emphysema, AV fistuale, pulmonary barotrauma,
venous air emboli
Symptoms: Dyspnoea, Haemoptysis, cough, chest pain
Signs: Tachypnoeic, hypoxic, cynosis, wheezing


X-Ray features similar to pulmonary contusion, with bihilar (butterfly
pattern) shadows
Can be life threatening

Gastrointestinal Tract blast injury
Colon visceral organ most frequently affected
Mesenteric ischemia from gas embolism may cause delayed rupture of
large or small intestine
Intestinal barotrauma more common with underwater air blast
Solid organ injury less likely
Signs and symptoms
Abdominal pain, nausea, vomiting, hematemesis
Rectal pain and tenesmus
Testicular pain
Unexplained hypovolemia

Other Primary Blast Injury
Primary blast injury to the eye
include rupture of the globe, serous retinitis, and hyphema lid laceration,
traumatic cataracts injury to optic nerve .

Primary blast injuries to the brain
include concussion as well as barotraumas caused by acute gas embolism.
Consider the proximity of the victim to the blast particularly when given
complaints of headache, fatigue, poor concentration, lethargy, depression,
anxiety, insomnia, or other constitutional symptoms. Loss of
consciousness and coup and countercoup injuries formerly were
considered secondary and tertiary injuries, but with the increased use of
body armor in the military, damage to the CNS after an explosion has been
increasingly attributed to the direct effects of the blast.


Secondary Blast Injury
Due to flying debris and bomb fragments
Penetrating ballistic or blunt injuries
Leading cause of death in military and civilian terrorist attacks except
in cases of major building collapse
Wounds can be grossly contaminated

Consider delayed primary closure and tetanus vaccinations



Tertiary Blast Injury

Due to persons being thrown into fixed objects by wind of explosions
Also due to structural collapse and fragmentation of building and vehicles
Structural collapse may cause extensive blunt trauma
Crush syndrome
Damage to muscles and subsequent release of myoglobin,
urates, potassium, and phosphates
Oliguric renal failure
Compartment syndrome
Edematous muscle in an inelastic sheath promotes local
ischemia, further swelling, increased compartment pressures,
decreased tissue perfusion, and further ischemia

Potential Intra-operative and Post-resuscitation Complications

Surgeons, Anesthesiologists, and Critical Care Specialists will need to be
aware of potential intraoperative and post-resuscitation complications
Occult pneumothorax
Occult compartment syndrome
Hyperkalemia
Crush syndrome
Rhabdomyolysis

Quaternary Blast Injuries

Explosion related injuries or illnesses not due to primary, secondary, or
tertiary injuries
Exacerbations of preexisting conditions, such as asthma, COPD,
CAD, HTN, DM, etc.
Burns (chemical and thermal)
White Phosphorous (WP) from munitions causes extensive
burns, hypocalcemia and hyperphosphatemia
Toxic inhalation
Radiation exposure
Asphyxiation (carbon monoxide and cyanide)






General Considerations
Information about the type of explosion and the target helps to predict the types
of injuries.
After an explosion in a confined space, such as a bus, one would
anticipate, in addition to penetrating injuries, more victims with primary
blast injuries and lung damage than would be expected after an explosion
in an open space.
Explosions in confined spaces (mines, building, or large vehicles) and or
structural collapse are associated with greater morbidity and mortality.
Land mine injuries are associated with a high risk of below and above the
knee amputations.
. Intensity of an explosion pressure wave declines with the cubed root of
the distance away from the actual explosive.
That is, a person 3m from an explosion experiences 9 times more
overpessure than a person who is 6m away. Thus, proximity of the person
to the explosion is an important factor in a primary blast injury. Note that
blast waves are also reflected by solid surfaces, and therefore, a person
standing next to a wall may sustain a greater primary blast injury.
Terrorist attacks in civilian settings tend to have a biphasic distribution of
mortality high immediate rates of death followed by low early and late
mortality rates.
. Initial stabilization of victims of blast injury like that of other trauma victims,
includes assessment and management of the airway, breathing, and
circulation. Half of all initial casualties will seek medical care over a one-
hour period. This can be useful to predict demand for care and resource
needs.
Expect an upside down triagethe most severely injured arrive after the
less injured, who bypass EMS triage and go directly to the closest
hospitals.
Another ominous consideration is the tactic of setting dual explosion, since
the initial explosion may be a ploy to attract law enforcement and resuce
personnel, followed by a second device designed to injure rescuers.
Moreover, EMS personnel should check for radiation and chemical
contamination at the scene of a deliberate attack.
Unfotunatly, few health professionals have experience with explosive-
related injuries







General Management

Treatment of patients after blasts focuses on two examinations.

First,

Otoscopic exam
Portable otoscopes are used to identify rupture of the tympanic membranes.
1- If the tympanic membranes are intact, serious primary blast injuries can be
conditionally excluded, in the absence of other symptoms such as dyspnea,
respiratory distress, and acute abdominal pain.
2- Patients with rupture of the tympanic membranes should undergo radiography
of the chest and should be observed for at least eight hours, as clinically
indicated, since primary blast injuries are notorious for their delayed onset.

Second,

Pulse oximetry

These victims should be monitored by sequentially measuring their oxygen
saturation by pulse oximetry. Decreased oxygen saturation probably signals early
blast lung even before symptoms begin.

Treatment of Blast Lung Injury
Treatment of blast lung is challenging in that ventilation with high peak
inspiratory pressures increases the risk of air embolism and pneumothorax.
Ventilation should use limited INSPIRATORY PRESSER and permissive
hypercapnia, when available,
High frequency ventilation may be of value.
Assume that a patients wheezing associated with a blast injury is due to
pulmonary contusions

Treatment of TM rupture
Generally expectant management
Most resolve spontaneously
Avoid irrigating or probing the auditory canal
Avoid swimming
Refer to ENT if no healing or complications occur
Complications include ossicle disruption, cholesteatoma,
perilymphatic fistula, and permanent hearing loss (1/3)
Steroids may be helpful in sensorineural hearing loss





Treatment for Acute Gas Embolism (AGE)

Patients thought to have acute gas embolism (AGE) require recompression
treatment.
Place patients on 100% oxygen by tight-fitting face mask and, if possible,
place them in the left lateral recumbent position.
Trendelenburg (head down) position is no longer recommended.
Of course, other causes of symptoms (eg, traumatic CNS injury) must be
excluded.
Hyperbaric oxygen (HBO) treatment is the definitive procedure.
Transfer of the patient may be required.
Research suggests that aspirin is helpful in AGE. Aspirin may reduce
inflammation-mediated injury in pulmonary barotrauma as well.
It may, however, be unwise to give an antiplatelet agent to a patient with
acute trauma.

Treatment of Eye Injuries

Up to 28 percent of blast survivors may have serious eye injuries,
particularly if the blast caused shattering glass.
Symptoms include eye pain or irritation, foreign body sensation,
altered vision, periorbital swelling or contusion, and findings can
include decreased visual acuity, hyphema, globe perforation,
subconjunctival hemorrhage, foreign body or lid laceration.
Objects penetrating the eye should not be removed in an
emergency setting.
The eye can be covered with a paper cup or other clean object
that will not exert pressure on the globe, and the patient can be
referred for definitive surgical treatment.

Special Populations

Children who are victims of terrorism require more resources of ICUs, have
higher ISS, and have longer hospital stays than children who survived traumatic
events unrelated to terrorism.
During pregnancy, the direct injury of the fetus by the blast is uncommon, as the
fetus is apparently protected by amniotic fluid. However, its attachment to the
placenta is at risk, if the blast wave affects the high-density uterine wall and the
lower-density placental medium, causing placental abruption. For women
exposed to blasts in the second and third trimester of pregnancy, admission to
the labor and delivery area for fetal monitoring is recommended



Guidelines for Disposition

Limited data prevent establishing the optimal duration of observation.
Persons exposed to open-space explosions who have no apparent
significant injury and with normal vital signs and unremarkable lung and
abdominal examinations generally can be discharged after 4 hours with
instructions to return to the ED if shortness of breath, abdominal pain,
vomiting, or other symptoms occur.

Persons exposed to significant closed-space explosions, in-water
explosions, and those who sustaine TM rupture are at higher risk of
delayed complications. These patients should receive more intensive
observation over a longer period.

Motivated, reliable, and completely asymptomatic patients may be sent
home after 4 hours of observation.

Guidelines for Admission
High risk patients who require admission
Significant burns
Suspected air embolism
Radiation
WP contamination
Abnormal vital signs
Abnormal lung examination findings
Clinical or radiographic evidence of pulmonary contusion or
pneumothorax
Abdominal pain or vomiting
Penetrating injuries to the thorax, abdomen, neck, or cranial cavity

















No obvious injuries Obvious Injuries
Otoscopic Exam
+
-
Observe
O2 Sat 6-8 hours
+
-
Admit D/C with
Abd Warnings
Release
+
-
Treat Injuries
as usual
Injury RX and
blast observation
(pulmonary/visceral)
Triage Algorithm
Otoscopic Exam












Heat syndromes



Heat cramps
Brief intermittent, often severe cramps in groups of muscles
subjected to physical exertion.

Heat oedema:
Mild swelling at the ankles appearing in the first 7- 10 days.
Disappearing after acclimatization.

Heat fatigue:
Transient deterioration of skills, improve after returninig to cool
place.

Heat syncope
Sensation of giddiness and or acute physical fatigue during
exposure to heat. It is self-limiting. Improves by moving to cool
place.













Heat syndromes
Minor
Heat cramps
Heat fatigue
Heat oedema

Heat syncope
Major
Heat exhaustion
Heat stroke



































H He ea at t e ex xh ha au us st ti io on n
Definition
It includes number of syndromes leading to collapse in hot weather.
The common features of the syndrome is cardiovascular insufficiency,
brought about by predominantly by dehydration and insufficient intake of
water , by salt depletion or both specially when great amount of sweating has
occurred. Left unattended, the condition may proceed to heat stroke.

Cardinal features
Patient is conscious.
Rectal temperature below 40 degrees centigrade.
Patient is sweating.

Clinical picture

Temperature below 40 degree
Fatigue
Giddiness
Frontal headache
Nausea
Vomiting
Muscle cramps
Management
Examine to exclude systemic illness.
Position the patient on his side.
Take vital signs ( rectal temp, BP, PR, RR).
Bl. for CBC, Urea& Electrolytes, Bl sugar, ECG,& chest X-rays
I.V line, NS 500 ml if unable to take plenty of liquids orally.
Expose the patient as much as you can by removing the clothing to
a minimum for better cooling.
Start cooling by covering patient with muslin gauze or wet bed sheet,
Spray the patient with water at the normal room temperature.
Fan the patient.
If the patient is tired and willing to sleep, let him have rest for a couple of
hours.
If improvement, discharge after 2-4 hours.
Resistant cases usually have underlying cause e.g, chest infection. Re-
examine and admit to medical ward.






H He ea at t s st tr ro ok ke e
Definition
It is a complex clinical condition in which an elevated body temperature
causes tissue damage. This elevated body temperature results from
overload or failure of the normal thermoregulatory mechanism following
exposure to hot environment.

It is characterized by:
Generalized anhydrosis.
Disturbance of consciousness.
Rectal temperature above 40
o
C.

Predisposing factors:
1. Extremes of age.
2. Dehydration.
3. Lack of acclimatization.
4. Lack of physical fitness.
5. Chronic disease e.g. DM.
6. Cardiovascular disease.
7. Obesity.
8. Fatigue &lack of sleep.
9. Sustained output of Muscular Metabolic Heat
10. Past hx.of heat illness.
11. Conditions that affect sweating.
12. Skin disease.
13. Use of drugs ( e.g. Barbiturates).
14. Leisions of hypothalamus, brain stem or spinal cord.
15. Acute infection.
16. During convalescence.
17. Recent intake of food.

Clinical features
Usually sudden onset may be preceded in some cases by short period of
confusional state.
Almost all patient present with coma or semicoma with or without
convulsions.
Hot,dry flushed skin.
Rectal temp more than 40
o
C.
TACHYCARDIA, HYPOTENSION is very common.
Tachypnea is always a rule.
Aspiration pneumonia may complicate the picture.


Vomiting may be present.
May be associated with diarrhea.
May present with bleeding tendency e.g. petechiae or ecchymosis,
epistaxis, bleeding from injection site, GIT bleeding etc..


Common laboratory findings.

Hypokalemia or hyponatremia.
Hyperglycemia.
Respiratory Alkalosis early and later Metabolic Acidosis.
Evidence of Disseminated Intravascular Coagulopathy e.g,
Low platelets
Low hemoglobin
Hypoprothrombinaemia
Hypofibrinoginaemia
High FDP.
Proteinuria with granular casts and RBCs.

Diagnosis of heat stroke

Hyperpyrexia: rectal temp. 40 deg. C. or more.
Altered consciousness: patient may be confused, delirious,
semicomatosed or comatosed, with or without convulsions.
Skin usually hot and dry but may be occasionally wet.
Any patient with rectal temp. 40 or more needs rapid cooling.

Deferential diagnosis
Look for:
Neck rigidity (meningitis),
Splenomegally ( malaria)
Head injury.
Stroke (pontine Hge).










M Ma an na ag ge em me en nt t o of f h he ea at t s st tr ro ok ke e

1. Remove all the clothing of the patient.
2. Manage airway
a) Make sure airway is patent.
b) Intubate if needed.
c) Give oxygen as required.
d) Do endotracheal suction if needed.
e) Ventilate, if required.
3. Establish IV line.
4. Bl. for investigations:
CBC, Clotting study, FDP, Serum osmolality, BS, Urea,Bl
Gases.,Calcium,Totals.Bil.ALB.AlkalinePhosphatase,CreatinineS.Elect
rolytes.,LDH,SGOT,SGPT,CPK.
5. NS .500ml infused followed by further infusion ,according to clinical
picture and laboratory results.
6. Monitor temperature both rectally and peripherally / 5min.
7. Insert Foley's catheter, take urine sample for exam.
8. Start cooling like heat exhaustion management.
9. Sedation( valium 5-10 mg. iv slowly ) for convulsions .
10. NGT may be inserted if needed.
11. Correct acid base abnormality and electrolytes according ABGs
results.
12. Stop cooling when temp is less than 39
o
C .

NB
DON'T GIVE INSULIN IF THERE IS HYPERGLYCEMIA ( ONLY IF
PATIENT IS KNOWN TO BE DIABETIC YOU CAN THEN MANAGE.)

DON'T GIVE ANTIPYRETIC OR ANTIBIOTICS IN THE FIRST 6 HOURS
WITHOUT CLEAR REASON.

MAJORITY OF HEAT STROKE PATIENTS GET DIARREA, SO TREAT
THE DIARRHEA AND DEHYDRATION BY FLUID ONLY, NO DRUG
TREATMENT.

WATCH FOR BLEEDING, CONVULSIONS AND SIGNS OF
NEUROLOGICAL COMPLICATIONS.






References:

1. Cummins RO, etal : Advanced Cardiac Life Support, Provider Manual. AHA 2011 .
2. Fundamental Critical Care Support: Society of Critical Care Medicine 5
rd
Edition
2011.
3. Advanced Trauma Life Support for Doctors : American College of Surgeons
Committee on Trauma 9th Edition 2012
4. Stone C. Humpries R. Current Emergency Diagnosis and Treatment 5th Edition
2004
5. Osler's Emergency medicine 3rd edition 2002
6. Markovchick V, Pons P. Emergency Medical Secrets.3
rd
Edition 2003.
7. Coterino J, Kahan s.In a Page of Emergency Medicine. 1
st
Edition 2003.
8. Lefor A. Critical Care on Call. 1
st
Edition 2002
9. Haist S, Robbins J. Internal Medicine on Call 3
rd
Edition 2002
10. Ma O.J, etal: Emergency Medicine Maual. 6th Edition 2004
11. Biddinger P,etal: Emergency Medicine . 2
nd
Edition 2003
12. Tallia A, etal: Swanson's Family Practice Review, A problem-oriented approach.
a. 5
th
Edition
13. Al-Khuwaiter T, etal: Guidelines for treatment of hypertensive emergencies 2004
14. Standards for Accident & Emergency Departments in Ireland. EMS in Ireland-2009
15. Emergency Policy & Procedures. MOH, KSA
16. Subash F, etal:Team Triage Improves Emergency Department Efficiency:
Emer.Med. J 2004
17. Beveridge R,etal: Reliability of the Canadian Emergency Department Triage and
Acuity Scale. Ann. Emergency Medicine Aug.1999
18. Cambell S, Sinclair D. Strategies for Managing a Busy Emergency Department
19. Guidelines for Cardiac Care Resuscitation council UK.2011
19.Unified forms (Physical ex, progress notes, nursing notes) General
Directorate of Quality, Ministery of Health & Population























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2013 /33597

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977-17-2585-7 : ISBN




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Dr. Hamid Shaalan
e-mail : hshaalan90@hotmail.com