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Emergency Medicine Notes 2019

BASIC UPDATED Emergency Medicine Notes, AS BACKGROUND FOR ER DOCTORS
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Emergency Medicine Notes 2019

  1. 1. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 1 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
  2. 2. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 2 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
  3. 3. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 3 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
  4. 4. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 4 RESUSCITATION
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  22. 22. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 22 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.
  23. 23. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 23 CARDIOLOGICAL EMERGENCIES
  24. 24. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 24 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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  38. 38. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 38 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.
  39. 39. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 39 CARDIOGENIC SHOCK
  40. 40. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 40 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:
  41. 41. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 41 (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
  42. 42. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 42 PREMATURE ATRIAL CONTRACTION Emergency Department Care and Disposition 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 Emergency Department Care and Disposition 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,
  43. 43. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 43 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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  47. 47. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 47 MULTIPLE ATRIAL TACHYCARDIA Emergency Department Care and Disposition 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 Emergency Department Care and Disposition 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.
  48. 48. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 48 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 Emergency Department Care and Disposition 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
  49. 49. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 49 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
  50. 50. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 50 Emergency Department Care and Disposition 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. Emergency Department Care and Disposition 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).
  51. 51. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 51 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. Emergency Department Care and Disposition 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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  57. 57. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 57 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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  62. 62. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 62 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
  63. 63. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 63 RESPIRATORY EMERGENCIES
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  70. 70. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 70 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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  75. 75. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 75 NEUROLOGICAL EMERGENCIES
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  81. 81. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 81 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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  96. 96. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 96 GASTRO INTESTINAL EMERGENCIES
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  99. 99. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 99 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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  103. 103. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 103 ER MANAGEMENT OF ACUTE PANCRETITIS
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  105. 105. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 105 ENDOCRINOLOGICAL EMERGENCIES
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  112. 112. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 112 MYXEDEMA CRISIS
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  114. 114. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 114 ADRENALCRISIS
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  116. 116. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 116 Medications in the Emergency Management of Hyperkalemia Step-Wise Approach to Emergency Management of Hyponatremia
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  118. 118. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 118 Management of hypernatremia
  119. 119. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 119 Hypocalcemia
  120. 120. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 120  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.
  121. 121. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 121 ENVIRONMENTAL EMERGENCIES&POISONING
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  124. 124. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 124 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
  125. 125. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 125 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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  132. 132. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 132 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.
  133. 133. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 133 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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  139. 139. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 139 Ca channel blocker toxicity
  140. 140. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 140 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.
  141. 141. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 141 ASPIRIN TOXICITY Emergency Department Care and Disposition 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
  142. 142. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 142 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
  143. 143. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 143 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. 144. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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.
  145. 145. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 145 Organo phosphorus poisoning
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  147. 147. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 147 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.
  148. 148. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 148 Hydrocarbon toxicity
  149. 149. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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 .
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  151. 151. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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.
  152. 152. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 152 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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  160. 160. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 160 HEAT EMERGENCIES
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  162. 162. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 162 Scorpion stang
  163. 163. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 163 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.
  164. 164. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 164 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)
  165. 165. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 165 Marine emergencies
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  171. 171. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 171 Chemical exposure
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  173. 173. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 173 PAIN MANAGEMENT
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  178. 178. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 178 TRAUMA MANAGEMENT
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  183. 183. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 183 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. 184. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 185. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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
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  192. 192. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 192 Brain injury
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  206. 206. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 207. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 208. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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.
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  228. 228. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 228 Trauma in Pediatrics
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  237. 237. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 237 Trauma in pregnancy
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  246. 246. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 246 Orthopedic
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  258. 258. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 258 MIS EMERGENCIES
  259. 259. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 259 Red eye
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  261. 261. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 262. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 263. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 264. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 265. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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. 266. Emergency Medicine Notes 2019 Dr Abd El Aal Elbahnasy 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

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