Unified Protocol for Management of Critical Cases Commonly Encountered in ED. Dr. Hamid Shaalan. FRCS

8/13/2019 Unified Protocol for Management of Critical Cases Commonly Encountered in ED. Dr. Hamid Shaalan. FRCS

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E E d d i i t t i i oonn 220 0 1144nn d d 22

R. HAM I SHAA LAN. FRCS Ed.

Consultant G. Surgery And Emergency Medicine.


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INTRODUCTION

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

Thousands of people attend ED every year for more than come into contactwith any other hospital service .Some of them are acutely ill or injured andneed immediate, sometimes life-saving treatment. Many of whose conditionare not so serious, require urgent assessment and treatment for their injuryor 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 theregion. For these reasons EDs have a high public profile and are viewed bymany as essential local service.

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

This plan suggests :

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

encountered in ED.IV) Algorithms.

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

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

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PART III

PROTOCOLS FOR MANAGEMENT OF CRITICALCASES COMMONLY ENCOUNTERED

IN ED


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Initial Assessment And Management OfPolytrauma

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 simultaneously4) Do not add further harm5) 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 injuredyou have less than 60 minutes to survive. You might not die right then; it maybe three days or two weeks later -- but something has happened in your bodythat is irreparable." Dr. R. Adams Cowley, Shock Trauma Center section of the University ofMaryland Medical Center


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1 Primary Survey And Resuscitation- Primary survey and resuscitation of vital functions are donesimultaneously.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 unconsciousor has any significant injury above the clavicles ) has a cervical spineinjury , until can be excluded.

Check the patient's responsiveness by gentle shaking them by theshoulder 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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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 O 2 (10L/min.) Ventilate with ambu-bag (a bag valuemask device) if

respiration is absent, impaired or inadequate

Chest decompression if tension pneumothorax is suspected. Seal open pneumothorax. Monitor the patient's arterial O 2 saturation with a pulse oximeter.And maintain saturation greater than 9 5%

1.3 Circulation With Control Of Hemorrhage : Assessment :

- Check the patient's Skin colour

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

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

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

antecubital veins >Central venous (femoral, subclavian, jugular ) > Cutdown for saphenous vein. In pedia, forearm > intraosseous > femoral > cutdown age less than 6 years.

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

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

- Splint any long bone fracture.- Consider using pneumatic anti-shock garment (PSAG).- Operative intervention.


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** Prevent hypothermia during assessment andmanagement

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 CO 2 Urinary & gastric catheters unless contraindicated. Urine output hourly. ECG X-ray (chest, pelvis &lat. Cervical spine( C7-T1 should be visualised) Ultrasound or DPL Consider early transfer

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

- Use time before transfer for resuscitation.Re-evaluate the patient :Before beginning secondary survey be sure that :

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

Remember : Life saving SHOULD BE initiated when the

problem is identified, rather than after the primary survey.


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Airway Adjuncts:1- Oropharyngeal Airway

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

2-Naso-pharyngeal Airway

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

Inserting the lubricated tube with bevel towards medial Direct upwards whileroling gemntly


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Bag-Valve Mask

Holding B/V Mask E/C Technique

Needle Cricothyrotomy

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

while aspirating

Aspirating air signifies entery into trachea, remove stylet with syringe and fix O 2 tube .Secure in place , Apply intermittened ventilation


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III Secondary Survey :

Components :

- History- Physical examination : Head-to-toe- Special diagnostic procedures.- Re-evaluation of the patient.Secondary survey can be summarized as tubes and fingers in everyorifice.

History :A- Allergies M- Medications currently used.P - Post illness/frequencyL- Last mealE- Events ( mechanism of injury)/Environment related to the injury.

Blunt trauma Penetrating injury Burns Chemicals, toxins, radiation


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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 tohave cervical spine fracture/or ligamentous injury .

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

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


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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, crepitation, abnormal movement,

peripheral pulses (presence, absence, equality)

Apply appropriate splinting for extremity fractures.- Pelvis fracture :

Suspected by ecchymosis over iliac wings, pubis, labia orscrotum

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

associated with pelvic fracture.- Back :

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


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Palpate for : tenderness, Bogginess, irregularity of the contourof 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 thepatient hemodynamic and ventilation status returned to normal.

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

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

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

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

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


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2- Rapid Sequence Intubation (RSI)

RSI refers to technique of simultaneous administration of a sedativeagent (induction) and neuromuscular blocker along with cricoidpressure designed to facilitate intubation and reduce the risk of gastricaspiration .

RSI should only performed if emergent intubation is necessary(respiratory failure, acute intracranial lesion, some overdose, statusepilepticus, combative trauma patient where behavior threatens life,

possible cervical spine fracture and immobilization is not possiblebecause delirium ), the patient may have a full stomach, theintubation is predicted to be successful.

Patients for whom intubation is likely to be difficult shouldnot have RSI

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

Steps:1. Preparations:

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

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

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

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 assistanttill the ETT is in place and cuff is inflated and proper position isconfirmed.

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, malignanthyperthermia, bardycardia (pretreat with atropine in children),hypotension, ICP , intraocular pressure, Histamine releasemay 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 directvisualization and confirm placement by primary and secondaryconfirmation.

8. Post-intubation management : secure tube, provide long-termparalysis 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--SS HHOOCCKK I Definition:

Shock is inadequate organ perfusion and tissue oxygenation.

In adults, a systolic 90 mmHg, a mean arterial BP 60mmHg or adecrease in systolic BP of 40 mmHg from the patient's baseline

pressure and a pulse pressure 20 mmHg constitutes significanthypotension .In children, if a child's BP 2 times the child age, pulse70, hypotension is present.

Evidence of hypoperfusion includesMental status change .Cyanosis, cold limbs.Oliguria or lactic acidosis.

Hypoperfusion may lead to organ dysfunction or death . Management should be directed towards correcting

hypoperfusion, NOT HYPOTENSION , as a primary endpoint.

II Pathophysiology In most cases, tachycardia is the first sign of shock.

Progressive vasoconstriction of cutaneous and visceralcirculation.

The release of catecholamines increases peripheral vascularresistance.

This increases diastolic blood pressure and decreases pulsepressure. Increase aldosterone secretions, which retain sodiumand water to expand blood volume.

Aerobic metabolism will be shifted to anaerobic one withdevelopment of metabolic acidosis.

III Types & common causes of shock:1. Hypovolemic shock

Loss of blood( Haemorrhagic shock )o Traumao Hematomao Hemothorax or hemoperitoneum


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Loss of plasma o Burnso Exfolutive dermatitis

Loss of fluids and electrolytes o Vomitingo Diarrheao Excessive sweatingo Ac. Pancreatitiso Ascitiso bowel obstruction

2.Cardiogenic shocko 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 vitalorgans are not getting sufficient O2, signs and symptoms ofshock 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 ofbrain, coagulative necrosis of the heart, acute tubular necrosisof the kidney, and diffuse alveolar damage of the lungs, Theaim of the first aider is to prevent the casualty reaching thisstage.

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%ofBl. Volume lost)

Decrease peripheral oforgans able to withstandprolonged ischaemia(skin, fat, muscles andbone)Ph is normal.

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

Moderate(20%-40% of Blvolume lost)

Decrease central

perfusion of organs ableto tolerate only briefischaemia (liver, kidney,gut).Ph : metabolic acidosis.

Thirst, supine hypotension,

tachycardia,oliguria or anuria.

Severe ( 40%of Bl .volumelost.)

Decrease perfusion ofheart and brain.Metabolic acidosis is

severe.

Respiratory acidosis mayalso be present.

Agitation,confusion,obtundation.Supine hypotension andtachycardia,Rapid, deep respiration.


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restore the oxygen-carrying capacity of the intravascular volume. Fully cross matched blood ispreferable but requires about 45 minutes, type specificblood can be prepared within 10 minutes. For lifethreatening blood loss, use of unmatched, type specificblood is preferable over type O blood. Fresh frozenplasma should be used only for correction ofcoagulopathy and not for volume replacement.

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 inaortic dissection.

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

ECHO to identify pericardial tamponade ofeffusion

Pulmonary artery catheterization revealsdecreased cardiac output index ( 2.2 L/min./m2), wedge pressure ( > 18 mmHg), systemicvascular 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, unlesscontraindicated.

Morphine IV in 2mg, repeated if needed. Hemodynamicparameters should be monitored.


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

to cause inotropy and vasoconstriction .

-Dobutamine(2.5-20mcg/kg/min)for normotensivepatientto cause inotropy. Nitroglycerine (5-100mcg/min) to preload

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

COP by of after load. Norepinephrine may be used if is no or poor

response to other pressors infusion. It should

be started at 2mcg/min and titrated to desiredeffect. PTCA( Percutaneous Transluminal Angiopathy

) is preferred method for reperfusion in cases ofcardiogenic shock following MI, Thromblyticsare much less effective in shock state.

Intra-aortic balloon pump placement may beused as temporizing measure to decrease afterload,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. Oftrauma, focal neurological deficit ).


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TREATMENTo ABC of resuscitation should be addressed.o Hemodynamic stabilization : rapid infusion of NS or RL

( 500ml every10 minutes ,(20ml/kg in children ), often6L(60ml/kg in children) is necessary.

o BP, mental status, pulse, capillary refill, urine output shouldbe monitored.

o If no response to fluid administration,- Systolic BP 70mmHg infuse norepinephrine 0.5-30 ug /min .- Systolic BP 70 90 mmHg Dopamin 5-20 ug/kg/min, Then

Dopamine can be combined with Dobutamine in dose of 5-20 ug/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 insome cases.

- acidosis is treated : O , ventilation and fluid replacement,NaHCO 3 1mEq/kg IV in metabolic acidosis.

-DIC should be treated with fresh-frozen plasma: 15-20ml/kginitially 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 otherinterventions-Bradycardia may be treated with atropine 0.5-1 mg/5min fortotal 3mg. A pacemaker may be used.

- Methylpredisolone (high dose) should be instituted within 8hours of injury, 30mg/kg bolus over 15 min. followed by aninfusion 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 Fluidresuscitation may improve cardiac output.


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Figure 2 Anaphylactic Reactions: Treatment Algorithm for Children by FirstMedical Responders

1 An inhaled beta 2-agonist such as salbutamol may be used as an adjunctive measure if bronchospasmis 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 recommendedonly for an experienced practitioner who can also obtain IV access without delay. Note the differentstrength 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 giveninstead of 120 micrograms, and 300 micrograms can be given instead of 250 micrograms or 500micrograms.

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 Adults

Consider when compatible history of severe allergic-typereaction with respiratory difficulty and/or hypotension

especially if skin changes present

Oxygen treatmentwhen available

Stridor, wheeze,respiratory distress orclinical signs of shock 1

Adrenaline (epinephrine) 2,31:1000 solution

0.5 mL (500 micrograms) IM

Repeat in 5 minutes if no clinicalimprovement

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

IN ADDITION If clinical manifestations of shock

For all severe or recurrent do not respond treatmentdrug reactions and patients give 1-2 litres IV fluid. 4 Hydrocortisone Rapid infusion or one repeatdose100-500 mg IM/or slowly IV may be necessary

1. An inhaled beta 2-agonist such as salbutamol may be used as an adjunctive measureif bronchospasm is severe and does not respond rapidly to other treatment.2. If profound shock judged immediately life threatening give CPR/ALS if necessary. Considerslow IV adrenaline (epinephrine) 1:10,000 solution. This is hazardous and is recommendedonly 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 onamitriptyline, imipramine, or beta blocker.4. A crystalloid may be safer than a colloid.


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AAnn gg iioo ee dd ee mm aa

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 adeficiency 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 apredilection 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 asdeterioration due to edema formation can be rapid.Medical therapy includes steroids, H 1 and H 2 histamine blockers, and s/c ori/m epinephrine.

Chronic angioedema responds better to corticosteroids and H 2 blockers .

Disposition depends on the severity and resolution of symptoms.I) Patients with symptomatic improvement or showing no worsening after 4

hours of observation may be discharged home. Discontinue suspectedmedications.II) Airway involvement requires admission to a monitored environment withsurgical airway equipments at bedside.

ADVICE:

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

2- Angioedema can also cause gastrointestinal and neurologic involvement.

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

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


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TTrraa uu mm aa TTee aa mm The trauma team is ideally made up of a group of doctors, nurses, operatingdepartment assistants, radiographers and other support personnel who haveno 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. Manycenters now have their trauma teams led by consultants.

Core Trauma Team is group of professionals that receives and treatsthe 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 ancillary services:

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

Blood Bank

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

Neurosurgeon Thoracic Surgeon Plastic Surgeon Radiologist

Certain areas need early notification of the trauma victim.

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

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

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

can be heard and assessments from team members can be relayedback to him.

Vital signs should be called out every five minutes and these must beheard 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 membersor passing senior staff.

This avoids confusion for team members of who to take direction fromand 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, orthopaedicsurgeon 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 EDphysician 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. Pelvisunless directed otherwise by the team leader.

Once these have been processed, other views may be required byevidence of other injuries.

The radiographer should also act as liaison to the CT scanningdepartment.

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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An injury to the eye or its surrounding tissues is the most common cause for

attendance at an eye hospital emergency department.

HistoryThe history of how the injury was sustained is crucial, as it gives clues as towhat to look for during the examination. If there is a history of any highvelocity injury (particularly a hammer and chisel injury) or if glass wasinvolved in the injury, then a penetrating injury must be stronglysuspected and excluded .If there has been a forceful blunt injury (such as a punch), signs of a

blowout fracture should be sought. Thecircumstances of the injury must be elicited and carefully recorded, as thesemay have important medicolegal implications. It may not be possible to getan accurate and reliable history from children if an injury is not witnessed byan adult. Such injuries should be treated with a high index of suspicion, as apenetrating eye injury may be present.

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

ExaminationA good examination is vital if there is a history of eye injury.Specific signs must be looked for or they will be missed. It isvital to test the visual acuity, both to establish a baseline valueand to alert the examiner to the possibility of further problems.However, an acuity of 6/6 does not necessarily exclude seriousproblemseven a penetrating injury. The visual acuity may alsohave considerable medicolegal implications. Local anaestheticmay need to be used to obtain a good view, and fluoresceinmust be used to ensure no abrasions are missed.


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Corneal abrasionsCorneal abrasions are the most common result of blunt injury. They mayfollow injuries with foreign bodies, fingernails, or twigs. Abrasions will bemissed if fluorescein is not instilled. TreatmentThe 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 dayor eye drops four times a day until the eye has healed and symptoms aregone. Ointment blurs the vision more but provides longer lasting lubricationcompared with eye drops. This will help prevent infection, lubricate the eyesurface, 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 theeye becomes uncomfortable with the pad, it can be removed and the eyetreated as per a small abrasion. The pad must be firm enough to keep theeyelid shut. Ointment or drops can then continue. If there is significant paincycloplegic eye drops (cyclopentolate 1% or homatropine 2%) may help,although this will further blur the vision. Oral analgesia such as paracetamolor stronger non-steroidal anti-inflammatory drugs can also be used. Patientsshould be told to seek futher ophthalmological help if the eye continues to bepainful, vision is blurred, or the eye develops a purulent discharge.

Recurrent abrasions Occasionally the corneal epithelium may repeatedlybreak down where there has been a previous injury or there is an inherentlyweak adhesion between the epithelial cells and the basement membrane.These recurrences usually occur at night when there is little secretionof tearsand the epithelium may be torn off. Treatment is long term and entails dropsduring the day and ointment at night to lubricate the eye. Occasionally, asurgical procedure (such as epithelial debridement or corneal stromalpuncture) may be carried out to enhance the adhesion between theepithelium and the underlying basement membrane.

Foreign bodiesIt is important to identify and remove conjunctival andcornealforeign bodies. A patient may not recall a foreignbody having entered the eye, so it is essential to beon the lookout for a foreign body if a patient has anuncomfortable red eye. It maybe necessary to uselocal anaesthetic both to examine the eye and toremove the foreign body. Although patients often

request them, local anaesthetics should never begiven to patients to use themselves, because theyimpede healing and further injury may occur to an


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anaesthetized eye. Small loose conjunctival foreign bodies can be removedwith the edge of a tissue or a cotton wool bud or they can be washed out withwater. 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 penetratinginjury is suspected. Corneal foreign bodies are often more difficult to removeif they are metallic, because they are often rusted on. They must beremoved as they will prevent healing and rust may permanently stain thecornea. A cotton wool bud or the edge of a piece of cardboard can be used. Ifthis does not work, a needle tip (or special rotary drill) can be used, but greatcare must be taken when using these as the eye may easily be damaged. Ifthere 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 theedge of a piece of cardboard

Radiation damageThe most common form of radiation damage occurs when welding has beencarried 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 knownas arc eye.) Radiation damage can also occur after exposure to largeamounts of reflected sunlight (for example, snow blindness) or afterultraviolet light exposure in tanning machines. Treatment is as for a cornealabrasion.

Chemical damageAll 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 immediatelywith copious amounts of water. Acute management should consist of thethree Is: Irrigate, Irrigate, Irrigate . Alkalis areparticularly damaging, and any loose bits such aslime should be removed from the conjunctival sac,with the aid of local anaesthetic if necessary.

The patient should then be referre immediately toan ophthalmic department. If there is any doubt,irrigation should be continued for as long aspossible 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 injuriesIf a large object (such as a football) hits the eye most of the impact is usuallytaken by the orbital margin. If a smaller object (such as a squash ball) hitsthe area the eye itself may take most of the impact. Haemorrhage may

occur and a collection of blood may be plainly visible in the anteriorchamber of the eye (hyphaema). Patients who sustain such injuries need tobe reviewed at an eye unit as the pressure in the eye may rise, and furtherhaemorrhages may require surgical intervention. Haemorrhage may also

occur into the vitreous or in the retina, and this may be accompanied by aretinal detachment. All patients with visual impairment after blunt injuryshould 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, asthis may be interpreted as (or mask) the dilated pupil that is suggestive ofan acute extradural haematoma. The lens may be damaged or dislocatedand acataract may develop.Damage to the drainage angle of the eye (which cannot be seen without aMirror contact lens and a slit lamp microscope) increases the chances of

glaucoma developing in later life. If the force of impact is transmitted to theorbit, an orbital fracture may occur (usually in the floor, which is thin and haslittle support). Clues to the presence of an inferior blowout fracture includediplopia, a recessed eye, defective eye movements (especially vertical), anipsilateral nose bleed, and diminished sensation over the distribution of theinfraorbital nerve. These patients need to be seen in an ophthalmicdepartment for assessment and treatment of eye damage, and a maxillofacialdepartment for repair of the orbital floor.

Penetrating injuries and eyelid lacerationsLacerations 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 themedial ends of the eyelids and it is likely that the lacrimal canaliculi will havebeen damaged, and these may need to be reapposed under the operatingmicroscope There is any suspicion of a foreign body or penetrating eyelid injury objects may easily penetrate the orbit and even the cranial cavity through theorbit.Penetrating injuries of the eye can be missed because they may sealthemselves, and the signs of abnormality are


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subtle. Any history of a high velocity injury (particularly a hammer and chiselinjury) should lead one strongly to suspect a penetrating injury. In that case,the eye should be examined very gently and no pressure should be broughtto bear on the globe. It is possible to cause prolapse of intraocular

contents and irreversible damage if the eye and orbit are not examinedwith great care .Signs to look for include a distorted pupil, cataract, prolapsed black uvealtissue on the ocular surface, and vitreous haemorrhage. The pupil should bedilated (if there is no head injury) and a thorough search made for anintraocular foreign body. If there is a suspicion of an intraocular or orbitalforeign body then orbital x ray photographs, with the eye in up and downgaze, should be taken. If the eye is clearly perforated it should be protectedfrom 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 thenormal fellow eye, is a potentially serious complication of any severepenetrating eye injury. The risk of this increases if a penetrating eye injury isleft untreated. All penetrating eye injuries should receive immediatespecialist ophthalmic management without delay .

RRee dd ee yyee The red eye is one of the most common ophthalmicproblems presenting to the general practitioner.An accurate history is important and should payparticular attention to vision, degree, and type of

discomfort and the presence of a discharge. Thehistory, and a good examination, will usually permitthe diagnosis to be made without specialist ophthalmic

equipment. Symptoms and signsThe most important symptoms are pain and visual loss;these suggest serious conditions such ascorneal ulceration, iritis,and acute glaucoma.A purulent discharge suggests bacterial

conjunctivitis; a clear discharge suggests aviral or allergic cause. A gritty sensation iscommon in conjunctivitis, but a foreign bodymust be excluded, particularly if only oneeye is affected. Itching is a common symptomin allergic eye disease, blepharitis, and topical drop hypersensitivity.

Corneal abrasions will be missed if fluorescein is not used


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Equipment for an eye examination Snellen eye chart Bright torch or ophthalmoscope with blue filter Magnifying aidfor example, loupe Paper clip to help lid eversion Fluorescein impregnated strips or eye drops

Conjunctivitis Conjunctivitis is one of the most common causes of anuncomfortable red eye. Conjunctivitis itself has many causes,including bacteria, viruses, Chlamydia , and allergies.Bacterial conjunctivitisHistory The patient usually has discomfort and a purulent

discharge in one eye that characteristicallyspreads to the other eye. The eye may bedifficult to open in the morning because thedischarge sticks the lashes together. Theremay be a history of contact with a personwith similar symptoms.

Examination The vision should be normal afterThe discharge has been blinked clear of thecornea. The discharge usually is mucopurulent and there is uniform

engorgement of all the conjunctival blood vessels. When fluorescein dropsare 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 thefirst 24 hours to hasten recovery, decreasing to four times a dayfor one week. Chloramphenicol ointment applied at night mayalso increase comfort and reduce the stickiness of the eyelids inthe morning. Patients should be advised about general hygienemeasures; for example, not sharing face towels.Viral conjunctivitisViral conjunctivitis commonly is associated with upperrespiratory tract infections and is usually caused by anadenovirus. This is the type of conjunctivitisthat occurs in epidemics of pink eye.

History The patient normally complainsof 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 longerthan bacterial conjunctivitis and may go on for many weeks; patients needto be informed of this. Photophobia and discomfort may be


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severe if the patient goes on to develop discrete cornealopacities.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 associatedopacities may give rise to pronounced symptoms, but these are difficult tosee without high magnification. There may be associated head and necklymphadenopathy with marked pre-auricular lymphadenopathy.Managemen t Viral conjunctivitis isgenerally a self Limiting condition, butantibiotic eye drops (for example,chloramphenicol) provide symptomatic

relief and help prevent secondary bacterialinfection. Viral conjunctivitis is extremelycontagious, and strict hygiene measuresare important for both the patient and thedoctor; for example, washing of hands andsterilising of instruments. The period ofinfection is often longer than with bacterial pathogens and patients should be

warned that symptoms may be present for several weeks. In some patientsthe 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, becauseof the real danger of causing cataract or irreversible glaucomatous damage.Furthermore, if long term steroids are required, patients should remain undercontinuous ophthalmological supervision.

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

Chlamydial conjunctivitisHistory Patients usually are young with ahistory of a chronicbilateral conjunctivitis with a

mucopurulent discharge. There may beassociated symptoms of venereal disease.Patients generally do not volunteer genitourinarysymptoms 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 theconjunctiva (follicles). The cornea usually is involved (keratitis) and aninfiltrate of the upper cornea (pannus) may be seen.


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Management The diagnosis is often difficult and special bacteriologicaltests may be necessary to confirm the clinical suspicions. Treatment with oraltetracycline 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 inchildren or pregnant women. Associated venereal disease should also betreated, and it is important to check the partner for symptoms or signs ofvenereal disease (affected females may be asymptomatic). It often is helpfulto 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 severescarring of the conjunctiva and the underlying tarsal plate. These cicatricialchanges cause the upper eyelidsto turn in (entropion) and permanently scar

the already damaged cornea. Worldwide, trachoma is still one of the majorcauses of blindness.

Conjunctivitis in infantsConjunctivitis in young children is extremely importantbecause the eye

defences are immature and a severe conjunctivitis with membrane formationand bleeding may occur. Serious corneal disease and blindness may result.Conjunctivitis in an infant less than one month old (ophthalmianeonatorum) is a notifiable disease . Such babies must be seen in an eyedepartment so that special cultures can be taken and appropriate treatmentgiven. Venereal disease in the parents must be excluded.

Allergic conjunctivitisHistory The main feature of allergic conjunctivitis is itching. Both eyesusually are affected and there may be a clear discharge. There may be afamily history of atopy or recent contact with chemicals or eye drops. Similarsymptoms may have occurred in the same season in previous years. It isimportant to differentiate between an acute allergic reaction and a more longterm chronic allergic eye disease.Examination The conjunctivae are diffusely injected and may beoedematous (chemosis). The discharge is clear and stringy. Because of thefibrous septa that tether the eyelid (tarsal) conjunctivae, oedema results inround swellings (papillae). When these are large they are referred to ascobblestones.Management Topical antihistamine and vasoconstrictor eye drops provideshort term relief. Eye drops that prevent degranulation of mast cells also areuseful, but they may need to be used for several weeks or months to achievemaximal effect. Oral antihistamines may also be used, particularly the newer

compounds that cause less sedation. Topical steroids are effective butshould not be used without regular ophthalmological supervision because of


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the risk of steroid induced cataracts and glaucoma, which may irreversiblydamage vision.

Cases of allergic eye disease in association with severe eczema will oftenneed careful combined ophthalmological and dermatological management.

Corneal ulcerationCorneal ulcers may be caused by bacterial, viral, or fungal infections; these

may occur as primary events or may be secondary to an event that hascompromised the eyefor example, abrasion, wearing contact lenses, or useof topical steroids.History Pain usually is a prominent feature as the cornea is an exquisitelysensitive structure, although this is not so when corneal sensation isimpaired; for example, after herpes zoster ophthalmicus. Indeed, this lack ofsensory innervation may be the cause of the ulceration. There may be cluessuch as similar past attacks, facial cold sores, a recent abrasion, or thewearing 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 waterydischarge due to reflex lacrimation or a mucopurulent discharge in bacterialulcers. Conjunctival injection may be generalised or localised if the ulcer isperipheral,giving a clue to its presence. Fluorescein must be used or an ulcereasily may be missed. Certain types of corneal ulceration are characteristic;for example, dendritic lesions of the corneal epithelium usually are caused byinfection with the herpes simplex virus. If there is inflammation in the anteriorchamber there may be a collection of pus present (hypopyon). The uppereyelid must be everted or a subtarsal foreign body causing cornealulceration may be missed. Patients with subtarsal foreign bodies sometimesdo not recollect anything entering the eye.Management Patients with corneal ulceration should be referred urgently toan eye department or the eye may be lost. Management depends on thecause of the ulceration. The diagnosis usually will be made on the clinical

appearance. The appropriate swabs and cultures should be arranged to tryto identify the causative organism. Intensive treatment then is started withdrops and ointment of broad spectrum antibiotics until the organisms andtheir sensitivities to various antibiotics are known. Injections of antibiotics intothe subconjunctival space may be given to increase local concentrations ofthe 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 tothe lens (posterior synechiae).


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

Acute angle closure glaucomaAcute angle closure glaucoma always should be considered in a patient overthe age of 50 with a painful red eye. The diagnosis must not be missed or theeye will be damaged permanently.History The attack usually comes on quite quickly, characteristically in theevening, when the pupil becomes semidilated. There is pain in one eye,which can be extremely severe and may be accompanied by vomiting. Thepatient complains of impaired vision and haloes around lights due to oedemaof the cornea. The patient may have had similar attacks in the past whichwere relieved by going to sleep (the pupil constricts during sleep, so relievingthe attack). The patient may have needed reading glasses earlier in life. Apatient with acute angle closure glaucoma may be systemically unwell, withsevere headache, nausea, and vomiting, and can be misdiagnosed as anacute abdominal or neurosurgical emergency. Acute angle closure glaucomaalso may present in patients immediately postoperatively after generalanaesthesia, and in patients receiving nebulised drugs (salbutamol andipratropium bromide) for pulmonary disease.Examination The eye is inflamed and tender. The cornea is hazy and thepupil is semidilated and fixed. Vision is impaired according to the state of thecornea. On gentle palpation the eye feels harder than the other eye. Theanterior chamber seems shallower than usual, with the iris being close to thecornea. If the patient is seen after the resolution of an attack the signs mayhave 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 itis not possible to get the patient to hospital straight away, intravenousacetazolamide 500 mg should be given, and pilocarpine 4% should beinstilled in the eye to constrict the pupil.

First the pressure must be brought down medically and then a hole made inthe iris with a laser (iridotomy) or surgically (iridectomy) to restore normalaqueous flow. The other eye should be treated prophylactically in a similarway. 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 beirreversibly damaged necessitating a full surgical drainage procedure.

Subconjunctival haemorrhageHistory The patient usually presents with ared eye which is comfortable and without anyvisual disturbance. It is usually the appearanceof the eye that has made the patient seek attention.

If there is a history of trauma, or a red eye after hammering or chiselling, thenocular injury and an intraocular foreign body must be excluded.Subconjunctival haemorrhages are often seen on the labour ward postpartum.

Examination There is a localised area ofSubconjunctival blood that is usually relativelywell demarcated. There is no discharge orconjunctival reaction. Look for skin bruisingand evidence of a blood dyscrasia.

Management It is worth checking the bloodpressure to exclude hypertension. If there areno other abnormalities the patient should bereassured and told the redness may take

several weeks to fade. If patients are anticoagulated with warfarin thenthe coagulation profile (international normalised ratio, INR) should bechecked. If abnormal bruising of the skin is present then consider checkingthe full blood count and platelets


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Definition Systolic Blood Pressure > 140 mmHg, Diastolic Blood Pressure > 90mmHg.

Hypertensive emergencies: SBP > 200mmHg & DBP > 120mmHg,with new or progressive end-organ damage(CNS, CVS orRenal)

Hypertensive Urgency: Severe hypertension without end-organdamage.

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.

Cardiovascularo Chest pain ( ischemic )o Acute aortic dissection

- Severe tearing chest pain- Pulse deficit

- New aortic regurgitation murmuro 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 Hgeand or Ppilledema etc.)

ECG if cardiac symptoms are present. CBC if BP is very high to check for microangiopathic hemolytic

of malignant hypertension Urea, creatinine and electrolytes to check for renal impairment (

as sign for end-organ damage or as a cause of hypertension) Urine analysis to investigate for secondary causes of

hypertension specially if patient has renal impairment CXR: Cardiomegaly, pulmonary edema or aortic dissection

Treatment : I. Hypertensive emergency

(very high BP with end-organ damage )

1) Sodium nitroprusside- patient needs continuous monitoring- solution and bottle should be covered by foil and should be

changed every 6h- start with 0.25 /kg/min and titrate up to of 1 /kg/min and reduce

the dose if BP is acceptable- do not allow BP to fall more than 25% of pre-treatment BP- CONTRA-IDICATED IN PRESENCE OF RENAL FAILURE

2)Hydralazine IV infusion- Used if nitroprusside is contra-indicated (i.e., renal failure)- May give 5-10 mg iv, slowly over 10 min. or im- Do not allow BP to drop more than 25% of the pre-treatment BP- DOSE MAY BE REPEATED IF NO EFFECT FROM FIRST DOSE- If BP drops to reasonable level start infusion at 1-10 mg/hour and

measure BP every 5-10 min, titrate dose up and down (do notallow 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 5 g/min. and titrate up until adequate control is

achieved ( maximum dose is 100 g/min.)

II. Hypertensive urgency


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( Very high BP with no end-organ damage )

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

Ask patient if he (she) missed his (her) medication, if yesresume their medication with possibility of increasing thedose.

Always aim for monothrapy, add other drug if no responsewith maximum dose of one drug or if side effect of the drugarises

The following are available option:

Nifedipine ( Adalat ) should not be given

sublingually May give Nifedipine retard 20mg BID ( maximumdose 40 mg TID ), if unavailable give Nifedipine10mg TID ( maximum dose 20mg TID )

If no contra-indicated to beta blocker (renal failure,bradycardia, or bronchial asthma ) may giveAtenolol( Cardol,Hypoten,or Tenormin) 50 -100mgOD

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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AAcc uu ttee PP uu llmm oo nn aa rryy EEdd ee mm aa

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

o Signs and symptoms represent the transference of fluids from thepulmonary capillaries into the pulmonary interstitial and alveolar airspaces.

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 inthe lower zones, 2cm long at least, that, on the contrary of bloodvessels reach the lung edge. Alveolar oedema (can be observed with its butterfly pattern)characterized by the central predominance of shadows with a clearzone at periphery lobes. Enlarged cardiac, silhouette may be present in chronic CHF.

ABG: May reveal hypoxemia ( PO 2 ) and respiratory alkalosis ( PCO 2 )due to Tachypnea. Respiratory acidosis ( PCO 2 ) is an ominous sign of tiring andimpending respiratory failure. P02 values 50 mmHg denotes severity and theneed of mechanical ventilation.

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

Blood studies: CBC, Electrolytes, BUN and Creatinine .

Treatment: (O 2, 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% O 2 by mask:

If hypoxia persist despite O 2 therapy, continuous positiveairway pressure (CPAP) or biphasic airway pressure shouldbe applied.

Immediate intubation is indicated for unconscious or visiblytiring 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 importantdecrease in BP


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

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

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

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 mayoccur 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 rapidvent. reasons is a contributory factor. The total dose 1-1.5 mg IV inthe first 24 hours.

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


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BB aa ss iicc LLiiffee SS uu pp pp oo rr tt o It is the simple procedures which prevent circulatory or respiratory

arrest or insufficiency prompt

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

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

the left in the 5 th intercostals space mid clavicular line.

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

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

minute Cardiac Output is around 5 L/min.

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

of the arterial carbon dioxide.

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

Room air contain 21%O 2 our expiration contain 16% O 2

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 ofoxygen, the brain cells are the most sensitive to the lack of oxygen.

o Brain damage occurs after 4 minute of cardio-respiratory

arrest .


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


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NNee aa rr DDrroo ww nn iinn gg ((SS uu bb mm ee rrss iioo nn ))

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 accountingfor 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, hemoglobinuria, ketonuria

ABG Hypoxemia,or combined metabolic& respiratory

acidosis.

CXR Pneumonitis or pulmonary edema.

C-spine X ray To exclude spine injury specially in diving injury TREATMENT Take the patient from the water to dry area, remove all wet clothes and avoid

hypothermia (cover him with blanket, warm atmosphere).

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

Resuscitation must start at scene rapidly. Do not waste time to drain water from thevictim'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, placethe victim supine, perform Hemlich Maneuver ) clear the victim's mouth with fingersweep.

Start rapid CPR , Rescue Breathing. Do not press over the abdomen or thrust asthese 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 adjunctsshould be used if the patient is hypothermic.

Hypothermic victims in Cardiac Arrest should undergo prolonged, aggressiveresuscitation 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 withGCS 3 survive with full neurological recovery ).

Poor prognostic indicators include fixed dilated pupils, need for cardiacmedications and GCS less than 5.

Long term sequelae include ischemic encephalopathy, aspiration pneumonia,ARDS and chronic lung disease.


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MMaa nn aa gg ee mm ee nn tt OO ff CCoo nn vvuu llss iioo nn IInn EEmm ee rrgg ee nn cc yy DDee pp aa rr ttmm ee nn tt

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 O 2 and glucose.

All body muscle tone increased leading to respiratory insufficiency oraspiration, which is the brain anoxia.

Sudden diaphragmatic contraction lead to vomiting and possibleaspiration, 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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TTrree aa mm ee nn tt OO ff TThh ee FFiitt

Protect the patient form injury during resuscitation .

1. Airway :Open airway, suction, protect from aspiration and put in recovery position

2. Breathing:

Supply O 2 through face mask or endotracheal intubation as needed, guided by pulse

oximeter to ensure O 2 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 timeso Paedia: 0.3 mg/kg/dose repeat twice every 5 minutes

In paedia, if no IV line, give valium rectally

If Diazepam fail to control the fit or after controlling the fit start

2. Phenytoin sodium

Adult: 15-20 mg/kg bolus over 20 min - repeat 10mg/kg if not controlled Paedia: loading dose 10 mg/kg/ repeat after 2 hours 5mg/kg, infuse1mg/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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MMaa nn gg ee mm ee nn tt OOff

SS ee vvee rree BBrroo nn cc hh iiaa ll AAss tthh mm aa

Clinical picture:

Severe shortness of breath.

Usual precipitating factors Non-compliance with medications.

Exposure to allergens or medications.

Sinus infection(URTI)

Stress.

HistoryShould include prior HX, of intubation, hypoxic seizure or

Documents

Unified Protocol for Management of Critical Cases Commonly Encountered in ED. Dr. Hamid Shaalan. FRCS