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CCP 222 Toxicology ☠️ Flashcards

1
Q

GOLDMARK (anion gap mnemonic)

a new mnemonic recommended to replace MUDPILES for causes of anion-gap metabolic acidosis

A

G - Glycols (ethylene glycol, propylene glycol)
O - Oxoproline (acetaminophen ingestion)
L - L Lactate
D - D Lactate (short bowel, propylene glycol)
M - Methanol
A - ASA
R - Renal failure
K - Ketoacidosis (DKA, starvation, alcoholism)

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2
Q

causes of NAGMA

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. GI (diarrhea, pancreatic fistula)
  2. Renal (RTA I, II, IV)
  3. Too much N/S (hyperchloremic)
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3
Q

causes of AGMA (KULT)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Ketones (starvation, DKA, alcoholism)
  2. Uraemia
  3. Lactate (L and D lactate)
  4. Toxins (ASA, methanol, ethylene glycol, toluene)
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4
Q

At what point do we intubate profound metabolic acidosis?

What indicates that someone with a metabolic acidosis is “failing”

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

When they start to develop a superimposed respiratory acidosis

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5
Q

Steps to preparing a bicarb infusion

🔥🔥🔥MEGA PEARL🔥🔥🔥

A
  1. Draw out 30cc of D5W from a 1L bag
  2. Put 3 amps of NaHCO3- in to replace it
  3. Standard infusion rate = 250mL/hr

this shit HAS to be in D5W. if you use 0.9% Saline or LR you will create a HYPERTONIC SOLUTION because the Na+ content will be too high. you will fuck up your patient

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6
Q

key physical findings when differentiating a toxic exposure (characterizing a toxidrome)

A
  1. odors
  2. Pupillary findings
  3. Neuromuscular abnormalities
  4. Mental status alterations
  5. Skin findings
  6. Temperature alterations
  7. Blood pressure and heart rate alterations
  8. Respiratory disturbances
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7
Q

what is covered on a “urine drug screen”

A
  1. Amphetamines
  2. Cocaine
  3. Marijuana
  4. Opiates
  5. Phencyclidine (PCP)
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8
Q

the guiding principle of medical toxicology

A

“treat the patient, not the poison”

Supportive care is key

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9
Q

Delirium tremens clinical findings

A
  1. Delirium
  2. agitation
  3. tachycardia
  4. hypertension
  5. fever
  6. diaphoresis
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10
Q

Delirium tremens time of onset from last drink

A

48 to 96 hours

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11
Q

Alcohol withdrawal seizures time of onset from last drink (different from full blown DT’s)

A

6 to 48 hours

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12
Q

fomepizole MOA

A
  1. Fomepizole prevents the formation of toxic alcohol metabolites via inhibition of alcohol dehydrogenase (primary enzyme involved in alcohol metabolism)
  2. toxic alcohols themselves aren’t toxic, it’s their metabolites/breakdown products
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13
Q

primary treatment for toxic alcohol poisoning

A
  1. Inhibition of alcohol dehydrogenase through either fomepizole or ethanol
  2. this prevents the development of toxic acid metabolites
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14
Q

How to set up a Bicarb infusion for profound metabolic acidosis

A
  1. mix sodium bicarbonate 8.4% 3 ampules (150 mEq) in 1L of D5W
  2. infuse at 250 mL/hour
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15
Q

primary toxic metabolite of methanol

A
  1. formate (derived from formic acid)
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16
Q

primary toxic metabolites of ethylene glycol (there’s three… 💎💎💎)

A
  1. glycolate
  2. glyoxylate
  3. oxalate
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17
Q

harmful manifestations of methanol poisoning

A
  1. blindness due to direct toxicity at the optic nerves

2. profound anion gap metabolic acidosis

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18
Q

major manifestations of Ethylene glycol poisoning

A
  1. acute kidney injury due to deposition of calcium oxalate crystals within the renal tubules
  2. profound anion gap metabolic acidosis

EHYLENE GLYCOL = OXALATE CRYSTALS = AKI (because the crystal plug up your GU system)

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19
Q

most common source of ethylene glycol (for ingestion)

A
  1. automotive antifreeze

this is oftentimes going to be a suicide attempt in teens/adults. kids are prone to accidental ingestion

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20
Q

most common sources of methanol (for ingestion)

A
  1. windshield washer fluid
  2. automotive antifreeze
  3. “moonshine” (impure home made alcohol)

classic case is people making home made hooch, their hooch ends up impure, and they get methanol toxic. this is the classic stereotype of the blind Appalachian hillbilly

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21
Q

classic “mixed picture” acid-base disturbance seen in Salicylate toxicity

A
  1. respiratory alkalosis (crosses blood brain barrier and stimulates tachypnea. it is NOT a compensatory tachypnea to the metabolic acidosis)
  2. metabolic acidosis.
  3. finally respiratory acidosis (when they start to get pooched and their ventilatory effort begins to fail)
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22
Q

Treatment goals for salicylate toxicity

A

“Alkalinize and dialyze”

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23
Q

key findings of a poisoning history

A
  1. time, route, and quantity of exposure
  2. coingestants
  3. onset of symptoms
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24
Q

key exam findings in salicylate toxicity

A
  1. Vitals: tachycardia, tachypnea/hyperpnea, hyperthermia
  2. Gastrointestinal (GI): nausea, vomiting, and abdominal pain
  3. CNS: tinnitus/hearing dysfunction, coma/seizures
  4. Pulmonary: non-cardiogenic pulmonary edema, acute respiratory distress syndrome
  5. Dermatologic: diaphoresis
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25
Q

pathophysiology of salicylate toxicity

A
  1. At a physiologic serum pH, salicylic acid exists in an ionized state as a weak acid
  2. in toxicity (acidic environment), salicylic acid is converted to an un-ionized (highly permeable) state
  3. ATP production becomes limited secondary to Krebs cycle interference.
  4. Energy is released in the form of heat as a result of uncoupling oxidative phosphorylation
  5. Renal hemodynamics are ultimately impaired, and anion gap metabolic acidosis ensues
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26
Q

key pearls for tubing a salicylate toxicity patient

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Don’t do it!
  2. Hold off until your hand is forced (deteriorating mental status, acute lung injury, agitation)
  3. If intubating maintain or exceed minute ventilation requirements
  4. pursue aggressive bag-valve mask procedures (delayed sequence intubation if possible)
  5. ensure adequate fluid loading and hydration prior to induction. these patients are usually dry! (also consider administering 1x amp D50 IV immediately before sedation to treat unrecognized neuroglycopenia, a sinister complication of salicylate toxicity)
  6. use amps of bicarb peri intubation (administer 2 mEq/kg IV bolus sodium bicarbonate)
  7. RSI with most experienced intubator and get the tube in quick
  8. adjust vent settings to maximize minute ventilation (e.g. 8-10 cc/kg breaths, high RR)
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27
Q

rescue therapy for acetaminophen toxicity

A

N-acetylcysteine (NAC)

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28
Q

N-acetyl-p-aminophenol (acetaminophen) abbreviation

A

APAP

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29
Q

toxic dose range for acetaminophen

A
  1. > 150 mg/kg or >10g in adults and adolescents

2. >200-250 mg/kg in infants and toddlers

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30
Q

Stage I of acetaminophen toxicity

A

quiescent phase…

2-24 hr post ingestion. usually asymptomatic. if symptoms present, usually GI-related (N/V, abdominal tenderness)

liver labs (AST/ALT) and coags (PT/INR) are typically normal, may become mildly elevated

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31
Q

Stage II of acetaminophen toxicity

A

1-2 days post ingestion, minimal symptoms. may develop RUQ pain

elevated AST/ALT, bilirubin, INR

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32
Q

Stage III of acetaminophen toxicity

A

72-96 hours post ingestion, Maximal stage of hepatotoxicity!

elevated AST/ALT, Abnormal LFT’s (rising PT/INR)

this is the full meal deal. full blown hepatic failure. this is the stage where these guys get super fucked up

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33
Q

Stage IV of acetaminophen toxicity

A

> 5 days post ingestion. progression to MODS/Death.

resolution of hepatotoxicity in survivors

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34
Q

what is the clinical utility of activated charcoal (AC) in toxic ingestion?

A
  1. Patients may benefit from the administration of activated charcoal (AC) in a single dose of 1 g/kg (maximum dose 50 g)
  2. Typically only works if given within one to two hours of ingestion
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35
Q

key clinical features of solvents, anesthetics, or sedatives (SAS) Toxidrome

A
  1. CNS depression
  2. decreased LOC (progressing to coma in some cases)
  3. hypoventilation
  4. ataxia (difficulty balancing and walking)
  5. hypothermia
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36
Q

key clinical features of anticholinergic toxidrome

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. dilated pupils (mydriasis) “blind as a bat”
  2. decreased sweating (anhidrosis) “dry as a bone”
  3. hyperthermia “hot as hell”
  4. delirium “mad as a hatter”
  5. flushed skin “red as a beet”
  6. decreased UO and decreased bowel sounds (urinary retention and constipation)
  7. tachycardia
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37
Q

key clinical features of cholinergic toxidrome

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

“DUMBBELLS”

  1. Diarrhea
  2. Urination
  3. Miosis
  4. Bradycardia (increased parasympathetic response)
  5. Bronchoconstriction
  6. Excitation (myoclonic twitches/seizures)
  7. Lacrimation (parasympathetic stimulation of lacrimal glands)
  8. Lethargy
  9. Salivation (parasympathetic stimulation of salivary glands)
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38
Q

key clinical features of opioid toxidrome

A
  1. pinpoint pupils (miosis)
  2. central nervous system depression
  3. respiratory depression
  4. hypothermia
  5. hypoactive bowel sounds
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39
Q

key clinical features of Sympathomimetic Toxidrome

A
  1. tachycardia
  2. tachypnea
  3. hypertension
  4. anxiety/agitation/delirium/hallucinations
  5. hyperthermia with diaphoresis
  6. dilated pupils (mydriasis)
  7. seizures
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40
Q

pathophysiology of cardiac toxicity associated with cocaine use

A
  1. Cocaine is an ester anesthetic that acts via sodium channel blockade
  2. leads to QRS widening and slowed conduction on ECG
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41
Q

key clinical differences between Acute sympathomimetic and anticholinergic toxidromes

A
  1. sympathomimetic and anticholinergic toxidromes have similar features of febrile agitated delirium with tachycardia and hypertension
  2. Major difference: Diaphoresis with sympathomimetics and dry skin with anticholinergics
  3. Minor differences: Reactive pupils with sympathomimetics and minimally reactive pupils with urinary retention in anticholinergics
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42
Q

mechanism of digoxin

A
  1. Cardiac glycosides inhibit sodium-potassium-ATPase
  2. levels of intracellular Na+ and extracellular K+ increase
  3. The increase in intracellular Na+ eventually results in an increase in intracellular Ca++, increasing cardiac contractility
  4. Digoxin increases vagal tone and shortens the refractory period of the myocardium
  5. This leads to bradycardia and increased automaticity
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43
Q

drug class of digoxin

A

cardiac glycoside

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44
Q

primary treatment modality for digoxin toxicity

A
  1. digoxin-specific antibody fragments (digoxin-Fab)

2. also known as “Digi-bind”

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45
Q

primary means of death in digoxin toxicity

A
  1. cardiac manifestations of toxicity
  2. brady-tachydysrhythmias
  3. hyperkalemia
  4. cariogenic shock
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46
Q

most common ECG finding indicating digoxin toxicity

A
  1. new onset PVC’s in the setting of a patient taking digoxin
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47
Q

signs of chronic/long term digoxin toxicity

A
  1. fatigue
  2. malaise
  3. nausea
  4. dizziness
  5. visual disturbances such as xanthopsia (yellow haloes)
  6. chromatopsia (color vision disturbances)
  7. scotomas (area of partial alteration in the field of vision)
  8. reduced visual acuity
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48
Q

common clinical syndrome seen in BB + CCB overdose

A
  1. refractory hypotension
  2. bradydysrhythmias (conduction blocks)
  3. cardiogenic shock
  4. death
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49
Q

primary clinical distinction between CCB OD and BB OD

A
  1. Hyperglycemia is common with CCB overdose (CCB block voltage gated Ca++ channels in pancreatic beta cells that are necessary for insulin release)
  2. hypoglycemia is common with BB overdose (BBs interfere with glycogenolysis and gluconeogenesis)
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50
Q

CCB mechanism

A
  1. CCBs block voltage-gated Ca++ channels responsible for excitation of the myocardium and smooth and skeletal muscle
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51
Q

Beta blocker mechanism

A
  1. BBs inhibit epinephrine and norepinephrine adrenergic stimulation on beta receptors
  2. beta receptors are found on the heart, smooth muscles, arteries, airways, kidneys, and other tissues.
52
Q

CCB toxicity pathophysiology

A
  1. Antagonism of the Ca++ channels decreases Ca++ influx, resulting in impaired muscle contraction.
  2. Ca++ channel antagonists impair insulin release, resulting in intracellular hypoglycemia (extracellular hyperglycaemia) rendering the cells less efficient at energy production
53
Q

beta blocker toxicity pathophysiology

A
  1. BBs antagonize beta receptors
  2. in beta receptor blockade cAMP production is reduced
  3. this inhibition results in a decrease in cardiac inotropy and chronotropy
  4. Antagonism of non-cardiac beta receptors impairs gluconeogenesis and glycogenolysis, resulting in hypoglycaemia
54
Q

what is the mechanism behind high-dose insulin therapy in BB and CCB overdose?

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. high-dose insulin improves hemodynamic parameters because of direct inotropic effects independent of cAMP
  2. also has anti-inflammatory effects, and antioxidant effects
55
Q

which antidepressants have the highest rate of mortality

A
  1. Tricyclic antidepressants (TCA’s)
  2. monoamine oxidase inhibitors (MAOI’s)
  3. dopamine and norepinephrine reuptake inhibitor’s (DNRI)
56
Q

characteristic findings in TCA overdose

A

Think “neuro-cardiac”

  1. CNS depression
  2. seizures
  3. hypotension
  4. dysrhythmias
57
Q

characteristic findings in MAOI overdose

A

Think “adrenergic crisis”

  1. adrenergic storm
  2. coma
  3. complete cardiovascular collapse
58
Q

characteristic findings in bupropion (wellbutrin) DNRI overdose

A

think “stimulant toxidrome”

  1. tachycardia
  2. tremor
  3. agitation/hallucination
  4. delayed onset seizures
59
Q

define Serotonin syndrome

A
  1. potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (CNS)
  2. presents with the clinical triad of autonomic instability, altered mental status, and neuromuscular findings (eg, hyperreflexia, clonus)
  3. must be in the context of exposure to a serotonergic agent
60
Q

explain the cardio toxicity of TCA overdose

A
  1. QRS complex widening occurs due to fast Na+ channel inactivation by ionized TCA binding to the Na+ channel
  2. Sinus tach occurs due to anticholinergic effects and increased norepinephrine
  3. QTc prolongation occurs secondary to QRS widening
  4. Hypotension occurs due to impaired cardiac conduction and peripheral alpha 1 blockade.
61
Q

explain CNS toxicity in TCA overdose

A
  1. Agitation and delirium occur due to antimuscarinic and antihistaminic effects.
  2. Seizures occur d/t increased norepinephrine, Na+ channel blockade, and GABA inhibition
62
Q

first-line treatment for cyanide poisoning

A
  1. Hydroxocobalamin
  2. 5 g IV over 30 min (may repeat dose × 1)
  3. Forms cyanocobalamin (vitamin B12)
63
Q

pathophysiology of cyanide toxicity

A
  1. Inhibition of cytochrome c oxidase within the electron transport chain halts ATP formation
  2. this results in the accumulation of H+ and profound acidemia
64
Q

diagnosing cyanide toxicity

A
  1. Diagnosis is clinical
  2. history of occupational or environmental exposure
  3. presence of rapidly progressive cardiovascular collapse
  4. presence of profound lactatemia
  5. “Cherry-red” skin color is unreliable. may be a late or postmortem finding
65
Q

clinical manifestations of cyanide toxicity

A
  1. Central nervous system: headache, agitation, confusion, seizures, coma
  2. Cardiovascular: tachy-brady dysrhythmias, hypotension, cardiovascular collapse
  3. Pulmonary: tachypnea, followed by bradypnea
  4. Gastrointestinal: nausea,vomiting, abdominal pain
  5. metabolic: Serum lactate >8-10 mmol/L is highly sensitive for cyanide toxicity
  6. Severe anion gap acidosis is anticipated in cyanide toxicity (hyperlactatemia)
66
Q

median toxic dose (TD50) definition

A
  1. the dose required to produce a defined toxic effect in 50% of subjects
67
Q

median lethal dose (LD50) definition

A
  1. the dose required to kill 50% of subjects
68
Q

median effective dose (ED50) definition

A
  1. the dose at which 50% of individuals exhibit the specified effect
  2. the dose of a drug that produces, on average, a specified all-or-none response in 50% of a test population
69
Q

therapeutic index definition

A
  1. the ratio of the TD50 to the ED50

2. a parameter which reflects the selectivity of a drug to elicit a desired effect rather than toxicity.

70
Q

therapeutic window definition

A
  1. the range between the minimum toxic dose and the minimum therapeutic dose
  2. the range of doses over which the drug is effective for most of the population and the toxicity is acceptable.
71
Q

key history features for EtOH usage/withdrawal

A
  1. time of last drink
  2. quantity
  3. daily allotment
  4. co-ingestants
  5. onset of symptoms
72
Q

Signs and symptoms of mild ethanol withdrawal

A
  1. Tremor
  2. anxiety
  3. insomnia
  4. sweating
  5. anorexia
73
Q

Signs and symptoms of moderate ethanol withdrawal

A
  1. Autonomic instability (increased heart rate, blood pressure, temperature)
  2. visual/tactile/auditory hallucinations
74
Q

Signs and symptoms of severe ethanol withdrawal

A
  1. Severe autonomic instability
  2. extreme agitation
  3. altered sensorium
  4. extreme tremors/seizures (delirium tremens)
75
Q

classic triad of wernicke encephalopathy

A
  1. mental status changes
  2. ophthalmoplegia
  3. ataxic gait
76
Q

define Wernicke encephalopathy

A
  1. acute brain disorder that results from thiamine deficiency
  2. Thiamine is a cofactor for several key enzymes important in energy metabolism
  3. thiamine deficiency initiates neuronal injury by inhibiting metabolism in brain regions with high metabolic requirements
  4. Thiamine deficiency in alcoholics results from a combo of decreased PO intake, reduced GI absorption, decreased hepatic storage, and impaired utilization
77
Q

define Korsakoff syndrome

A
  1. a late neuropsychiatric manifestation of Wernicke encephalopathy (WE)
  2. characterized by profound anterograde and retrograde amnesia
  3. most frequently in alcohol abusers after an episode of WE
  4. most patients with KS show typical WE lesions
  5. 80 percent of alcohol abusers recovering from classic WE exhibit amnesia of KS
78
Q

Z-drugs

A
  1. Zolpidem, zopiclone, and zaleplon

2. structurally unrelated to benzodiazepines but bind to the benzodiazepine site on the GABA-A receptor

79
Q

describe flumazenil

A
  1. GABA-A receptor antagonist
  2. rapid onset of action and a high affinity for the benzodiazepine binding site on the GABA-A receptor
  3. will not reverse the effects of other sedative-hypnotics such as barbiturates or other sedatives such as ethanol
80
Q

“2 salt and a sticky BUN”

this is for CALCULATED serum osmolarity

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

Calculated Serum osmolarity = “2 salt and a sticky BUN”

Calculated osmolarity = (2 x Na) + Glucose + BUN + (1.25 x ETOH)

81
Q

What is the normal osmolar gap?

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

Osmolar Gap = Measured Serum Osmolality - Calculated Serum osmolarity (Og = Om - Oc)

normal osmolar gap is arbitrarily set at 10. But can range from -15 to 10 in population

82
Q

define osmolar gap

A

the difference between measured serum osmolality and calculated serum osmolality

83
Q

define an osmole

A
  1. an osmole is the amount of a substance that yields the number of particles that would depress the freezing point of the solvent by 1.86K (such as volatile alcohols)
  2. a good way of thinking about this is with antifreeze. antifreeze is usually ethylene glycol (an alcohol) which has a very low freezing point (approx -40 Celsius)
84
Q

most common toxicological causes of an elevated osmolar gap

A
  1. methanol
  2. ethylene glycol
  3. isopropanol (Isopropyl alcohol)
  4. ethanol
85
Q

name the three types of cholinergic receptors

A
  1. central
  2. muscarinic
  3. nicotinic
86
Q

effects of Excess acetylcholine at muscarinic receptors

A
  1. symptoms increased secretions
  2. bronchoconstriction
  3. bradycardia
  4. vomiting
  5. abdominal cramping
87
Q

effects of Excess acetylcholine at nicotinic receptors

A
  1. muscle fasciculations or paralysis d/t activation of the neuromuscular junction
88
Q

CNS effects of excess acetylcholine

A
  1. headache
  2. drowsiness
  3. confusion
  4. dizziness
89
Q

three main methods of GI decontamination in toxic ingestion

A
  1. Gastric lavage
  2. Activated charcoal
  3. Whole-bowel irrigation
90
Q

MOA for organophosphate toxicity

A
  1. blocks the action of Ach esterase at the neuromuscular junction.
  2. Ach acts on nicotinic and muscarinic receptors
91
Q

muscarinic effects of organophosphate poisoning

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Muscarinic receptors in heart, eye, lung, GI, skin and sweat glands
  2. Bradycardia/hypotension
  3. Miosis
  4. Bronchorrhea / Bronchospasm
  5. Hyperperistalsis (SLUDGE)
  6. Sweating
  7. Vasodilation
92
Q

nicotinic effects of organophosphate poisoning

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. fasciculations, flaccid paralysis

2. tachycardia, hypertension

93
Q

dializable drugs

A 
I - Isopropanol (Isopropyl alcohol) 
S - salicylate
T - theophyline 
U - urea 
M - metformin/methanol
B - barbiturates 
L - lithium
E - ethylene glycol
D - dabigatran
94
Q

The Rumack-Matthew nomogram (acetaminophen tox)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

determines toxic 4 hour level + Calculates NAC dosing for acetaminophen overdose

MUST HAVE:

  1. Acute, single ingestions (where entire ingestion occurs within an 8-hour period).
  2. A known time of ingestion.
  3. Immediate release formulation.
  4. Absence of formulations or coingestants that alter absorption and bowel motility (e.g. anticholinergics, opioids).

Notes:

  1. An acetaminophen concentration obtained prior to 4 hours post-ingestion cannot be plotted on the Rumack-Matthew nomogram, and only confirms acetaminophen exposure, not toxicity
  2. Get an accurate time of ingestion: the Rumack-Matthew nomogram is entirely dependent on knowing time of ingestion.
  3. Start NAC treatment within 8 hours post-ingestion to ↓ the risk of hepatotoxicity (AST or ALT > 1000 IU/L).
  4. In patients presenting 8-24 hours post-ingestion, start NAC while awaiting the acetaminophen concentration; once this is resulted, NAC can be continued or discontinued depending on the level.
95
Q

describe the classic “mixed picture” acid-base disturbance seen in Salicylate toxicity

A

respiratory alkalosis followed by metabolic acidosis.

96
Q

pathophysiology of salicylate toxicity

A

Salicylates uncouple oxidative phosphorylation, impair ATP synthesis, and promote lipolysis

  1. At a physiologic serum pH, salicylic acid exists in an ionized state as a weak acid; in toxicity (acidic environment), it is converted to an un-ionized (highly permeable) state
  2. ATP production is limited secondary to Krebs cycle interference
  3. Energy is released in the form of heat d/t uncoupling oxidative phosphorylation
  4. Renal hemodynamics are ultimately impaired, and AGMA ensues
97
Q

physical exam findings seen in salicylate toxicity

A

Vitals: tachycardia, tachypnea/hyperpnea, hyperthermia (late, severe toxicity)
GI: nausea, vomiting, and abdominal pain
CNS: tinnitus/hearing dysfunction, coma/seizures (late, severe toxicity)
Pulmonary: non-cardiogenic pulmonary edema, ARDS
Dermatologic: diaphoresis

98
Q

treatment pathway for salicylate toxicity

A
  1. Support ABCs, prevent further organ toxicity by encouraging salicylate elimination
  2. Alkalinize the serum/urine (1-2 mEq/kg sodium bicarb. IV bolus followed by sodium bicarb. infusion (3 amps into 1L D5W) @ 1.5-2 X maintenance rate) goal serum pH ~7.5; goal urine pH >7.5
  3. Salicylate overdose + IV sodium bicarbonate therapy = potential hypokalemia. Avoid hypokalemia because it prevents alkalization of the urine, prolonged elimination of salicylate (goal K+ 4.0 to 4.5 mEq/L)
  4. Monitor Ca++ levels (ionized/total); IV NaHCO3– can cause hypocalcemia
  5. Consider glucose supplementation if altered mental status (Serum glucose may be normal but CNS levels may be low d/t effects of salicylates)
  6. CCP transport for emergent hemodialysis
99
Q

classic ABG findings in salicylate toxicity

A
  1. Primary respiratory alkalosis followed by a mixed acid-base disorder (respiratory alkalosis and metabolic acidosis).
  2. The metabolism of salicylates causes an increase in the anion gap. Salicylate is the primary unmeasured anion; however, lactic acid is also produced from anaerobic metabolism, which contributes to the anion gap.
  3. Many chemistry analyzers report a false elevation of chloride in the setting of salicylate toxicity, which can skew the anion gap
100
Q

pathophysiologic pathway of methanol metabolism in the body

A
  1. Methanol is metabolized in the liver to formaldehyde by alcohol dehydrogenase.
  2. The formaldehyde is then metabolized by aldehyde dehydrogenase to formic acid.
  3. The formic acid inhibits cytochrome-C in the mitochondria, shifting the cell to anaerobic glycolysis → lactic acid accumulation
101
Q

M in the MUDPILES mnemonic

A

Methanol ingestion

elevated anion gap metabolic acidosis (formic acid buildup and lactic acid buildup)

102
Q

pathophysiologic pathway of Ethylene glycol metabolism in the body

A
  1. Ethylene glycol is metabolized in the liver to glycoaldehyde by alcohol dehydrogenase.
  2. Glycoaldehyde is converted to glycolic acid by aldehyde dehydrogenase, which is then converted to glyoxylic acid, then to oxalic acid.
  3. oxalic acid combines with serum calcium to form the classic calcium oxalate crystals found in the urine of patients who have consumed ethylene glycol
103
Q

E in the MUDPILES mnemonic

A

Ethylene glycol ingestion

elevated anion gap metabolic acidosis

104
Q

most commonly ingested toxic alcohol

A

Isopropanol (Isopropyl alcohol)

105
Q

most common sources of Isopropanol (Isopropyl alcohol)

A

solvents, disinfectants, mouthwashes, lotions, rubbing alcohol, hand sanitizers

106
Q

pathophysiologic pathway of Isopropanol (Isopropyl alcohol) metabolism in the body

A
  1. hepatically metabolized by alcohol dehydrogenase to acetone.
  2. The acetone does not undergo further metabolism, and no acid byproducts are formed.
  3. This means that isopropanol is the only toxic alcohol that does not cause an elevated anion gap acidosis
107
Q

define and describe Osmolar gap

A
  1. difference between the Measured Serum Osmolality minus the Calculated Serum Osmolarity
  2. equate to the amount of particles present in the serum that are not accounted for by the calculated Osmolarity formula

Calculated Serum osmolarity = “2 salt and a sticky BUN”
Calculated osmolarity = (2 x Na) + Glucose + BUN + (1.25 x ETOH)

Osmolar Gap = Measured Serum Osmolality - Calculated Serum osmolarity (Og = Om - Oc)

normal osmolar gap is arbitrarily set at 10. But can range from -15 to 10 in population

108
Q

the only substances that consistently increase the serum Osm gap

A

ethanol, methanol, ethylene glycol, isopropyl alcohol, acetone, mannitol, and glycerol

109
Q

toxic end product of methanol metabolism

A

formic acid

110
Q

toxic end products of ethylene glycol metabolism

A

glycolic and oxalic acid

111
Q

what is the distinguishing feature which differentiates TOXIC alcohol poisoning from ethanol toxicity

A

elevated osmolar gap

112
Q

specific manifestations of ethylene glycol toxicity

A
  1. significant renal failure d/t oxalate crystal deposition in the kidneys and glycolic acid, which is directly nephrotoxic
  2. hypocalcemia and tetany can result d/t oxalate binding to calcium.
113
Q

specific manifestations of methanol toxicity

A

MeOH toxicity classically causes visual disturbances (“snowfield” vision) due to formic acid-induced optic neuropathy

114
Q

specific manifestations of Isopropanol toxicity

A

causes ketosis without acidosis (no lactic acid formed!)

Usually benign clinical course but can occasionally cause hemorrhagic gastritis.

Fomepizole and HD not usually indicated

115
Q

specific manifestations of Propylene glycol toxicity

A

often due to IV medication preparations containing this alcohol (e.g., diazepam, lorazepam, esmolol, nitroglycerin, phenobarbital, phenytoin)

can result in severe lactic acidosis.

116
Q

MOA of fomepizole

A
  1. competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol.
  2. It is given to prevent the buildup of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid) whose deposition in tissues can cause irreparable damage
117
Q

discuss the role for vitamin supplementation in toxic alcohol poisoning

A
  1. Give folic or folinic acid to patients with Methanol toxicity to divert metabolism away from formic acid to carbon dioxide and water.
  2. Give folic acid, pyridoxine, and thiamine to patients with ethylene glycol toxicity to divert metabolism to nontoxic metabolites
118
Q

in what clinical picture should one suspect toxic alcohol poisoning

A

unexplained elevated anion gap metabolic acidosis and elevated osmolar gap

119
Q

Goals of management in toxic alcohol poisoning

A
  1. Block the toxic metabolites with fomepizole or ethanol
  2. Correct pH to 7.2 with bicarb
  3. Eliminate toxic metabolites with dialysis (especially methanol)
120
Q

describe an approach to intubation for toxic alcohol patient (hint: severe metabolic acidosis)

A

Consider DSI with ketamine and beware of the acidosis; match the pre-intubation respiratory rate with post intubation respiratory rate and consider bicarbonate boluses to avoid worsening acidosis and cardiovascular collapse

121
Q

Indications for fomepizole or ethanol in toxic alcohol poisoning

A
  1. Known ingestion of methanol, ethylene glycol or diethylene glycol without access to rapid serum osmolality
  2. AG metabolic acidosis or elevated osmolar gap plus strong suspicion of ingestion
  3. Serum methanol >8 mmol/L
  4. Serum ethylene glycol >3.2 mmol/L
  5. Suspicion of toxic alcohol ingestion with evidence of end organ damage (ocular, renal)
122
Q

Lab clues for toxic alcohol poisoning

A
  1. AG metabolic acidosis (caused by toxic alcohol +/- elevated lactate and renal failure)
  2. High osmolality +/- osmolar gap (note that osmolality decreases with time)
  3. Low ethanol level in intoxicated patient
  4. Hypocalcemia with prolonged QT
123
Q

when/how is The Rumack-Matthew nomogram used to determine the risk of APAP-induced hepatoxicity ?

A

Use after a single acute ingestion only (not for chronic or repeated ingestions) to determine if treatment is req’d

the nomogram starts at 4 hours post-ingestion

Obtain serum APAP level at 4 hours post ingestion: If the APAP plots above the treatment line, or “150-line”, treat with NAC

124
Q

MOA for NAC in acetaminophen toxicity

A
  1. The non-toxic route of APAP metabolism gets saturated in overdoses, which leads to the formation of the toxic metabolite NAPQI.
  2. N-acetylcysteine acts as a glutathione precursor and substitute to aid the conversion of N-acetyl-p-benzoquinoneimine to non-toxic metabolites.
  3. NAC helps replenish glutathione stores to conjugate the toxic metabolite, and assists with other routes of liver metabolism as well
125
Q

4 stages of acetaminophen toxicity

A 
Stage 1 (0.5-24 hrs): mild nausea, emesis, weakness
Stage 2 (24-72 hrs): hepatotoxicity +/- nephrotoxicity => RUQ abdominal pain
Stage 3 (72-96 hrs): hepatotoxicity peaks => nausea, vomiting, jaundice, coagulopathy
Stage 4 (4 days -2 wks): recovery or decompensation resulting in death
126
Q

sources of salicylate overdose OTHER than aspirin

A

oil of wintergreen (methyl salicylate)
BenGay (topical methyl salicylate)
PeptoBismol (bismuth subsalicylate)

127
Q

discuss the approach to sodium bicarb in TCA toxicity

A
  1. Sodium bicarbonate is the primary treatment for QRS widening, arrhythmias, or hypotension associated with TCA overdoses.
  2. administering sodium bicarbonate for QRS > 100-120 ms is appropriate
  3. Bicarbonate is administered at 1-2 meq/kg IVP. This dose may be repeated q5 minutes, until the QRS interval narrows and the hypotension resolves.
  4. After 3 rounds of bicarb, start a bicarbonate drip (3 amps in 1L D5W) at a rate of 250 cc/hr. continued 12-24 hours after the EKG has normalized

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