24395804 Study Notes Emergency Medicine

Study Notes Emergency Medicine James Lamberg 28Jul2010

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Textbooks: Adams Emergency Medicine, Emergency Medicine Secrets, First Aid for Emergency Clerkship -------------------------------------------------------------------------------------------------------------------------------------------- Common Problems in Emergency Medicine Undifferentiated: Shortness of Breath, Chest Pain, Shock, Altered Mental Status, Headache, Syncope, Abdominal Pain, Fever, "Unwell" Patient, GI Bleeding, Vaginal Bleeding, Abnormal Behavior, Seizure Respiratory: Asthma, COPD, Pulmonary Embolism, Airway Obstruction, Pneumothorax, Pneumonia Cardiovascular: Acute Coronary Syndromes, Congestive Heart Failure, Cardiac Dysrhythmias, Hypertensive Emergency, Aortic Dissection, Aortic Aneurysm Neurological: Stroke, Transient Ischemic Attack, Seizure, Meningitis, Cerebral Hemorrhage HEENT: Corneal Abrasion, Eye Foreign Body, Epiglottitis, Epistaxis Gastrointestinal: Gastritis, Peptic Ulcer Disease, Upper GI Bleed, Lower GI Bleed, Acute Cholecystitis, Bowel Obstruction, Appendicitis Genitourinary: UTI, STD, Vaginal Bleeding, Ectopic Pregnancy, Nephrolithiasis, Testicular Torsion, Acute Urinary Retention Musculoskeletal: Trauma, Ankle Sprain/Strain, Common Fractures, Common Dislocations -------------------------------------------------------------------------------------------------------------------------------------------- Procedures: NEJM Videos In Clinical Medicine: http://www.nejm.org/multimedia/videosinclinicalmedicine -------------------------------------------------------------------------------------------------------------------------------------------- Kaplan Videos (2001) Emergency Medicine with Dr. Asher Kornbluth, MD --------------------------------------------------------------------------------------------------------------------------------------------See the current American Heart Association (AHA) guidelines for cardiopulmonary resuscitation (CPR), basic life support (BLS), pediatric advanced life support (PALS), and advanced cardiac life support (ACLS). --------------------------------------------------------------------------------------------------------------------------------------------Cardiac: Ventricular Arrhythmias & Sudden Death * 54yo man is at the opera when he suddenly jumps up clutching his chest. He falls to his side in the lap of the woman sitting next to him. Etiology is most likely cardiac, often in the setting of ischemic heart disease. First, assess if the patient is truly unresponsive, gentle shaking or prodding. Do not shake the head or neck if possible cervical spine injury. Next, call for help (need defibrillator and medications). Now, lay patient on a firm flat surface. Now do ABCs, check if airway is open via jaw thrust or a head-tilt chin-lift (if no c-spine injury). Check breathing by looking for chest movement, listening at the mouth, and feeling for air movement. If no breathing, give two breaths. Check circulation at the carotids or femorals. If no pulse, start compressions at a rate of 80-100 compressions per minute. Ratio (per 2005 AHA) is 30:2 compressions to breaths. * 54yo man is at the opera when he suddenly jumps up clutching his chest. He falls to his side in the lap of the woman sitting next to him. After confirming that he is unresponsive, opening the airway, performing chest compressions and ventilation, an ECG arrives and shows no evidence of electrical activity. This is asystole. Next step is to confirm lead placement and confirm asystole in a second lead. Now, continue CPR and start an IV. IV is started before intubation because patient is currently getting respirations. Medications to give are epinephrine and atropine every 3-5 minutes. Epinephrine dose is normally 1mg or possibly 0.1mg/kg, so 7mg for a 70kg person. Atropine dose is normally 1mg. Bicarbonate (HCO3) is not a first-line agent; it should only be used if you know the patient has a severe underlying acidosis, such as sepsis or renal failure without dialysis. The general agreement is a pH of 7.1 before getting an amp of bicarb. * 54yo man is at the opera when he suddenly jumps up clutching his chest. He falls to his side in the lap of the woman sitting next to him. ECG shows ventricular fibrillation. He has no spontaneous respirations. Most common cause of spontaneous death is ventricular fibrillation (vfib). Next step is defibrillation, usually 200J dose. Continue CPR for 5 cycles. If vfib still, next dose is 300J, continue CPR, next shock dose is 360J. CPR is stopped while shocking, have people stand back. Now you can worry about the IV, if it was not started during CPR. Medication to give is epinephrine 1mg or 0.1mg/kg. Next step is 360J shock again with immediate CPR after. If this does not work, antiarrhythmics may be used including amiodarone or lidocaine. * Bicarbonate useful for phenothiazine or aspirin overdose. * 54yo man is at the opera when he suddenly jumps up clutching his chest. He falls to his side in the lap of the woman sitting next to him. He is awake but confused. He complains of dyspnea and lightheadedness. His exam reveals jugular venous distension (JVD) and a blood pressure of 114/80. ECG shows ventricular tachycardia at a rate of 180. Ventricular tachycardia is usually a rate of 160-240 with wide complex > 0.12s and no p-waves. If all QRS complexes are identical, it is called monomorphic (versus polymorphic). For hemodynamically stable patients, give IV antiarrhythmic, such as amiodarone. If patient is hemodynamically unstable, synchronized cardiovert.



* If patient has Torsades de Pointes (polymorphic twisting ECG), give magnesium. Most likely cause is long QT interval, such as from an anticholinergic overdose, phenothiazine overdose, quinidine, procaine, and others. Example would be a patient taking medications for atrial fibrillation who develops kidney failure and then has sudden death. Answer is likely the atrial fibrillation medication if it prolongs the QT. * If patient had a symptomatic run of ventricular tachycardia, they should have electrophysiologic studies (EPS) and be placed on an antiarrhythmic medication for life. If the presentation is sudden death, the patient gets an automatic implantable cardioverter defibrillator (ICD). If patient does not respond to antiarrhythmic therapy, they get an ICD. * Patient leaps up, grabs his chest, falls to the ground. We follow basic life support protocol for a patient with no pulse and no respirations. ECG shows an organized narrow-complex rhythm. This is pulseless electrical activity (PEA). Causes of PEA are the Hs and Ts: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypoglycemia, hypothermia, toxins, tamponade (cardiac), tension pneumothorax, thrombosis, trauma. Tension pneumothorax comes with distended neck veins, no signs of heart failure, unilateral absence of lung sounds, and midline shifting such as apical cardiac pulse or PMI movement. So, treatment for PEA is the same as asystole (epinephrine, atropine) as well as treating the underlying cause. Treatment would be fluid for hypovolemia, emergency pericardiocentesis for cardiac tamponade, needle thoracentesis or chest tube for tension pneumothorax, and fibrinolytics for pulmonary embolism. Only use fibrinolytics if you are sure it is a pulmonary embolism, such as from DVT history, no bleeding diathesis, ECG showing S1Q3T3 with signs of right ventricular strain. --------------------------------------------------------------------------------------------------------------------------------------------Cardiac: Atrial Arrhythmias * Atrial fibrillation is irregularly irregular. Atrial flutter, like afib, will also have normal looking QRS complexes. * Supraventricular tachycardia (SVT) is usually due to atrioventricular nodal reentrant tachycardia (AVNRT). * If patient is asymptomatic, whether it is afib, aflutter, or SVT, do not do acute treatments (e.g. cardioversion). * Milder presentation includes lightheadedness and palpitations, but not hemodynamic compromise. * Atrial contractions (atrial kick, S4 sound) most important in patients with underlying cardiovascular compromise, especially in mitral valve stenosis. Symptoms usually due to poor filling time. * Treatment of symptomatic atrial arrhythmia (e.g. SVT) is to slow down the rhythm to improve ventricular filling time. Agent of choice to block AV node is adenosine, which has quick onset and fast metabolism. In patients with underlying CHF or pulmonary edema, digoxin is a good choice. Other choices are calcium channel blockers and beta-blockers; do not use these in CHF. These slow the ventricular rate and are not meant to convert to sinus rhythm. * Treatment of stable patient with atrial arrhythmia is to attempt physiologic maneuvers before using adenosine. So carotid sinus massage (CSM) and valsalva maneuver to increase vagal tone and slow the AV node. CSM is done on one side only and after listening to rule out a carotid bruit. * If patient has unstable SVT, hypotensive, unconscious, ischemia, and so forth, answer is synchronized cardioversion. Normal cardioversion doses are 25-50J. * For stable conversion of SVT to sinus rhythm, usual course is quinidine, or procainamide, or amiodarone. Elective cardioversion is the next step after that, involving mild sedation. * In patients who have long-term atrial fibrillation, anticoagulation (warfarin) is used to prevent clots that form due to stasis, usually in the atrial appendage. It is necessary to anticoagulate prior to cardioversion. Anticoagulants should not be used in a new-onset situation with atrial fibrillation, atrial flutter, or supraventricular tachycardia. --------------------------------------------------------------------------------------------------------------------------------------------Cardiac: Brady Arrhythmias & Heart Blocks * In a healthy patient with sinus bradycardia, the answer is no treatment. Do not choose pacemaker, atropine, or any other stimulant in this case. Marathon runners may have pulse rates normally in the low 40s. * If bradycardia is producing hemodynamic instability, give anticholinergic medication atropine. This is an anti-vagal medication, meaning it removes the brakes for the heart. We can use epinephrine as well if we are close to cardiac arrest. Transcutaneous pacing is the next option if atropine 0.5mg is failing. * Check patients medications to determine if they are making the patient bradycardic. Meds could include beta-blockers for their hypertension or calcium channel blockers for coronary heart disease. * First-degree heart block is simply prolonged PR interval and will not have symptoms. If a patient is on beta-blockers and the question says they have first-degree block and should you lower the dose, the answer is no. * Second-degree Mobitz Type-1 heart block (Wenckebach) involves a prolonging PR interval with a dropped beat. This rarely produces symptoms and does not require treatment. * Second-degree Mobitz Type-2 heart block involves a dropped beat at regular intervals. This requires treatment. If hemodynamically unstable, give atropine and pacemaker. Eventually, permanent pacemaker. * Third-degree (complete) heart block has p-waves and QRS complexes that do not correlate (AV dissociation). This



occurs almost always in the presence of underlying heart disease. It can be differentiated from atrial flutter as the QRS complexes come slowly. Typical presentation is syncope. Answer is pacemaker. --------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Common Substances * 25yo medical student goes home after class and finds no messages on his answering machine from his girlfriend. In a fit of despair, he takes a full bottle of pills then tears the label off the bottle of pills to prevent any attempt to reverse the poison he just took. Immediately after doing this his girlfriend calls. He goes to the Emergency Department 30 minutes later, deciding he wants to live, but cannot share the type of medication he took. What is the next best step in management? Obtain a detailed history, which can include calling family members. * A patient who is very depressed may likely overdose on their antidepressant medications. Phenothiazines are the antidepressants to worry about, but are not commonly used due to their side effects. Cyclic antidepressants (formerly tricyclic, TCAs) are also worrisome. * If the patient is diabetic and unconscious, think about low blood glucose. If the patient has strange cellulitis or endocarditis without a known cause, think about IV drug abuse. * Gastric emptying methods are only appropriate if you know the ingestion is within the last hour or so. After two hours, assume the stomach has emptied. If patient is awake and alert with no risk of aspiration and just recently ingested pills, you can give ipecac to cause vomiting. Gastric lavage is another option using a large Ewald tube, but comes with a risk of aspiration. Ewald tube is rarely used, but can be done in a patient with decreased mental status (e.g. somnolent) after patient is intubated. * Most frequently, the patient arrives to the ED hours after ingestion. Activated charcoal is a good approach until we know what the agent is. Charcoal is a non-specific binding agent. Then, add a laxative to evacuate the GI tract. * If were several hours after ingestion, pills are present on x-ray, and theyre further down from the stomach, we can give a rapid flush of charcoal with an electrolyte lavage laxative (polyethylene glycol, PEG). * Rarely do we attempt to remove the toxins via dialysis, as this is a slow option, unless it is certain toxins. * Forced diuresis (e.g. furosemide) is also not an effective route. Exceptions are phenobarbital and aspirin. * Unconscious patients should get the coma cocktail. This includes naloxone, dextrose (D50), and thiamine. Mnemonic is DONT for dextrose, oxygen, naloxone, and thiamine. --------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Acetaminophen * 38yo man comes to the ED four days after the ingestion of a full bottle (60 tabs) of extra strength acetaminophen and is complaining of vomiting and RUQ pain. Patient has elevated bilirubin, AST (SGOT), and increased prothrombin time. This is acute liver failure, mostly because PT is increased. 60 tabs times 500mg is 12grams. For acetaminophen, toxicity occurs after 140mg/kg. * Signs of acetaminophen toxicity early on include GI tract irritation, such as nausea and vomiting. It takes several days, 3-4 days usually, to develop liver disease symptoms. There is a window, such as 24-48 hours, where the patient looks surprisingly well, but dont be fooled. * When measuring acetaminophen levels, it is important to measure levels at different time frames. Follow the nomogram (Rumack-Matthew nomogram). So even a normal looking level could be toxic if were at 24 hours out. * Antidote for acetaminophen is N-acetylcysteine (NAC). This is given orally ever 4 hours as soon as we know the patient has an acetaminophen overdose. Normally, 17 doses of NAC are given. --------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Alcohol * At the opera, you go to see the three tenors. All three tenors exhibit confusion, ataxia, lethargy, drowsiness, and slurred speech. How do we differentiate methanol intoxication from ethanol intoxication? A desperate alcoholic may drink anything that smells like or sounds like alcohol, including wood alcohol (methanol). Methanol intoxication presents with acute visual changes, even to the point of blindness. Ethylene glycol (in antifreeze) is another substance that may be swallowed. Ethylene glycol intoxication presents with oxalate crystals (rhomboid-shaped) in the urine and possibly renal insufficiency. Rubbing alcohol (isopropyl alcohol) intoxication can occur also, and presents with an elevated anion gap ketosis without acidosis. Lab ethanol level may be zero as another clue. * Methanol is metabolized to formic acid. Reaction is catalyzed by alcohol dehydrogenase. Treatment is to give ethyl alcohol IV solution so alcohol dehydrogenase will preferentially work on that. Fomepizole is a competitive inhibitor of alcohol dehydrogenase, so it may be used instead of IV ethanol. * Ethylene glycol is metabolized to oxalic acid. Reaction is catalyzed by alcohol dehydrogenase. Treatment is to give ethyl alcohol IV solution so alcohol dehydrogenase will preferentially work on that. Fomepizole is a competitive inhibitor of alcohol dehydrogenase, so it may be used instead of IV ethanol.



--------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Acetylsalicylic Acid * An elderly woman with osteoarthritis comes to the ED with dyspnea, intractable nausea, vomiting, and tinnitus. Patient is fully alert and has a history of hypertension. Her husband says she was in so much pain lately that she took half a bottle of extra pills a half hour ago. If question is management, were in the window to give gastric lavage via ipecac. Answer for overdose is aspirin (acetylsalicylic acid). Quinidine also causes tinnitus. * The dyspnea here is from tachypnea as aspirin stimulates the respiratory drive via the metabolite salicylic acid. The tachypnea will cause a respiratory alkalosis initially. The salicylic acid metabolite will lead to a metabolic acidosis. If the pH is given to you as part of an overdose question, think aspirin. * This will be a metabolic acidosis with anion gap, due to the extra acid floating around. Anion gap calculated by Na+ plus HCO3- minus serum Cl-, normally about 4-12 value. Typical high anion gap will be > 12, likely around 15, maybe even higher. Obtain an aspirin level. * Other things that can cause high anion gap in overdose are methanol and ethylene glycol. Isopropyl alcohol produces ketones with a high anion gap, but does not produce acid so the serum bicarb and pH will be normal. * To clear residual aspirin if were outside the gastric window, give charcoal. * Specific treatment for aspirin is sodium bicarbonate, alkalizing the urine to convert the aspirin to a more soluble form, then giving furosemide to get rid of the aspirin products. --------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Cyclic Antidepressants * 28yo man with a history of depression comes to the ED one hour after a suicide attempt with his tricyclic antidepressants and benzodiazepines. He is stuporous with a respiratory rate of 7. If the question is not this specific, and just says a depressed person found unconscious, think about antidepressants. Since this is one hour, give ipecac, unless the patient is lethargic or obtunded. So in this patient we intubate then clear stomach with Ewald gastric lavage tube. He has a wide QRS, what do we do next? Wide QRS is specific for cyclic antidepressants, which can also prolong the QT and cause Torsades de Pointes. Answer for next step is give bicarbonate, because it protects the cardiac conduction system against the affects of the cyclic antidepressants. * Cyclic antidepressants also have anticholinergic effects, so the question might say dry mouth, urinary retention, tachycardia, flushed but dry skin, dilated pupils. Pinpoint pupils suggests opioids. * Cyclic antidepressants slow down peristalsis, so ipecac may be an option even after a few hours. * Antidote for benzodiazepines is flumazenil, but be very careful if the patient has been chronically on benzodiazepines because you risk seizures. --------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Carbon Monoxide * You are the chief resident of a great metropolitan training program at the time of the bombing of the World Trade Center. A total of 2,500 people come to your emergency department at the same time to be treated for smoke inhalation. Among them is a 68yo man with a history of aortic stenosis who had to walk down 90 flights of stairs. What is the most important initial test for this man? This is not meant as a case dealing with lactic acidosis from exercise, forward failure, or backward failure. Focus on the smoke inhalation within a close space. Answer is to check a carbon monoxide level. * The risk is for anyone who is exposed to a smoking fire in an enclosed space. Carbon monoxide binds strongly to hemoglobin, so oxygen cannot bind. Hemoglobin and hematocrit levels will look normal on labs. There will be tissue hypoxia throughout the body, so you go into an anaerobic metabolism mode. A byproduct of that anaerobic metabolism is lactic acidosis. Symptoms will include shortness of breath, tachypnea, obtunded, confusion, encephalopathy, arrhythmias, hypotension, and chest pain. * People may attempt to commit suicide by closing their garage and running their car. The carbon monoxide from the car exhaust will fill the car. Unfortunately, the person may forget to realize the garage is connected to their house, leading to death of their sleeping family members. * People who live in busy cities or who are chronic smokers may have an increased carbon monoxide levels, up to 10%. Mild CO poisoning is 10-30% and these patients clear quickly with treatment. Levels of 30-50% is more saturated hemoglobin and potentially very sick patient. A CO level over 50% is considered potentially fatal. * Management is to remove patient from the CO environment. Next step is to compete with the hemoglobin binding sites, which is done by giving 100% oxygen by facemask. More severe cases are treated with intubation and 100% oxygen directly into the system. Very severe cases are treated with hyperbaric oxygen if available. * Half time of carboxy-hemoglobin (until 50% is dissociated) is about 4-6 hours. If youre giving the patient 100% oxygen, the half time is about 40 to 80 minutes (about an hour). If you put the patient in a hyperbaric chamber, the half time is about 15-30 minutes.



--------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Under The Sink Products * Products can be acidic such as toilet cleaners and pool cleaners, or alkaline such as liquid drain cleaner. * Alkaline products cause more severe injury because there is less acid in the blood to act as a buffer. * Patient will appear uncomfortable, have drooling, have severe oral pain, and odynophagia. * Esophagus will develop strictures from the alkaline and lead to dysphagia. * Answer for test to order is endoscopy to rule out acute esophageal perforation. Do not give these patients antiemetic agents such as ipecac. Do not place a nasogastric tube, as the esophagus may be friable. * The stomach contains low pH so there is some natural buffering of the alkaline. Do not give the patient something to ingest as a buffering agent. If the patient ingested lye, do not give them dilute acid (e.g. citrus fruit drinks) as it will cause more thermal reactions and lead to further injury. * Management includes intravenous fluids. No prophylactic antibiotics or steroids are needed. We do attempt to dilute the solution with plain water. If the eyes are exposed, rinse them with water. If they swallowed a caustic agent, try to give them water to dilute the agent. * These patients may presents years later with mechanical dysphagia. Motility dysphagia occurs with any ingested substance including hard, soft, and liquids. Mechanical dysphagia is typically a progression as the lumen is getting blocked, so initially trouble with large foods, then softer foods, then finally liquids. Mechanical dysphagia to liquids may have a lumen the size of a pinhole. Ask about smoking, drinking, and other risk factors of esophageal cancer. * Steakhouse Syndrome occurs when a patient has trouble swallowing a large piece of steak out of the blue. This is likely a Schatzki ring at the lower esophagus. * So this case would not involve a 30-year history of GERD with likely adenocarcinoma. It would more likely talk about a patient with a history of suicide attempts, and maybe even say one attempt involved substance ingestion. * These lye strictures are premalignant and have risk for esophageal cancer of the squamous type. --------------------------------------------------------------------------------------------------------------------------------------------Toxicology: Digoxin * Typically seen in an older patient, possibly due to a suicide attempt. * Exam may say patient is on several medication and list them all, including digoxin. Or, it might just say the patient is on several medications that they cannot remember but they are for heart disease. * Digoxin used in congestive heart failure that has a dilated ventricle (with volume overload and S3, systolic dysfunction), not the patient with a hypertrophic ventricle (with S4). Digoxin also used for atrial fibrillation to slow the rhythm (ventricular rate by blocking the AV node), not to convert the rhythm. Digoxin also used in supraventricular tachycardias, such as AVNRT or atrial flutter. * Digoxin is metabolized and excreted through the kidneys. So a patient with CHF with poor BUN and creatinine may be likely to have a high digoxin level. If the patient has a creatinine of 2.0 and you start them on 0.25mg/day of digoxin, you may be going too high. Typical starting dose is 0.25, but if there is risk you start at 0.125mg, or if very advanced renal disease you can start at 0.0625mg. Patients CHF or diabetes may worsen as well, so digoxin dose has not changed but their excretion has gotten worse (e.g. saying patients creatinine went from 1.2 to 1.9). * Classic drug-drug interaction with digoxin is with quinidine. Quinidine is also used in atrial fibrillation. * Increased risk of dig tox with decreased renal function, quinidine, and hypokalemia. * Symptoms of digoxin toxicity are non-specific GI symptoms (N/V/D) and CNS symptoms (confusion, forgetfulness, new blue-green color changes/blindness). Cardiac arrhythmias include PVCs, paroxysmal atrial tachycardia with varying amounts of AV node block (specific symptom), and eventually high-grade bradycardias due to the AV block, so escape rhythms and non-p-wave rhythms (e.g. nodal bradycardia). * Treatment includes determining what is correctable, such as hypokalemia. You want to correct the potassium rapidly, but you cant give it intravenously very rapidly (i.e. stops heart). Give large doses of oral potassium. * To treat the symptomatic bradycardia, give atropine and if prolonged then transcutaneous pacing. * To treat multiple PVC that could lead to life-threatening ventricular arrhythmias, give Digibind digoxin antibody. So, Digibind is reserved for digoxin toxicity with life threatening arrhythmias. * Drugs that also work for digoxin-induced ventricular arrhythmias are phenytoin and lidocaine. --------------------------------------------------------------------------------------------------------------------------------------------Toxicity: Opiates & Opioids (Narcotics) * OxyContin is a form of morphine with long action. Sometimes these pills are ground up and taken all at once, as the grinding removes the time-release action of the pill. * The specific finding that suggests narcotic overdose is symmetric pinpoint pupils (miosis). If you toss in obtunded and decreased breathing then you can be pretty sure this is a narcotic overdose, disregarding any other history. * Part of the coma cocktail is naloxone to reverse the opioid overdose.



* Other symptoms follow the depressant actions of the drug, so hypotensive, bradycardia, and hypothermia. There might be a history of endocarditis (specifically tricuspid valve regurgitation), or presence of cellulitis on the arms (Staph aureus). If the patient licks the needle to facilitate injection, there may also be oral flora present. Tricuspid regurgitation will present as a pan-systolic murmur at the left sternal border that increase with inspiration (right sided murmurs, Carvallo Sign). --------------------------------------------------------------------------------------------------------------------------------------------Toxicity: Cocaine * Clues for IV drug abuse would be homelessness, schizophrenia or other mental disorders, and prison. * Clues for cocaine use would be a well-dressed banker who is brought in by a friend because of agitation. Further clues would be tachycardia, dilated pupils, and perforation of the nasal septum. * Most likely way to get cocaine overdose is by smoking it, such as if it is baked down into a small rock and smoked in a pipe (crack cocaine). * Systemic signs of cocaine overdose are almost the opposite of heroin overdose. Cocaine works by inhibiting norepinephrine reuptake at the synapses. So there is an overload of norepinephrine, like a norepinephrine-secreting tumor (e.g. pheochromocytoma). Will see tachycardia, hypertension, and agitation. * Norepinephrine can stimulate alpha-receptors, so you get coronary vasospasm. So healthy bankers and doctors spending their riches on cocaine will present with chest pain and no history of coronary disease. * Cocaine can also cause ventricular arrhythmias. * No specific antidote for cocaine. Treat symptoms. Norepinephrine stimulates alpha-receptors and binds to beta-receptors. So ideal drug for hypertension would be a beta-blocker as well as alpha-blocker, namely labetalol due to blockage of both alpha and beta. If you gave atenolol or propranolol (pure beta-blocker), the alpha-receptors are unopposed so there will be more coronary vasospasm and more diffuse peripheral vasospasm, therefore keeping the blood pressure up. So drug of choice for cocaine overdose to lower BP and HR would be labetalol. * Very high blood pressure can lead to a subarachnoid or intra-parenchymal hemorrhage. So, patient with cocaine use, altered mental status, and focality on neurologic exam should clue you into a stroke. * If patient has neck stiffness, hypertension, worst headache my life, think subarachnoid hemorrhage. * With CNS hyperactivity, there may be tremors that progress to a grand-mal seizure. Seizure may be so bad that the patient develops rhabdomyolysis (CPK > 5x upper limit of normal, give lots of fluids). --------------------------------------------------------------------------------------------------------------------------------------------Toxicity: Benzodiazepines * Patient has a history of a panic disorder (or anxiety or severe insomnia). People are rarely successful in killing themselves with pure benzodiazepine overdose (e.g. diazepam); it is usually a poly-substance overdose. * Benzodiazepines bind to GABA receptors increasing frequency of chloride channel opening. * If the overdose is within the first hour of presentation, do gastric emptying (e.g. ipecac). If more than one hour, try to bind the agent with charcoal. Antidote for overdose is flumazenil, a benzodiazepine antagonist. * Patient comes in to the ED lethargic, received coma cocktail by paramedics, but still unconscious. Patient is hemodynamically stable but not arousal. Here, flumazenil can be used as a diagnostic test to help determine if benzodiazepines are part of the patient presentation (while you figure out what else the patient might have taken). * Have caution here as many patients taking benzodiazepines are on them chronically. So reversing with flumazenil can cause an acute withdrawal syndrome and precipitate agitation and seizures. * You are called to the recovery room after an endoscopy procedure. The patient is hypercapnic, high PCO2. History reveals the patient only received benzodiazepines during the procedure. Next step should be to look at the medication list and ensure the patient has not been on chronic benzos. If on chronic benzos, next step is give oxygen. * Also, be cautious using naloxone in chronic narcotic patients. However, narcotic overdoses are much more likely to be life-threatening compared with benzodiazepine overdoses. --------------------------------------------------------------------------------------------------------------------------------------------Toxicity: Barbiturates * Patient has a history of seizure disorders and presents lethargic with respiratory depression. The seizure medication to think about is phenobarbital. Phenobarb is not used commonly for seizures due to the risk of chronic abuse and the risk of overdose. * As a side note for actual practice, you should be sending a urine or blood toxicology screen for all of these patients. The board exam is going to expect a diagnosis from the initial presentation and ask what to do next. * Barbiturates bind to GABA receptors increasing duration of chloride channel opening. * The CNS depression in barbiturate overdose may be so severe that the patients EEG will appear as if the patient is dead (flat-line EEG). Treatment is usually more aggressive than with benzodiazepine overdose.



* Management is to increase phenobarbital excretion with bicarbonate. This alkalizes the patient, then induce diuresis. Next, support the patient hemodynamically with fluids and pressor if needed. * If phenobarbital overdose is suspected, do not give up treatment initially as the patient may simulate death. --------------------------------------------------------------------------------------------------------------------------------------------Toxicity: Marijuana & Hallucinogens (LSD, Mescaline, Peyote, Mushrooms) * Cocaine patients may be grandiose, but will not be delusional as seen in patients taking hallucinogens. * Hallucinogens generally have anticholinergic properties, with symptoms including flushing, warm skin, dry skin, mouth is dry, and dilated pupils. Patients may be behaviorally agitated, but hemodynamically stable in general. * Phencyclidine (PCP, angel dust) gives typical marijuana-like behavior but additional violent agitation and nystagmus. Patient might not even know they ingested PCP; they may say they smoked marijuana but did not know it was laced with phencyclidine. * Treat agitation with short-acting intravenous benzodiazepines. --------------------------------------------------------------------------------------------------------------------------------------------Toxicity: Lead & Mercury * Seen more commonly in children living in old buildings in urban areas (e.g. Section 8 housing). * In the past, adults presented with lead poisoning after drinking homemade alcohol. This is only really seen these days in areas of the country where people make moonshine (almost 200 proof) alcohol. In the past, the home alcohol process involved using old truck radiators, which contained a great deal of lead in those days. The specific overdose finding was renal insufficiency. * 80-90% of lead (Pb) ends up in the bones. About 10% in red blood cells. Presenting complaint will be anemia. * The commonly seen method of poisoning these days is children in poor housing who are hungry and ingest paint chips that contain lead. * Symptoms will be increasing lethargy. Chronically the lead can cause irreversible CNS damage, thus it is looked for in all children with learning disabilities, especially in poor urban areas. * Mercury poisoning cases will involve a patient being exposed to a broken thermometer or a blood pressure sphygmomanometer column. Some paints also contain mercury, but not as common. * Mercury is very effective at entering the CNS. Patients present with excitability, tremors, and seizures. * Treatment for mercury poisoning is chelation with dimercaprol or penicillamine. * Treatment for lead poisoning is chelation with dimercaprol (BAL). * Dimercaprol is mixed in peanut oil, so ask about peanut allergies. --------------------------------------------------------------------------------------------------------------------------------------------Burns & Thermal Injury * 32yo fireman is caught in a fire and is briefly trapped under a burning staircase. He is quickly extracted and brought to the emergency department. He has a respiratory rate of 14. He is fully alert. He weights 220lbs and has soot in his mouth, nose, and face. His sputum is carbonaceous. The nasal hairs are singed. He has no stridor or hoarseness. His lungs are clear to auscultation. He has first-degree burns to his right leg and second/third-degree burns on his right arm and chest. * Think about carbon monoxide poisoning first, not the severe burns. PO2 on blood gas is not reflective of carbon monoxide poisoning, so measure a CO blood level. Give 100% oxygen. * The next step is assessing respiratory burns. Have a low threshold for intubating the patient early. Their larynx will progressively become edematous and close off. Treatment is early intubation prior to laryngeal edema progression. * Largest insulator against fluid loss is the skin, so we must worry about fluid loss with burns. * Rule of 9s: Face is 18%, Front Torso is 18%, Back Torso is 18%, Arms are 9%, Legs are 18%, Genitals are 1%. * Another rule is using the patients hand for 1% burn area. * First degree burn is superficial, third degree burn is full thickness. Example of a first-degree burn is a sore red sunburn. The skin will be tender generally without blisters, nerves are still intact. Second-degree burns are partial or full thickness of dermis, painful with blistering, skin appendages still intact (sweat glands, hair follicles, nerves). Third-degree burn is deeper and does involve skin appendages, full thickness necrosis, not painful at site although it will likely be surrounded by second and first-degree burns. Third-degree burns may be black, white/gray, waxy. * Rarely admit first-degree, sometimes admit second-degree, always admit third-degree burns. * Parkland Formula for fluid requirements in burns: Fluids = BSA * weight(kg) * 4mL. So remember 4mL. * Fireman is 220lbs (100kg) with 25% burns. Fluids needed are 100 * 25% * 4mL is 10L needed. * The fluid of choice is Lactated Ringers, secondary is 0.9% Normal Saline. * Give fluids over first 24 hours. Half over first 8 hours, next half over last 16 hours. * So for our fireman, give 5L over first 8 hours (625mL/hour) and 5L over next 16 hours (312.5mL/hour). * After first 24 hours, give enough fluids to ensure adequate renal function, so gauged by urinary output. Rule is to



maintain 1mL/kg/hour of urinary output. Patient weights 100kg so we want 100mL of urine per hour or 2.4L/day. * Patient has burns over 30% of body and weighs 60kg. How much fluid do they get in the first 8 hours? So we do 30% * 60kg * 4mL = 7200mL, for first 8 hours we give half so answer is 3600mL in first 8 hours. * Also ensure these patients are transferred to dedicated burn units, which typically contains surgeons who have done advanced training in burn injury patients. * For burn wounds, apply sterile hydration and dress the wounds. Several times a day we remove the bandages, rehydrate the skin, and re-bandage. Any areas that look infected or necrotic get topical (not systemic) antibiotics. Typical antibiotic used is silver sulfasalazine (Silvadene). Areas that remain necrotic will eventually need to undergo debridement and replaced with skin grafts. No prophylactic systemic antibiotics are needed. * Early skin grafts should be used to prevent contractions. Have particular concern for burns around joints as the contraction can prevent future joint movement. * Circumferential burns are at risk for vascular compression, ischemia, and compartment syndrome. In this case, call for a surgeon to perform an escharotomy to relieve circumferential tension. --------------------------------------------------------------------------------------------------------------------------------------------Head Trauma, Epidural, & Subdural Hemorrhage * Any patient with a focal defect after trauma should raise the question of a bleed causing a mass effect. * It is misleading to attempt to gauge the severity of internal head trauma based on what you find on head exam. * Head trauma can be a concussion, with temporary loss of consciousness, confusion, agitation, but no focal findings. Scanning will not show any kind of blood. * For scanning, the best choice is head CT scan without contrast. The CAT scan is better than MRI in this scenario. You are looking for a collection of blood, whether it be epidural or subdural. Blood can be seen on a CT scan of the head without contrast. If you can avoid something like contrast, avoid it, especially if renal failure is present. * The CT scan will also help with skull fractures. A skull x-ray will tell you where the fractures are, but not help with sources of bleeding. * Symptoms may include a headache, which is a mild finding. They may have a mild loss of consciousness, which may be normal or may be transient as in an epidural bleed. The patient may have a waxing and waning of their consciousness, which is indicative of a subdural hematoma. * Focal findings are the most worrisome. Patients may develop amnesia. Retrograde amnesia is where the patient does not remember the events prior to the trauma. The duration of memory loss is a good indicator of the severity of the traumatic injury. So forgetting minutes before a head injury is less worrisome than forgetting 12 hours before. Patient may even forget days, weeks, or months prior to trauma. When a patient recovers memory from retrograde amnesia, they will start by recovering the most distant memory. Antegrade amnesia is where the patient does not have memory between the traumatic event and when they present to the hospital. The degree of amnesia is again correlated to the degree of injury. * Patient may present after a minor car injury but does not recall the events. Any indication of head or neck injury, such as pain at the posterior pillars, immobilize the patients neck and do cervical spine films (three view). This is done prior to CT scan unless the patient is unconscious in a coma (then straight to CT scan) because youre worried about a large hematoma with mass effect so the hematoma needs to be evacuated. Keep cervical spine rigid. * Initial management for any trauma is ABCs. For airway in head trauma, do not extend the neck, use a jaw thrust. If there is any evidence of facial trauma or basilar skull fracture (Battle signs, raccoon eyes) do not use any nasal tubes, including nasal intubation, nasogastric tube, or nasal pharyngeal airway. * If there is a penetrating wound on physical exam, do not remove the object. If there is an object sticking out of the patients head, assume it is tamponading some vessel. You can do much more harm by removing the object. * After ABCs, do focused neurological exam for focal deficits. Any new focality in head trauma implies expanding hematoma, do head CT without contrast. The first nerve to be affected is the oculomotor nerve, so you might see oculomotor palsies as your first sign of a mass lesion (hematoma in this setting). * Management of concussion (with transient loss of consciousness from seconds to minutes) with negative CT scan is to have someone observe the patient at home, waking them up every few hours to ensure no major neurological deficits. If the patient has no reliable person at home, they must stay in the hospital to ensure the concussion is not masking an underlying hematoma. * If a patient with concussion has a negative CT scan for blood but even a hairline skull fracture, keep the patient in the hospital because they are at an increased risk for infection and bleeding. * Epidural hematomas are often associated with skull fractures that cross the (middle) meningeal artery. These patients may have a lucid period where they seem normal, then decline (talk and die). * With epidural hematomas, patient may develop an uncal herniation, which will lead to certain death if not managed. Patient will have a severe decline in mental status that can progress rapidly to coma, ipsilateral pupillary



dilatation, and contralateral focality that results in a hemiparesis. Patient may even have a step-off on the skull. On the scale of severity, it does not get much worse than this. You need a head CT scan and neurosurgery consult now. Neurosurgery will promptly evacuate the hematoma to save the patients life. * With subdural hematomas on CT scan, question is if the hematoma is acute or not. If acute, contact neurosurgery for prompt evacuation of the hematoma. The common case of chronic subdural hematoma would be either no description of head injury or head injury (or fall) that occurred days before. Management does not necessarily include hematoma evacuation. Management depends on neurologic status and presence of focal deficits. * If patient is on a blood thinner like warfarin and had a fall, assume they have a bleed. They may have developed a progressive change in mental status with slowly developing dementia. In that case, the CT will likely show a chronic hematoma and may not require an evacuation. Just seeing a CT scan of a subdural hematoma or a question saying specifically subdural hematoma does not mean to do a neurosurgical evacuation. If the patient is stable with progressing neurologic findings or focality and has a chronic subdural hematoma, do not operate, just observe. * Teenager playing football gets hit hard while running with the ball. Skull x-ray shows a fracture. There is risk of epidural hematoma and CNS infection with skull fracture. The case may not give you an x-ray. Signs of skull fracture include CSF from the ear (otorrhea), CSF from the nose (rhinorrhea), hematoma on the tympanic membrane, ecchymosis over the post-auricular/mastoid area (Battle sign), and ecchymosis around the orbits (Raccoon eyes). These patients should go for CT scan to assess both fractures and hematomas. * For suspected uncal herniation (ipsilateral pupil dilation, contralateral hemiparesis), lower intracranial pressure (ICP). Do this by intubating and hyperventilating patient to pCO2 of 30-35mmHg. Give the patient an osmotic diuretic, namely mannitol, to decrease ICP. Keep blood pressure between systolic 110-160. Ideally, want mean arterial pressure 60 points higher than mean ICP pressure. ICP measured via intracerebral transducer placed by neurosurgery. If pressure is higher than 160 systolic, it increases ICP predisposing to more bleeding. At the same time, do not drop below 110 systolic to prevent hypoxic ischemia due to poor brain perfusion. * Elevate the head of the bed to 30-degrees for venous drainage. Never place in trendelenburg. Steroids will be an option on exams, but it is always the wrong answer for lowering ICP. --------------------------------------------------------------------------------------------------------------------------------------------Subarachnoid Hemorrhage * Occurs typically in a patient bleeding for an intracerebral aneurysm, can be fusiform aneurysm, saccular aneurysm, does not matter here. These often occur around the circle of Willis. * Pertinent history is a patient or patients relatives with polycystic kidney disease (PKD). About 10% of these patients have berry aneurysms in the brain, which are at risk for rupture. These patients are predisposed to hypertension as well, as the cysts press on the renal artery decreasing flow and leading to a high renin, high aldosterone state, and thus increased blood pressure. * Classic symptom is abrupt onset headache, thunderclap headache, worse headache of my life. Everybody with headaches will have a worst headache at some point, so anyone who walks into the office with a bad headache does not necessarily have a subarachnoid hemorrhage. Patient might not have a history of headaches. * Subarachnoid hemorrhages are rare, but it is a diagnosis you cannot afford to miss. * About 50% of patients with subarachnoid hemorrhage will have a change in mental status, which implies increased intracranial pressure. This situation is a life-threatening emergency. * Patient may have symptoms similar to meningitis, like fever, nuchal rigidity, and photophobia. There is meningeal irritation from the blood, similar to the meningeal irritation/inflammation that occurs from bacterial infection. * If you suspect subarachnoid hemorrhage, the lumbar puncture (LP) is not the first test as there may be increased ICP and the tap would cause brain herniation. In contract, spinal tap would be done first for suspected meningitis without signs of increased ICP. Next step in management is suspecting subarachnoid hemorrhage is head CT without IV contrast. No need to expose the patient to the risks of contrast if youre looking for blood. * Head CT scan is about 90-95% sensitive. If you have a suspicion of a diagnosis, even with a negative CT scan, do not exclude the diagnosis. Next step if you still suspect subarachnoid hemorrhage is lumbar puncture looking for blood. A flow cytometer of the CSF showing hundreds of RBCs should strongly suggest subarachnoid hemorrhage here. A traumatic tap could also put RBCs into your CSF sample. To rule out traumatic tap, you collect serial CSF tube samples and number them sequentially. The lab will see the number of RBCs declining across the tubes if the tap was traumatic. If the number of RBCs is constant, subarachnoid would be most likely given the presentation. * Management for subarachnoid hemorrhage is angiography to guide the neurosurgeon to bleeding aneurysm. Most subarachnoid hemorrhages stop on their own, so the patient is not bleeding in the ED or in the OR. * Stabilization prior to the OR is maintaining systolic BP between 110 and 160. * Cerebral vasospasm is a specific worry in subarachnoid hemorrhage. As a response to the localized bleed, the vessels will go into spasm causing decreased perfusion. Treatment is nimodipine calcium channel blocker. Care



should be taken not to drop BP too much. The nifedipine class calcium channel blocker prevents vasospasm. The subsequent hypoperfusion stroke from vasospasm may be the must devastating injury. * If CT scan demonstrates hydrocephalus, patient may need a shunt to relieve the pressure. --------------------------------------------------------------------------------------------------------------------------------------------Heat Disorders (Exertional & Non-Exertional) * Syndromes range from mild head cramps, to heat exhaustion, to heat stroke (most severe). * Typically a patient exercising on a hot day and not drinking much. Or, might be a marathon run in the fall. * Symptoms of heat cramps are generally mild and the patient is still able to sweat. If you can sweat you can dissipate heat. Patient is dry, feels dehydrated, mild tachycardia, and minimal or no temperature elevation. * Manage heat cramps with PO fluids and electrolyte solutions (e.g. sports drinks with Na+ and K+). * Symptoms of heat exhaustion are moderate dehydration, minor temperature elevation (100F, 101F), and are still able to sweat and therefore can dissipate heat. May have mild changes in mental status (e.g. confusion). * Manage heat exhaustion with PO fluids (if they can drink) and electrolyte solutions (e.g. sports drinks). * Heat stroke is very serious; cases can include 25yo healthy patients in peak athletic shape who die. Be worried if the patient is hot (>104F) and not sweating, as they have lost their ability to dissipate heat. * Symptoms of heat stroke are severe confusion, high temperature, and not sweating. These patients are very dehydrated, can be hemoconcentrated, develop rhabdomyolysis, myobloginuria, and renal failure. Renal failure because they are dehydrated and become pre-renal while also plugging up renal tubules with myoglobin. * Manage heat stroke with aggressive IV fluid administration, normal saline with added potassium. * Do not dump these patients in ice baths as it can cool them too rapidly. * Place patient in cool environment, spray with cool water and fan them to dissipate the heat (simulates sweating). * Patient might begin shivering, which we can treat with diazepam or chlorpromazine, but watch BP. * Non-exertional hyperthermia is split into, malignant hyperthermia and neuroleptic malignant syndrome. * Malignant hyperthermia (MH) is commonly related to halothane and succinylcholine. Treatment is dantrolene. This is an idiosyncratic reaction so a patient may have previously normal surgeries prior to an episode. * Typical MH case is a patient undergoing anesthesia who has a dangerous rise in temperature after induction. * Neuroleptic malignant syndrome (NMS) is commonly related to phenothiazines (e.g. chlorpromazine) and butyrophenones (e.g. haloperidol). Treatment is dantrolene or bromocriptine. * Typical NMS is psych patient who has a dangerous rise in temperature in a short period of time. --------------------------------------------------------------------------------------------------------------------------------------------Hypothermia * Typical case is a patient with cold exposure who is drunk or intoxicated with another recreational substance. * Homeless patient is found on a park bench and is brought to the ED obtunded, temperature is 92F. * Without aggressive treatment, severe organ shutdown may occur. Treat aggressively. * Symptoms include temperature < 35C (< 95F), mental status changes, and ventricular arrhythmias. * On ECG, look for diffuse J-point elevation (simulates ST elevation), also known as Osborn waves. * Treatment is to warm up the patient. Get a core temperature by esophageal probe or rectal thermometer. * Cover patient with blankets. If they are very cold, use warmed IV fluids, warmed oxygenation. Rewarming the patient too quickly can lead to arrhythmias. So, bring the patient up gradually and keep them on an ECG monitor. * Hypothermic patient without a pulse might still be resuscitated. Warm patients will have some form of neurologic damage after 4 minutes of pulselessness. Hypothermic patients cannot be declared dead until they are rewarmed. --------------------------------------------------------------------------------------------------------------------------------------------Radiation Injury * Unit for nuclear radiation is gray = 100 rads. Radiation is destructive to DNA, causing changes (e.g. cancer). * Most live if exposure is < 2gray. Most die if exposure is > 10gray. * Symptoms include GI complaints in 2-3gray range and early bone marrow suppression. PMNs most vulnerable, platelets vulnerable, and RBCs least vulnerable. Treat these patients with G-CSF (granulocyte colony-stimulating factor), platelet transfusions, and rarely RBC transfusions. Long-term DNA changes lead to leukemia. * Gonads affected with testes more susceptible than ovaries. At 2-3gray, testes temporarily decrease sperm count. At 5rads the patient can become permanently infertile. --------------------------------------------------------------------------------------------------------------------------------------------Near-Drowning * Often in the setting of alcohol or drug intoxication, or due to trauma while swimming. Can also be seen in patients who have an MI or arrhythmia while swimming. Seizure patients should not swim unsupervised. * Freshwater (lake, stream, pool) near drowning involves hypotonic fluid entering the lungs. These patients become hemodiluted, can hemolyze, get damaged surfactant leading to alveolar collapse, hypoxia, and hypercapnia.



* Salt water (sea) near drowning involves hypertonic fluid entering the lungs. These patients become hemoconcentrated as body fluids pour into lungs in an effort to dilute the concentrated seawater. Alveoli become flooded, patient becomes get hypoxia and hypercapnia (increased pCO2). * These patients will be obtunded, tachypneic, tachycardic, have crackles/rhonci on lung exam. * Treatment is to provide an adequate airway (CPAP or intubation with PEEP) and deliver air under pressure into the lungs. In the freshwater case, the pressurized air is forcing the alveoli to open. In the saltwater case, the pressurized air forces the fluid back into the bloodstream. * Treatments that do not work are abdominal thrusts, antibiotics generally, and steroids. --------------------------------------------------------------------------------------------------------------------------------------------Electric Injury * Electrical electricity conducts much more effectively if you are wet. The low resistance conduits in your body are nerves and blood vessels. So you are better off if you are dry and get hit by lightning; causes local injury. * If local injury, treat with burn care. If systemic injury, treat cardiac conduction disturbances (e.g. vfib). * Treatment is ABCs, adequate hydration, wound care, and cardiac monitoring. --------------------------------------------------------------------------------------------------------------------------------------------Anaphylaxis * Mild allergic reaction involves mild rash and urticaria. Immune sensitivity is through skin so it could be a new perfume, a new cream, through inhalation (e.g. seasonal allergies). Localized mast cell release of histamine causes bronchospasm and leads to wheezing. Itching is due to histamine as well. Treatment here is an antihistamine like diphenhydramine. Tends to make patient drowsy. * For anaphylaxis, it could be a very mild exposure such as a single peanut. These patients should be carrying an epinephrine auto-injector (epi-pen). Allergy can be to any food substance. * Severe reactions include bronchospasm leading to laryngospasm (stridor). Stridor is a life-threatening situation because it indicates the airway is about to close. Aggressively treat with anti-histamines and steroids. If life threatening give epinephrine. Epinephrine is a rough drug, causes tachyarrhythmias, can induce VT. If the airway closes, the patient will likely need a cricothyroidotomy. * Most severe anaphylactic response is hypotension (vasomotor collapse, vessels all dilate). This patient will die soon if they are not treated. Do not give antihistamine in this case, it will further lower blood pressure. Answer for next step in management in this case is epinephrine. Steroids take too long to work. --------------------------------------------------------------------------------------------------------------------------------------------Venom Exposure * Rattlesnakes are the most prevalent venomous snakes in the United States. * Snake venom contains endotoxins, neurotoxins, and/or hemolytic toxins. * Susceptibility depends on body weight. Certain areas are more prone to develop severe reactions, such as the trunk and the face. The depth of the bite also determines who will get sick (deeper is sicker). * Immediate treatment should be to immobilize the patient. Activity will further circulate the venom. * There are specific anti-venoms, usually held by a single hospital in a region. * Management also includes isolation of the area of venom bite, such as with compression bandages. * Treat associated complications, such as paralysis (neurotoxin) and hemolysis (hemolytic toxin). * Never ever suck out venom from a wound. -------------------------------------------------------------------------------------------------------------------------------------------- Emergency Medicine: A National Perspective (Keaton, MD from EMRA Medical Student Survival Guide) Our specialty was born out of adversity a little over three decades ago in places like Lansing, Michigan, and Alexandria, Virginia. Americans had a better chance of surviving serious illness and injury on the battlefields of Vietnam than on the streets of our major cities. The physicians who staffed the emergency rooms of the day were there as punishment. The workforce was made up of physicians who were at the beginning, end, or low point of their careers. How times have changed. We are now the most sought-after specialty, and our residency graduates are the best and the brightest American medicine has to offer. When we look at the external environment, were faced with unprecedented challenges. With them come opportunities to transform our health care system into one that can provide high-quality care for all Americans, regardless of their age, sex, race, creed, color, primary language, or ability to pay. When the government or organized medicine puts together a team to take on a tough challenge, emergency physicians are among the first to be asked to step forward. Instead of being a fly on the wall, we have a seat at the table, often a seat at the head of the table. Although we are relatively small in number compared to other specialties, we are disproportionately represented in leadership roles.



The same skills set that makes us good at what we do clinically makes us the perfect docs to bridge the gaps between medicine, business, and the government. Our knowledge base is miles wide, and were able to speak intelligently about almost any aspect of medicine. We see the big picture and are good at cutting through the minutiae to focus on what is really important. We thrive in stressful environments where decisions must be made with less than complete information. Were good stewards of precious resources. We tend to be good politicians. Were seen by the public as healers more concerned about doing whats in their best interest than ours. Theres a universal connection to what we do and a natural desire to associate with us because every person we meet is just a heartbeat from being one of our patients. We heal sick people, band-aid sick systems, and hold the greatest promise to resuscitate our flawed health care system. Economic, demographic, and social factors are forcing fundamental change in our health care system. Emergency medicine has long been the safety net, and as a result has borne the brunt of the health care systems woes. Concerns to our specialty include: ensuring universal access to emergency medical services; ensuring the highest quality of care is provided to all our patients; improving the liability climate to ensure both emergency physicians, and the consultants who they rely on, can provide needed emergency care; easing the crowded conditions in which emergency physicians provide care; improving our emergency departments and hospitals ability to respond to natural and terrorist disasters; and ensuring adequate reimbursement for the services provided by physicians, much of which is uncompensated. The spectrum of disease witnessed by the emergency physician is unparalleled and is often the draw for medical students choosing a career in emergency medicine. Your future training goes well beyond the bedside, however. As suggested, the challenges before the American health care system are significant. However, there is no group better prepared to lead this transformation than emergency physicians. Patients have spoken with their feet, seeking our care in unprecedented numbers. We are the ones you come to when youre really sick, possibly sick, or kind of sick and in need of rapid evaluation, diagnosis, and treatment. We are the place you come to when you cannot or will not wait for others to find a place in their schedules for you, and the site of medical refuge when you dont know where else to turn. Despite limited resources, unrealistic expectations, and impossible demand, emergency medicine delivers on our promise to provide the best possible care to every patient regardless of their ability to pay or what time of day they choose to seek care. Alan Kay once said, The best way to predict the future is to invent it. Were in an inventing mode and are being presented with a historic opportunity to define both the future of our specialty and of American medicine. The opportunities in emergency medicine are endless and by choosing this career you will become a leader and a champion for the health care needs of your patients. The challenges before our health care system and emergency medicine are significant, but the rewards and honor of providing care to our communities are limitless. --------------------------------------------------------------------------------------------------------------------------------------------

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