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DR. HAMID SHAALAN. FRCS Ed. Consultant G. Surgery And Emergency Medicine.

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بسم اهللا الرحمن الرحيم)اً َجِميع النـاسَ أَْحيـَا َفَكأَنَما أَْحيـَاَها َوَمنْ )

صدق اهللا العظيم

INTRODUCTION

The emergency department (ED) is an integral unit of a hospital and the experience of patients attending the ED significantly influences the public image of the hospital offering medical service. Thousands of people attend ED every year or more come into contact with one or any other hospital service .Some of them are acutely ill or injured and need immediate, sometimes life-saving treatment. Many of whose condition are not so serious, require urgent assessment and treatment for their injury or sickness. Non-urgent visits comprise a significant proportion of total pts., attending ED , but still their medical conditions have to be evaluated and managed. The ED also providers for reception and management of disaster plan in the region. For these reasons EDs have a high public profile and are viewed by many as essential local service. To achieve our goal towards offering best service according to accepted standards, this proposed plan for developing and evolution EDs. is created. This plan suggests :

I ) Structure and Manpower Standards . II ) Policies and Procedures. III ) Protocols for management of critical cases commonly

encountered in ED. IV) Algorithms.

V) Procedural skills.

The purpose of these standards is to establish an organized, safe, efficient and customer service focused utilization of the Emergency Depatment….. Here are the 2nd updated revised edition of third part , that I think they are very important pillars in ED protocol implementation's success.

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PART III

PROTOCOLS FOR MANAGEMENT OF CRITICAL CASES COMMONLY ENCOUNTERED

IN ED

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Initial Assessment And Management Of Polytrauma

Objectives :

1. To identify the correct sequence of assessing the polytrauma patient. 2. To apply the Guidelines of priorities for the primary and secondary

survey. 3. To resuscitate and manage life threatening injuries.

General principles

1) Follow ( A, B, C and D ) 2) Maintain spinal stabilization at all times. 3) Evaluate and treat simultaneously 4) Do not add further harm 5) The primary and secondary survey should be repeated at

the time and adverse change is identified. 6) In actual clinical situation, may of these activities occur in

parallel or simultaneously.

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

I. Rapid primary survey and resuscitation. II. Adjuncts to primary survey. III. Detailed secondary survey. IV. Adjuncts to secondary survey. V. Re-evaluation VI. Definitive care.

"There is a Golden hour between life and death. If you are critically injured you have less than 60 minutes to survive. You might not die right then; it may be three days or two weeks later -- but something has happened in your body that is irreparable." Dr. R. Adams Cowley, Shock Trauma Center section of the University of

Maryland Medical Center

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

Primary survey :

1.1 Airway with C-Spine protection - Initial assessment should be done without moving the neck . (if possible) • It must be assumed that the casualty (especially if they are unconscious

or has any significant injury above the clavicles ) has a cervical spine injury , until can be excluded.

• Check the patient's responsiveness by gentle shaking them by the shoulder or giving a command.

• If the patient is able to communicate verbally, the airway is not likely to be obstructed.

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

• Chin left or jaw thrust maneuver: clear the airway of foreign bodies. • Insert an oropharyngeal or nasopharyngeal airway. • Establish a definitive airway.

- Orotracheal or nasotracheal intubation. - Surgical cricothyroidotomy.

- Apply a rigid cervical collar and only remove it to examine the neck further while maintaining full spinal immobilization.

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• Soft collar - In general, this decreased rotation by 8 degrees but insignificantly protected against flexion and extension.

• Hard collars - A variety of collars available . They all allowed about 8% flexion, 18% lateral movement, and 2% rotation. The Philadelphia collar allowed the least extension.

• Sandbags and tape - Surprisingly, this was the best. It allowed no flexion and only a few percent movement in any other direction.

1.2 Breathing With O 2 Supplementation - A) Assessment

• Expose the neck and the chest. • Determine the rate and depth of respiration. • Look for tracheal deviation, chest movement, asymmetry, use of

accessory muscles and signs of injury • Listen for movement of air on both sides of the chest. • Percussing for dullness or hyper-resonance.

- B) Management • Administer high flow O2 (10L/min.) • Ventilate with ambu-bag (a bag 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 9 5%

Sizing and fitting Cervical Collar

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

d) fitting anterior part e) stretching the strip and fix to anterior f) put head suppot or sand bags on both sides

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Tension pneumothorax is a clinical diagnosis

• History of penetrating trauma, positive pressure ventilation or airways disease

• Air hunger • Hypotension • +/- distended neck veins • +/- hyperresonant on tension pneumothorax side

Do NOT x-ray - this is a clinical diagnosis

• Immediate needle decompression.

• Confirm side clinically.

• Inform patient.

• 14G cannula .

• 2nd intercostal space

• Insert vertically while aspirating

• Note air bubbling.

• Protect with gauze.

• Tape and leave in situ.

• Prepare chest drain for insertion.

1.3 Circulation With Control Of Hemorrhage : � Assessment : - Check the patient's

• Skin colour • Pulse • Bp • Identify source of external major hemorrhage. • Identify any evidence of hypovolemic shock.

� Management : - Basic and advanced cardiac life support if needed. - Apply direct pressure to external bleeding site. - Vascular access by inserting 2 large bore peripheral IV cannulae

(14-16gauge). The desirable sites in adult are the forearm or antecubital veins >

- Central venous(femoral, subclavian, jugular ) if not in profound hypovokemia to avoid complications > Cutdown for saphenous vein.

- In pedia , forearm > intraosseous > femoral > cutdown age less than 6 years.

- Obtain blood sample for CBC, Bio-Chemistry – type & cross match, blood gases.

a) Locate 2

nd ICS midclvicular line b) While aspirating insert vertically a

Sterile using Betadine 14G cannula a,ached to a syringe with NS

c) Protect and tape

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- Fluid therapy with warm Ringer's Lactate, normal Saline, (Initially 1-2 liters for an adult, and 20 ml/kg for pediatric patient in first 10 minutes.) and blood replacement.

- Splint any long bone fracture. - Consider using pneumatic anti-shock garment (PSAG). - Operative intervention. ** Prevent hypothermia during assessment and management

1.4 Disability - Rapidly assess the patient's central (brain)

and peripheral (spinal cord) neurological status.

- CNS : • AVPU scale( Alert ,responds to Verbal command,respnds to Pain

,Unresponsive) • The pupils : size, equality and reactivity.

- Peripheral nervous system • Ask the patient if he can feel : Fingers, toes. • Ask the patient to squeeze your hand with his fingers.

1.5 Exposure/Environment Control : - The patient should be completely undressed.

Prevent hypothermia ****** II Adjuncts to Primary Survey : • Vital sign • ABGs • Pulse oximeter and exhaled CO2 • Urinary & gastric catheters unless contraindicated. • Urine output hourly. • ECG • X-ray (chest, pelvis &lat. Cervical spine( C7-T1 should be visualised) • Ultrasound or DPL • Consider early transfer

- Referring doctor receiving communication is essential. - Don't delay transfer for diagnostic tests. - Use time before transfer for resuscitation.

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Re-evaluate the patient : Before beginning secondary survey be sure that :

- The primary survey is completed. - The ABCD are reassessed. - Vital functions are normal

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

Airway Adjuncts: 1- Oropharyngeal Airway

A correctly positioned O/P Airway O/P Airway showing flange , body ,and tip Sizing O/P Airway .Measured from

incisors to angle of the jaw

Step –by- step guide

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

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2-Naso-pharyngeal Airway

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

Inserting the lubricated tube with bevel towards medial Direct upwards while rolling gently

Bag-Valve Mask

Holding B/V Mask E/C Technique

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Needle Cricothyrotomy

Papate Cricothyroid mem brane Puncture midsagitally with a 12-14 canula attached to a syringe .Direct caudally at angle 45 °° while aspirating

Aspirating air signifies entery into trachea, remov e stylet with syringe and fix O 2 tube .

Secure in place , Apply intermittened ventilation

III Secondary Survey :

Components : - History - Physical examination : Head-to-toe - Special diagnostic procedures. - Re-evaluation of the patient. Secondary survey can be summarized as tubes and fin gers in every orifice.

History : A- Allergies M- Medications currently used. P- Post illness/frequency L- Last meal

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E- Events ( mechanism of injury)/Environment related to the injury. � Blunt trauma � Penetrating injury � Burns � Chemicals, toxins, radiation

Physical examination : 1. Head :

• GCS • Monitor the level of consciousness at regular intervals • Look for

- Any obvious injury - Mastoid staining/bruising - CSF leakage : Rhinorrhea, otorrhea - Eye : injury, Hge, foreign body

• Palpate for – lacerations, swellings, depression, fractures at the base of lacerations.

• Hemorrhage from the scalp should be stopped with pressure dressing.

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2. Maxillo-facial :

Palpate the face for deformities and tenderness. - If there is facial injury :

• Check for loose or lost teeth. • Grasp the upper incisor and check for the maxilla (suggesting a

middle third fracture).

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

Cervical Spine & Neck :

• Patients with maxillofacial or head trauma should be presumed to have cervical spine fracture/or ligamentous injury .

• Stabilize the neck in a semi-rigid cervical collar and a rigid spine board until the patient reaches the hospital.

• Repeat the neurological examination to assess motor power, sensation and reflexes.

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3. Chest : - Inspect the anterior, lateral and posterior chest w all for:

� Tracheal deviation ( a late sign) � Signs of resp. obstruction : stridor, intercostal recession � Asymmetrical chest movement. � Wounds � Bruising

- Palpate for : � Tenderness & crepitus over the ribs & sternum, clavicle. � Subcutaneous emphysema. � Blunt & penetrating injury

- Percussion for hyperresonance or dullness. - Auscultation : breath & heart sounds Management :

o Tension pneumothorax : needle decompression, chest tube o Flail chest : Intubation and ventilation o Open chest wound : Cover with an occlusive dressing and

tape down on three edges. o Cardiac tamponade : Pericadiocentesis

4 . Abdomen : - Inspect: the anterio r and posterior abdomen for : Brusing,

movement and open wounds and distension. - Palpate for : Tenderness, involuntary muscle guarding, rebound

tenderness - Auscultate: for bowel sounds - Investigations :

• X-ray pelvis • DPL or FAST if haemodynamically unstable. • CT IF the patient haemodynamically stable.

- Put 2 IV infusion with large bore cannulae. - Transfer the patient to the operating room if indic ated.

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5 . Perineum/Rectum/Vagina : • Perineum : Laceration, contusion, hematomas, urethral

bleeding • Rectum : Rectal blood, anal sphincter tone, bowel wall

integrity, pelvic fracture, prostate position • Vagina : Vaginal laceration, blood in vaginal vault

6. Musculoskeletal : - Extremities :

• Inspect for laceration, contusion, deformity, burns. • Palpate for : tenderness, crepitations, abnormal movement,

peripheral pulses (presence, absence, equality) • Apply appropriate splinting for extremity fractures.

- Pelvis fracture : • Suspected by ecchymosis over iliac wings, pubis, labia or

scrotum • Palpable for : tenderness, mobility, leg length uneven • X-ray pelvis • Apply the pneumatic antishock garment for control of Hge

associated with pelvic fracture. - Back :

• Log roll the patient, if a spinal injury is suspected. • Inspect for : laceration, contusion deformity

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• Palpate for : tenderness, Bogginess, irregularity of the contour of spinous process

• Auscultate the back of the chest. • Immobilization of the back.

7. neurological Examination : - Re-evaluate the patient level of consciousness, papillary size and

response. - Re-determine GCS. - Evaluate the upper & lower extremities for motor & sensory

functions. - Early neurological consultation if needed. - Adequate oxygenation ventilation and perfusion. - Immobilization of the entire patient - Document any neurological deficits when identified.

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

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

V . Re-evaluation : - Revaluate the patient constantly to minimize missed injures and

to discover any deterioration. - Continuous monitoring of vital sings, urine output, cardiac

monitoring, pulse oximeter - Relief sever pains by I.V. opiates or anxiolytics

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

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Management of Multiple Trauma

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2- Rapid Sequence Intubation (RSI)

� RSI refers to technique of simultaneous administration of a sedative

agent (induction) and neuromuscular blocker along with cricoid pressure designed to facilitate intubation and reduce the risk of gastric aspiration.

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

� Patients for whom intubation is likely to be diffic ult should

not have RSI

� Features of possible difficult intubation: obesity, short neck , short or long chin, airway deformity, limited oral opening, and limited neck mobility.

� Steps: 1. Preparations:

Ensure that all needed items are available (IV line,O2,monitor, suction, different sizes endotracheal tube, laryngoscope, assess airway, draw medications.

2. Pre-oxygenation: 100%O2 for 3 minutes by mask, if ventilatory assistance is necessary, ventilate gently to avoid stomach inflation and possible regurgitation.

3. Pre-medication: depending on the underlying condition of the patient.

• Fentanyl: 2-3 mcg/kg IV for analgesia in a wake patient. • Midazolam (sedation, amnesia, hypnosis, NO analgesia) 0.1-

0.3mg/kg IV, onset 30 seconds, last 15-20 minutes. • Atropine: 0.01 mg/kg IV for children or adolescent if there is

bradycardia. • Lidocaine : 1-2 mg/kg IV, to suppress response in HTN, IHD

ICP. • Morphine: 0.1mg/kg in pulmonary edema.

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4. IV induction agent

• Thiopental (provides sedation, amnesia, hypnosis) - A short acting highly lipid soluble barbiturate. - Dose 1-4mg/kg, Onset: 60 seconds, duration 5-50 min. - Side effects: Respiratory depression, apnea myocardial depression, hypotension anaphylactoid reaction - Advantage: ICP and cerebral 02 consumption, rapid onset &

short duration, consider an alternative drug in pregnancy. - Effect antagonized by aminophylline.

• Propofol • Ketamine • Etomidate

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

6. paralysis (neuromuscular blocking agent): • Succinylcholine (Scoline): dose: 1-1.5 mg/kg in adults, 1.5-2

mg/kg in children, depolarizing neuromuscular blocker, rapid onset < 60 see, short duration (6min). Side effects: Fasciculation (pre treat with small dose(1-2mg) of Pancuronium or vecuronium), hyperkalaemia (e.g. in renal failure, crush injury, burns, mitral stenosis) trismus, malignant hyperthermia, bardycardia (pretreat with atropine in children), hypotension, ICP , intraocular pressure, Histamine release may cause bronchospasm or anaphylactoid reaction. Contraindications:

� Risk factors for hpyerkalaemia � Hereditary pseudocholinesterase deficiency � Penetrating ocular trauma or glaucoma.

• Recuronium: (esmeron) - A rapid onset, short acting a nondepolarising neuromuscular

blocking agent (NDNMB). - Dose: 0.6 mg/kg, 1-2 minutes, duration 30 minutes - Excellent choice for NDNMB, good alternative for use when

succinylcholine is contraindicated.

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

8. Post-intubation management : secure tube, provide long-term

paralysis and sedation as indication mechanical ventilation. N.B 1. To calculate approximate tube size:

• For children: (age in years/4)+4 • For adults (> 12 years): 7-8 cuffed.

2. Long term paralysis • Pancuronium (pavulon)

- A longer-acting NDNMB. - Dose: 0.05-0.2 mg/kg onset 1-3 minutes. Duration dose

dependant, averaging 60-90 minutes. - Main use is prolonged blockade after intubation is complete - No elevated intracranial pressure or fasciculation - Contraindication: hypersensitivity to Pancuronium, IHD,

HTN. • Atracurium (Tracurim)

- Dose : 0.4 mg/kg, onset 3-5 minutes, duration 20-25 minutes

- Contraindications: Hypotension – Bronchial asthma - Advantage: best in renal failure – liver failure.

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33--SSHHOOCCKK

I Definition:

� Shock is inadequate organ perfusion and tissue oxyg enation.

� 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 d eath.

� Management should be directed towards correcting hypoperfusion , NOT HYPOTENSION, as a primary endpoint.

II Pathophysiology

• In most cases, tachycardia is the first sign of shock. Progressive vasoconstriction of cutaneous and visceral circulation.

• The release of catecholamines increases peripheral vascular resistance.

• This increases diastolic blood pressure and decreases pulse pressure. Increase aldosterone secretions, which retain sodium and water to expand blood volume.

• Aerobic metabolism will be shifted to anaerobic one with development of metabolic acidosis.

III Types & common causes of shock:

1. Hypovolemic shock

� Loss of blood( Haemorrhagic shock )

o Trauma o Hematoma o Hemothorax or hemoperitoneum

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� Loss of plasma

o Burns o Exfolutive dermatitis

� Loss of fluids and electrolytes

o Vomiting o Diarrhea o Excessive sweating o Ac. Pancreatitis o Ascitis o bowel obstruction

2.Cardiogenic shock o Dysrhythmia

- Tacharrhythmia - Bradyarrhythmia

o Pump failure

- MI - Cardiomyopathy

o Acute valvular dysfunction

3.Obstrutive shock � Tension pneumothorax � Pericardial disease( tamponad,constriction) � Disease of pulmonary vasculature

- Massive pulmonary embolism -Pulmonary hypertension

� 0bstructive valvular disease - Aortic stenosis - Mitral stenosis

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

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I. Stages of shock

3 Main stages:

STAGE I : Compensation stage:

The body is able to compensate for loss in the circulation.

Reflex sympathetic activation leads to tachycardia and

peripheral vasoconstriction, so maintaining BP and cardiac

output.

Signs and symptoms of shock may be minimal as the

compensation is effective

( Volume loss up to 15% of COP. Pulse < 100, urine output > 30ml/hr ,BP

normal, CNS normal or anxious).

STAGE II : Decompensation stage: The body's compensation functions are working at full

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

STAGE III : Irreversible stage

When prolonged shock has produced irreversible cellular

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

IV Symptoms and signs of shock: General symptoms

� Anxiety & nervousness. � Dizziness. � Weakness.

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� Confusion. � Fainting. � Nausea &vomiting. � Decreased or no urine output. � Excessive thirst.

Symptoms associated with specific cause • Symptoms associated with hypovolemia. • External (bleeding) or internal Hge . • Pain of burn. • Pain of Pancreatitis. • Chest pain-{cardiogenic}. • Fever, rigors,{ septic shock}.

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

Type

Pathophysiology

Clinical manifestation

Mild(‹ 20%of Bl. Volume lost)

Decrease peripheral of organs able to withstand prolonged ischaemia (skin, fat, muscles and bone) Ph is normal.

Patient complains of feeling cold, postural hypotension, tachycardia. Cool, pale, moist skin. Collapsed neck veins, Concentrated urine.

Moderate(20%-40% of Bl volume lost)

Decrease central perfusion of organs able to tolerate only brief ischaemia (liver, kidney, gut). Ph : metabolic acidosis.

Thirst, supine hypotension, tachycardia, oliguria or anuria.

Severe ( › 40% of Bl .volume lost.)

Decrease perfusion of heart and brain. Metabolic acidosis is severe. Respiratory acidosis may also be present.

Agitation,confusion,obtundation. Supine hypotension and tachycardia, Rapid, deep respiration.

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

V. Management of shock:

A.General management of shock ( all types ) i. Airway ii. Breathing iii. Circulation iv. Disability

( See INITIAL ASSESSMENT & MANAGEMENT )

B.Specific treatment :

1- Hypo-volaemic shock • Treatment of hypovolaemic shock should be aggressive and

directed by response to therapy than by initial classification of Hge.

• Crystalloids (e.g. 0.9% NaCl & LR ) and colloids ( e.g. 5% Albumin and hetastarch ) are equally effective if given in sufficient amount for restoration of intravascular volume .

An initial fluid bolus is given as rapidly as possible. The usual dose is 1-2 Liters for an adult and 20ml/kg for a pediatric patient. A rough guideline for total amount of crystalloid volume acutely required to replace each ml of blood with 3ml of crystalloid fluid ( 3 for 1 rule ). Dextrose 5% should not be used to treat hypovolemic shock as it is rapidly distributed throughout body fluid compartment.

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

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

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1. Cardiogenic shock

� Diagnosis • ECG may reveal arrhythmia, MI, ischemia,

electrolyte abnormalities. • CXR can show signs of CHF (vascular

congestion, Kerley B lines), wide mediastinum in aortic dissection.

• Cardiac enzymes for MI as troponin & CPK-MB., and Troponin I

• ECHO to identify pericardial tamponade of effusion

• Pulmonary artery catheterization reveals decreased cardiac output index (< 2.2 L/min./m2), ↑ wedge pressure (> 18 mmHg), ↑ systemic vascular resistance, ↑ peripheral O2 extraction.

• CBC, • Coagulation profile • Bl. chemistries.

� Treatment • Airway control with intubation or CPAP as necessary • IV access, pulse oximetry, cardiac monitoring • Rhythm disturbances, hypoxia,hypovolemia, and electrolyte

abnormalities should be identified and treated immediately. Monitor urine output hourly.

• Patient should chew and swallow Aspirin 160-325 mg, unless contraindicated.

• Morphine IV in 2mg, repeated if needed. Hemodynamic parameters should be monitored.

• IV Inotrope administration: -Dopamine(2.5-20mcg/kg/min.)for hypotensive patients

to cause inotropy and vasoconstriction. -Dobutamine(2.5-20mcg/kg/min)for normotensivepatient

to cause ↑inotropy.

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• Nitroglycerine (5-100mcg/min) to ↓ preload

→↑COP. • Na nitroprusside (0.5-10mcg/kg/min) to improve

COP by ↓ of after load.

• Norepinephrine may be used if is no or poor response to other pressors infusion. It should be started at 2mcg/min and titrated to desired effect.

• PTCA( Percutaneous Transluminal Angiopathy ) is preferred method for reperfusion in cases of cardiogenic shock following MI, Thromblytics are much less effective in shock state.

• Intra-aortic balloon pump placement may be used as temporizing measure to decrease after load,so improving perfusion and cardiac arrest.

NB: - Drugs causing preload reduction :loop diuretics( furosemide or bumetanide) and vasodilators (nitroglycerine and morphine). - Drugs causing afterload reduction ACE inhibitors,nitroprusside. 3- Distributive shock

• Hypotension. • Wide pulse pressure. • Mental status changes. • Warm extremities. • ↓ Urine output.

� Septic shock ( Temperature ↑ 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.

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

o SEPTIC SHOCK - Remove source of infection e.g. catheter, I&D abscess. - Blood, urine and sputum for culture. -Empiric antibiotic therapy IV against gram-positive and gram-

negative organisms. Anaerobic organisms may be considered in some cases.

- acidosis is treated : O2, ventilation and fluid replacement, 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.

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Figure 2 Anaphylactic Reactions: Treatment Algorit hm 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.

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Anaphylactic Reactions: Treatment Algorithm for Adu lts

Consider when compatible history of severe allergic-type

reaction with respiratory difficulty and/or hypotension especially if skin changes present

Oxygen treatment when available

Stridor, wheeze, respiratory distress or clinical signs of shock1

Adrenaline (epinephrine)2,3

1:1000 solution 0.5 mL (500 micrograms) IM

Repeat in 5 minutes if no clinical improvement

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

IN ADDITION If clinical manifestations of shock

For all severe or recurrent do not respond treatment drug reactions and patients give 1-2 litres IV fluid.4 Hydrocortisone Rapid infusion or one repeatdose

100-500 mg IM/or slowly IV may be necessary

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

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TTrraauummaa TTeeaamm The trauma team is ideally made up of a group of doctors, nurses, operating department assistants, radiographers and other support personnel who have no other commitment that day than to receive and treat trauma patients. This is a very expensive arrangement. If the doctors involved are residents, senior consulting staff should be immediately available if necessary. Many centers now have their trauma teams led by consultants. Core Trauma Team is group of professionals that re ceives and treats the patient:

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

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Additional staff need to be mobilized to provide an cillary services:

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

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

� Neurosurgeon � Thoracic Surgeon � Plastic Surgeon � Radiologist

Certain areas need early notification of the traum a victim.

� CT Scanner � Intensive Care � Theatres � The core trauma team comprises 10 people working around a single

patient. � everyone must know their place and their tasks, and has the skills,

equipment and support to accomplish these. � The trauma room should be quiet so that the voice of the team leader

can be heard and assessments from team members can be relayed back to him.

� Vital signs should be called out every five minutes and these must be heard by everyone.

Trauma Team Tasks The Team Leader Responsibilities

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

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� Record audit information. � Dismiss and debrief team members. � Educate trauma team. � The trauma team leader should be the most experienced team member

present before the patient arrives in hospital. � The leader's role should not be superseded by late arriving members

or passing senior staff. � This avoids confusion for team members of who to take direction from

and who to report to. Anaesthetist Responsibilities

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

General Surgeon Responsibilities

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

Orthopaedic Surgeon

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

Emergency Room Physician

� Intravenous access. � Venous and arterial blood samples. � Thoracostomy. � Urinary Catheter. � Assist with diagnostic peritoneal lavage

Some overlap is necessary between the general surgeon, orthopaedic surgeon and emergency department physician to ensure that tasks continue simultaneously and no time is lost and no hands wasted.

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Nursing staff

� If their is no anaesthetic assistant , one nurse should be solely dedicated to the anaesthetist.

� Nurses should attach themselves to each hands-on surgeon or ED physician and assist in their tasks

� Nurses should not have to leave the resuscitation room to fetch equipment or run samples to the labs.

� Ancillary staff should be outside the main resus. area to provide this. Radiographer

� Radiographer should immediately start with the trauma series of X-rays,

I. Cervical Spine, II. Chest,

III. Pelvis unless directed otherwise by the team leader.

� Once these have been processed, other views may be required by evidence of other injuries.

� The radiographer should also act as liaison to the CT scanning department.

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

passing through the leader is then passed to the scribe

Records � Time of arrival. � Mechanism of injury. � Personnel present at call � Physical findings � Vital signs; Urine output, Glasgow Coma Scale. Results of X-rays and

other investigations. � Fluids administered. � Drugs administered. � Previous Medical History. � Summary of injuries. � Disposal of patient

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

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AAnnggiiooeeddeemmaa

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

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

It is either hereditary, allergic, or idiopathic.

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

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

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

(ACE) inhibitor-induced angioedema Hereditary angioedema

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Emergency department treatment and disposition

Airway protection remains the primary focus of emergency treatment.

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

Medical therapy includes steroids, H1 and H2 histamine blockers, and s/c or i/m epinephrine.

Chronic angioedema responds better to corticosteroids and H2 blockers . Disposition depends on the severity and resolution of symptoms. I) Patients with symptomatic improvement or showing no worsening after 4 hours of observation may be discharged home. Discontinue suspected medications. II) Airway involvement requires admission to a monitored environment with surgical airway equipments at bedside. ADVICE: 1- Do not underestimate the degree of airway involvement, act early to preserve airway patency.

2- Angioedema can also cause gastrointestinal and neurologic involvement.

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

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

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EEyyee iinnjjuurr iieess

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

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

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

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

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

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

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

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

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Dealing with chemical damage to the eye ● Immediately wash out eye with water ● Remove loose particles ● Refer patient to ophthalmic department ● Beware alkalis

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

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

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Penetrating injuries of the eye can be missed because they may seal themselves, and the signs of abnormality are subtle. Any history of a high velocity injury (particularly a hammer and chisel injury) should lead one strongly to suspect a penetrating injury. In that case, the eye should be examined very gently and no pressure should be brought to bear on the globe. It is possible to cause prolapse of intraocular contents and irreversible damage if the eye and orbit are no t examined with great care . Signs to look for include a distorted pupil, cataract, prolapsed black uveal tissue on the ocular surface, and vitreous haemorrhage. The pupil should be dilated (if there is no head injury) and a thorough search made for an intraocular foreign body. If there is a suspicion of an intraocular or orbital foreign body then orbital x ray photographs, with the eye in up and down gaze, should be taken. If the eye is clearly perforated it should be protected from any pressure by placing a shield over the eye, and the patient should be sent immediately to the nearest eye department. Sympathetic ophthalmia, in which chronic inflammation develops in the normal fellow eye, is a potentially serious complication of any severe penetrating eye injury. The risk of this increases if a penetrating eye injury is left untreated. All penetrating eye injuries should receive immediate specialist ophthalmic management without delay .

RReedd eeyyee

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

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

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than bacterial conjunctivitis and may go on for many weeks; patients need to be informed of this. Photophobia and discomfort may be severe if the patient goes on to develop discrete corneal opacities. Examination —Both eyes are red with diffuse conjunctival injection (engorged conjunctival vessels) and there may be a clear discharge. Small white lymphoid aggregations may be present on the conjunctiva (follicles). Small focal areas of corneal inflammation with erosions and associated opacities may give rise to pronounced symptoms, but these are difficult to see without high magnification. There may be associated head and neck lymphadenopathy with marked pre-auricular lymphadenopathy. Managemen t—Viral conjunctivitis is generally a self Limiting condition, but antibiotic eye drops (for example, chloramphenicol) provide symptomatic relief and help prevent secondary bacterial infection. Viral conjunctivitis is extremely contagious, and strict hygiene measures are important for both the patient and the doctor; for example, washing of hands and sterilising of instruments. The period of infection is often longer than with bacterial pathogens and patients should be warned that symptoms may be present for several weeks. In some patients the infection may have a chronic, protracted course and steroid eye drops may be indicated if the corneal lesions and symptoms are persistent. Steroids must only be prescribed with ophthalmological supervision, because of the real danger of causing cataract or irreversible glaucomatous damage. Furthermore, if long term steroids are required, patients should remain under continuous ophthalmological supervision. Topical steroids should not be prescribed or continued without continuous ophthalmological supervision potentially blinding complications may occur Chlamydial conjunctivitis History —Patients usually are young with a history of a chronicbilateral conjunctivitis with a mucopurulent discharge. There may be associated symptoms of venereal disease. Patients generally do not volunteer genitourinary symptoms when presenting with conjunctivitis; these need to be elicited through questioning. Examination —There is bilateral diffuse conjunctival injection with a mucopurulent discharge. There are many lymphoid aggregates in the

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conjunctiva (follicles). The cornea usually is involved (keratitis) and an infiltrate of the upper cornea (pannus) may be seen. Management —The diagnosis is often difficult and special bacteriological tests may be necessary to confirm the clinical suspicions. Treatment with oral tetracycline or a derivative for at least one month can eradicate the problem, but poor compliance can lead to a recurrence of symptoms. Systemic tetracycline can affect developing teeth and bones and should not be used in children or pregnant women. Associated venereal disease should also be treated, and it is important to check the partner for symptoms or signs of venereal disease (affected females may be asymptomatic). It often is helpful to discuss cases with a genitourinary specialistbefore commencing treatment, so that all relevant microbiological tests can be performed at an early stage. In developing countries, infection by Chlamydia trachomatis results in severe scarring of the conjunctiva and the underlying tarsal plate. These cicatricial changes cause the upper eyelidsto turn in (entropion) and permanently scar the already damaged cornea. Worldwide, trachoma is still one of the major causes of blindness. Conjunctivitis in infants Conjunctivitis in young children is extremely importantbecause the eye defences are immature and a severe conjunctivitis with membrane formation and bleeding may occur. Serious corneal disease and blindness may result. Conjunctivitis in an infant less than one month old (ophthalmia neonatorum) is a notifiable disease . Such babies must be seen in an eye department so that special cultures can be taken and appropriate treatment given. Venereal disease in the parents must be excluded. Allergic conjunctivitis History—The main feature of allergic conjunctivitis is itching. Both eyes usually are affected and there may be a clear discharge. There may be a family history of atopy or recent contact with chemicals or eye drops. Similar symptoms may have occurred in the same season in previous years. It is important to differentiate between an acute allergic reaction and a more long term chronic allergic eye disease. Examination —The conjunctivae are diffusely injected and may be oedematous (chemosis). The discharge is clear and stringy. Because of the fibrous septa that tether the eyelid (tarsal) conjunctivae, oedema results in round swellings (papillae). When these are large they are referred to as cobblestones. Management —Topical antihistamine and vasoconstrictor eye drops provide short term relief. Eye drops that prevent degranulation of mast cells also are useful, but they may need to be used for several weeks or months to achieve maximal effect. Oral antihistamines may also be used, particularly the newer compounds that cause less sedation. Topical steroids are effective but

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

Corneal ulceration

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

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

Acute angle closure glaucoma Acute angle closure glaucoma always should be considered in a patient over the age of 50 with a painful red eye. The diagnosis must not be missed or the eye will be damaged permanently. History —The attack usually comes on quite quickly, characteristically in the evening, when the pupil becomes semidilated. There is pain in one eye, which can be extremely severe and may be accompanied by vomiting. The patient complains of impaired vision and haloes around lights due to oedema of the cornea. The patient may have had similar attacks in the past which were relieved by going to sleep (the pupil constricts during sleep, so relieving the attack). The patient may have needed reading glasses earlier in life. A patient with acute angle closure glaucoma may be systemically unwell, with severe headache, nausea, and vomiting, and can be misdiagnosed as an acute abdominal or neurosurgical emergency. Acute angle closure glaucoma also may present in patients immediately postoperatively after general anaesthesia, and in patients receiving nebulised drugs (salbutamol and ipratropium bromide) for pulmonary disease. Examination —The eye is inflamed and tender. The cornea is hazy and the pupil is semidilated and fixed. Vision is impaired according to the state of the cornea. On gentle palpation the eye feels harder than the other eye. The anterior chamber seems shallower than usual, with the iris being close to the cornea. If the patient is seen after the resolution of an attack the signs may have disappeared, hence the importance of the history. Features of acute angle closure glaucoma ● Pain ● Hazy cornea ● Haloes around lights ● Age more than 50 ● Impaired vision ● Eye feels hard ● Fixed semidilated pupil ● Unilateral Management —Urgent referral to hospital is required. Emergency treatment is needed if the sight of the eye is to be preserved. If it is not possible to get the patient to hospital straight away, intravenous acetazolamide 500 mg should be given, and pilocarpine 4% should be instilled in the eye to constrict the pupil. First the pressure must be brought down medically and then a hole made in the iris with a laser (iridotomy) or surgically (iridectomy) to restore normal aqueous flow. The other eye should be treated prophylactically in a similar way. If treatment is delayed, adhesions may form between the iris and the

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

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HHyyppeerrtteennssiioonn &&hhyyppeerrtteennssiivvee eemmeerrggeenncciieess

� 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

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� 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.)

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

� No urgency to lower BP to near normal in emergency department, BP can be normalized in 24-48hs

� Ask patient if he (she) missed his (her) medication, if yes resume their medication with possibility of increasing the dose.

� Always aim for monothrapy, add other drug if no response with maximum dose of one drug or if side effect of the drug arises

� The following are available option:

• Nifedipine ( Adalat ) should not be given sublingually

• May give Nifedipine retard 20mg BID ( maximum dose 40 mg TID ), if unavailable give Nifedipine 10mg TID ( maximum dose 20mg TID )

• If no contra-indicated to beta blocker (renal failure, bradycardia, or bronchial asthma ) may give Atenolol( Cardol,Hypoten,or Tenormin) 50 -100mg OD

• If no contra-indication to ACEI (Renal artery stenosis, hyperkalemia), may give Captopril( Capoten) 12.5mg-50mg TID

• Indipamide (Natrilix) 205mg is good add on drug to Captopril

• Furosimide (Lasix) is good diuretic if edema is present (use initially small dose 20mg OD to BID

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AAccuuttee PPuullmmoonnaarryy EEddeemmaa

o It is one of the most common medical emergencies and very life

threatening. o Signs and symptoms represent the transference of fluids from the

pulmonary capillaries into the pulmonary interstitial and alveolar air spaces.

o Causes: • Cardiac:

� MI / Ischaemia. � Valvular disease (miteral, aortic stenosis). � Cardiomyopathy. � Pericardial effusion. � Constrictive pericarditis. � Hypertensive emergencies.

• Non- cardiac: � Sepsis. � Trauma. � Inhalation injuries. � Near drowning. � Drug (e.g. opioids,

salicylates). � Inhaled toxins.

� Renal failure. � DIC. � High altitudes. � Airway obstruction (croup,

FB). � Aspiration pneumonia. � Lung re-expansion. � ARDS.

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

peripheral oedema and cardiac murmur or rub.

� Differential diagnosis :

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

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� Diagnosis: • Pulse oximeter : may reveal hypoxemia. • Chest x-ray:

� Mild congestion may result in cephalization of pulmonary vessels, pleural effusion.

� Interstitial oedema (Kerley B lines) i.e. horizontal lines seen laterally in the lower zones, 2cm long at least, that, on the contrary of blood vessels reach the lung edge.

� Alveolar oedema (can be observed with it’s “butterfly” pattern) characterized by the central predominance of shadows with a clear zone at periphery lobes.

� Enlarged cardiac, silhouette may be present in chronic CHF. • ABG:

� May reveal hypoxemia (↓ PO2 ) and respiratory alkalosis (↓PCO2 ) due to Tachypnea.

� Respiratory acidosis (↑ PCO2 ) is an ominous sign of tiring and impending respiratory failure.

� P02 values <50 mmHg and Pco2>50 mmHg denotes severity and the need of mechanical ventilation.

� • ECG: vent, hypertrophy, conduction abnormalities and Ischaemia /

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

� Treatment: • (O2, preload reducers, diuretics, after load reducers and in tropic

agents). 1. Put the patient in sitting position with legs dangling over the side of the

bed in order to make perspiration easier and to reduce venous return. 2. Administer 100% O2 by mask:

� If hypoxia persist despite O2 therapy, continuous positive airway pressure (CPAP) or biphasic airway pressure should be applied.

� Immediate intubation is indicated for unconscious or visibly tiring patients.

3. Nitroglycerine: o Decrease hydrostatic pressure by

venodilatation. o 0.4 mg SL (can be repeated twice every 5

minutes as long as there is no important decrease in BP

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

4. Furosemide (40-80 mg IV bolus) causes venodilatation, decrease after load by volume reduction.

5. Morphine (2-3 mg IV) and repeat as needed reduce anxiety, sympathetic activity, venodilatation, its use is controversial, may cause respiratory depression and add little to O2, diuretics and nitrates.

6. In tropes( congestion by cardiac output). � Dopamine (5-10 mcg / kg / min.) and titrate to a systolic BP 90-100

mmHg. � Dobutamine (provided the patient is not in server Cardiogenic shock)

start 3 mcg / kg / min. and titrate to desired response. 7. Inhaled B2 agonist or aminophylline IV to treat bronchospam that may

occur in response to pul. Oedema. (Aminophylline renal blood flow, excretion of Na, cardiac contraction, venodilatation – side effects: Tachycardia and supraventricular arrhythmia).

8. Digoxin ( 0.25 mg in a slow IV push) can be given if AF and rapid vent. reasons is a contributory factor. The total dose 1-1.5 mg IV in the first 24 hours.

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

63

BBaassiicc LLii ffee SSuuppppoorrtt

o It is the simple procedures which prevent circulato ry or respiratory

arrest or insufficiency prompt

Basic knowledge o BLS at this level can be considered primarily a public community

responsibility.

o Our heart position is behind lower two third of the sternum with its apex to

the left in the 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-respir atory

arrest .

64

To start CPR The patient is

- Unresponsive

- Breathlessness

- Pulselessness

Once life threatening condition recognized Chain Of Survival

( Sequences of action linked together too tightly w ith no gap ) should be followed

The links include the following:

• Immediate recognition of cardiac arrest and activation of the

emergency response system.

• Early CPR with an emphasis on chest compressions • Rapid defibrillation • Effective advanced life support • Integrated post–cardiac arrest care

65

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

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70

71

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73

NNeeaarr DDrroowwnniinngg ((SSuubbmmeerrssiioonn))

General consideration

• Drowning : Death from suffocation following submersion.

• Near drowning: Survival after suffocation following submersion

• Secondary drowning : Death due to complication > 24h after submersion

• Wet drowning : Consists of aspiration of water into lungs causing washout of

surfactant, which results in diminished alveolar gas transfer, atelectasis and

ventilation perfusion mismatch. Non-cardiogenic pulmonary edema results from

moderate to severe aspiration.

• Dry drowning : results from laryngospasm causing hypoxemia and different degree

of neurologic insult and represents up to 20% of submersion injuries.

• The rapid sequence events after submersion (hypoxia, laryngospasm, fluid

aspiration, ineffective circulation, brain injury and brain death) may occur within 5-

10 minutes.

• The difference in the pathophysiology of fresh water ( hypotonic ) and sea water (

hypertonic ) usually have little clinical significance in humans ,because the amount

of fluid aspirated in most patients is small. The primary effect in both instances is

disruption of vascular endothelium and dilution of pulmonary surfactant, with

resulting atelctasis and perfusion of poorly ventilated alveoli.

• Hypoxia, acidosis and hypo-perfusion of vital organs are common factors accounting for high incidence of illness and death associated with drowning.

• Resuscitation can extend longer time than other cases of arrest due to hypothermia.

Clinical findings:

The victim of near-drowning may present with wide range of clinical manifestations:

� Spontaneous return of consciousness often occurs in healthy individuals when

submersion is brief. Others may respond promptly to immediate artificial ventilation.

� Patient with more severe near-drowning may experience frank pulmonary failure,

pulmonary edema, shock, anoxic encephalopathy, cerebral edema or cardiac arrest.

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� 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, hemoglo binuria, ketonuria

• ABG Hypoxemia,or co mbined metabolic& respiratory

acidosis.

• CXR Pneumonitis or pulmonary edema.

• C-spine X ray To exclude spine inj ury specially in diving injury

TREATMENT

• Take the patient from the water to dry area, remove all wet clothes and avoid hypothermia (cover him with blanket, warm atmosphere).

• Immobilize him on long spinal board with cervical collar assuming he has spinal injury

• Resuscitation must start at scene rapidly. Do not waste time to drain water from the victim's lungs or stomach as there is only a minimal volume of water in the lungs.( however, if a tense, water-filled stomach prevents adequate lung expansion, place the victim supine, perform Hemlich Maneuver ) clear the victim's mouth with finger sweep.

• Start rapid CPR, Rescue Breathing. Do not press over the abdomen or thrust as these will make complications.

• Intubate for hypoxia, poor respiratory effort, decline respiratory status.

• If pulse can't be detected, start chest compression according to ACLS protocols.

• Core temperature should be monitored, warmed IV. NS. and warming adjuncts should be used if the patient is hypothermic.

• Hypothermic victims in Cardiac Arrest should undergo prolonged, aggressive resuscitation until they are normothermic or considered nonviable.

• Antibiotics, steroids are not indicated for prophylactic pulmonary protection

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• 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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MMaannaaggeemmeenntt OOff CCoonnvvuullssiioonn

IInn EEmmeerrggeennccyy DDeeppaarrttmmeenntt

� 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

Investigation s:

• 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).

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TTrreeaammeenntt OOff TThhee FFii tt

Protect the patient form injury during resuscitatio n.

1. Airway :

Open airway, suction, protect from aspiration and put in recovery position

2. Breathing:

Supply O2 through face mask or endotracheal intubation as needed, guided by pulse

oximeter to ensure O2 saturation > 94%.

3. Circulation :

Insert peripheral line and take blood sample for the above-mentioned investigation

4. Drugs .

1. Diazepam (Valium)

o Adult: 5-10 mg/dose - repeat 5 min as needed for 3 times

o Paedia: 0.3 mg/kg/dose – repeat twice every 5 minutes

In paedia, if no IV line, give valium rectally

• If Diazepam fail to control the fit or after contr olling the fit start

2. Phenytoin sodium

° Adult: 15-20 mg/kg bolus over 20 min - repeat 10mg/kg if not controlled

° Paedia: loading dose 10 mg/kg/– repeat after 2 hours 5mg/kg, infuse

1mg/kg/min

If seizures persist may need intubation

3. Phenobarbital

° Adult:l15-20 mg/kg over 30 min. if persist, second dose 7mg/kg

° Paedia: 2-5 mg/kg over 15 min

If seizures persist need intubation

4. Thiopentone sodium

2-3 mg/kg/dose, maintenance 1 mg/kg as needed

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MMaannggeemmeenntt OOff

SSeevveerree BBrroonncchhiiaall AAsstthhmmaa

Clinical picture:

Severe shortness of breath.

Usual precipitating factors

• Non-compliance with medications.

• Exposure to allergens or medications.

• Sinus infection(URTI)

• Stress.

History Should include prior HX, of intubation, hypoxic seizure or ICU admission.

On Examination:

1. Cannot complete one sentence

2. Respiratory rate > 25/min

3. Heart rate > 110/min

4. On auscultation, bilateral wheezes with respiratory distress

5. Arterial blood gas respiratory alkalosis, then in prolonged severe attack it

becomes acidosis

6. Treatment:

o Start 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.

o Those who fail to respond to initial β-agonist therapy should be given IV or oral corticosteroids, start with methylprednisolone 125mg IV

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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).

Moderate persistent

• Daily symptoms.

• Exacerbation affects activity and sleep.

• Night symptoms > once/week.

• PEF 60-80% of predicted.

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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.

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HHooww ttoo rreeaadd EECCGG

P Wave : Atrial depolarization.

QRS Complex: Ventricular depolarization.

PR Interval: Conduction time from atrium to ventricles.

T Wave: Ventricular repolarization

ECG. Interpretatiion ( For arrhythmia & ischemia )

o Rhythm Regular R-R equal distance.

Irregular R-R unequal distance.

° Rate If regular rhythm use 300 .

Number of big square bet.R-R

If irregular a) Count 30 big square

b) Count number of R Waves inside 30

big square

c) Number of R X 10 = HR/MIN

° R Wave present or no , width must be less than 3 small

squares otherwise it is wide.

Normal Absent R (VF)

wide

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° 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.

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CCaarrddiiaacc IIsscchheemmiiaa

Definition of the terms: o Arteriosclerosis means thickening and lost elasticity. o Atherosclerosis means arteriosclerosis plus irregular inner wall

due to fat deposits. So blood flow is reduced. o Coronary heart disease means coronary atherosclerosis plus

angina or history of acute MI. o Ischemic heart disease is a more general term (poor oxygen

supply to the myocardium).

RISK FACTORS: ° Non-Changeable Risk factors

Heredity – sex – race – age.

° Changeable & controlable risk factors

SMOKING – HYPERLIPIDEMIA – DIABETES - HIGH BP.

° Contributing risk factors

STRESS – OBISITY - LACK OF EXERCISE.

Clinical syndromes of coronary heart disease

° Variable presentation, presumptive diagnosis. Exam. May be normal and nonspecific.

° Coronary artery lesion may rapidly evolve through plaque disruption and vessel occlusion.

° Hypoxemia, shock, anemia, etc. may reduce Myocardial oxygen supply.

° Increased myocardial demandial O2 .Demand may exceed supply capability.

° Angina pectoris is transient retrosternal (crushing, pressing,

constricting or heaviness) may radiate to lt. shoulder or both,

inner of lt. arm, neck and jaw, epigastrium and back. Pain is

induced by effort or stress and lasts 2-15 min. Pain relieved by rest and/or

nitroglycerine

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° Acute myocardial infarction due to severe narrowing or complete blockage

of a diseased coronary artery. It leads to injury to myocardium then death of

the muscle. Pain is severe MAY OCCURE AT REST OR DURING

SLEEPING and may be associated with nausea and sweating. Chest pain

may be atypical not relieved by rest or nitroglycerine. Usually lasts for more

than 15 min.

° It may show signs of complications ( hypotension, bradycardia, arrhythmia,

heart failure ).

° Sudden cardiac death (cardiac arrest), in 80% is due to ventricular

fibrillation , 15% asystole and 5% pulseless electrical activity.

° Cardiac enzymes : CK rises4-6 hours after infarction, CK-MB more

specific. SGOT and LDH will rise later on.

° Echocardiogram.

° ECG FINDINGS

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Arrhythmia

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90

MMaannaaggeemmeenntt ooff IIsscchheemmiicc AAttttaacckk

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.

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AApppprrooaacchh TToo SSuurrggiiccaall CCaauusseess OOff AAbbddoommiinnaall PPaaiinn

• Although abdominal pain is common and often trivial, acute and severe pain nearly always is a symptom of intra-abdominal disease.

• Abdominal pain is one of the most common presentations in emergency department. The most important concern is to decide if the condition requires surgical intervention or can be managed medically

• Common causes of abdominal pain are listed in the following illustrations.

Initial Evaluation History Physical exam Investigations Sound interpretation

• Diagnosis can be made most of the time by a good history and a proper physical examination.

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

History (AMPLEHF) • Allergy to drug or asthma. • Medication or History of drugs taken . • Previous surgery , blood transfusion & past Medical history • Last meal & last menses in female. • Event that could have led to the problem ( in patient opinion.) • History of Present illness • Family History

Pain The Most Important Symptom History of pain should include:

• Location ( site , radiation & reference ) • Quality (character & severity ) • Time (onset , Duration, course & Change in nature of Pain) • Aggravating or alleviating factors • Associated symptoms. • Other relevant symptoms of same affected system.

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

1) Extra-abdominal causes e.g.

• Otitis media & upper respiratory tract infection specially in children. • Sudden raised intracranial pressure & intraocular pressure. • Pneumonia specially basal and in children. • Hip arthritis .

2) Metabolic & blood diseases e.g.

• Diabetic keto-acidosis • Hypercalcemia • Lead poisoning • Porphyria • Sickle cell crises • Uremia & acidosis.

Is it truly difficult ? • The history and physical examination are crucial to determine the most

likely causes of an acute abdomen. • The precise location of abdominal pain and tenderness helps the

practitioner to make a differential diagnosis. Although there are many acute abdominal conditions, only a few causes are common

3) Abdominal pain ( the key )

• The location of referred abdominal pain is based on the embryological origin of the affected organ.

• The location of peritoneal irritation (somatic pain ) depends on the anatomical position of the diseased organ.

• In cases where the diagnosis is not clear, repeated physical examination at frequent intervals will often clarify the diagnosis

Peritoneal irritation • Peritoneal irritation can be localized or generalized. Findings that are

important indications for surgery, are: • Abdominal tenderness , suggesting inflammation of an underlying

organ ::Rebound abdominal tenderness elicited by percussion, which confirms peritoneal irritation :: Involuntary contraction of the abdominal wall, a sign of peritoneal irritation, which presents as local guarding or generalized rigidity .

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Referred abdominal pain • Fore gut pain (stomach, duodenum, gall bladder) is referred to the

upper abdomen • Mid gut pain (small intestine, appendix, right colon is referred to the mid

abdomen • Hind gut pain (mid transverse, descending, sigmoid colon and rectum)

occurs in lower abdomen • Diseased retroperitoneal organs (kidney, pancreas) may present with

back pain • Ureteric pain radiates to the testicle or labia • Diaphragmatic irritation presents as shoulder tip pain.

Onset of Pain • Sudden onset pain which wakes up the patient from sleep

e.g.. perforation or strangulation of bowel • Slow insidious Onset

e.g.. Inflammation of visceral peritoneum. • Crampy or colicky pain

Biliary colic, Ureteric colic or Intestinal colic

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

Associated Bowel Symptoms

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

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

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Nausea & vomiting � Frequency of vomiting � Character of vomiting: projectile, non-projectile or self-induced � Nature of vomiting: a. Bilious vomiting of small bowel obstruction b. Non-bilious vomiting in obstruction proximal to ampulla of Vater c. Feculent vomiting in distal small gut obstruction, large bowel

obstruction , strangulation � Vomiting is very prominent in.

1. Acute gastritis, 2. Acute pancreatitis. 3. High intestinal obstruction. 4. Biliary colic & acute cholecystitis. 5. Ureteric colic. 6. Acute appendicitis. (Anorexia with pain is usually seen or infrequent

vomiting ) Relevant items in history

• Past Surgical history: previous operations- leading to adhesions • Past Medical history: Sickle cell disease, Diabetes or Cancer or Renal

failure • Menstrual History in females

(i) Missed period- ectopic pregnancy (ii) Mid of period-ovulation pain (Mittel- schmetz) (iii) With heavy periods- endometriosis

• Family history of colon cancer, any other malignancy or inflammatory bowel disease

Physical examination

Look , Feel , Listen

• When doing a physical examination: Determine the vital signs – Rapid respiration may indicate pneumonia – Tachycardia and hypotension indicate patient decompensation Irregular pulse (AF, POSSIBLE MESENTERIC ISCHEMIA) – Temperature is elevated in gastrointestinal perforation and normal in gastrointestinal obstruction

• Look for abdominal distension • Percuss to differentiate gas from liquid

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• Palpate the abdomen – Start away from the site of tenderness – Check for masses or tumors – Determine the site of maximum tenderness – Check for abdominal rigidity

• Guarding- involuntary spasm of muscles during palpation • Rigidity- when abdominal muscles are tense & board-like. Indicates

usually surgical cause. • Listen for bowel sounds

– Absence is a sign of peritonitis or ileus – High pitched tinkling indicates obstruction

• Always examine: – Groin for incarcerated hernia – Rectum for signs of trauma, abscess, obstruction – Vagina for pelvic abscess, ectopic pregnancy, distended pouch of Douglas.

• Abdominal examination is never complete without back ,PR & hernial orifices exam.

Helping examples a. Anxious Patient lying motionless: (i) Acute appendicitis (ii) Peritonitis b. Rolling in bed & restless: (i) Ureteric Colic (ii) Intestinal colic c. Writhing in Pain: Mesenteric Ischemia d. Bending Forward: stooping Pancreatitis e. Jaundiced: CBD obstruction f. Dehydrated (i) Peritonitis (ii) Small Bowel obstruction

• Ruptured AAA or ectopic pregnancy can lead to -Pallor -Hypotension -Tachycardia -Tachypnea

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

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High grade temp . is seen with - Salpingitis - Abscess , pyelonephritis Very High Grade Temp .with increasing lethargy seen in - Imminent septic shock - Peritonitis - Acute cholangitis - Pyonephrosis

Systemic Examination

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

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

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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

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Non-specific abdominal pain • It is the most common cause of abdominal pain in late childhood and

early adolescence. It is a colicky pain with some localization that becomes worse after meals. Bowel sounds may be increased and a palpable mass of feces may be present in right or left iliac fossa. The causes commonly are constipation, irritable bowel and chronic spasm.

• The treatment consists of antispasmodics

INVESTIGATIONS Laboratory

• Complete Blood Count with differential • Blood sugar. • Electrolyte ,Blood Urea , Creatinine • Urine dipstick • Amylase or Lipase • Liver Function Test Radiology 1) Upright X ray chest for - Basal Pneumonia - Ruptured Esophagus - Elevated Hemi- diaphragm - Free Gas under diaphragm 2) Abdominal X ray film • Air-Fluid Levels - Stones - Ascites - Eggshell calcification in AAA - Air in Biliary tree. - Obliteration of Psoas Shadow in retro- peritoneal disease - Right lower quadrant sentinel loop in acute appendicitis Other Investigations - USG - CT abdomen for AAA, Pancreatic disease, or ureteric colic (non-

Contrast) - IVU - Mesenteric Angiography for Ischemia, Hemorrhage

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DDiiaabbeett iicc KKeettooaacciiddoossiiss Precipitating factors

• Intercurrent medical illness (60%) • Omission of treatment • Emotional factors and stress

FEATURES: • Nausea, vomiting and abdominal pain.( mainly in children) • Unexplained tachycardia • Dehydration • Kaussmul respiratory pattern • Pain, coma and shock.

LABORATORY FINDING • Blood Sugar 500-600 mg/dl • 15% could be less than 350 mg/dl • Anion gap is high. • Metabolic acidosis, • Na could be low • K could be high, • Mg is low, and low pH • S. creatinin is elevated • Positive ketones in urine

TREATMENT • Insulin

0.1 unit/kg IV (10 UNITS) Regular insulin 0.1 unit/kg 1hour after Then follow the insulin infusion protocol 1- Standard insulin conc. 1 unit Regular insulin/10ml NS ( 25units

mixed with 250 ml NS ) 2- Capillary glucose measured hourly for the first 6-8 hours while

receiving insulin infusion. If Bl S. is stable, less frequent monitoring (every 2 hours) is acceptable.

3- Algorithm:

Capillary BS Action > 350 6 units/hour

301-350 5units/hour 251-300 4 units/hour 201-250 3 units/hour 151-200 2 units/hour 100-150 1 unit/hour

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• If the blood sugar is still very high, not responding to the above

mentioned dose, its dose can be doubled. • If blood sugar reduction is more than 100-150 mg/hour, the dose of

infused insulin should be reduced.

• Fluid replacement:

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

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

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

Give 10-30 mEq of potassium in each litre fluid to maintain serum potassium at 4-5 mEq/L IF SERUM POTASSIUM 1S> 3.3 mEq/L, insulin treatment should be

delayed till serum K is restored by IV potassium infusion

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

• IF pH< 7.0 ( 100ml of sod bicarb. Over 20-30min to maintain

• PCO2 =10-12 mmHg serum HCO3 10-12 mEq/L) • HCO3 < 5mEq/L

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

Ca & tetany

� Complication of DKA

INFECTION VASCULAR THROMBOSIS CEREBRAL EDEMA ARDS

103

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

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

� Delay in eating meals. � Unusual physical exertion. � Excessive dose of exogenous insulin. � Unusual fluctuation in insulin absorption from varying

injection sites. � Impaired counterregulatory mechanisms due to autonomic

neuropathy. Oral hypoglycaemic drugs which don't cause hypoglyc aemia:

� 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.

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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.

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.

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CCoommaa Definitions : � Coma has been defined as unarousable and unresponsiveness to

stimulation, although reflex movements and posturing may be present. � Other terms used to decreased level of consciousness:

� Stupor: severely impaired arousal with some response to vigorous stimuli.

� Lethargy: a state in which arousal, though diminished, is spontaneously maintained or requires only light stimulation.

� Obtundation : a lesser state of decreased arousal with some response to touch or voice.

Etiology: � Based on the anatomic location of the lesion and the mecahanisms by

which neurologic diseases produce coma, the causes of coma can be classified into four major groups:

1. Metabolic and diffuse cerebral disorders. Hypoxia, ischaemia, hypoglycaemia, endogenous and exogenouns toxins, meningitis, concussion, post-ictal state, metabolic and electrolyte disorders.

2. Supratentorial lesions. Epidural haematoms, subdural haematoma, cerebral Hge, cerebral infraction, tumour and abscess.

3. Infratentorial lesions. Brain stem or cerebellar infraction, Hge, tumour and abscess.

4. Psychogenic coma. Up to 75% of patients in a comatose state, without obvious cause, will likely have a diffuse systemic disorder. Structural lesions make up the remaining causes of coma; supratentorial lesions are more common than subtentorial lesions.

Clinical features:

1. Metabolic encephalopathy: � Hypoventilation, abnormal respiratory pattern. � Reactive pupils (a midbrain function) in the presence of impaired

function of the lower brain stem (e.g. hypoventilation, loss of extraocular movements)

� Symmetric neurologic findings. � No focal hemispheric lesions (hemiparesis, hemisensory loss,

aphasia) before loss of consciousness. � Random eye movements, but not persistant ocular deviations. � Tremors, asterixis, multifocal myoclonic jerks and seizures.

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

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

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

� When progressive, signs of transtentorial herniation.

� Uncal herniation (herniation of the medial portion of the temporal lobe i.e. the uncus across the cerebellar tentorium produces midbrain signs)

• Ipsilateral (unilateral) pupil dilatation and oculomotor nerve paralysis.

• Progressive impairment of the level of consciousness.

� Central herniation. � Loss of consciousness. � Marked unilateral papillary dilatation, loss of light

reactivity and oculocephalogyric reflex. � Decerebrate posturing.

3. Infratentorial lesions: � Coma (sudden onset) � Conjugate gaze toward lesion i.e. the eyes are directed away

from the side of the lesion and towards the hemisphere. � Disconjugate eye movements with 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.

inhibitors and opiates also produce pinpoint pupils. holinesteraseCN.B:

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

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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:

� Thiamine 100mg IV. � Glucose: 50ml D 50% W (in children 2ml / kg of D25W) IV. � Naloxone: 0.4-2mg IV.

N.B: Flumazenil is not included in the coma cocktail because of its ability to induce seizures and cardiac arrhythmias. It should be used only if coma is definitively caused by benzodiazepine use

5. The history is vital and should include: � Onset (sudden or gradual). � The evaluation of the clinical picture. � The state of the patient health prior to the onset of coma. � The patient accessibility to drugs or poisons. � Inquiry concerning condition, that commonly cause coma (trauma,

epilepsy, drug abuse, CV diseases, pulmonary disease, cerebravascular disease, metabolic disorders, infections, neoplasm).

� History of psychiatric illness. � Occupational or environmental exposures e.g. CO. cyanide,

organic solvents, lead… � Past medical history: DM, HTN, epilepsy, liver, renal, respiratory

failure, endocrine disorder.

6. Physical Examination: A. Vital Signs.

1. Temperature: • Fever may suggest: infection, thyroid storm, heat

stroke, anticholinergic toxicity. • Hypothermia suggests: myxoedema, cold exposure,

intoxication with ethanol or barbiturates .

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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 bre athing)

indicates involvement of the brain stem between the midbrain and pons.

B. Skin. � Jaundice, spider angiomata, palmar erythema point to hepatic

encephalopathy. � Petechiae and ecchymoses suggest a coagulation abnormality

or thrombocytopenia. � A maculohemorrhagic rash suggests meningococcal infection,

staphylococcal endocarditis. � Cherry-red skin suggests carbon monoxide poisoning. � Needle marks on extremities indicate possible drug abuse. � Check skin turgor.

C. Odor of the breath: � A fruity odor suggests diabetic keto-acidosis. � A uriniferous odor is found in uremia.

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

D. Body orifices: � Bleeding from the ears or nose suggests cranial trauma. � Bleeding from other orifices suggests a bleeding disorder or

haemorrhage as the cause of coma.

E. Central nervous system: � Posture in bed:

• Decorticate rigidity characterized by flexion of arms and elbows with hyperextension of the legs, signifies bilateral hemispheric dysfunction with the brain stem intact.

• Decerebrate rigidity in which the arms and legs are in an extended position, it reflects damage to the midbrain and upper pons.

� Meningeal signs: • Resistance to passive flexion of the neck without resistance to

other neck movements is evidence of meningities or subarachnoid Hge.

• Restriction of movement of the neck in all directions may occur in generalized rigidity or disease of the cervical spine.

• Positive 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.

� Eye movements: • When eyelids are opened, if the eyes flutter upwards,

exposing only the scalera, suspect psychogenic coma. • In comatose patients without involvement of the neural

pathways influencing ocular movements, the eyes usually directed straight ahead or display slow roving (spontaneous eye) movements.

• Sustained, involuntary conjugate deviation of the eyes toward the unaffected side suggests a hemispheric lesion; towards the paralyzed side, a pontine lesion.

• Absence of oculocephalic (doll’s eye movement) and corneal reflexes indicates pontine dysfunction.

• Oculovestibular reflexes (cold calorics) may be lost in brain stem lesion.

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� Pupils: • Equal, round, reactive pupils exclude midbrain damage as a cause

and suggest metabolic abnormality. • Reactive pupils in association with absent oculocephalic and

corneal reflexes generally signify a metabolic encephalopathy or drug overdose.

• Pinpoint pupils (<1mm) may indicate opiate, pilocarine or pontine lesion.

• A unilateral, fixed and dilated pupil suggests ipsilateral temporal lobe herniation.

• Bilateral, fixed and dilated pupil suggest anticholinergic poisoning, anoxia, severe midbrain lesion or brain death. Also in response to some drugs as atropine or glutethimide.

� Motor system: • Hemiplegia, hyperreflexia and an extensor plantar response

indicate a structural lesion of the brain as the cause of coma. • Hyporeflexia without paralysis and with preservation of normal

planter response suggests a metabolic cause or drug ingestion.

� Sensory system: • Sensory loss may be suspected if the patient exhibits variations in

responsiveness to noxious stimuli.

7. Investigations: � CBC. � Biochemistry: glucose, urea, Creatinine, bilirubin, alkaline

phophatase, transaminases, Ca, magnesium, (serum glucose can be rapidly checked with a glucometer).

� Platelets and coagulation profile. � Blood and urine culture if infection is suspected. � ABG. � Toxicology screening. � Chest films . � ECG. � CT Scan of the head specially in the presence of focal neurologic

signs, papilledema or in the absence of any other etiology.

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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.

� 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 .

1Repeated doses, up to 5–10 mg, may be required. 2Do not give if patient has coingested a tricyclic antidepressant

or other convulsant drug or has a seizure disorder.

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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, 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.

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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.

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AAnniimmaall BBii ttee

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

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

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

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

� Clinical picture • Initial manifestations: fever, headache, sore throat, pain and

parasthesia at the wound site. • CNS symptoms develop 1-2 weeks after the prodrome

Encephalitic form: bulbar and peripheral muscle spasms, opisthotonus, agitation, and hydrophobia.

Paralytic form: symmetric, ascending flaccid paralysis. • Coma, apnea, death usually 4-7 days after the onset of CNS

symptoms.

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

� Treatment:

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

2. Vaccination of non-immunized patients.

a) Passive immunization - Human rabies immunoglobulin: 20 IU/Kg half of the

dose infiltrated locally at the exposure site and the remaining should be injected IM distant from the wound.

- Equine rabies antiserum 40 I.U/Kg can be used after skin test of horse serum sensitivity, if human rabies immunoglobulin is not available.

b) Active immunization: - Human diploid cell vaccine (HDCV), given as 5

injections of 0.5 ml IM in the deltoid muscle (anterolateral region of the thigh muscle in children).

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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.

NB: � Schedule of vaccination is the same for adults and for children. � Rabies immunoglobulin and rabies vaccine should never be given in

the same syringe or the same site.

117

MMaannaaggeemmeenntt ooff SSccoorrppiioonn sstt iinngg

black scorpion yellow scorpion � Androctonus Crassicaude (black scorpion) and Leiurus quinquestriatus

(yellow scorpion) have been found the two most dangerous scorpions and two of the most toxic in the world.

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

� Investigations

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

� Management � Give scorpion antivenom to all patients confirmed to have

scorpion sting after a skin test. (This is done by injecting 0.1 ml of antivenom intrademally).

� 5 x 1 ml ampules polyvalent scorpion antivenom diluted in a 20-50 ml 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.

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- 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

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Management of Snake Bite � There are 2 main types of poisonous snakes:

Rattlesnake Copra Snake

• Crotalids or pit vipers (hemotoxic venom) : causing haemolysis, necrosis, DIC e.g. rattlesnakes.

• Elapids (Neurotoxic venom) : disrupt neuromuscular activity e.g. coral snakes, cobras.

� Presentation � Crotalids

Puncture marks (may have 1-4). Local symptoms (pain, swelling, erythema, necrosis, oedema, ecchymoses).

Systemic symptoms (weakness, nausea, vomiting, numbness, tingling, perioral parasthesia, bruising, tachycardia, shock, death.

Coral snakes Multiple, painless small wounds. Local symptoms of numbness & fasciculations. Systemic symptoms: slurred speech, weakness cranial never palsies, dysphagia, ptosis, diplopia, diaphoresis, impaired consciousness, respiratory failure & death.

Do not handle dead snakes as reflex biting may occu r.

� 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.

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• Lab. Investigations may be abnormal in crotalid bites (but usually

normal with neurotoxic venom). CBC: haemolysis PT/PTT, DIC Screen: Coagulation abnormalities. Renal function: May reveal acute renal failure. Electrolytes & LFTs: may be abnormal.

Treatment:

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

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

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

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

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

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

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

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

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

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

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- NB: Polyvalent Crotalidae Immune Fab (CroFab), a new sheep-derived antivenom has generally replaced Antivenom polyvalent, an equine-derived product.

- Antivenom is the only specific antidote available at present time for the treatment of venomous snake bite.

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

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

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

Ingestion of an unknown

drug

Unconscious pt.

Conscious pt. Patient

Stabilization

Airway Breathing Circulation Altered mental status

Stomach Evacuation

Physical exam. Baseline Lab Investigations

Coma Cocktail: *** Naloxone Glucose + thiamine

Ipecac* or Gastric Lavage

Activated Charcoal + MgSo4**

Symptomatic Management

* Ipecac dosing: Adults: 15-30 ml, Child> 1yr: 15 ml, Child < 1yr: 10 ml ** Activated charcoal Adults: 60-100 mg Child: 1-2 mg/kg MgSo4: Adult: 16 gm Child: 250 mg/kg *** Coma cocktail: Naloxone: opioid antagonist Adult/Child: 0.2-2 mg IV; repeat at 2-3 minutes intervals until desired effect or a total dose of 10-15 mg. Careful in opioids-dependent patient. Flumazenil: Benzodiazepine antagonist. Adult: 0.2 mg IV over 30 seconds, then 0.3 mg, then 0.5 mg (every 30 seconds) up to 3 mg. Child: 0.01 mg/kg, titrate up to 1 mg Careful use in case of mixed ingestion, may precipitate seizures or arrhythmias Glucose: Adults: 50-100 ml of 50% Child: 2-4 ml/kg of 25% Thiamine 100 mg is indicated concomitantly for alcoholic or malnourished patients.

Insectici de Exposure

Pyrethroids Caramate Organophophate

Carbamate

No Yes

- Dermal,Eye, Inhalation

Dermal + Eye 1. Removal of clothes 2. Local Irrigation of the

exposed are Inhalation: 1. Remove to fresh air. 2. Give oxygen if required

If any symptomaticManifestations refer to oral Exposure management

Oral

No Antidote Symptomatic

Treatment only LD: 10-100 mg

Suction of secretions until Full atropinization

Establish an airway

Is the patient 1. Comatosed 2. Convulsing 3. Without a gag reflex

1. Endotracheal Intubation

2. Gastric Lavage

Induction of Emesis

Activated Charcoal + MgSo4*

Mild Symptoms Severe Symptoms with/or without

1. Weakness 2. Respiratory Depression

Atropine Therapy alone

Atropine + Pralidoxime (for Carbamate give atropine only) Atropinization should be performed adequately & rapidly**

* Refer for dosing to the section: management of unknown ingestion ** Treatment Guidelines:

Atropine: for treatment of muscrinic effects. 1. Diagnostic dose: IV/IM adult: 1 mg; child: 0.25 mg (0.02 mg/kg).

If patient exhibit toxic effects of atropine (dry mouth, dilated pupil, and rapid pulse) then probably not seriously poisoned.

2. Dosage: IM/IV Mild symptomology, initially 2-4 mg (child 0.05 mg/kg) further 2 mg doses may be given every 10 minutes to maintain full atropinization.

Severe symtomatology, initially 4-6 mg (child 0.05 mg/kg), followed by 2 mg every 5-10 minutes to maintain full atropinization (not to exceed 50 mg/24 hours for adults). 3. Therapeutic endpoint: Administer until full atropinization (dry mouth,

pulse) (130-140/minute, and dilated pupil, clearing of rales). Maintain some degree of atropinization fpr 48 hours.

Pralidoxime: for treatment of nicotinic manifestations, use as adjunct and not a substitute to atropine.

Adult: 1-2 GM/IV in 100 ml NS 0.9% at 15-30 minutes. 1. Child: 20-40 mg/kg IV. Alternatively doses may be administered IM or SC. 2. Administration may be repeated x 3 or as needed at an interval of 8-12

hours if muscle weakness has not been relieved.

119

Management of acute burn

Burn injury is a common cause of morbidity and mortality. Proper evaluation and management,coupled with appropriate

early referral to a specialist, greatly help in minimizing suffering and optimizing results.

INITIAL EVALUATION AND RESUSCITATION Before management of the burn wound can begin, the patient should be properly and completely evaluated

Evaluation of the burn patient is organized into primary survey and secondary survey .

Primary survey

A Airway . B Breathing . C Circulation. D Disability. E Expose patient. F Fluid resuscitation

1- First evaluate the airway; early recognition of imp ending airway compromise, followed by prompt intubation, c an be lifesaving .

2- Obtain appropriate vascular access . 3- Place monitoring devices.

4-Complete a systematic trauma survey, including indi cated 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 inhalatio n 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 a re obtunded.

Carboxyhemoglobin levels can be misleading in thos e ventilated with oxygen

Patients trapped in buil dings or those caught in an explosion are at higher risk for inhalation injury. These patients m ay have facial burns,

singeing of the eyebrows and nasal hair, pharyngeal burns, carbonac eous sputum, or impaired mentation. A change in voice qu ality, stridorous respirations, or wheezing may be noted

The upper airway may be visualized by laryngoscopy, and the tracheobronchial tree should be evaluated by bronch oscopy. Chest radiography is not sensitive for detecting inhalati on 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 de oxyhemoglobin are detected

Co-oximetry measurements are necessary to confirm t he diagnosis of CO poisoning. Patients exposed to CO should receive 10 0% oxygen using a nonrebreather face mask.

Hyperbaric oxygen (HBO) therapy reduces the half-li fe 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 leve ls of 15% or greater.

� After evaluation of the burn wound, begin fluid res uscitation and make decisions concerning outpatient or inpatient m anagement or transfer to a burn center

� Pathology tests: full blood count, urea, electrolyt es, proteins (at time of canula insertion)

� Analgesia, preferably IV � Routine medication: Tetanus toxoid, Cimetidine ? � After evaluation of the burn wound, begin fluid res uscitation and

make decisions concerning outpatient or inpatient m anagement or transfer to a burn center

� Pathology tests: full blood count, urea, electrolyt es, 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% t otal body surface area

(TBSA) in patients younger than 10 years or older t han 50 years. greater than 20% in persons of other age groups

2. Second- or third-degree burns that involve the face, hands, feet, genitalia, perineum, or major joints .

3. Third-degree burns greater than 5% TBSA . 4. Electrical burns, Chemical burns . 5. Inhalational injury . 6. Burn injury with preexisting medical disorder. 7. Any patients with burns and concomitant trauma. 8. A lack of qualified personnel (care taker ).

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

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

Extent of burn An accurate estimate of burn size is important for treatment and transfer

decisions. Burn size or extent can be estimated in a number of ways. The “rule of nines.” in adults is easy but less ac curate in children because

their body proportions are different from those of adults. For areas of irregular or nonconfluent burns, the palmar surface of the

patient's hand can be used. For a wide age range, the area of the palm without the fingers represents

0.5% of the body surface.

% BSA .OF BODY PARTS ADULT CHILD

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

Burn depth Burn depths are routinely underestimated during the initial examination.

Devitalized tissue may appear viable for some time after injury, and often, some degree of progressive microvascular thrombosis is observed on the wound periphery. Consequently, the wound appearance changes over the days following injury. Serial examination of burn w ounds can be very useful.

First-degree burns are usually red, dry, and painfu l. (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 pa inful.Their depth, ability to heal, and propensity to form hypertrophi c scars vary enormously

Third-degree burns are generally leathery in consis tency, dry, insensate, and waxy. These wounds will not heal, except by con traction and limited epithelial migration, with resulting hypertrophic a nd unstable cover

Burn blisters can overlie both second- and third-de gree burns. Fourth-degree burns involve underlying subcutaneous tissue, tendon, or

bone.

Severity Severity determines if the burn is critical, modera te or minor.

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

Moderate burns - adults � A. Full - thickness burns of 2% to 10% of the body surface area,

excluding critical areas � B. Partial - thickness burns of 15% to 30% of the body surface area � C. Superficial burns of greater than 50% of the body surface area

Minor Burns - adults � a. Full - thickness burns of less than 2% of the body surface area � b. Partial - thickness burns of less than 15% of the body surface area Critical burns - infant and children � a. Full - thickness or partial thickness burns covering more than 20 %

of the 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 conti nuous reevaluation and adjustment of infusions based on resuscitation targ ets

The modified Brooke or Parkland formulas are reason able and are used to help determine the initial volume of infusion.

Half of the total calculated 24-hour volume is adm inistered in the first 8 hours post injury. Should the resuscitation be dela yed, this volume is administered so that infusion is completed by the e nd of the eighth hour post injury.

After 18-24 hours, capillary integrity generally r eturns and fluid administration should be decreased .

Volume = weight x percent burn area x 4ml

First 8 hrs - give half of total next 16 hrs - give half of total next 24 hrs - give half of total

Type of fluid is Hartmann's solution Adjust volume for each patient according to urine o utput ( 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 administra tion 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, phosphoro us, and magnesium levels should be monitored and kept within physiolo gic range.

Ideally, begin enteral feedings during resuscitatio n, except in patients with massive injuries or those who are underresuscitated and less likely to tolerate tube feedings because of ileus secondary t o splanchnic underperfusion

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

CChheemmiiccaall bbuurrnnss

� May occur from any toxic substance that comes in contact with the skin

� Mostly caused by Alkaline (alkali) and acid � Protect yourself from exposure or injury

Emergency Care

Stop the burning process

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

Dry chemicals Reaction with water can worsen burn

)1 “Brush - then flush” 2) Remove victims clothing (shoes & socks 3) Cover with dry sterile dressing or clean sheet Special care of the eyes

Gently /continuously flush For direct eye injury hold lids open and irrigate the eye

Dry lime victim Industrial shower for chemical removal

Electrical Burns

� May be more serious than it seems � Entry wound is usually a small burn area � Look for an extensive exit wound � Possible tissue damage underneath (current spreads out as it travels

through the body) � Possible Cardiac arrest(VF or VT) � Possible Respiratory arrest � Treat any major complications first � Splint possible fractures � Treat wounds with a dry, sterile dressing (Entry wound on hand ,Exit

wound on foot) Infection Control

Hand-washing BEFORE and AFTER touching each patient Aseptic techniques for dressing and procedures Environmental controls, such as air filtration and balanced ventilation Microbiological screening of wounds, nose, throat, perineum and axillae Isolation of infected patients Early nutritional support Early excision of deep burns Use of topical antimicrobials, where applicable, to reduce wound

colonization Conclusions

Proper early management of burns is crucial A systematic approach to burn management is vital Superficial burns heal by regeneration within weeks Deep burns require surgery

BBllaasstt IInnjjuurryy

1. Classification of Explosives – Explosives are categorized as 1- High-order explosives That produce a defining supersonic over-pressurization shock wave. Examples of HE include TNT, C-4, Semtex, nitroglycerin, dynamite, and ammonium nitrate fuel oil. 2- Low- order create a subsonic explosion and lack HE’s over- pressurization wave

Examples of LE include

pipe bombs, gunpowder, Molotov cocktails or aircraft improvised as

guided missiles.

Types of Blast Injuries: Primary (Direct effects of pressure of the blast wave , either overpressurization and such as

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

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

Quaternary (burns, asphyxia, and exposure to toxic inhalants

infections, crush injuries, delayed collapse ).

Primary Blast Injuries

• Unique to high explosives • Due to impact of over-pressurization wave with body surfaces • Most commonly involve air-filled organs and air-fluid interfaces

– Middle ear – Lungs – Gastrointestinal tract

• Types of injuries – Tympanic Membrane (TM) rupture – Blast lung – Intestinal hemorrhage and perforation – Globe rupture – Traumatic brain injury (TBI) without physical signs of head injury

Middle Ear Injury • TM - structure most frequently injured by blast • Most sensitive organ in barotrauma • As little as 5 psi above atmospheric pressure • Temporary neuropraxia is common

INJURIES: – TM rupture ( spontaneous healing in 50 % - 80 % ) – Ossicle dislocation – Disruption of oval or round window (Permanent hearing loss can

occur with disruption of the oval or round windows in the cochlea ) • Symptoms may include

Hearing loss, tinnitus, vertigo, bleeding from external canal, mucopurulent otorrhea

• Otologic exam and audiometry for all is essential . • TM rupture is sensitive marker, but absence does not exclude other organ

injury as blst lung injury may occurs in absence of TM rupture

Blast Lung Injury ( B L I ) • Second most susceptible organ • Direct consequence of blast wave on the body • Overpressure needed is about 40 psi • At 80 psi- 50 % have severe pulmonary damage (at 200 psi-fatal) • Most common CRITICAL Injury in victims close to bomb • Can be life threatening • May not have obvious external injury to the chest • Can be associated with pneumothorax, haemothorax • Air embolism from pulmonary disruption (fatal) • Results in tearing, haemorrhage, contusion and oedema • Microhaemorrhages in alveoli • Disruption and weakening of alveolar walls • Disruption of perivascular and peribronchial tissue • Resultant Ventilation-Perfusion mismatch • Pulmonary contusions – multifocal hemorrhages • Pulmonary C-fiber receptor injury causes vagal nerve-mediated cardiogenic

shock, pulmonary edema • Other injuries: traumatic emphysema, AV fistuale, pulmonary barotrauma,

venous air emboli • Symptoms : Dyspnoea, Haemoptysis, cough, chest pain • Signs : Tachypnoeic, hypoxic, cynosis, wheezing

• X-Ray features similar to pulmonary contusion, with bihilar (butterfly pattern) shadows

• Can be life threatening

Gastrointestinal Tract blast injury • Colon – visceral organ most frequently affected • Mesenteric ischemia from gas embolism may cause delayed rupture of

large or small intestine • Intestinal barotrauma more common with underwater air blast • Solid organ injury less likely • Signs and symptoms • Abdominal pain, nausea, vomiting, hematemesis • Rectal pain and tenesmus • Testicular pain • Unexplained hypovolemia

Other Primary Blast Injury

• Primary blast injury to the eye • include rupture of the globe, serous retinitis, and hyphema lid laceration,

traumatic cataracts injury to optic nerve .

• Primary blast injuries to the brain • include concussion as well as barotraumas caused by acute gas embolism.

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

Secondary Blast Injury • Due to flying debris and bomb fragments • Penetrating ballistic or blunt injuries

– Leading cause of death in military and civilian terrorist attacks except in cases of major building collapse

– Wounds can be grossly contaminated Consider delayed primary closure and tetanus vaccinations

Tertiary Blast Injury

• Due to persons being thrown into fixed objects by wind of explosions • Also due to structural collapse and fragmentation of building and vehicles • Structural collapse may cause extensive blunt trauma

– Crush syndrome • Damage to muscles and subsequent release of myoglobin,

urates, potassium, and phosphates • Oliguric renal failure

– Compartment syndrome • Edematous muscle in an inelastic sheath promotes local

ischemia, further swelling, increased compartment pressures, decreased tissue perfusion, and further ischemia

Potential Intra-operative and Post-resuscitation Co mplications

• Surgeons, Anesthesiologists, and Critical Care Specialists will need to be

aware of potential intraoperative and post-resuscitation complications – Occult pneumothorax – Occult compartment syndrome – Hyperkalemia

• Crush syndrome • Rhabdomyolysis

Quaternary Blast Injuries

• Explosion related injuries or illnesses not due to primary, secondary, or

tertiary injuries – Exacerbations of preexisting conditions, such as asthma, COPD,

CAD, HTN, DM, etc. – Burns (chemical and thermal)

• White Phosphorous (WP) from munitions causes extensive burns, hypocalcemia and hyperphosphatemia

– Toxic inhalation – Radiation exposure – Asphyxiation (carbon monoxide and cyanide)

General Considerations Information about the type of explosion and the target helps to predict the types of injuries.

• After an explosion in a confined space, such as a bus, one would anticipate, in addition to penetrating injuries, more victims with primary blast injuries and lung damage than would be expected after an explosion in an open space.

• Explosions in confined spaces (mines, building, or large vehicles) and or structural collapse are associated with greater morbidity and mortality.

• Land mine injuries are associated with a high risk of below and above the knee amputations.

• . Intensity of an explosion pressure wave declines with the cubed root of the distance away from the actual explosive.

• That is, a person 3m from an explosion experiences 9 times more overpessure than a person who is 6m away. Thus, proximity of the person to the explosion is an important factor in a primary blast injury. Note that blast waves are also reflected by solid surfaces, and therefore, a person standing next to a wall may sustain a greater primary blast injury.

• Terrorist attacks in civilian settings tend to have a biphasic distribution of mortality – high immediate rates of death followed by low early and late mortality rates.

• . Initial stabilization of victims of blast injury like that of other trauma victims, includes assessment and management of the airway, breathing, and circulation. Half of all initial casualties will seek medical care over a one-hour period. This can be useful to predict demand for care and resource needs.

• Expect an upside down triage—the most severely injured arrive after the less injured, who bypass EMS triage and go directly to the closest hospitals.

• Another ominous consideration is the tactic of setting dual explosion, since the initial explosion may be a ploy to attract law enforcement and resuce personnel, followed by a second device designed to injure rescuers. Moreover, EMS personnel should check for radiation and chemical contamination at the scene of a deliberate attack.

• Unfotunatly, few health professionals have experience with explosive-related injuries

General Management Treatment of patients after blasts focuses on two examinations .

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

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

Treatment of Blast Lung Injury Treatment of blast lung is challenging in that ventilation with high peak inspiratory pressures increases the risk of air embolism and pneumothorax.

• Ventilation should use limited INSPIRATORY PRESSER and permissive hypercapnia, when available,

• High frequency ventilation may be of value. • Assume that a patient’s wheezing associated with a blast injury is due to

pulmonary contusions

Treatment of TM rupture • Generally expectant management

– Most resolve spontaneously – Avoid irrigating or probing the auditory canal – Avoid swimming – Refer to ENT if no healing or complications occur

• Complications include ossicle disruption, cholesteatoma, perilymphatic fistula, and permanent hearing loss (1/3)

• Steroids may be helpful in sensorineural hearing loss

Treatment for Acute Gas Embolism (AGE )

• Patients thought to have acute gas embolism (AGE) require recompression treatment.

• Place patients on 100% oxygen by tight-fitting face mask and, if possible, place them in the left lateral recumbent position.

• Trendelenburg (head down) position is no longer recommended. • Of course, other causes of symptoms (eg, traumatic CNS injury) must be

excluded. • Hyperbaric oxygen (HBO) treatment is the definitive procedure. • Transfer of the patient may be required. • Research suggests that aspirin is helpful in AGE. Aspirin may reduce

inflammation-mediated injury in pulmonary barotrauma as well. • It may, however, be unwise to give an antiplatelet agent to a patient with

acute trauma. Treatment of Eye Injuries

• Up to 28 percent of blast survivors may have serious eye injuries,

particularly if the blast caused shattering glass. • Symptoms include eye pain or irritation, foreign body sensation,

altered vision, periorbital swelling or contusion, and findings can include decreased visual acuity, hyphema, globe perforation, subconjunctival hemorrhage, foreign body or lid laceration.

• Objects penetrating the eye should not be removed in an emergency setting.

• The eye can be covered with a paper cup or other clean object that will not exert pressure on the globe, and the patient can be referred for definitive surgical treatment.

Special Populations

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

Guidelines for Disposition

• Limited data prevent establishing the optimal duration of observation. • Persons exposed to open-space explosions who have no apparent

significant injury and with normal vital signs and unremarkable lung and abdominal examinations generally can be discharged after 4 hours with instructions to return to the ED if shortness of breath, abdominal pain, vomiting, or other symptoms occur.

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

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

Guidelines for Admission

• High risk patients who require admission – Significant burns – Suspected air embolism – Radiation – WP contamination – Abnormal vital signs – Abnormal lung examination findings – Clinical or radiographic evidence of pulmonary contusion or

pneumothorax – Abdominal pain or vomiting – Penetrating injuries to the thorax, abdomen, neck, or cranial cavity

No obvious injuries Obvious Injuries

Otoscopic Exam

+

-Observe

O2 Sat 6-8 hours

+ -Admit D/C with

Abd Warnings

Release+

-Treat Injuries

as usual

Injury RX andblast observation

(pulmonary/visceral)

Triage Algorithm

Otoscopic Exam

Heat syndromes

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

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

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

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

Heat syndromes

Minor Heat cramps

Heat fatigue Heat oedema

Heat syncope

Major Heat exhaustion

Heat stroke

HHeeaatt eexxhhaauusstt iioonn 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.

HHeeaatt sstt rrookkee 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. Predisposing factors:

1. Extremes of age. 2. Dehydration. 3. Lack of acclimatization. 4. Lack of physical fitness. 5. Chronic disease e.g. DM. 6. Cardiovascular disease. 7. Obesity. 8. Fatigue &lack of sleep. 9. Sustained output of Muscular Metabolic Heat

10. Past hx.of heat illness. 11. Conditions that affect sweating. 12. Skin disease. 13. Use of drugs ( e.g. Barbiturates). 14. Leisions of hypothalamus, brain stem or spinal cord. 15. Acute infection. 16. During convalescence. 17. Recent intake of food.

Clinical features Usually sudden onset may be preceded in some cases by short period of confusional state.

Almost all patient present with coma or semicoma with or without convulsions.

Hot,dry flushed skin. Rectal temp more than 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..

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).

MMaannaaggeemmeenntt ooff hheeaatt sstt rrookkee

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 .

10. NGT may be inserted if needed. 11. Correct acid base abnormality and electrolytes according ABGs

results. 12. Stop cooling when temp is less than 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.

References:

1. Cummins RO, etal : Advanced Cardiac Life Support, Provider Manual. AHA 2011 .

2. Fundamental Critical Care Support: Society of Critical Care Medicine 5rd Edition

2011.

3. Advanced Trauma Life Support for Doctors : American College of Surgeons

Committee on Trauma 9th Edition 2012

4. Stone C. Humpries R. Current Emergency Diagnosis and Treatment 5th Edition

2004

5. Osler's Emergency medicine 3rd edition 2002

6. Markovchick V, Pons P. Emergency Medical Secrets.3rd Edition 2003.

7. Coterino J, Kahan s.In a Page of Emergency Medicine. 1st Edition 2003.

8. Lefor A. Critical Care on Call. 1st Edition 2002

9. Haist S, Robbins J. Internal Medicine on Call 3rd Edition 2002

10. Ma O.J, etal: Emergency Medicine Maual. 6th Edition 2004

11. Biddinger P,etal: Emergency Medicine . 2nd Edition 2003

12. Tallia A, etal: Swanson's Family Practice Review, A problem-oriented approach.

a. 5th Edition

13. Al-Khuwaiter T, etal: Guidelines for treatment of hypertensive emergencies 2004

14. Standards for Accident & Emergency Departments in Ireland. EMS in Ireland-2009

15. Emergency Policy & Procedures. MOH, KSA

16. Subash F, etal:Team Triage Improves Emergency Department Efficiency:

Emer.Med. J 2004

17. Beveridge R,etal: Reliability of the Canadian Emergency Department Triage and

Acuity Scale. Ann. Emergency Medicine Aug.1999

18. Cambell S, Sinclair D. Strategies for Managing a Busy Emergency Department

19. Guidelines for Cardiac Care Resuscitation council UK.2011

19.Unified forms (Physical ex, progress notes, nursing notes) General Directorate of Quality , Ministery of Health & Population

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Dr. Hamid Shaalan

e-mail : hshaalan90@hotmail.com