Emergency Medicine Flashcards

1
Q

When is gastric lavage the right answer after toxic ingestion?

A

When ingestion is extremely recent (can be attempted up to 2 hours after ingestion)

One hour after ingestion = 50% effective

2 hours after ingestion = 15% effective

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2
Q

When is gastric lavage dangerous (i.e., contraindicated)?

A

Patients with altered mental status (may cause aspiration)

Caustic ingestion (causes burning of the esophagus and oropharynx)

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3
Q

What is ipecac?

A

Used to induce vomiting

Always the WRONG ANSWER in the ED (needs 15-20 minutes to work and delays the administration of antidotes)

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4
Q

When is whole bowel irrigation indicated?

A

Placing a gastric tube and flushing out the GI tract with polyethylene glycol-electrolyte solution (GoLYTELY) is almost always the wrong answer

Indications = massive iron ingestion, lithium, and swallowing drug-filled packets

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5
Q

Gastric emptying of any kind is always wrong with:

A

Caustics (acids and alkali)

AMS

Acetaminophen overdose

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6
Q

When the answer is not clear and the cause of overdose is asked, say:

A

Acetaminophen or

Aspirin

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7
Q

What is the most appropriate next step when a patient presents after overdose confused, disoriented, and lethargic?

A

The best initial management of AMS of unclear etiology is an opiate antagonist (Naloxone) and glucose (dextrose)

Opiate ingestion and diabetes are extremely common; naloxone and glucose work instantaneously and have no adverse effects (if they do not work, perform intubation)

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8
Q

Difference between the management of opiate and benzodiazepine overdose

A

Opiate overdose is fatal = give naloxone immediately

BZ overdose by itself is not fatal and acute withdrawal after chronic use causes seizures = do NOT give flumazenil

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9
Q

True/False

Charcoal is benign and should be given to anyone with a pill overdose

A

True

It may not be effective for every overdose, but it is not dangerous in anyone (removes toxic substances even after they have been absorbed)

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10
Q

Toxicity of acetaminophen may occur with ingestions greater than…

A

8-10 grams (approximately 0.5 grams per pill, 16 pills = toxic)

12-15 grams may be fatal (24 pills)

Note: alcoholism decreases the amount of acetaminophen needed to cause toxicity

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11
Q

If a clearly toxic amount of acetaminophen has been ingested (more than 8-10 grams/16 pills), what is the next step?

A

Give N-acetylcysteine

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12
Q

If acetaminophen overdose was more than 24 hours ago when the patient presents, what is the next step?

A

There is no therapy

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13
Q

If the amount of acetaminophen ingestion is unclear, what is the next step?

A

Drug level

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14
Q

Does charcoal make N-acetylcysteine ineffective?

A

No

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15
Q

Overdose of unknown substance

Tinnitus

Hyperventilation

A

Aspirin overdose

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16
Q

How does aspirin cause metabolic acidosis?

A

Aspirin interferes with oxidative phosphorylation and results in anaerobic glucose metabolism, which produces lactate

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17
Q

Treatment for aspirin overdose

A

Sodium bicarb

Alkalinizing the urine = increased rate of excretion

ASA is a weak acid; charged particles, which ASA would be in an alkaline enviroment, are not reabsorbed in the tubules (i.e., excreted)

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18
Q

Blood gas in aspirin overdose

A

Look for respiratory alkalosis progressing to metabolic acidosis*

pH 7.46, pCO2 22, HCO2 16

*ASA directly stimulates the respiratory center (hyperventilation = respiratory alkalosis), its interference with oxidative phosphorylation leads to metabolic acidosis

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19
Q

A patient ingested multiple toxic substances. You know for certain that this is the first time they took BZs. You give flumazenil and the patient immediately seizes. What happened?

A

BZs can prevent seizures from TCA toxicity. When you reverse BZs, you remove the suppression and can induce a seizure

Flumazenil will only cause seizures with chronic BZ dependence

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20
Q

What is the best initial test for suspected TCA toxicity

A

EKG

TCA toxicity is rapidly detectable on EKG (will show widening of the QRS complex that progresses to Torsades)

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21
Q

What is the treatment for TCA overdose

A

Sodium bicarbonate

Unlike for aspirin, bicarbonate will not increase urinary excretion of TCAs but it does protect the heart (competes for binding on Na fast channels)

If EKG shows torsades, give Magnesium

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22
Q

Dyspnea

Lightheadedness

Confusion

Seizures

MI

Pt was in a burning house

A

CO poisoning

The LV cannot distinguish between anemia, carboxyhemoglobin, and a stenosis of the coronary arteries (why death from CO is often from MI)

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23
Q

Blood gases for CO poisoning

A

pH 7.35, pCO2 26, HCO3 18

Prevents O2 release to tissues, so lactic acidosis develops

Note: pO2 is normal

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24
Q

When is hyperbaric oxygen indicated (over 100% oxygen via nonrebreather) for CO poisoning

A

For severe disease:

CNS symptoms

Cardiac symptoms

Metabolic acidosis (low bicarb and low pH)

It shortens the half-life of carboxyhemoglobin even more than 100% O2

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25
Difference between methemoglobinemia and CO poisoning?
In methemoglobinemia, hemoglobin will never pick up the oxygen; with carboxyhemoglobin, the oxygen is picked up, but will not release is to tissues CO = abnormally red blood Methemoglobinemia = abnormally brown blood
26
What causes methemoglobinemia
Idiosyncratic reaction of hemoglobin to certain drugs (oxidized hemoglobin gets locked into the ferric state) such as: Benzocaine and other **anesthetics** **Nitrites** and nitroglycerin Dapsone
27
Test and Treatment for Methemoglobinemia
Most accurate test = methemoglobin level Best initial therapy = 100% oxygen Most effective therapy = **methylene blue**
28
Cyanosis normal pO2
Methemoglobinemia
29
Salivation Lacrimation Polyuria Diarrhea Bronchospasm and respiratory arrest
Organophosphate (insecticide) poisoning and nerve gas It causes a massive increase in the level of ACh by inhibiting its metabolism
30
Treatment for organophosphate poisoning?
Give **atropine** first (blocks the effects of ACh that is already increased) Then give **pralidoxime** (reactivates acetylcholinesterase, but does not work as instantaneously as atropine)
31
How are potassium and digoxin related
They compete for binding at the same site on the Na/K ATPase **Hypokalemia** predisposes to digoxin toxicity Digoxin toxicity causes **hyperkalemia**
32
Diagnostic testing for digoxin toxicity
Best initial test = potassium level and EKG (**downsloping of the ST segment** in all leads) Most accurate = digoxin level
33
What are the strongest indications for giving digoxin-binding antibodies?
CNS and cardiac involvement
34
Abdominal pain ATN Anemia Wrist drop Memory loss
Lead poisoning
35
Diagnostic test for lead poisoning
Best initial = increased level of **free erythrocyte protoporphyrin\*** Most accurate = **lead level** *\*The free erythrocyte protoporphyrin (FEP) test measures the concentration of nonheme protoporphyrin in red blood cells. Protoporphyrin comprises the predominant porphyrin in red blood cells, which combines with iron to form the heme portion of hemoglobin.*
36
Treatment for lead poisoning
Chelating agents **Succimer** is the only oral form of lead chelator **EDTA (ethylenediaminetetraacetic acid)** and **BAL (dimercaprol)** are parenteral agents
37
Difference between mercury poisoning from oral ingestion vs inhaled?
Oral = neurological problems (nervous, jittery, twitchy, and hallucinations) Inhaled = lung toxicity that presents as interstitial fibrosis
38
Treatment for mercury poisoning
There is **no therapy to reverse pulmonary toxicity** (inhaled) Chelating agents such as **dimercaprol** and **succimer** are effective for neurological toxicity (can prevent progression of pulmonary disease)
39
Difference between Methanol and Ethylene Glycol intoxication
_Methanol_ From wood alcohol, cleaning solutions, and paint thinner Toxic metabolite = formic acid/formaldehyde **Presentation = ocular toxicity (retinal inflammation on exam)** _Ethylene Glycol_ From antifreeze Toxic metabolite = oxalic acid/oxalate **Presentation = renal toxicity (look for hypocalcemia 2/2 precipitation of calcium in oxalate crystals\*)** *\*Calcium oxalate crystals are enveloped shaped*
40
Treatment for methanol and ethylene glycol intoxication
Both give an osmolar gap and are treated with fomepizole and dialysis **Fomepizole** inhibits alcohol dehydrogenase and prevents production of the toxic metabolites **Dialysis** effectively removes methanol and ethylene glycol from the body
41
Death from bites is from:
Hemolytic toxin: hemolysis and DIC Neurotoxin: respiratory paralysis
42
Treatment for snake bites
Pressure, Immobilization (decreases movement of venom), and Antivenin *Ineffective/dangerous treatment = tourniquet, ice, and incision/suction*
43
Difference between black widow and brown recluse bite?
_Black widow_ Abdominal pain, **Hypocalcemia** Treat with *calcium and antivenin* _Brown recluse_ Local **skin necrosis** Treat with *debridement, steroids, and dapsone*
44
Management of dog, cat, and human bites
Amoxicillin/clavulanate Tetanus vaccination booster if more than 5 years since last injection * Dog and Cats = Pasteurella multocida* * Humans = Eikenella corrodens (most damaging)*
45
True/False Both epidural and subdural hematomas are associated with a lucid interval
True
46
Treatment for large subdural/epidural hematomas
1. **Intubation and hyperventilation** (cerebral circulation constricts when the pCO2 is low; a small decrease in volume results in a large decrease in pressure) 2. **Mannitol** 3. **Drainage (evacuation)**
47
What are clear indications for stress ulcer prophylaxis with a PPI?
Head trauma Burns Intubation Coagulopathy (platelets \< 50,000 or INR \> 1.5) with respiratory failure
48
When to intubate a burn patient?
Any signs of airway injury: stridor hoarseness wheezing burns insides the nasopharynx or mouth
49
How to calculate fluid replacement for burn patients
(4 mL) x (% BSA burned) x (weight in kg) Give one-half in the first 8 hours, then give the second half over the next 16 hours
50
How to estimate BSA in burns
Head = 9% Arms = 9% each Legs = 18% each Chest or back = 18% each * Each hand width is one percent of BSA* * For children, Head = 18% and each Leg = 14%*
51
The most common cause of death from hypothermia is...
**cardiac arrhythmia** look for an intoxicated person with a low body temp best initial step = EKG
52
What does the EKG show for hypothermia
Marked **elevation of the J point** J waves are where the QRS hits the ST segment
53
What is always the wrong answer for management of patients recovering from drowning?
Seroids and Abx Correct answer = positive pressure ventilation
54
Besides CPR, therapy for asystole is with...
epinephrine (vasopressin is an alternative) by constricting blood vessels in tissues (like the skin), they shunt blood into critical central areas
55
The best initial therapy for v fib
immediate, unsynchronized cardioversion (aka defibrillation) followed by the resumption of CPR if not effective *Only VF and VT without a pulse get unsynchronized cardioversion*
56
When is amiodarone given for v fib
After shock, epi, shock, epi, shock (order is shock, drug, shock, drug, shock...and amiodarone is given after 2 doses of epi are unsuccessful)
57
Hemodynamically stable vs unstable VT
Stable = amiodarone, then lidocaine, then procainamide (cardiovert if medical therapy fails) Unstable = electrical cardioversion several times, followed by medications
58
What constitutes hemodynamic instability
Chest pain Dyspnea Hypotension Confusion
59
Why do we synchronize the delivery of electricity in the cardioversion of VT
To prevent worsening of the arrhythmia into ventricular fibrillation or asystole
60
normal EKG and no pulse
PEA Give CPR and correct the underlying cause (tamponade, tension pneumo, massive PE, potassium disorders)
61
Irregularly irregular rhythm
Think a fib
62
Atrial fibrillation vs Atrial flutter
Fibrillation = irregular rhythm Flutter = regular rhythm *Flutter will either go back into sinus rhythm or deteriorate into fibrillation*
63
What defines chronic atrial fibrillation
Lasting for more than 2 days The distinction is important because acute a fib does not need anticoagulation prior to cardioversion, whereas chronic a fib does
64
Why is cardioversion of chronic atrial fibrillation (even after anticoagulation) not routinely indicated?
Most will revert to fibrillation *Shocking the patient into sinus rhythm does not correct a dilated LA (chronic a fib is caused by anatomic abnormalities of the atria or from HTN or valvular heart disease)*
65
Treatment for a fib
**Rate control** and **anticoagulation** (same for atrial flutter) _Best initial therapy = beta blocker, CCB, or digoxin_ Once the rate is under 100 per minute, the most appropriate next step is to give warfarin, dabigatran, or rivaroxaban
66
Is heparin necessary prior to starting warfarin on a patient with a fib?
No (unless there is evidence of an existing clot)
67
CHADS Score
C: CHF or cardiomyopathy H: hypertension A: age \> 75 D: diabetes S: stroke or TIA (2 points) When CHADS score is 1 or less use aspirin 2 or more use warfarin, dabigatran, rivaroxaban, or apixaban
68
Best initial step for SVT
Look for a patient with palpitations who is hemodynamically stable 1. Vagal maneuvers (carotid massage, valsalva, ice immersion) 2. Adenosine 3. Beta blockers (metoprolol), CCB (diltiazem), or digoxin
69
Narrow complex tachycardia without P waves, fibrillatory waves, or flutter waves
SVT
70
SVT alternating with ventricular tachycardia SVT that gets worse after diltiazem or digoxin Observing the delta wave on the EKG
WPW Syndrome
71
Most accurate test for WPW
Cardiac electrophysiology (EP) studies *They will tell you where the anatomic defect is*
72
Acute and chronic therapy for WPW
Acute = procainamide or amiodarone Chronic = radiofrequency catheter ablation
73
Why are digoxin and CCBs dangerous in WPW
They block the normal AV node and force conduction into the abnormal pathway
74
3 different P-wave morphologies and associated with COPD
MAT Treat as you would atrial fibrillation, but _AVOID beta blockers for rate control because of their lung disease_
75
Treatment for sinus brady
Asymptomatic = no treatment Symptomatic: best initial = atropine most effective = pacemaker
76
Wenckebach block
aka Mobitz I Progressively lengthening PR interval that results in a "dropped" beat Often a sign of normal aging of the conduction system
77
Mobitz II
Drops a beat **without the progressive lengthening** of the PR interval Mobitz II progresses, or deteriorates into third-degree AV block _EVERYONE gets a pacemaker, even if they are asymptomatic_
78
P waves and T waves have no fixed relationship to each other
Third-degree or complete heart block Pacemaker
79
What determines the risk of recurrence of a ventricular arrhythmia?
Ejection fraction (get an echo) A normal ejection fraction = low risk of recurrence
80
The most common cause of death in the 72 hours surrounding an acute MI
Ventricular arrhythmia If the arrhythmia is from ischemia, correct the ischemia (angiography and angioplasty or bypass)
81
Most appropriate next step in a patient with multiple episodes of syncope and an EKG showing ventricular tachycardia
Implantable defibrillator (will prevent the next episode of sudden death or syncope) Metoprolol is NOT sufficient when syncope or sudden death has occurred
82
HEART Score
Used to predict the risk of a MACE (major adverse cadiac event) within the next month * History* * EKG* * Age* * Risk Factors* * Initial Troponins* 0-3 = low risk, \>7 = 50-65% risk
83
Wells Criteria
Objectifies risk of PE Clinical signs and symptoms PE is #1 diagnosis HR \> 100 Immobilization Previous PE/DVT Hemoptysis Malignancy w/ treatment within the last 6 months *The original intent of this tool was to determine who was low risk (\<2 points) enough to rule out testing with a d-dimer*
84
PERC
The PERC rule can be applied to patients where the diagnosis of PE is being considered, but the patient is deemed low-risk * Age \> 50* * HR \> 110* * SaO2 \< 95* * Unilateral leg swelling* * Hemoptysis* * Recent surgery/trauma* * Prior DVT/PE* * Hormone use* If no criteria are positive and clinician’s pre-test probability is \<15%, PERC Rule criteria are satisfied. PERC negative patients do not require utilization of the d-dimer, which has a high sensitivity but low specificity.