Toxic Alcohols and Poisonings
A patient presents with blurred vision, headache, confusion, high anion gap metabolic acidosis, and an elevated osmolar gap after ingesting windshield washer fluid.
What is methanol poisoning?
Point: Visual symptoms are the hallmark of methanol toxicity.
A critically ill patient develops facial twitching when the facial nerve is tapped and carpal spasm when a blood pressure cuff is inflated.
What are Chvostek and Trousseau signs of hypocalcemia?
Point: Classic board finding.
This ventricular arrhythmia is classically associated with severe hypomagnesemia.
What is torsades de pointes?
Point: One of the highest-yield magnesium questions on any board exam.
A phosphate level below this threshold generally warrants intravenous rather than oral phosphate replacement.
What is phosphate less than 1.0 mg/dL?
Point: Board-level treatment cutoff.
This urinary sediment finding is considered pathognomonic for nephritic syndrome.
What are red blood cell casts?
In the early stages of methanol or ethylene glycol ingestion, this laboratory abnormality is often present before the development of a significant anion gap metabolic acidosis.
What is an elevated osmolar gap?
Point: Early = parent alcohol predominates → elevated osmolar gap. Later = toxic metabolites accumulate → elevated anion gap. The classic board question.
This ECG abnormality is most commonly associated with clinically significant hypocalcemia.
What is a prolonged QT interval?
Point: Hypocalcemia prolongs QT; hypercalcemia shortens QT.
An alcoholic patient has persistent hypomagnesemia. This deficiency proves them at high risk for this electrolyte abnormality.
What is hypokalemia?
Point: If potassium won't correct, check magnesium.
A malnourished ICU patient develops profound hypophosphatemia shortly after enteral nutrition is started.
What is refeeding syndrome?
Point: One of the most common ICU phosphate questions.
This syndrome is characterized by edema, hypoalbuminemia, heavy proteinuria, and hyperlipidemia.
What is nephrotic syndrome?
This toxic alcohol causes "ketosis without acidosis," often produces a fruity odor on the breath, and results in a high osmolar gap but a normal anion gap.
What is isopropyl alcohol poisoning?
Point: Isopropanol → acetone. Elevated osmolar gap, ketosis, but no significantnmetabolic acidosis.
A patient receives 12 units of packed red blood cells during a massive transfusion protocol and subsequently develops hypotension and tetany.
What is citrate-induced hypocalcemia?
Point: Frequently tested ICU scenario. Stored blood contains citrate which binds calcium.
A patient receiving magnesium sulfate for eclampsia develops absent deep tendon reflexes and bradycardia.
What is hypermagnesemia?
Point: Loss of reflexes is often the first clue.
A mechanically ventilated patient on CRRT repeatedly fails spontaneous breathing trials despite normal cardiac and pulmonary function. What is the cause?
What is respiratory muscle weakness from hypophosphatemia?
Point: Extremely high-yield PCCM board concept.
A patient presents with hematuria, hypertension, edema, and declining renal function.
What is nephritic syndrome?
A patient presents with tinnitus, tachypnea, nausea, and an ABG showing pH 7.46, PaCO2 24 mmHg, HCO3− 17 mEq/L.
What is salicylate poisoning causing a mixed respiratory alkalosis and metabolic acidosis?
Point: One of the most tested acid-base patterns on the boards. Salicylates stimulate the medullary respiratory center while simultaneously generating an anion gap metabolic acidosis.
A 65-year-old smoker presents with confusion, constipation, calcium of 15.2 mg/dL, and a suppressed PTH.
What is hypercalcemia of malignancy?
Point: Severe hypercalcemia (>13 mg/dL) is malignancy until proven otherwise.
This medication is the immediate treatment for life-threatening ECG abnormalities due to hypermagnesemia.
What is intravenous calcium gluconate?
Point: Calcium antagonizes magnesium's cardiac effects.
A patient with tumor lysis syndrome develops hyperphosphatemia. This calculation helps predict the risk of soft tissue calcium-phosphate precipitation.
What is the calcium-phosphate product?
Point: Risk becomes substantial when the product exceeds 70.
A patient with volume depletion has a BUN of 60 mg/dL and creatinine of 2 mg/dL.
What is a BUN:Creatinine ratio greater than 20:1 suggesting prerenal azotemia?
Point: Increased proximal urea reabsorption.
A patient presents 18 hours after ingesting antifreeze. Laboratory studies reveal severe metabolic acidosis, AKI, and calcium oxalate crystals in the urine.
What is ethylene glycol poisoning?
Point: Methanol attacks the eyes; ethylene glycol attacks the kidneys. Calcium oxalate crystals remain a classic board clue.
A patient with severe hypercalcemia requires immediate therapy while awaiting bisphosphonate effect. This medication lowers calcium within hours.
What is calcitonin?
Point: Calcitonin = rapid onset; bisphosphonates = delayed onset (1–2 days).
A dialysis patient presents with magnesium 13 mg/dL, apnea, and complete heart block. The most effective therapy is this.
What is hemodialysis?
Point: Severe hypermagnesemia with organ dysfunction = dialysis.
This hormone decreases phosphate reabsorption in the proximal tubule.
What is parathyroid hormone (PTH)?
Point: A favorite physiology pearl tested repeatedly.
A patient with nephrotic syndrome suddenly develops flank pain and hematuria. This thrombotic complication should be suspected.
What is renal vein thrombosis?
Point: Particularly associated with membranous nephropathy.
A critically ill patient presents after a suspected toxic alcohol ingestion. The osmolar gap is 70 mOsm/kg and the anion gap is normal. Twelve hours later, the osmolar gap has fallen to 20 mOsm/kg while the anion gap has increased to 32 mEq/L. What is the mechanism?
What is metabolism of the parent alcohol into toxic organic acids?
Point: This is the quintessential ABIM toxic alcohol question. As methanol or ethylene glycol is metabolized by alcohol dehydrogenase:
Osmolar gap decreases (less parent alcohol)
Anion gap increases (more formic acid or glycolic/oxalic acid)
The two gaps move in opposite directions over time.
An ICU patient has a calcium of 7.4 mg/dL and phosphate of 9 mg/dL due to tumor lysis syndrome. This common intervention should be avoided unless absolutely necessary.
What is intravenous calcium administration?
Point: Calcium can precipitate with phosphate causing tissue deposition. Classic board point.
This hormone becomes functionally impaired in hypomagnesemia, contributing to concurrent hypocalcemia.
What is parathyroid hormone (PTH)?
Point: Low magnesium causes PTH resistance and impaired secretion. ABIM loves this relationship.
A patient with severe respiratory alkalosis develops acute hypophosphatemia despite normal phosphate stores. The mechanism is this.
What is intracellular phosphate shifting due to stimulated glycolysis?
Point: This is one of the trickier ABIM questions that distinguishes fellows from residents.
A patient develops AKI, eosinophilia, fever, and a rash one week after starting a proton pump inhibitor.
What is acute interstitial nephritis?
Point: Drug-induced AIN remains an ABIM favorite.