Emergency Medicine Notes 2019

Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy
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EMERGENCY MEDICINE notes 2019
2nd
edition
EDITED&COLLECTED BY
DR.ABD ELAAL MOHAMED ELBAHNASY
Master Degree in Emergency Medicine
Tanta University, Egypt
HEAD OF EMERGENCY DEPARTMENT
SOUTH QUNFUDAH GENERAL HOSPITAL
MINISTRY OF HEALTH, SAUDI ARABIA

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Dear colleagues,
IT IS MY PLEASURE TO PRESENT THIS NOTEBOOK
FOR ALL DOCTOR WORKING IN EMERGENCY
DEPARTMENTS ALLOVER THE WORLD AS BASIC
KNOWLEDGE ENABLE DOCTORS FROM DEALING
AND THINKING WITH MOST OF FAMOUS AND
CRITICAL CASES IN ER
I HOPE FROM MY GOD YOU FOUND THESE NOTES
USEFUL AND FRUITFUL TO SAVE MORE AND
MORE LIVES ALL OVER THE WORLD
WITH MY BEST WISHES
ABD ELAAL ELBAHNASY
EMERGENCY MEDICINE SPECIALIST
EGYPT

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contents
subject No.
1 Resuscitation 4
2 Cardiology 23
3 Respiratory 62
4 Neurological 74
5 Gastro entrology 95
Endocrine/ electrolyte 104
6 Environmental &poisoning 120
Pain management 172
7 Trauma 177
9 Orthopedic 245
10 Miscellaneous 257

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RESUSCITATION

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LOCAL ANTHESIA TOXICITY
1 If symptoms or signs of toxicity appear during procedure stop giving local anesthetic.
2 Call for help and specifically request the LAST kit.
3 Maintain airway, give 100% O2 and consider intubation.
4 Confirm intravenous access is established.
5 If cardiac arrest, start CPR but use < 1 mcg/kg epinephrine.
6 Treat seizures with benzodiazepines as first line therapy.
7 Administer 20% intravenous lipid emulsion.
8 Prepare for prolonged CPR and alert the nearest ECMO facility.
Symptoms
circumoral and/or tongue numbness, metallic taste, light-headedness, dizziness visual/auditory
disturbance, drowsiness, disoriented
Signs
muscle twitching, convulsions, unconsciousness, coma, respiratory depression,
dysrhythmias, cardiovascular depression, collapse
Cardiopulmonary resuscitation
Follow ACLS algorithm but use reduced dose epinephrine (< 1 mcg/kg) and give
intralipid early. Avoid beta-blockers, Ca2+ channel blockers, lidocaine and vasopressin.
Drugs for seizure termination
 Reduce the risk of LAST by using correct local anesthetic dosing, aspirating
before injecting, fractionating doses and using ultrasound.
 Always be prepared for LAST when blocking patients. Consider stocking a
LAST kit anywhere nerve blocks are performed and know the location. The
kit should include 20% lipid emulsion and a LAST checklist.
 Neurological signs, which can be non-specific, depressive or excitatory, often
but not always precede cardiovascular signs.

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CARDIOLOGICAL EMERGENCIES

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Chest pain
Classic Chest Pain Terms such as “typical” and “atypical” symptoms are
misleading because symptoms among patients with acute coronary
syndrome vary and may not include classic findings. Classic cardiac chest
pain is retrosternal left anterior chest crushing, squeezing, tightness, or
pressure. Cardiac chest pain is often brought on or exacerbated by exertion
and relieved by rest
Nonclassic presentations include chest pain lasting for seconds, constant
pains lasting for 12 to 24 hours or more without waxing and waning
intensity, or pain worsened by specific body movements or positions, such
as twisting and turning of the thorax. Reports of stabbing, welllocalized,
positional, or pleuritic chest pain are uncommon with acute coronary
syndrome but do not exclude it with certainty.
Investigation:
1- ECG
2- CBC
3- cardiac enzyme
4- troponine

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ER MANAGEMENT OF ACUTE PULMONARY EDEMA
1. Establish IV access and consider arterial line placement.
2. Start NIPPV using 100% O2 and settings listed opposite.
3. Give NTG 200-400 mcg IV bolus over 1 min and repeat in 2 min if BP remains
high.
4. Start 100 mcg/min NTG infusion and titrate up to 400 mcg/min.
5. If hypotension develops, reduce or turn off NTG and consider a 250 mL fluid
bolus.
6. Avoid giving diuretics early.
7. Avoid morphine.
8. Perform bedside echo/US assessment of cardiovascular system.
9. Screen for ischemia with serial ECGs and cardiac enzymes.
10. Once stable, transfer to ICU or CCU as appropriate
NIPPV settings
 Patients require primarily CPAP/EPAP. Start at 5 cm H2O and titrate up to 15
cm H2O.
 IPAP is supplementary.
 Diuretics should not be given early. Acute diuresis with furosemide may lead
to an increase in afterload due to neurohormonal mechanisms (increase in
sympathetic and renal angiotensin). Morphine leads to greater intubation rates
and doesn’t improve the primary problem.
 If the patient is not hypertensive then treatment is directed more towards
cardiogenic shock or other causes of edema rather than SCAPE.
 Bedside echocardiography can determine cardiac function, valvular function
and monitor pulmonary edema.

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CARDIOGENIC SHOCK

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General Approach to dysrhythmias
Asking these three questions will help classify any tachydysrhythmia in most cases.
1. Regular or irregular?
2. Narrow or wide QRS?
3. Are there P waves? P-QRS relationship? How many P waves for each QRS?
Sinus Tachycardia
Clinical Features
The ECG characteristics of sinus tachycardia are:
 normal sinus P waves and PR intervals
 an atrial rate usually between 100 and 160 beats/min.
Sinus tachycardia is in response to three categories of stimuli:

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(a ) physiologic (pain or exertion),
( b ) pharmacologic (sympathomimetics, caffeine, or bronchodilators),
( c ) pathologic (fever, hypoxia, anemia,hypovolemia, pulmonary embolism, or hyperthyroidism).
In many of these conditions, the increased heart rate is an effort to increase cardiac output to match
increased circulatory needs.
Emergency Department Care and Disposition
Diagnose and treat the underlying condition.
SVT
Treatment

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PREMATURE ATRIAL CONTRACTION
1. Discontinue precipitating drugs (alcohol, tobacco, or coffee) or toxins.
2. Treat underlying disorders (stress or fatigue).
3. PACs that produce significant symptoms or initiate sustained tachycardias can be suppressed with
agents such as β-adrenergic antagonists (eg, metoprolol 25 to 50 milligrams PO 3 times daily), usually in
consultation with a follow-up physician.
ATRIAL FIBRILATION
1. Treat unstable patients with synchronized cardioversion (50-100 J).
2. Stable patients with Afib for longer than 48 hours should be anticoagulated with heparin (80
units/kilogram IV followed by an infusion of 18 units/kilogram/h IV) before cardioversion. Consider a
transesophageal echocardiogram to rule out atrial thrombus before cardioversion.
3. Control rate with diltiazem. Administer 20 milligrams (0.25 milligram/kilogram) IV over 2 min
followed by a continuous IV infusion, 5 to 15 milligrams/h, to maintain rate control. Give a second
dose of 25 milligrams
(0.35 milligram/kilogram) in 15 min if the first dose fails to control rate. Alternative rate control agents
for patients with normal cardiac function include verapamil , 5 to 10 milligrams IV, metoprolol , 5 to
10 milligrams IV, and digoxin , 0.4 to 0.6 milligram IV. Treat patients with preexcitation syndromes
(eg, WPW) with procainamide, 17 milligrams/ kilogram IV, over 30 min up to 50 milligrams/kilogram
or until 50% QRS widening is noted. Avoid β-adrenergic or calcium channel blockers (ie, verapamil)
due to the risk of causing degeneration to VF.
4. In patients with impaired cardiac function (EF < 40%), use amiodarone,

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5 milligrams/kilogram IV over 30 min, followed by 1200 milligrams over 24 hours (contra
indicated in patients with iodine or shellfish allergy; increased risk of rhabdomyolysis if co-
administered with simvastatin) or digoxin 0.4 to 0.6 milligram IV.
5. Patients with Afib for shorter than 48 hours may be chemically or electrically cardioverted in the
emergency department. Use amiodarone, ibutilide (see comments for atrial flutter),
procainamide, flecainide, or propafenone in patients with normal cardiac function. Ibutilide is
dosed at 0.01 milligram/kilogram IV up to 1 milligram, infused over 10 min. A second ibutilide
dose may be given if there is no response in 20 min. Ibutilide should not be administered to
patients with known structural heart disease, hypokalemia, prolonged QTc intervals,
hypomagnesemia, or CHF because of the possibility of provoking torsades de pointes.
Monitor for 4 to 6 hours after giving ibutilide. Patients with impaired cardiac function may be
cardioverted with amiodarone or electrically

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MULTIPLE ATRIAL TACHYCARDIA
1. Treat the underlying disorder.
2. Specific antiarrhythmic treatment is rarely indicated. Rate control may be achieved with verapamil 5 to
10 milligrams IV, or diltiazem 10 to 20 milligrams IV in patients with acute COPD or CHF exacerbations.
3. Magnesium sulfate 2 grams IV over 60 seconds followed by a constant infusion of 1 to 2 grams/h may
decrease ectopy and convert MAT to sinus rhythm in some patients.
4. Replete potassium levels to greater than 4 mEq/L to increase myocardial membrane stability
JUNCTIONAL RTHYTHM
1. Isolated, infrequent junctional escape beats usually do not require specific treatment.
2. If sustained junctional escape rhythms are producing symptoms, treat the underlying cause.
3. In unstable patients, give atropine 0.5 milligram IV every 5 min to a total of 2 milligrams. This will
accelerate the SA node discharge rate and enhance AV nodal conduction.

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Premature Ventricular Contractions
Clinical Features
Premature ventricular contractions (PVCs) are due to impulses originating from single or multiple areas in
the ventricles.
The ECG characteristics of PVCs are:
( a ) a premature and wide QRS complex;
( b ) no preceding P wave;
( c ) the ST segment and T wave of the PVC are directed opposite the preceding major QRS deflection;
( d ) most PVCs do not affect the sinus node, so there is usually a fully compensatory post-ectopic pause,
or the PVC may be interpolated between 2 sinus beats;
( e ) many PVCs have a fixed coupling interval (within 0.04 second) from the preceding sinus beat; and
( f ) many PVCs are conducted into the atria, thus producing a retrograde P wave
If 3 or more PVCs occur in a row, patients are considered to have nonsustained ventricular tachycardia.
PVCs are very common, occurring in most patients with ischemic heart disease and acute MI. Other
common causes of PVCs include digoxin toxicity
1. Stable patients require no treatment.
2. Patients with 3 or more PVCs occur in a row should be managed as VT.
3. For hemodynamically unstable patients with PVCs, consider lidocaine 1 to 1.5 milligrams/kilogram IV (up
to 3 milligrams/kilogram) unless the patient is allergic to amide anesthestics

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Atrioventricular (AV) Block
First-degree AV block is characterized by a delay in AV conduction, manifested by a prolonged PR interval
(> 0.2 second).
It can be found in normal hearts and in association with increased vagal tone, digoxin toxicity, inferior MI,
amyloid, and myocarditis.
 First-degree AV block needs no treatment.
 Second-degree AV block is characterized by intermittent AV nodal conduction: some atrial
impulses reach the ventricles, whereas others are blocked, thereby causing “grouped beating.”
These blocks can subdivided into nodal blocks which are typically reversible and infranodal blocks
which are due to irreversible conduction system disease.
 Third-degree AV block is characterized by complete interruption in AV conduction with resulting
AV dissociation.
Second-Degree Mobitz I (Wenckebach) AV Block
Clinical Features
 Mobitz I AV block is a nodal block causing a progressive prolongation of conduction through the AV
node until the atrial impulse is completely blocked. Usually, only one atrial impulse is blocked at a
time.
 After the dropped beat, the AV conduction returns to normal and the cycle usually repeats itself
with the same conduction ratio (fixed ratio) or a different conduction ratio (variable ratio). Although
the PR intervals progressively lengthen before the dropped beat, the increments by which they
lengthen decrease with successive beats causing a progressive shortening of each successive R–
R interval before the dropped beat .This block is often transient and usually associated with an
acute inferior MI, digoxin toxicity, or myocarditis or can be seen after cardiac surgery. Because the
blockade occurs at the level of the AV node itself rather than at the infranodal conducting system,
this is usually a stable rhythm

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1. Specific treatment is not necessary unless slow ventricular rates produce signs of hypoperfusion.
2. In cases associated with acute inferior MI, provide adequate volume resuscitation before initiating further
interventions.
3. Administer atropine 0.5 milligram IV repeated every 5 min. Titrate to the desired heart rate or until the
total dose reaches 2 milligrams.
4. Although rarely needed, transcutaneous pacing may be used.
Second-Degree Mobitz II AV Block
Clinical Features
Mobitz II AV block is typically due to infranodal disease, causing a constant PR interval with intermittent
non-conducted atrial beats .
One or more beats may be non-conducted at a single time. This block indicates significant damage or
dysfunction of the infranodal conduction system;
therefore, the QRS complexes are usually wide coming from the low His-Purkinje bundle or the ventricles.
Type II blocks are more dangerous than type I blocks because they are usually permanent and may
progress suddenly to complete heart block, especially in the setting of an acute anterior MI, and almost
always require permanent cardiac pacemaker placement.
When second-degree AV block occurs with a fixed conduction ratio of 2:1, it is not possible to differentiate
between a Mobitz type I (Wenckebach) and Mobitz type II block.
1. Atropine 0.5 to 1 milligram IV bolus repeated every 5 min as needed up to 2 milligrams total dose is
first-line treatment for symptomatic patients. All patients should have transcutaneous pacing pads
positioned and ready for use in the case of further deterioration into complete heart block.
2. Initiate transcutaneous cardiac pacing (see section on sinus bradycardia) in patients unresponsive to
atropine
3. If transcutaneous pacing is unsuccessful, initiate transvenous pacing (0.2 to 20 mA at 40 to 140
beats/min via a semi-floating or balloontipped pacing catheter).

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Third-Degree (Complete) AV Block
Clinical Features
In third-degree AV block, there is no AV conduction. The ventricles are paced by an escape pacemaker
from the AV node or infranodal conductionsystem at a rate slower than the atrial rate .When third-
degree AV block occurs at the AV node, a junctional escape pacemaker takes over with a ventricular rate
of 40 to 60 beats/min; and, because the rhythm originates from above the bifurcation of the His bundle,
the QRS complexes are narrow.
Nodal third-degree AV block may develop in up to 8%of acute inferior MIs and it is usually transient,
although it may last for several days.
When third-degree AV block occurs at the infranodal level, the ventricles are driven by a ventricular escape
rhythm at a rate slower than 40 beats/ min.
Third-degree AV block located in the bundle branch or the Purkinje system invariably has an escape
rhythm with a wide QRS complex. Like Mobitz type II block, this indicates structural damage to the
infranodal conduction system and can be seen in acute anterior MIs. The ventricular escape pacemaker is
usually inadequate to maintain cardiac output and is unstable with periods of ventricular asystole.
1. Perform transcutaneous cardiac pacing in unstable patients until a transvenous pacemaker can be
placed.
2. In stable patients, apply transcutaneous pacing pads. Treat the same as second-degree Mobitz II AV
block.

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General principles for lowering BP rapidly in the ED
1. Blood pressure should almost never be rapidly lowered (except in aortic dissection).
2. Lower pressure by no more than 25%, to avoid ischemia in organs auto-regulated to higher
BP.
3. Therapies that correct the cause (e.g. phentolamine if the BP is elevated by catecholamines)
will be most effective.
4. Monitor the symptoms to determine whether the BP has been adequately lowered.

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ER MANAGEMNET OF AORTIC DISSECTION
1. Establish large bore IV access and titrate FiO2 to SpO2 ≥ 90%.
2. Place right radial arterial line and use left arm for NIBP.
3. Use fentanyl and esmolol as first line therapy to control pain, keep HR < 60 and
reduce SBP < 120 mmHg.
4. If additional control is needed, use the agents listed (in order of preference) in
the table opposite.
5. Prepare for rapid CT angiogram but use bedside TEE or TTE as alternatives if
unstable or while waiting for CT.
6. Notify blood bank, request blood products and activate massive transfusion
protocol if indicated 06 .
7. Seek early consultation with CT surgeon for decision on imaging, blood
pressure, and heart rate control.
8. Notify theatre early if surgery is indicated.
9. If hypotensive, consider tamponade, myocardial infarction, aortic valve
incompetence or aortic rupture.
10. Prepare for transfer to ICU or the OR.
OUR AIM IN ER
DECRESE PAIN
DECREASE BP
DECRESE HR

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RESPIRATORY EMERGENCIES

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ECG Findings in Pulmonary Embolism
1. sinus tachycardia
2. RV strain pattern
3. incomplete RBBB
4. flipped T waves in anterior leads
5. S1Q3T3 (poor sensitivity & specificity)
6. flipped T waves in anterior and inferior leads, an uncommon finding
which has been shown to be highly specific for PE

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NEUROLOGICAL EMERGENCIES

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APPROACH TO VERTIGO IN THE ED
4 types of dizziness (there’s always one that predominates):
1. Syncope / pre‐syncope: feeling of passing out
2. Vertigo: hallucination of rotation or linear movement; spinning
3. Disequilibrium: cannot walk properly, staggering
4. Non‐specific light‐headedness
4 types of vertigo (based on duration of symptoms):
1. Less than 60sec: Positional event (MARKEDLY worse with movement)
2. Minutes (few to 30): If not positional: migraine (in young, low‐risk patients) or TIA/CVA (in
older, at‐risk patients)
3. Many hours: Vestibulopathy, Ménière’s disease
4. Days: Labyrinthitis, or stroke
Approach to vertigo
The easiest way to rule out an ominous central cause is by ruling in a benign peripheral cause:
1. BPPV: <1min, normal in between attacks, Dix‐Hallpike positive , Epley maneuver cures it in
50% of cases
2. Vestibular neuronitis: acute severe constant vertigo, positive head‐thrust manoeuvre
3. Ménière’s disease: >20mins to hrs in combination with tinnitus, ear fullness or decreased
hearing
Vertigo History
Features suggestive of posterior circulation ischemia: diplopia, ataxia (especially between episodes),
dysarthria (slurred speech) and dysphagia – and central cause: non‐positional or bidirectional
nystagmus, inability to ambulate, focal neurological deficit and cerebrovascular risk factors
Note: all causes of vertigo can be worsened by head movement
Vertigo Physical examination
 Unidirectional horizontal nystagmus is usually peripheral in nature, whereas vertical, pure
torsional and/or bidirectional nystagmus, limb ataxia and pinprick sensation asymmetry are
usually central
Medications for Vertigo
 Antihistamines (eg, dimenhydrinate), antidopaminergic (prochlorperazine ‐ Stemetil™),
and/or anticholinergic (atropine 0.4‐0.6mg IM or Scopolamine 0.5mg patch) may be
triedSerc™ (betahistine) should ONLY be prescribed for Ménière’s disease

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GASTRO INTESTINAL EMERGENCIES

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Er Management of abdominal pain
Unstable patients should be resuscitated immediately, then diagnosed clinically with
emergent surgical consultation.
1. NBO
2. IV HYDRATION RL
3. Consider morphine 0.1 milligram/kilogram IV, which can be reversed
by naloxone (0.4 to 2 milligrams SC/IV) if necessary
4. . Antiemetics, such as ondansetron 4 milligrams IM/IV, or
metoclopramide 10 milligrams IM or slow IV
5. Surgery consultation and obs gyn for female

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ER MANAGEMENT OF ACUTE
PANCRETITIS

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ENDOCRINOLOGICAL EMERGENCIES

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MYXEDEMA CRISIS

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THYROID STORM

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ADRENALCRISIS

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Medications in the Emergency Management of Hyperkalemia
Step-Wise Approach to Emergency Management of
Hyponatremia

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Management of hypernatremia

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Hypocalcemia

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 Regimens can be 500 to 3000 milligrams of elemental calcium by
mouth daily, in one dose or up to three divided doses. The dose
must be individualized for each patient, according to the cause and
severity of hypocalcemia.
 IV calcium is recommended only in cases of symptomatic or
severe hypocalcemia2 (ionized [Ca2+] <1.9 mEq/L or <0.95
mmol/L), because IV Ca2+ administration causes vasoconstriction
and possible ischemia, especially in patients with low cardiac
output who already have significant peripheral vasoconstriction. IV
calcium gluconate is preferred over IV calcium chloride in
nonemergency settings due to the dangers of extravasation with
calcium chloride (calcinosis cutis).
 With severe acute hypocalcemia, 10 mL of 10% CaCl2 (or 10 to 30
mL of 10% Ca2+ gluconate) may be given IV over 10 to 20
minutes and repeated every 60 minutes until symptoms resolve or
followed by a continuous IV infusion of 10% CaCl2 at 0.02 to 0.08
mL/kg/h (1.4 to 5.6 mL/h in a 70-kg patient).
 IV Ca2+ should be used with caution in patients taking digitalis,
because hypercalcemia can potentiate digitalis toxicity.

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ENVIRONMENTAL
EMERGENCIES&POISONING

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EMERGENCY DEPARTMENT CARE OF POISONED CASE
1. Protect your self first
2. ABCDE
3. O2
4. Monitoring the patient with vital signs plus RBS
5. Treat arrhythmia if present according to ACLS PROTOCOL
6. Airway protection before GI decontamination
7. Antidote
8. Coma cocktail for unconscious patients( o2- naloxone (0.2 to 2.0
milligrams IV/IO/IM), glucose (1 to 1.5 grams/ kilogram IV/IO), and
thiamine (10 to 100 milligrams IV/IO in the adult patient).
9. Treat seizures by . Lorazepam (0.05 to 0.1 milligram/kilogram IV/IO
in children or 1 to 2 milligrams IV/IO in adults) is a reasonable first-
line agent. Phenytoin is generally not effective in toxin-induced
seizures and may exacerbate dysrhythmias in some poisonings
10. Once stabilized, surface decontamination is the next priority in
care. If not previously done, completely disrobe the patient. Dermal
toxins must be removed from the skin by irrigation. Ocular exposure
often requires pain control with topical agents such as 0.5%
tetracaine. Copiously irrigate the eye with isotonic crystalloid. This
may require several liters before restoration of physiologic pH.
11. Gastrointestinal decontamination is achieved via removal of the
toxin from the stomach, binding toxin within the GI tract, or
enhancing transit time through the gut.
 Gastric lavage
 Activated charcoal binds a large number of xenobiotics and
prevents their absorption across the GI tract. The dose is typically 1
gram/ kilogram in children or 25 to 50 grams in adults. The minimal
dose should be no less than a 10:1 ratio of AC to drug. Only the first
dose of AC should be used with a cathartic, and only if diarrhea is not
expected. An awake, alert, and cooperative patient may drink the
mixture. Alternatively, AC can be infused through an NG tube.
 Whole-bowel irrigation (WBI) is best accomplished through
placement of an NG tube and instilling polyethylene glycol at a rate
1 to 2 L/h until rectal effluent is clear. Indications for WBI include
sustained-release tablets, certain metals, and drugs carried by body
stuffers/packers Contraindications include diarrhea, decreased bowel
sounds, or intestinal obstruction.
12. Considerations for enhanced elimination depend on the specific
toxin and response to standard treatment. Urinary alkalinization and

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hemodialysis are the 2 most frequently utilized modalities. Forced
dieresis has essentially no role in enhancing elimination.
13. Early toxicology consultation

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Take Home Points for Management of Massive TCA Overdose
1. Use a QRS > 100 msec, a target pH of 7.5-7.55 and serum sodium
of 150-155 mmol/L to guide sodium bicarbonate bolus therapy in
TCA overdose. After 4 amps of sodium bicarbonate, if these targets
are not met, consider adjunctive therapies.
2. Intralipid (20% lipid emulsion) should be considered in
hemodynamically unstable TCA overdose patients, those with
refractory ventricular dysrhythmias following adequate sodium
bicarbonate therapy or lidocaine, and those with refractory seizures.
3. Adjunctive therapies for massive TCA overdose include hypertonic
saline, lidocaine, magnesium sulfate and ECMO where available.

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Serotonin syndrome (SS)
 Often rapid onset (vs. more prolonged in NMS) as a result of overdose
or, most commonly, combination of prescription (eg, SSRI, MAOIs) and
non‐prescription drugs (recreational such as
‘ecstasy’/methamphetamine, or OTC)
o Mnemonic “SHIVERS”:
 Shivering
 Hyper‐reflexia (myoclonus vs. “lead‐pipe”rigidity in NMS)
 Increased temperature
 Vital signs instability (high BP, HR, RR)
 Encephalopathy (or any altered LOC)
 Restlessness
 Sweating
o Clonus in the setting of ‘Ecstasy’/methamphetamine use should
prompt the diagnosis of SS!
o ‘Ecstasy’ is now the most common trigger of SS in Ontario, Canada
o Also beware of dilutional hyponatremia in people participating in
‘Rave Parties’, where they drink LOTS of water
 Drugs associated with SS: anti‐depressants – SSRIs, SNRIs, MAOIs,
TCAs; pain medications – Demerol, fentanyl, tramadol; headache
medications – maxeran, triptans; weight loss drugs; drugs of abuse –
amphetamines; as well as dextromethorphan (in Tylenol Cold©),
linezolid, ondansetron and granisetron
 Treatment: mainly supportive with activated charcoal as necessary,
external and/or internal cooling, benzodiazepines, and consider
olanzapine, chlorpromazine (DO NOT use if NMS is considered), and the
antidote cyproheptadine in conjunction with a toxicology consultation
(do not give both charcoal and cyproheptadine as it is an oral
medication!)

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Ca channel blocker toxicity

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1. Administer activated charcoal, 1 gram/kilogram within 1 to 2 hours of ingestion if
no contraindications exist
2. Atropine 0.5 to 1 milligram (0.02 milligram/kilogram, minimum dose 0.1 milligram)
and calcium may be of limited benefit in cases of severe toxicity; give calcium
gluconate or calcium chloride [10 mL of 10% (0.15 mL/kg) repeated 3 to 6 times as
necessary].
3. Use norepinephrine 2 to 30 micrograms/kg/min, epinephrine 1 to 20
micrograms/kilograms/min , dopamine 2.5 to 20 micrograms/kilograms/ min, for
refractory bradycardia and hypotension.
4. Hyperinsulinemia-euglycemia (HIE) therapy can improve myocardial contractility
and blood pressure .Bolus regular insulin (1 unit/kg IV) followed by continuous
infusion (0.5 to 1 unit/kg/h). Monitor serum glucose and potassium frequently.
5. Glucagon is variably successful in the treatment of calcium channel blocker toxicity.
Administer as an IV bolus of 3 to 5 mg (0.05 milligram/ kilogram) followed by
continuous infusion of 1 to 10 milligrams/h.
6. IV fat emulsion (20% solution) has shown promising success in the treatment of
severe toxicity. Administer as a bolus of 1.5 mL/kg I followed by a continuous infusion
of 0.25 mL/kg/min.
7. Patients who develop bradycardia, hypotension, or conduction disturbances should
be managed in an ICU. Patients who remain asymptomatic 6 hours after ingestion of an
immediate release agent can be medically cleared. Admit patients who have ingested a
sustained release preparation or sotalol to a monitored setting due to concern for
delayed toxicity.

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ASPIRIN TOXICITY
1. Institute cardiac monitoring and support the ABCs. Establish intravenous (IV) or
intraosseous (IO) access early. Careful airway management is critical in ASA-
poisoned patients: a sudden drop in serum pH due to respiratory failure can
precipitously worsen ASA toxicity, and careful ventilation guided by acid-base
status is essential in the intubated patient. Respiratory acidosis frequently occurs
shortly after a mechanical ventilator is set to a “normal” rate and volume
parameters, and is typically a premorbid event.
2. Administer activated charcoal 1 gram/kilogram PO. Whole-bowel irrigation
may effectively decontaminate the GI tract in the setting of large overdoses,
enteric-coated, or sustained-release preparations.
3. Administer IV normal saline (NS) to patients with evidence of volume
depletion. During initial resuscitation, monitor urine pH, ASA level, electrolytes,
glucose, and acid-base status hourly. Add dextrose to parenteral fluids after initial
NS resuscitation. Consider 10% dextrose in the setting of hypoglycemia or
neurologic symptoms. Add potassium 40 mEq/L after establishing adequate urine
output (1 to 2 mL/kg/h), if not contraindicated by initial electrolytes and renal
function.
4. Alkalinize the serum and urine to enhance ASA protein binding and

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urinary elimination: administer a bolus of 1 to 2 mEq/kg of sodium bicarbonate ,
then add 150 mEq (3 ampules) of sodium bicarbonate to 1 L 5% dextrose in water
and infuse at 1.5 to 2.0 times the patient’s maintenance rate; adjust the infusion to
maintain urine pH > 7.5 if possible. Bicarbonate may worsen hypokalemia and
precipitate arrhythmias.
5. Consider hemodialysis for all cases with ASA levels in excess of 100
milligrams/dL. Indications for hemodialysis may be significantly lower in the
setting of chronic toxicity (60 to 80 milligrams/dL). Also consider hemodialysis for
clinical deterioration despite supportive care and alkalinization, renal insufficiency
or failure, severe acid-base disturbance, improving clinical status. 4 to 6 hours until
the level is nontoxic.
6. Enteric-coated and sustained-release preparations result in delayed peak serum
levels (0 to 60 hours postingestion) and their ingestion requires.
7. Discharge a patient from the ED if there is progressive clinical improvement, no
significant acid-base abnormality, and a decline in serial ASA levels toward the
therapeutic range. In deliberate overdoses, obtain a psychiatric consultation before
discharge. altered mental status, or adult respiratory distress syndrome. Check
serial ASA levels every 2 hours until they begin to fall

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Iron toxicity
1. ABCDE Place the patient on supplemental oxygen and a cardiac monitor,
and establish 2 large-bore IVs.
2. Administer vigorous intravenous (IV) crystalloid infusion to help correct
hypovolemia and hypoperfusion.
3. Perform gastric lavage in patients who present within 60 min of ingestion.
Activated charcoal is not recommended.
4. Whole-bowel irrigation with a polyethylene glycol solution is efficacious.
Administration of 250 to 500 mL/h in children or 2 L/h in adults via
nasogastric tube may clear the GI tract of iron pills before absorption occurs.
5. Administer antiemetics such as ondansetron (4 milligrams IV in adults; 0.1
milligrams/kilogram to a maximum dose of 4 milligrams in pediatric
patients) or promethazine 25 milligrams IV in adults.
6. Correct coagulopathy with vitamin K 1 (5 to 10 milligrams SC) and fresh
frozen plasma (10 to 25 mL/kg in adults; 10 mL/kg in pediatric patients).
Order blood for type and screen or crossmatch as necessary.

144
7. Deferoxamine is a chelating agent that can remove iron from tissues and
free iron from plasma. Deferoxamine is safe to administer to children and
pregnant women.
Indication of Deferoxamine therapy:
 systemic toxicity,
 metabolic acidosis,
 worsening symptoms,
 or a serum iron level predictive of moderate or severe toxicity.
Dose: The recommended initial dose is 1000 milligrams IV. Since
hypotension is the rate-limiting factor for IV infusion, it is
recommended to begin with a slow IV infusion at 5
milligrams/kilogram/hour . The deferoxamine infusion rate can be
increased to 15 milligrams/ kilogram/h, as tolerated, within the first hour
of treatment. The recommended total amount of deferoxamine is 360
milligrams/kilogram or 6 grams during the first 24 hours. Initiate
deferoxamine therapy without waiting for the serum iron level in any
clinically ill patient with a known iron ingestion.
Evaluate the efficacy of deferoxamine treatment through serial urine samples.
As ferrioxamine is excreted, urine changes to a classic vin ros appearance.
Clinical recovery is the most important factor guiding the termination of
deferoxamine therapy.
8. Patients who remain asymptomatic after 6 hours of observation, have a
normal physical examination, and have a reliable history of an insignificant
ingestion may be considered for discharge. Patients initially symptomatic who
become asymptomatic should be admitted for further evaluation since this
may represent the second stage of iron toxicity.
9. Admit all patients who receive deferoxamine therapy to an intensive
care setting. Assess all patients for suicide risk. Consider child abuse or
neglect in pediatric cases.

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Organo phosphorus poisoning

146

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HYDROGEN SULFIDE
Hydrogen sulfide is a colorless gas used in the petrochemical industry
and can emanate from sewage or manure. Although it has a distinct
“rotten egg” odor, this olfactory warning is lost with extended exposure
and high concentrations.
Hydrogen sulfide causes cellular asphyxia that leads to lactic
acidosis. In high concentrations, rapid loss of consciousness, seizures,
and death can occur after only a few breaths. Treat with 100% oxygen,
followed by administration of sodium nitrite IV, as with cyanide
poisoning. The resultant methemoglobin enhances formation of less
toxic sulfmethemoglobin from sulfide.

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Hydrocarbon toxicity

149
Caustics
Decontamination
1. Remove contaminated clothing and irrigate exposed skin with copious amounts
of water. Alkali burns may require local debridement and removal of devitalized
tissue followed by additional irrigation.
2. Perform aggressive ocular decontamination with normal saline for a minimum of
15 min with frequent monitoring of ocular pH until a Ph of 7.5 to 8.0 is achieved.
3. Gastric decontamination in the form of activated charcoal, ipecac, or gastric
lavage is contraindicated. Intentional strong acid ingestions may benefit from
gastric decontamination with a nasogastric tube if performed within 30 min of
ingestion.
4. Dilution or neutralization is generally reserved for immediate prehospital or
home care of the unintentional pediatric ingestion and is not recommended more
than 30 min post-ingestion.
Supportive Care
1. Perform early awake oral intubation with direct visualization in symptomatic
patients with stridor, significant drooling, or dysphonia. Blind nasotracheal
intubation is contraindicated.
2. Obtain IV access and administer isotonic IV fluids for hypotension.
3. Obtain surgical consultation for suspected or confirmed peritonitis or free air.
Special Considerations
1. Treat hydrofluoric acid dermal exposures with topical calcium gluconate gel
(3.5 grams mixed with 150 mL water-soluble lubricant). Consider intradermal 5%
calcium gluconate for large burns and calcium gluconate infusion into the radial
artery over 4 hours or given as a Bier block (10 mL of 10% calcium gluconate in
40 mL saline or 5% dextrose) for refractory distal extremity burns.
2. Oral ingestions of hydrofluoric acid within an hour can be suctioned via
nasogastric tube followed by instillation of up to 300 mL of 10% calcium
gluconate . High doses of IV calcium and magnesium may be needed to treat
systemic deficiencies and dysrhythmias.
3. Disc batteries lodged in the esophagus require emergent endoscopic removal .

150

151
1. Administer fomepizole 15 milligrams/kilogram IV load followed by 10
mg/ kilogram every 12 hours. Fomepizole is a potent inhibitor of alcohol
dehydrogenase with greater affinity and fewer side effects than ethanol. If
fomepizole is not available, or the patient is allergic, use ethanol 800
milligrams/kilogram IV load, followed by a continuous infusion of 100
milligrams/kilogram/h inAdjust the infusion accordingly to maintain a blood
ethanol level at 100 to 150 milligrams/dL. If resources are limited, oral therapy
with commercial 80 proof liquor can be initiated. A load of 3 to 4 oz with
maintenance of 1 to 2 oz/h is a typical dose for a 70 kilograms patient.
2. Monitor serum glucose during treatment with ethanol as hypoglycemia may be
induced, especially in children. Treat hypoglycemia with 1 mL/kg 50% dextrose in
water in adults and 4 mL/kg 10% dextrose in water in children.
3. Dialysis eliminates both methanol and ethylene glycol and their toxic
metabolites. Indications are listed in Table 104-2. Fomepizole or ethanol treatment
do not alter the indications for dialysis; however, both fomepizole and ethanol are
dialyzed and, therefore, increase the dosing interval of fomepizole to every 4 hours.
Double the infusion rate of ethanol during dialysis and adjust accordingly to
maintain the level at 100 to 150 milligrams/dL.
4. Continue dialysis, fomepizole, or ethanol treatment until the methanol or
ethylene glycol level is < 20 milligrams/dL and the metabolic acidosis has
resolved.
5. In methanol poisoning, administer folate 50 milligrams IV. In ethylene glycol
poisoning, administer pyridoxine 100 milligrams IV and thiamine 100 milligrams
IV.
6. Administer sodium bicarbonate 1 to 2 mEq/kg and titrated to maintain a normal
pH in methanol toxicity to increase renal excretion of formic acid.
7. Treat documented and symptomatic hypocalcemia in ethylene glycol toxicity
with calcium gluconate or calcium chloride.
8. Consult a medical toxicologist or regional poison control center to aid in the
management of symptomatic methanol or ethylene glycol ingestion.
9. Patients with suspected ethylene glycol ingestion who are asymptomatic after 6
hours with no ethanol detected and no osmolar gap or metabolic acidosis may be
safely discharged. Since methanol toxicity and coingestion
of ethanol may result in delayed symptoms, these patients should be observed for a
minimum of 12 hours. Patients with significant signs and symptoms should be
admitted to an intensive care unit.

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ER management of Amphetamine toxicity
1. ABCD
2. Benzodiazepines are the mainstay of treatment for cardiovascular and CNS
effects. Administer lorazepam 2 milligrams IV (0.1 milligram/ kilogram)
for agitation, hypertension, and tachycardia and titrate to effect. Avoid
antipsychotic medications, which may precipitate seizures, hyperthermia,
and dysrhythmias.
3. Treat seizures with benzodiazepines. Phenobarbital (15 to 20 milligrams/
kilogram) and neuromuscular blockade with continuous EEG monitoring
may be necessary for status epilepticus.
4. Treat cardiac ischemia or infarction with aspirin, nitrates, morphine, and
benzodiazepines. -blockers are contraindicated due to unopposed -
receptor stimulation. Fibrinolytic therapy should be used with great caution
because of the risk of cocaine-associated intracranial hemorrhage.
5. Treat cocaine-induced wide complex tachydysrhythmia and QRS interval
prolongation with sodium bicarbonate 1 to 2 mEq/kg titrated to a serum pH
of 7.45 to 7.5. Acidification of the urine for amphetamine intoxication is
contraindicated.
6. Treat hypertension unresponsive to benzodiazepines with nitroprusside (0.3
microgram/kilogram/min IV) or phentolamine (2.5 to 5.0 milligrams IV)
.
7. Treat asymptomatic “body packers” with whole-bowel irrigation using
polyethylene glycol . Symptomatic patients with presumed rupture of
ingested packets are treated for acute toxicity as above and immediate
surgical consultation for possible laparotomy.

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158

159

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HEAT EMERGENCIES

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Scorpion stang

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Snake bite
1. Assess the ABC and initiate the appropriate resuscitation measures.
2. Inspect the area of the bite and document evidence of fang marks, abrasions or lacerations.
Document the size of the eryhema and edema surrounding the site of bite.
3. Clean the site immobilize and splint thebitten limb.
4. Determine the extent of local and Systemic Reaction (table1)
5. The following lab test should be done:
 CBC,PT ,PTT & INR, Bleeding Time,CPK,LFT,KFT,RBS,Urine Analysis.
 Type and screen, Cross match 2 units of PRBC and hold
 D Ddimer if needed
6. Start IV NS,not in the affected limb
7. 12 Lead ECG keep monitoring ABP, cardiac rhythm, urine color, O/P.
8. Also observe the local edema, erythema and blister. Document the changes.
9. Assess tetanus status and update immunization as necessary.
Haemotoxic Snake Bite
Horned Viper, Sand scaled Viper, Carpet Viper
Neurotoxic Snake Bite
Arabian Cobra, Black Desert Cobra, Male Viper
1. Spontaneous systemic bleeding
2. Local swelling involving more than half the bitten limb
3. Extensive blistering or bruising
4. Marked thrombocytopenia ≤ 50,000/mm3
5. Hypotension, shock and abnormal ECG
6. Prolonged bleeding time
7. Hematouria
8. Rhabdomyolysis
Neurotoxicity
1. Ptosis, External ophtalmoplegia
2. Progressive paralysis of face, palate, jaws,
tongue, vocal cords, neck muscles and
muscles of degilution
3. Impaired consciousness
4. Progressive Respiratory failure
Serious Local Envenomation : Local swelling involving more than half of the bitten limb, extensive bruising or
blistering with rapid progression of swelling.

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10. If no local/ systemic signs of envenomation observe for 24 hours.
11. Snake bite patients will be admitted under internal medicine/pediatrics (below 14 years).
12. If signs of serious local or systemic envenomation are present start in Emergency
Department with 40 ml antivenom (4ampules, 10 ml each) diluted in 5ml NS and titrate over
60min.
13. Children must be given the same dose of antivenom as adults.
14. Those patients will be admitted to ICU/PICU.
15. The dose of Antivenom should be repeated every 4-6 hours till definite improvement
Table 2: Adjunctive Therapy for Snake Bite Envenomation:
Neurotoxic Envenomation
Bulbar and respiratory paralysis may lead to death from aspiration, airway
obstruction or respiratory failure mechanical measures should be taken to
maintain lung ventilation i.e. endotracheal intubation and mechanical
ventilation
Anticholinesterases are potentially useful in these cases (physisotagmin)
Hypotension and Shock
Fresh whole blood, fresh frozen plasma or plasma expander can be used.
Dopamine infusion can be used in cases of persistent or profound
hypotension
Oliguria and Renal Failure
Cautious rehydration, diuretics, peritoneal/haemodialysisor haemofiltration
may be undertaken
Local Infection at the site of bite
Penicillin, erythromycin or a broad spectrum antibiotic together with a
booster dose of tetanus toxoid should be given in cases of wound infection.
An aminoglycoside and metronidazole should be added if there is evidence
of local necrosis.
Fasciotomy is indicated only for those patients with objective evidence of
elevated compartment pressure.
Reference: The Antivenom and Vaccine Production Center (AVPC).K SA
16. Available is Polyvalent Snake Antivenom (AVPC polyvalentEquine).
17. If anaphylactiod reaction happens to the anitvenom (it can occur within 10-180 min) take the
following steps:-SQ Adrenaline (1mg/ml solution 0.5-1 ml for pediatrics. 0.01ml/kg) repeat the dose
if necessary -Chlorphenirarminemaleate10 mg IV (for pediatrics 0.2 mg/kg. IV)—
Hydrocortisone100-200 mg IV.Thosepatients will be admitted to ICU
18. Late reaction (serum sickness / immune complex) may develop 5- 24 days (7 days average), treat
with Prednisolone (5mg/ 6 hours / 7 days for adults. 0.7 mg/ kg/ day in divided doses for peds.) Add
Chlorphenirarminemaleate 2mg /6/hours for adults.(for pediatric 0.25 mg/ kg /day in divided
doses)

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Marine emergencies

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167

168

169

170

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Chemical exposure

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173
PAIN MANAGEMENT

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175

176

177

178
TRAUMA MANAGEMENT

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180

181

182

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Work up of any case of trauma:
LAB
1-cbc
2-blood chemistry (renal-liver-cardiac)
3-coagulation profile
4- Blood group, cross matching if multiple trauma patient
IMAGING:
1-x ray cervical vertebra
2-x ray chest
3-x ray pelvis
4-Abd U/S with report
INDICATION OF CT IN TRAUMA PATIENT:
CT HEAD FOR HEAD TRAUMA IF:
1-old age more than 65
2- Patient on warfarin
3- Loss of conscious level after trauma
4-GCS less than 15 for 2 hours
5-suspected depressed skull fracture
6-signs of basal skull fracture
7-pediatric with signs of increase ICT
8-convulsion after trauma
9-dangerous trauma
10-polytraumatized patient
CT CHEST IF:
1-chest pain after trauma
2-chest contusion
3-decrease air entry
4-any change in o2 sat
5-suspecting rib fracture
6-polytraumatized patient
CT abdomen for trauma patient must be with
contrast

184
Tetanus immunization protocol
Tetanus is preventable by vaccination through the administration of tetanus toxic (TT)
At regular basis.Also through the administration of tetanus immune globulin (TIG).
Source: Australian Technical Advisory Group on Immunisation. The Australian
Immunisation Handbook. 10th ed. Canberra: Australian Government Department of
Health and Ageing; 2013. p.404

185
ANY PATIENT OF TRAUMA LIKE RTA, FALL DOWEN
FROM HIGHT, SEVER ASSULT MUST BE EVALUTED
BY SURGERY DOCTOR AND DISCHARGED FROM ER
BY SURGERY SPECIALIST

186

187

188

189

190

191

192
Brain injury

193

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196

197

198

199

200

201

202

203

204

205

206
ER MANAGEMENT OF INCREASE ICP
Clinical signs of elevated ICP/herniation
altered mental state
pupil abnormalities - unilateral, fixed, dilated pupil or bilateral non reactive
midposition pupils
cranial nerve palsy
loss of upward gaze
stroke syndromes from vessel compression
cushing’s response - hypertension and bradycardia, erratic respiratory pattern
Diagnosis
 Urgent CT Scan
 Ultrasound of optic nerve sheath diameter:
outer diameter > 6mm in high risk patient - likely elevated ICP
outer diameter < 5mm in low risk patient - likely normal ICP
1 Optimize oxygenation, ventilation and blood pressure.
2 Use the neuroprotective protocol for intubation .
3 Correct any coagulopathy and consider correction of platelet function or
reversal of anti-platelet therapy.

207
4 Confirm there is elevated ICP by urgent CT scan, ocular nerve sheath
diameter, clinical examination or ICP monitoring.
5 Notify neurosurgeon for surgical intervention if indicated.
6 Position head of bed to 30 degrees, place head midline, and check cervical
collar is not impeding jugular blood flow.
7 Minimize pain and agitation with short acting agents.
8 Maintain PaCO2 at 35-40 mmHg.
9 Treat seizures and administer seizure prophylaxis.
10 If signs of herniation:
 hyperventilate to PaCO2 of 30 mmHg
 give osmolar therapy (23.4% hypertonic saline preferred)
 arrange for immediate operative intervention
Intubation
 is for airway protection and CO2 control.
 Aim to avoid hypotension, hypoxemia and hypo/hypercapnia
 Ketamine 1-2 mg/kg is a suitable alternative to etomidate in hypotension.
 PaCO2 should be maintained at 35-40 mmHg unless herniation
Osmolar therapy
 hypertonic saline: 500 mL 3% or 30-60 mL 23.4%
 mannitol: 1 g/kg if not hypotensive and no ESRD
 Insert IDC (Foley) and replace urinary losses with normal saline to avoid
hypotension.
Seizure treatment
 Use IV midazolam 2-4 mg or IV lorazepam 2-4 mg.

208
 Prophylaxis options: levitarecetam 1g BID (preferred), or fosphenytoin 20
mg/kg load,then 100 mg TID.
 Surgical intervention may include ventricular drain or more specific
procedures such as
 evacuation of hematomas, resection of tumor or SOL lesions, and
craniectomies.
 Do not use steroids in traumatic brain injury (TBI) or intracranial
hemorrhage (ICH).
 Do not adjust ventilation on EtCO2 only - set to EtCO2 ≤ 35 and then use
PaCO2.

209

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211

212

213

214

215

216

217

218

219

220
Musclo skeletal

221

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223

224

225

226

227

228
Trauma in Pediatrics

229

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231

232

233

234

235
Trauma in Geriatrics

236

237
Trauma in pregnancy

238

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240

241

242

243

244

245

246
Orthopedic

247

248

249

250

251

252

253

254

255

256

257

258
MIS EMERGENCIES

259
Red eye

260

261
Immediate Ophthalmologic Consultation;
1. Corneal Ulcer
2. Complicated Hyphema
3. Corneal Perforation
4. Endopthalmitis
5. Severe hyperacute conjunctivitis and gonococcal conjunctivitis (i.e. corneal involvement)
6. Central retinal artery occlusion
7. Severe chemical/thermal injury
8. Central retinal vein occlusion and branch retinal vein occlusion
9. Eyelid laceration (+/‐)
Nasal Fractures
Nasal fracture is a clinical diagnosis suggested by the injury mechanism,
swelling, tenderness, crepitance, gross deformity, and periorbital ecchymosis.
Radiographic diagnosis usually is not necessary in the ED. Intermittent ice
application, analgesics, and over-the-counter decongestants are the normal
treatment. ENT follow-up within 6 to 10 days for reexamination and possible
fracture reduction is prudent.
The nose should be examined for a septal hematoma. If left untreated, a septal
hematoma may result in abscess formation or necrosis of the nasal septum.

262
The treatment is local incision and drainage with subsequent placement of
an anterior nasal pack.
A fracture of the cribriform plate may violate the subarachnoid space
and cause cerebrospinal fluid rhinorrhea. Symptoms may be delayed for
several weeks. If a cribriform plate injury is suspected, CT and immediate
neurosurgical consultation should be obtained.
Epistaxis Management
Step 1: Visualize the bleed “Ensure proper orientation up-down orientation of nasal speculum
(see image). If bleeding, ask pt to blow nose gently to clear clots.
Step 2: Anesthetize “ Apply cotton pledget with 1:1 mix of oxymetazoline (Dristan or Afrin)
& lidocaine, which may be more effective than cocaine (& less side effects), using bayonet forceps.
Leave in place for 5–10 minutes with the nose *firmly* clamped.
Step 3: Cauterize “Remember eye and face protection, as silver nitrate causes sneezing.
Cauterize dry edges of bleeding site (ie around the site, not on it), for 10–15 seconds maximum.
Never cauterize both sides of the septum! Moisturize the area with petrolatum after cautery is
complete.
Step 4: If bleeding continues, tamponize “Consider wrapping tampon on balloon-type in
gelfoam or surgicel, which may encourage clotting in coagulopathic patients. Nasal balloons have
greater patient satisfaction than tampons.
Management Pearls: Apply ice to the palate (popsicles, ice in the mouth) to reduce nasal blood
flow up to 25%. Tranexamic acid (0.25mL IV which is 25mg) applied topically may also help anterior
bleed. Can apply IV formulation, as a slurry with gelfoam.
Does elevated blood pressure cause epistaxis?
There is no evidence that hypertension causes nosebleeds. Usually high BP results from pain or
anxiety. Our experts recommend treating these symptoms to manage hypertension in epistaxis
patients.
Posterior Epistaxis
More rare, but can have more serious consequences. Suspect posterior bleeds in elderly patients,
patients with brisk bleeds that cannot be directly visualized, or patients who have ongoing
bleeding despite bilateral anterior packing. These patients require aggressive treatment in a
monitored setting (if bleeding is severe, packing procedures may trigger vagal response), IV
access, fluids, and ENT consultation for admission and IV antibiotics. Packing requires both anterior
and posterior packing, usually by double packing balloons. Avoid overinflating, and secure anterior
packs centrally to avoid alar necrosis.

263
1 Establish two large bore IVs or place introducer sheath.
2 Consider intubation if the airway is at risk.
3 Have patient blow nose to clear clots from nares.
4 Insert dual-balloon pack or Foley catheter.
5 Slowly inflate the posterior balloon and apply traction.
6 Inflate the anterior balloon or pack the anterior nares.
7 Administer sedation and analgesia as needed.
8 Place gauze between exterior nares + catheter, then secure.
9 Discuss case with ENT specialist and prepare for admission.
10 Reverse any coagulopathy and review need for antibiotics.
Signs of posterior bleeding
heavy bleeding
bleeding in the posterior pharynx
bleeding not controlled with an anterior pack
Procedure can be painful so judicious use of sedation and analgesia is recommended.
Slow inflation of the balloons can allow hemostasis while minimizing pain.
Familiarity with the devices prior to an emergent event is essential as inflation substance (air/water)
and volumes are unique to the devices. A dedicated pre-made ENT kit containing all needed supplies
will improve management of these cases.
Treatment of any coagulopathy should be directed by the coagulation panel.
Posterior packing with Foley(s)
Intubation is preferable. For epistaxis due to trauma, use Foleys (12-14F) in preference to commercial
devices.
Procedure
Witness passage into the posterior pharynx by both Foleys with laryngoscope.

264
Inflate using smaller volume first (6-8 mL) and apply traction until balloon wedges in posterior
choana.
Inflate to 20 mL, apply traction and secure.
Reapply the anterior packs bilaterally

265
Rhabdomyolysis
EMERGENCY DEPARTMENT CARE AND DISPOSITION
1. The primary focus of therapy should be aggressive intravenous (IV) hydration
with crystalloids. The exact recommendations vary, but a rapid correction of
fluid deficits, followed by supraphysiologic maintenance fluids should be
performed. Some advocate 2.5 cc/kilogram/h of maintenance fluids, while
others target a urine output of 200 to 300 cc/h.
Urinary alkalinization or forced dieresis have not been clearly proven to
improve outcome. Patients with significant comorbidities require close
observation and titration of fluids to prevent fluid overload.
2. Electrolytes should be monitored. In general, asymptomatic early
hypocalcemia does not require specific therapies, and phosphorus
correction should only occur with levels > 7 milligrams/dL or < 1
milligram/dL. Hyperkalemia, in contrast, may require aggressive therapy
3. Placement of a urinary catheter may be needed in critically ill individuals in
order to accurately monitor urine output.
4. The use of nephrotoxic drugs, including nonsteroidal anti-inflammatory
(NSAID) medications should be avoided, if possible.
5. Patients without significant comorbidities with mild, exertional
rhabdomyolysis can be hydrated in the emergency department, and often
released. Those with significant elevations in the CK, those with acute
kidney injury, and those with underlying comorbidities should be admitted
for continued hydration and evaluation of renal function.

266
REFERRENCES
1- EMERGENCY MEDICINE ALGORITHMS,AFEM 2014
2- EMERGENCY MEDICICINE CASES. website
3- AMERICAN HEART ASSOCIATION GUIDELINES,2015
4- ATLS 10TH
EDITION
5- ATLS 9TH
EDITION
6- Tintinallis emergency medicine textbook, 8th
edition
7- Tintinallis emergency medicine,manual ,8th
edition
8- Nailing the written emergency medicine,Springer International
Publishing Switzerland 2016
9- Maine medical center protocols
10- The Resuscitation Crisis Manual,1st
edition 2018
With my best wishes,
Your colleague,
Dr. Abd Elaal Mohamed Elbahnasy
Er specialist, Egypt
Er_redsea@yahoo.com

Emergency Medicine Notes 2019

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