PROTOCOL of Management of Critical Cases

Arab Republic of Egypt
Ministry of Health & Population

Curative & Critical Care Sector
EMERGENCY DEPARTMENT
UNIFIED PROTOCOL
o Critical Conditions Commonly Encountered In ED
o Algorithms
Prepared By
WÜA [tÅ|w f{ttÄtÇA
Revised & Approved by

cÜÉyA atzãt XÄ [Éáá|xÇç WÜA [tÇç `ÉÜÉ
Supervised by
cÜÉyA atááxÜ etáÅ|A WÜA TuwâÄÄt{ ^twwt{
Cover designed by
WÜA `É{tÅxw fâÄàtÇ
Cairo2008
This publication is free, not for sale

Critical Cases Commonly Encountered In ED
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2
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 for more than come into
contact with 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.
The purpose of these standards is to establish an organized, safe,
efficient and customer service focused utilization of the Emergency
Depatment…..
Here are the third & forth parts, that I think they are very important
pillars in ED protocol implementation's success.
WÜA[tÅ|w f{ttÄtÇ
Vt|ÜÉ? ]tÇA ECCK
PART III
Protocols For Management

Of Critical Cases Commonly Encountered
In Ed
4
1- 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 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
5
I. 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.
1. 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.
6
1.2 Breathing With O2 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 value–mask 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%
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) > 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.
- 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.
7
** 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
• The pupil : 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 !!!
2 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.
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.
8
II 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 :(AMPLE)
A- Allergies
M- Medications currently used.
P- Post illness/frequency
L- Last meal
E- Events/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.
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).
9
- 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.
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: 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 U/S if haemodynamically unstable.
• CT IF the patient haemodynamically stable.
10
- Put 2 IV infusion with large bore cannulae.

- Transfer the patient to the operating room if indicated.
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, crepitation, 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 He
associated with pelvic fracture.
- Back :
• Log roll the patient, if a spinal injure is suspected.
• Inspect for : laceration, contusion deformity
• 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.
11
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
VI. Definitive Care :
- Rational for patient transfer.
- Direct doctor-to-doctor communication
- Transfer procedures.
- Patients needs during transfe
12
13
14
2- Rapid Sequence Intubation (RSI)
¾ 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.
¾ 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.
¾ Patients for whom intubation is likely to be difficult should not

have RSI
¾ Features of possible difficult intubation: obesity, short neck ,
short or long chin, airway deformity, limited oral opening, and
limited neck mobility.
¾ 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
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.
15
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 (Kellick'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.
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.
16
N.B
To calculate approximate tube size:
• For children: (age in years/4)+4
• For adults (> 12 years): 7-8 cuffed.
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.
17
3-SHOCK
I. Definition:
Shock is inadequate organ perfusion and tissue oxygenation.
‹
In adults, a systolic 90 mmHg, a mean arterial BP ‹60mmHg
or a decrease in systolic BP of 40 mmHg from the patient's
‹
baseline pressure and a pulse pressure 20 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
Loss Of Plasma
o Burns
o Exfolutive dermatitis
18
• 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
19
I. Stages of shock
3 main stages:
STAGE 1 : 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 2 : 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 3 : 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.
Confusion.
Fainting.
Nausea &vomiting.
Decreased or no urine output.
Excessive thirst.
20
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

Decrease peripheral of Patient complains of feeling cold,
Mild(‹ 20%of Bl. organs able to withstand postural hypotension, tachycardia.
Volume lost) prolonged ischaemia Cool, pale, moist skin. Collapsed
(skin, fat, muscles and neck veins,
bone) Concentrated urine.
Ph is normal.
Decrease central
Moderate(20%- perfusion of organs able Thirst, supine hypotension,
40% of Bl to tolerate only brief tachycardia,
volume lost) ischaemia (liver, kidney, oliguria or anuria.
gut).
Ph : metabolic acidosis.
Decrease perfusion of Agitation,confusion,obtundation.
Severe ( › 40% heart and brain. Supine hypotension and
of Bl .volume Metabolic acidosis is tachycardia,
lost.) severe. Rapid, deep respiration.
Respiratory acidosis may
also be present.
* These clinical findings are most consistently observed in

hemorrhagic shock but apply to other types of shock as well.
21
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 )
• Colloids ( e.g. 5% Albumin and hetastarch )
Both 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.
• 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.
22
2.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.
• 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, 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.
• 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.
23
• 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 after load reduction
(ACEinhibitors,nitroprusside).
3. Distributive Shock
• Hypotension.
• Wide pulse pressure.
• Mental status changes.
• Warm extremities.
• ↓ Urine output.
Septic Shock ( Temperature ↑ 38°C or ↓ 36°C,
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.
- 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
24
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, NaHCO3 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.
25
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.
26
27
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.
28
4.Hypertension &Hypertensive Emergencies
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
29
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 µ/kg/min and titrate up to of 1 µ/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 5µg/min. and titrate up until adequate control is
achieved ( maximum dose is 100 µg/min.)
30
II. Hypertensive Urgency

( Very high BP with no end-organ damage )
9 No urgency to lower BP to near normal in emergency

department, BP can be normalized in 24-48hs
9 Ask patient if he (she) missed his (her) medication, if
yes resume their medication with possibility of
increasing the dose.
9 Always aim for monothrapy, add other drug if no
response with maximum dose of one drug or if side
effect of the drug arises
9 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
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5- Acute Pulmonary Edema

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:
D MI / Ischaemia.
D Valvular disease (miteral, aortic stenosis).
D Cardiomyopathy.
D Pericardial effusion.
D Constrictive pericarditis.
D Hypertensive emergencies.
Non- cardiac:
D Sepsis. D Trauma.
D Inhalation injuries. D Near drowning.
D Drug (e.g. opioids, D Inhaled toxins.
salicylates).
D Renal failure. D DIC.
D High altitudes. D Airway obstruction (croup, FB
D Aspiration pneumonia. D Lung re-expansion.
D 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.
32
Diagnosis:
• Pulse oximeter: may reveal hypoxemia.
• Chest x-ray:
D Mild congestion may result in cephalization of pulmonary vessels,
pleural effusion.
D 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.
D Alveolar oedema (can be observed with it’s “butterfly” pattern)
characterized by the central predominance of shadows with a clear
zone at periphery lobes.
D Enlarged cardiac, silhouette may be present in chronic CHF.
• ABG:
D May reveal hypoxemia (↓ PO2 ) and respiratory alkalosis (↓PCO2
) due to Tachypnea.
D Respiratory acidosis (↑ PCO2 ) is an ominous sign of tiring and
impending respiratory failure.
D P02 values <50 mmHg and Pco2>50 mmHg denotes severity and
the need of mechanical ventilation.
D
• 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:
• Decrease hydrostatic pressure by venodilatation.
• 0.4 mg SL (can be repeated twice every 5 minutes as
long as there is no important decrease in BP
• If there is no response or ECG show ischaemia or
infraction given IV drips (10 mcg / min.) and titrated.
33
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. Inotropes( congestion by cardiac output).
D Dopamine (5-10 mcg / kg / min.) and titrate to a systolic BP
90-100 mmHg.
D Dobutamine (provided the patient is not in server Cardiogenic
shock) start 3 mcg / kg / min. and titrate to desired response.
7. Inhaled β2 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).
34
6-Basic Life Support

o It is the simple procedures which prevent circulatory or respiratory
arrest or insufficiency prompt and intervention.
o These simple procedures include:
• Open and clear airway ( Head tilt, Chin lift )
• Mouth to mouth breathing (through a barrier OR Ambu-baging )
• External cardiac compression
: 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 5th 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.
35
o The ABCD of CPR

Airway ( Assessment & management ) and then,
Breathing (Assessment & management) then,
Circulation ( Assessment &management) then,
Defibrillation (Assessment & management)
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
: Activate code blue.
: Start CPR until Defibrillator and team arrive
: Defibrillation if indicated
: Advanced cardiac life support actions to be followed
i.e. intubation, IV line for fluids and drugs etc….
Check the following algorithm, and keep it in your mind all the time
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Phone123
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7-Near Drowning (Submersion)
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

see 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.
41
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.
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
42
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
• 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.
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8-Management Of Convulsions In E D
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 O2 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).
44
9-Treament Of The Fit

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
IV 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 intubate
4. Thiopentone sodium
2-3 mg/kg/dose, maintenance 1 mg/kg as needed
45
10-Mangement Of Severe Bronchial Asthma
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
Treatment:
o Start β-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 ) 500µg might be added to
ventolin nebulizer.
46
o Those who fail to respond to initial β-agonist therapy should be

given IV or oral corticosteroids, start with methylprednisolone
125mg IV 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 β-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 β-agonist (Serevent) or steroid inhaler+ PRN
( Ventolin).
47
Moderate persistent
• Daily symptoms.
• Exacerbation affects activity and sleep.
• Night symptoms > once/week.
• PEF 60-80% of predicted.
TX. Inhaled long acting β-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 β-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 β-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.
48
11- How TO Read ECG

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.RR
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 square

otherwise it is wide.
Normal Absent R (VF) wide
49
° 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.
50
12-Cardiac Ischemia
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 – Obesity - 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
° 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.
51
° Pain is severe may occur 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
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Arrhythmia
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13- Management of Ischemic Attack

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.
57
Acute Coronary Syndromes Algorithm

1
Chest discomfort suggestive of
2 ischemia
EMS assessment and care and hospital preparation:

• Monitor, support ABCs. Be prepared to provide CPR and defibrillation
• Administer oxygen aspirin, nitroglycerin, and morphine if needed
• If available, obtain 12-lead ECG: if ST-elevation
- Notify receiving hospital with transmission or interpretation
- Begin fibrinolytic checklist (Figure 2)
• Notified hospital should mobilize hospital resources to respond to STEMI
3
Immediate ED assessment (<10 min) Immediate ED general treatment
• Check vital signs: evaluate oxygen • Start oxygen at 4 L/min:
saturation • Maintain O2 sat > 90%
Establish IV access • Aspirin 160 to 325 mg (if not given by EMS)
• Obtain/review 12-lead ECG • Nitroglycerin sublingual, spray, or IV
• Perform brief, targeted history, physical • Morphine IV if pain not relieved by
exam check contraindications (Table 1) nitroglycerin
• Obtain initial cardiac marker levels, initial
electrolyte and coagulation studies
4 Review initial 12-lead ECG
5 9 13
ST elevation or new or presumably ST depression or dynamic T-wave Normal or nondiagnostic changes
new LBBB; strongly suspicious for inversion; strongly suspicious for in ST segment or T wave
injury ischemia
10
6 14
Start adjunctive treatment as indicated
Start adjunctive treatment as (see text for contraindications) Develops high or intermediate risk
indicated (see text for • Nitroglycerin criteria (Tables 3. 4)
contraindications) • ß-Adrenergic receptor blockers OR
Do not delay reperfusion • Clopidogrel troponin-positive
• ß-Adrenergic receptor blockers • Heparin (UFH or LMWH)
• Clopidogrel • Glycoprotein llb/llla inhibitor 15
• Heparin (UFH or LMWH)
11 Consider admission to
7 ED chest pain unit or to
Time from onset of Admit to monitored bed
Assess risk status (Tables monitored bed in ED
symptoms ≤ 12 hours
3 4) Follow:
8 12 • Serial cardiac markers
Reperfusion strategy: High-risk patient (Tables 3, 4 for risk (including troponin)
Therapy defined by patient and center stratification):
• Repeat ECG/continuous ST
criteria (Table 2) • Refractory ischemic chest pain
• Recurrent/persistent ST deviation segment monitoring
• Be aware of reperfusion goals:
- Door-to-door balloon inflation • Ventricular tachycardia • Consider stress test
(PCI) goal of 90 min • Hemodynamic instability
- Door-to-needle (fibrinolysis) • Signs of pump failure 16
goal of 30 min • Early invasive strategy, including Develops high or
• Continue adjunctive therapies and: catheterization and revascularization for shock intermediate risk
- ACE inhibitors/angiotensin within 48 hours of an AMI criteria (Tables 3. 4)
receptor blocker (ARB) within 24 Continue ASA, heparin, and other therapies as OR
hours of symptom onset indicated. troponin-positive?
- HMG CoA reductase inhibitor • ACE inhibitor/ARB 17
(statin therapy) • HMG CoA reductase inhibitor (statin therapy) If no evidence of ischemia
• Not a high risk: cardiology to risk-stratify or infarction, can
discharge with follow-up
58
14-Approach To Surgical Causes Of Abdominal

Pain
• 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 medicall
• 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 (AMPLE)
• 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.
Abdominal pain ( The Dilemma )
1) Abdominal causes
2) Extra-abdominal causes
3) Metabolic & blood diseases
59
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.
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.
60
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
1. Progressive intestinal obstruction from a neoplasm or inflammatory
bowel disease
2. Paralytic Ileus
3. Post Operative
4. 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
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 )
61
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
• 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 & hernia orifices examination
62
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
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)
63
-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
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
• Rovsing’s Sign in Acute Appendicitis
• Obturator Sign in Pelvic Appendicitis
• Psoas Sign
- Retrocaecal appendicitis
- Crohn’s 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
64
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 retroperitoneal 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
65
15-Diabetic Ketoacidosis
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
100-150 1 unit/hour
• If the blood sugar is still very high, not responding to the above
mentioned dose, its dose can be doubled.
66
• 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
67
16- Hypoglycaemia
Biochemically, Hypoglycemia is defined as decrease of blood glucose
levelbelow40mg/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 (32.5OC-35oC) 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.
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 µg .
6. Oral feeding of fruit juice should be given as soon as the patient regain
consciousness.
68
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.
69
17- Coma
Definitions:
¾ Coma has been defined as unarousable and unresponsiveness to
stimulation, although reflex movements and posturing may be present.
¾ Other terms used to decreased level of consciousness:
D Stupor: severely impaired arousal with some response to vigorous
stimuli.
D Lethargy: a state in which arousal, though diminished, is
spontaneously maintained or requires only light stimulation.
D Obtundation: a lesser state of decreased arousal with some response
to touch or voice.
Etiology:
¾ 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.
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.
70
Signs of bilateral hemispheric dysfunction (e.g.decorticate posturing).

When progressive, signs of transtentorial herniation.
D 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.
D 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 doll’s eye or caloric testing
strongly suggest a subtentorial lesion.
Pinpoint pupils, non reactive, are often present in pontine or
cerebellar Hge or infarction.
N.B: cholinesterase inhibitors and opiates also produce pinpoint pupils.
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.
Approaches to Coma patient.
1. Evaluation of the comatose patient should progress as for any
patient in the ED.
2. Priorities include the initial ABC’s 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:
D Thiamine 100mg IV.
D Glucose: 50ml D 50% W (in children 2ml / kg of D25W) IV.
D Naloxone: 0.4-2mg IV.
71
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
2. Heart rate:
• Bradycardia, hypertension and bradypnea may indicate ICP
(Cushing’s 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.
72
B. Skin.
¾ Jaundice, spider angiomata, palmar erythema point to hepatic
encephalopathy.
¾ Petechiae and ecchymoses suggest a coagulation abnormality
or thrombocytopenia.
¾ A maculohemorrhagic rash suggests meningococcal infection,
staphylococcal endocarditis.
¾ Cherry-red skin suggests carbon monoxide poisoning.
¾ Needle marks on extremities indicate possible drug abuse.
¾ Check skin turgor.
C. Odor of the breath:
¾ A fruity odor suggests diabetic keto-acidosis.
¾ A uriniferous odor is found in uremia.
¾ Fetor hepaticus points to hepatic encephalopathy.
¾ The odor of alcohol is characteristic.
¾ A burnt almond odor is found with cyanide toxicity.
¾ A garlic scent maybe seen in arsenic poisoning.
D. Body orifices:
¾ Bleeding from the ears or nose suggests cranial trauma.
¾ Bleeding from other orifices suggests a bleeding disorder or
haemorrhage as the cause of coma.
E. Central nervous system:
¾ 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.
¾ 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 brudzinki’s sign i.e. flexion of the hips on passive flexion of
the neck.
• Positive Kernig’s sign i.e. pain or resistance of the hamstrings when
the knees are extended with the hips flexed at 90 degree.
¾ 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.
73
• Absence of oculocephalic (doll’s eye movement) and corneal reflexes

indicates pontine dysfunction.
• Oculovestibular reflexes (cold calorics) may be lost in brain stem
lesion.
¾ 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.
¾ 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.
¾ 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 cilture 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.
COMA In summary
Assessment & Complications
Coma is commonly associated with ingestion of large doses of
antihistamines, barbiturates, benzodiazepines and other sedative hypnotic
drugs, γ-hydroxybutyrate (GHB), ethanol, opioids,
phenothiazines, or antidepressants.
The most common cause of death in comatose patients is respiratory
failure, which may occur abruptly.
74
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%, 50–100 mL IV (unless bedside glucose
is normal).
Thiamine, 100 mg IM or IV.
Naloxone, 0.45 – 2 mg IV 1.
And consider flumazenil, 0.2 – 0.5 mg IV 2.
1
Repeated doses, up to 5–10 mg, may be required.
2
Do not give if patient has coingested a tricyclic antidepressant or other
convulsant drug or has a seizure disorder.
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 CO2 tension is useful in determining the adequacy of
ventilation. The arterial blood PO2 determination may reveal
hypoxemia, which may be caused by respiratory arrest,
75
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, 50–100 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 2–3 minutes intravenously.
B. Narcotic antagonists
Naloxone, 0.4–2 mg intravenously, may reverse opioid-induced respiratory
depression and coma.
If opioid overdose is strongly suspected, give additional doses of naloxone
(up to 5–10 mg may be required to reverse potent opioids
Caution:
Naloxone has a much shorter duration of action (2–3 hours) than most common
opioids; repeated doses may be required, and continuous
observation for at least 3–4 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, 0.2–0.5 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 (2–3 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 disorder—because its use in these
circumstances may precipitate seizures. In most circumstances, flumazenil is not
advised as the potential risks outweigh its benefits.
76
18- Animal Bite

¾ Rabies is a fatal disease, due to infection of CNS by a rhabdo virus.
¾ Transmitted by inoculation with infectious saliva or by salivary contact with
a break in the skin or mucus membrane.
¾ Foxes, cats, dogs, horses, camels, raccoons are more likely to be
infected.
¾ Rats, mice, rabbits, guinea pigs rarely transmit the virus to humans.
¾ 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.
¾ Differential diagnosis: Guillain-Barre syndrome, tetanus, meningitis,
encephalitis, polio, and brain abscess.
¾ 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). Don’t 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.
77
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.
78
19- Management of Scorpion sting

¾ 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.
¾ The toxins causes local pain, tenderness and swelling and rarely systemic
manifestations like vomiting, Dyspnea, hyperthermia, hypertension,
convulsion, acidosis and shock.
¾ Investigations
• CBC: lecucocytosis
• Biochemistry: blood glucose, CPK, LDH, amylase: ↑
• Electrolytes: Na, Ca: ↓ K ↑
• ABG: Acidosis
• ECG
• X-ray chest
¾ 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 ½
NaCl given IV over a period of 20 minutes. ¼ 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.
- 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
79
20-Management of Snake Bite

¾ There are 2 main types of poisonous snakes:
• Crotalids or pit vipers (hemotoxic venom): causing haemolysis,
necrosis, DIC e.g. rattlesnakes.
• Elapids (Neurotoxic venom): disrupt neuromuscular activity e.g. coral
snakes, cobras.
¾ 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.
¾ 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.
• 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.
80
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.
- 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.
81
82
Ingestion of an unknown
drug
Unconscious pt.
Conscious pt.
Patient
Stabilization
Stomach Physical exam.
Evacuation Baseline Lab
Investigations
Airway Breathing Circulation Altered mental status
Coma Cocktail: *** Ipecac* or Activated

Naloxone Glucose + thiamine Gastric Charcoal + Symptomatic
Lavage MgSo4** 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 mg
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
- Dermal,Eye, Inhalation
Oral
Dermal + Eye
Pyrethroids Caramate Organophophate
1. Removal of clothes
2. Local Irrigation of the
exposed are
Carbamate
Inhalation: No Antidote Suction of secretions until Establish an
1. Remove to fresh air. Symptomatic Full atropinization airway
2. Give oxygen if required Treatment only
LD: 10-100 mg
If any symptomaticManifestations refer to oral Is the patient
Exposure management 1. Comatosed
2. Convulsing
* Refer for dosing to the section: management of unknown ingestion 3. Without a gag reflex
** Treatment Guidelines:
Atropine: for treatment of muscrinic effects.
1. Diagnostic dose: IV/IM adult: 1 mg; child: 0.25 mg (0.02 mg/kg).
No Yes
If patient exhibit toxic effects of atropine (dry mouth, dilated pupil, and
rapid pulse) then probably not seriously poisoned. Induction of Emesis 1. Endotracheal
2. Dosage: IM/IV Mild symptomology, initially 2-4 mg (child 0.05 mg/kg) Intubation
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
Activated Charcoal + MgSo4*
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. Severe Symptoms with/or
Pralidoxime: for treatment of nicotinic manifestations, use as without Mild Symptoms
adjunct and not a substitute to atropine. 1. Weakness
Adult: 1-2 GM/IV in 100 ml NS 0.9% at 15-30 minutes.
2. Respiratory Depression
1. Child: 20-40 mg/kg IV.
Alternatively doses may be administered IM or SC. Atropine + Pralidoxime (for Carbamate give Atropine Therapy
2. Administration may be repeated x 3 or as needed at an interval of 8-12 atropine only) Atropinization should be alone
hours if muscle weakness has not been relieved. performed adequately & rapidly**
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 sufferin
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 ).
86
Burn injuries can be classified on the basis of the extent or 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.
87
% S.A .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
Superficial burns of greater than 50% of the body surface area
88
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 body’s 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
89
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.
21- Chemical Burns

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
22- 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
90
23- 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
91
Heat syndromes
Heat syndromes
Minor Major
Heat cramps Heat syncope Heat exhaustion
Heat fatigue Heat stroke
Heat oedema
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.
92
24- Heat Exhaustion

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.
93
25-Heat Stroke
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 40o C.
Pre-disposing 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 40oC.
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..
94
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).
95
26-Management of Heat Stroke

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.Electrolytes.,
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 .
1 0. NGT may be inserted if needed.
11. Correct acid base abnormality and electrolytes according ABGs results.
12. Stop cooling when temp is less than 39oC .
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.
96
Appendix
Algorithms
97
98
BRAYCARDIA ALGORITHM
1
PULSELESS ARREST
Heart rate <60 bpm and
inadequate for clinical
condition
2
• Maintain patent airway; assist breathing as needed
• Give oxygen
• Monitor ECG (identify rhythm), blood pressure, oximetry
• Establish IV access
3
Signs or symptoms of poor perfusion caused by the bradycardia?
(e.g. acute altered mental status, ongoing chest pain; hypotension or other
signs of shock)
4A 4
• Prepare for transcutaneous pacing;
Observe/Monitor use without delay for high-degree block
(type II second-degree block or third-
degree AV block)
• Consider atropine 0.5 mg IV while
awaiting pacer. May repeat to a total
dose of 3 mg. If ineffective, begin
pacing.
• Consider epinephrine(2 to 10 µg/min)
or dopamine (2 to 10 µg/kg per minute)
infusion while awaiting pacer or if
Reminders pacing ineffective
• If pulseless arrest develops, go to Pulseless Arrest

Algorithm 5
• Search for and treat possible contributing factors: • Prepare for transvenous pacing
• Treat contributing causes
- Hypovolemia - Toxins • Consider expert consultation
- Hypoxia - Tamponade, cardiac
- Hydrogen ion - Tension pneumothorax
(acidosis) - Thrombosis (coronary or
- Hypo- pulmonary
/hyperkalemia - Trauma (hypovolemia,
- Hypoglycemia increased ICP)
- Hypothermia
99
ACUTE CORONARY SYNDROMES ALGORITHM

1
Chest discomfort suggestive of
ischemia
2
EMS assessment and care and hospital preparation:
• Monitor, support ABCs. Be prepared to provide CPR and defibrillation
• Administer oxygen aspirin, nitroglycerin, and morphine if needed
• If available, obtain 12-lead ECG: if ST-elevation
- Notify receiving hospital with transmission or interpretation
- Begin fibrinolytic checklist (Figure 2)
• Notified hospital should mobilize hospital resources to respond to STEMI
3
Immediate ED assessment (<10 min) Immediate ED general treatment
• Check vital signs: evaluate oxygen • Start oxygen at 4 L/min: maintain O2 sat >
saturation 90%
• Establish IV access • Aspirin 160 to 325 mg (if not given by EMS)
• Obtain/review 12-lead ECG • Nitroglycerin sublingual, spray, or IV
• Perform brief, targeted history, physical • Morphine IV if pain not relieved by
exam check contraindications (Table 1) nitroglycerin
• Obtain initial cardiac marker levels, initial
electrolyte and coagulation studies
4 Review initial 12-lead ECG
5 9 13
ST elevation or new or presumably ST depression or dynamic T-wave Normal or nondiagnostic changes
new LBBB; strongly suspicious for inversion; strongly suspicious for in ST segment or T wave
6 injury ischemia
10 14
Start adjunctive treatment as Start adjunctive treatment as indicated
indicated (see text for (see text for contraindications) Develops high or intermediate risk
contraindications) • Nitroglycerin criteria (Tables 3. 4)
Do not delay reperfusion • ß-Adrenergic receptor blockers OR
troponin-positive
• ß-Adrenergic receptor blockers • Clopidogrel
• Clopidogrel • Heparin (UFH or LMWH)
• Heparin (UFH or LMWH) • Glycoprotein llb/llla inhibitor 15
7 11 Consider admission to
Time from onset of ED chest pain unit or to
Admit to monitored bed
symptoms ≤ 12 hours Assess risk status (Tables monitored bed in ED
3 4) Follow:
8 12 • Serial cardiac markers
Reperfusion strategy: High-risk patient (Tables 3, 4 for risk (including troponin)
Therapy defined by patient and center stratification):
• Repeat ECG/continuous ST
criteria (Table 2) • Refractory ischemic chest pain
• Recurrent/persistent ST deviation segment monitoring
• Be aware of reperfusion goals:
- Door-to-door balloon inflation • Ventricular tachycardia • Consider stress test
(PCI) goal of 90 min • Hemodynamic instability
- Door-to-needle (fibrinolysis) • Signs of pump failure 16
goal of 30 min • Early invasive strategy, including Develops high or
• Continue adjunctive therapies and: catheterization and revascularization for shock intermediate risk criteria
- ACE inhibitors/angiotensin within 48 hours of an AMI (Tables 3. 4)
receptor blocker (ARB) within 24 Continue ASA, heparin, and other therapies as OR
hours of symptom onset indicated. troponin-positive?
- HMG CoA reductase inhibitor • ACE inhibitor/ARB
17
(statin therapy) • HMG CoA reductase inhibitor (statin therapy) If no evidence of ischemia
• Not a high risk: cardiology to risk-stratify or infarction, can
discharge with follow-up
100
Goals for Management of Patients With Suspected Stroke Algorithm.

1 Identify signs of possible
stroke
2
NINE D’S Critical EMS assessments and actions
• Support ABCs; give oxygen if needed
TIME • Perform prehospital stroke assessment (Tables 1 and 2)
GOALS • Establish time when patient last known normal (Note: therapies
may be available beyond 3 hours from onset)
• Transport; consider triage to a center with a stroke unit if
appropriate; consider bringing a witness, family member, or
caregiver.
• Alert hospital
• Check glucose if possible.
ED Arrival
10 min 3
Immediate general assessment and stabilization
• Assess ABCs, vital signs
• Provide oxygen if hypoxemic
• Obtain IV access and blood samples
• Check glucose; treat if indicated
• Perform neurologic screening assessment
• Activate stroke team
• Order emergent CT scan of brain
• Obtain 12-lead ECG
ED
Arrival
25 min
4
Immediate neurologic assessment by stroke team or designee
• Review patient history
• Establish symptom onset
• Perform neurologic examination (NIH Stroke Scale or Canadian Neurologic
ED Scale)
Arrival
45 min 5
Does CT scan show any haemorrhage?
No Haemorrhage Haemorrhage
6
7
Probable acute ischemic stroke; consider fibrinolytic Consult neurologist or
therapy neurosurgeon; consider transfer if
• Check for fibrinolytic exclusions (Table 3) not available
• Repeat neurologic exam: are deficits rapidly improving
8 9
Patient remains candidate for Not a Administer aspirin
fibrinolytic therapy? Candidate
ED Arrival
60 min 10 • 11Begin stroke pathway
Candidate • Admit to stroke unit if available
Review risks/benefits with patient and family: • Monitor BP; treat if indicated (Table 4)
If acceptable – • Monitor neurologic status; emergent CT if
• Give tPA deterioration
• No anticoagulants or antiplatelet treatment for 24 • Monitor blood glucose; treat if needed
hours • Initiate supportive therapy; treat
comorbidities
101
Paediatric Healthcare Provider BLS Algorithm. Note that the boxes

with underlined text are performed by healthcare providers and not
by lay rescuers.
1
No movement or response
Send someone to phone EMS, get AED
2
Lone Rescuer: For SUDDEN COLLAPSE, PHONE
EMS, Get AED
3
Open AIRWAY, check BREATHING
4
If not breathing, give 2 BREATHS that make chest rise
5 5A
If no response, check pulse: Definite • Give 1 breath every 3
DEFINITE pulse Pulse seconds
within 10 seconds. • Recheck pulse every
2 minutes
6 No Pulse
One Rescuer: Give cycles of 30 COMPRESSIONS and 2 BREATHS
Push hard and fast (100/min) and release completely Minimize interruptions in
compressions
Two Rescuers: Give cycles of 15 COMPRESSIONS and 2
BREATHS
If not already done, PHONE EMS , for child get AED/defibrillator

Infant (<1 year): Continue CPR until ALS responders take over or victim starts to move
Child (>1 year): Continue CPR; use AED/defibrillator after 5 cycles of CPR
(Use AED as soon as it is available for sudden, witnessed collapse)
8 Child > 1 year:

Check rhythm
Shockable rhythm?
9 Shockable Not Shockable
10
Give 1 shock Resume CPR immediately for 5 cycles
Resume CPR immediately 5 cycles; continue until ALS providers
for 5 cycles take over or victim starts to move
102
103
104
105
ACLS PULSELESS ARREST ALGORITHM

1
PULSELESS ARREST
• BLS Algorithm: Call for help, give CPR
• Give oxygen when available
• Attach monitor/defibrillator when available
2
Shockable Not Shockable
Check rhythm
3 Shockable rhythm? 9
VF/VT Asystole/PEA
4 10
Give 1 shock
• Manual biphasic: device Resume CPR immediately for 5 cycles
specific (typically 120 to 200 J) When IV/IO available, give vasopressor
Note: if unknown, use 200 J • Epinephrine 1 mg IV/IO
• AED: device specific Repeat every 3 to 5 min , or
• Monophasic: 360 J • May give 1 dose of vasopressin 40 U IV / IO to replace first
Resume CPR immediately or second dose of epinephrine
• Consider atropine 1 mg IV/IO for asystole or slow PEA rate
5 Give 5 cycles of CPR* • Repeat every 3 to 5 min (up to 3 doses)
Check rhythm No
Shockable rhythm?
Give 5 cycles of
6 CPR*
Continue CPR while defibrillator is charging 11
Give 1 shock Check rhythm
• Manual biphasic: device specific (the same as Shockable rhythm?
first shock or higher dose)
Note: if unknown, use 200 J
• AED: device specific
Not
• Monophasic: 360 J Shockable Shockable
Resume CPR immediately after the shock
When IV/IO available, give vasopressor during
CPR (before or after the shock)
• Epinephrine 1 mg IV/IO
Repeat every 3 to 5 min 12
or
• May give 1 dose of vasopressin 40 U IV/IO to • If asystole, go to Box 10 13
replace first or second dose of epinephrine • If electrical activity, check pulse.
• If no pulse, go to Box 10 Go to
Box 4
7 Give 5 cycles of CPR* • If pulse present, begin
postresuscitation care
Check rhythm No
Shockable rhythm? CPR
• Push hard and fast (100/min)
• Ensure full chest recoil
8 Shockable
• Minimize interruptions in chest compressions
Continue CPR while defibrillator is charging • One cycle of CPR: 30 compressions then 2 breaths; 5 cycles – 2 min
Give 1 shock • Avoid hyperventilation
• Manual biphasic: device specific (the same as first shock or • Secure airway and confirm placement
higher dose) • After an advanced airway is placed rescuer no longer deliver cycles of CPR.
Note: if unknown, use 200 J • Give continuous chest compressions without pauses for breaths.
• AED: device specific • Give 8 to 10 breaths/minute.
• Monophasic: 360 J • Check rhythm every 2 minutes.
Resume CPR immediately after the shock • Rotate compressors every 2 minutes with rhythm checks
Consider antiarrhythmics after the shock (before or after the • Search for and treat possible contributing factors:
shock) • Hypovolemia
amiodarone (300 mg IV/IO once, then consider additional • Hypoxia
150mg IV/IO once) or lidocaine (1 to 1.5 mg/kg first dose, then • Hydrogen ion (acidosis)
0.5 to 0.75 mg/kg IV/IO, maximum 3 doses or 3 mg/kg) • Hypo/hyperkalemia
Consider magnesium, loading dose 1 to 2 g IV/IO • Hypoglycemi
for torsades de pointes
• Hypothermia
After 5 cycles of CPR,* go to Box 5 above
106
107
108
109
110
111
112
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.
113
114
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.
115
116
117
118
119
120
121
122
123
124
125
126
127
128
129
References:
1. Cummins RO, etal : Advanced Cardiac Life Support, Provider Manual. AHA 2006 .
2. Fundamental Critical Care Support: Society of Critical Care Medicine 3rd Edition
2001.
3. Advanced Trauma Life Support for Doctors : American College of Surgeons
Committee on Trauma 6th Edition 1997
4. Stone C. Humpries R. Current Emergency Diagnosis and Treatment 5th Edition
2004
5. Markovchick V, Pons P. Emergency Medical Secrets.3rd Edition 2003.
6. Coterino J, Kahan s.In a Page of Emergency Medicine. 1st Edition 2003.
7. Lefor A. Critical Care on Call. 1st Edition 2002
8. Haist S, Robbins J. Internal Medicine on Call 3rd Edition 2002
9. Ma O.J, etal: Emergency Medicine Maual. 6th Edition 2004
10. Biddinger P,etal: Emergency Medicine . 2nd Edition 2003
11. Tallia A, etal: Swanson's Family Practice Review, A problem-oriented approach.
a. 5th Edition
12. Al-Khuwaiter T, etal: Guidelines for treatment of hypertensive emergencies 2004
13. Standards for Accident & Emergency Departments in Ireland. EMS in Ireland-2001
14. Emergency Policy & Procedures. MOH, KSA
15. Subash F, etal:Team Triage Improves Emergency Department Efficiency:
Emer.Med. J 2004
16. Beveridge R,etal: Reliability of the Canadian Emergency Department Triage and
Acuity Scale. Ann. Emergency Medicine Aug.1999
17. Cambell S, Sinclair D. Strategies for Managing a Busy Emergency Department
18. Guidelines for Cardiac Care Resuscitation council UK.200
19.Unified forms (Physical ex, progress notes, nursing notes) General
Directorate of Quality, Ministery of Health & Population
130
‫‪Critical Cases Commonly Encountered In ED‬‬
‫ﺷﻜﺮ ﺧﺎﺹ ﳌﻨﻈﻤﺔ ﺍﻟﺼﺤﺔ ﺍﻟﻌﺎﳌﻴﺔ ﳌﺴﺎﳘﺘﻬﺎ ﰲ ﻃﺒﺎﻋﺔ ﻫﺬﺍ ﺍﻟﺪﻟﻴﻞ‬
‫ﻫﺬﺍ ﺍﻟﺪﻟﻴﻞ ﳎﺎﱐ ﻭ ﻏﲑ ﻣﺼﺮﺡ ﺑﺒﻴﻊ‬
‫ﲨﻴﻊ ﺍﳊﻘﻮﻕ ﳏﻔﻮﻇﺔ‬

‫ﻻﳚﻮﺯ ﻃﺒﺎﻋﺔ ﺃﻭ ﻧﺴﺦ ﻫﺬﺍ ﺍﻟﺪﻟﻴﻞ ﻛﻠﻴﺎ ﺃﻭ ﺟﺰﺋﻴﺎ ﺇﻻ ﺑﻌﺪ ﻣﻮﺍﻓﻘﺔ ﻛﺘﺎﺑﻴﺔ ﻣﻦ ﺍﳌﺆﻟﻒ‬
‫‪E-mail : hshaalan90@ hotmail.com‬‬
‫‪131‬‬

PROTOCOL of Management of Critical Cases

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PROTOCOL of Management of Critical Cases

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Ministry of Health & Population

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‫מ‬ ‫א‬ ‫א‬

Non-urgent visits comprise a significant proportion of total pts.,

The ED also providers for reception and management of disaster

To achieve our goal towards offering best service according to

Protocols For Management

1- Initial Assessment And Management Of

I. Primary Survey And Resuscitation

1.2 Breathing With O2 Supplementation

1.3 Circulation With Control Of Hemorrhage :

** Prevent hypothermia during assessment and

1.5 Exposure/Environment Control :

Re-evaluate the patient :

Remember : life saving SHOULD BE initiated when the problem

- If Maxillofacial injury or fracture compromises the airway :

- Put 2 IV infusion with large bore cannulae.

IV Adjuncts To The Secondary Survey :

2- Rapid Sequence Intubation (RSI)

¾ RSI refers to technique of simultaneous administration of a

¾ Patients for whom intubation is likely to be difficult should not

• Loss of fluids and electrolytes

 Symptoms Associated With Specific Cause

Type Pathophysiology Clinical manifestation

* These clinical findings are most consistently observed in

• Indices Of Successful Resuscitation

• Blood : Whale blood or packed red blood cells is indicated in

• PTCA( Percutaneous Transluminal Angiopathy

Figure 2 Anaphylactic Reactions: Treatment Algorithm for Children by First

1 An inhaled beta2-agonist such as salbutamol may be used as an adjunctive measure if bronchospasm

Anaphylactic Reactions: Treatment Algorithm for Adults

Consider when compatible history of severe allergic-type

Repeat in 5 minutes if no clinical

1. An inhaled beta2-agonist such as salbutamol may be used as an adjunctive measure

4.Hypertension &Hypertensive Emergencies

II. Hypertensive Urgency

9 No urgency to lower BP to near normal in emergency

• Nifedipine ( Adalat ) should not be given

5- Acute Pulmonary Edema

• COPD. • Pulmonary embolism.

• Blood studies: CBC, Electrolytes, BUN and Creatinine.

4. Furosemide (40-80 mg IV bolus) causes venodilatation, decrease

6-Basic Life Support

o These simple procedures include:

• Open and clear airway ( Head tilt, Chin lift )

• Mouth to mouth breathing (through a barrier OR Ambu-baging )

• External cardiac compression

o External cardiac compression give 25% of original Cardiac Output.

o It contract around 70 times/min, every contraction ejects 70 ml of blood,

o Respiratory center is located in the brain which is stimulated by the

o Adult respiratory rate is about 12-15 times/min.

Room air contain 21%O2 – our expiration contain 16% O2

o Brain damage occurs after 4 minute of cardio-respiratory arrest.

o The ABCD of CPR

 Breathing (Assessment & management) then,

 Circulation ( Assessment &management) then,

 Defibrillation (Assessment & management)

7-Near Drowning (Submersion)

• Drowning: Death from suffocation following submersion.

• Near Drowning: Survival after suffocation following submersion

• Secondary Drowning: Death due to complication > 24h after

• Wet Drowning: Consists of aspiration of water into lungs causing

Symptoms Associated With Specific Cause

Breathing (Assessment & management) then,

Circulation ( Assessment &management) then,

Defibrillation (Assessment & management)

Spontaneous return of consciousness often occurs in healthy individuals

Patient with more severe near-drowning may experience frank pulmonary

A few patients may be asymptomatic during the recovery period, only

The most common cause of convulsion is Epilepsy.

° Rate If regular rhythm use _300____

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

Aspiration of gastric contents may also occur, especially in victims who