Study Notes – Emergency Medicine James Lamberg 28Jul2010

Textbooks: Adams Emergency Medicine, Emergency Medicine Secrets, First Aid for Emergency Clerkship
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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
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Procedures: NEJM Videos In Clinical Medicine: http://www.nejm.org/multimedia/videosinclinicalmedicine
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Kaplan Videos (2001) – Emergency Medicine with Dr. Asher Kornbluth, MD
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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).
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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.

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Study Notes – Emergency Medicine James Lamberg 28Jul2010

* 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.
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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.
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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 patient’s 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

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Study Notes – Emergency Medicine James Lamberg 28Jul2010

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.
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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 we’re several hours after ingestion, pills are present on x-ray, and they’re 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.
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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 don’t 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 we’re 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.
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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.

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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, we’re 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 we’re 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.
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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.
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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 you’re 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.

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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.
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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. Patient’s CHF or diabetes may worsen as well, so digoxin dose
has not changed but their excretion has gotten worse (e.g. saying patient’s 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 can’t 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.
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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.

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Study Notes – Emergency Medicine James Lamberg 28Jul2010

* 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).
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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).
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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.
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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 patient’s EEG will appear as if the patient is
dead (flat-line EEG). Treatment is usually more aggressive than with benzodiazepine overdose.

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* 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.
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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.
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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.
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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 patient’s 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 Ringer’s, 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

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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.
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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 patient’s 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 you’re 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
patient’s 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

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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 patient’s 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.
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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 patient’s 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 you’re 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

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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.
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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.
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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.
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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.
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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.

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* 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.
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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.
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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.
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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.
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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, we’re 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.

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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 we’re 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. We’re good stewards of precious resources. We tend to be good politicians.
We’re seen by the public as healers more concerned about doing what’s in their best interest than ours. There’s 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 system’s 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 department’s and hospital’s 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
you’re 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 don’t 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.” We’re 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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