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A 54-year-old man with a history of chronic alcohol misuse is brought to the emergency department unconscious. He was found collapsed at home with an empty bottle of "windscreen washer fluid" beside him. On examination: GCS 9 (E2V3M4), RR 28 and deep (Kussmaul), BP 96/58, HR 118, Sat 96% on air. Fundoscopy is difficult but the pupil reactions are sluggish.[1]
Investigations: venous gas pH 7.12, PaCO2 22 mmHg, HCO3 7 mmol/L, base excess minus 22. U&E Na 142, K 5.0, Cl 98, urea 9.1, creatinine 160. Glucose 5.8 mmol/L, lactate 4.2 mmol/L, serum osmolality 340 mOsm/kg. Urine microscopy: needle/ envelope-shaped crystals.[1]
Questions
a) Interpret the blood gas systematically and calculate the anion gap and osmolar gap. (3 marks)[1]
Stepwise approach:
- pH 7.12 — severe acidaemia (under 7.35).
- HCO3 7 mmol/L (low) drives the primary disorder — metabolic acidosis. PaCO2 is also low (compensatory).[1]
- Anion gap = Na minus (Cl + HCO3) = 142 minus (98 + 7) = 37 mmol/L — high (normal 8 to 12).[1]
- Winter's check (compensation adequacy): expected PaCO2 = 1.5 x HCO3 + 8 = 1.5 x 7 + 8 = 18.5 mmol/L (range 16.5 to 20.5). Measured 22 is slightly higher — mild concurrent respiratory acidosis (reduced conscious state, hypoventilating relative to need).[1]
- Osmolar gap = measured minus calculated osmolality. Calculated = 2 x Na + glucose + urea = 2 x 142 + 5.8 + 9.1 = 298.9. Osmolar gap = 340 minus 299 = 41 mOsm/kg — high (normal under 10).[1]
High anion gap + high osmolar gap = toxic alcohol ingestion. The needle/envelope crystals are calcium oxalate — this is ethylene glycol poisoning.[1]
b) What is the mechanism of the acidosis in ethylene glycol poisoning, and why does the osmolar gap fall while the anion gap rises over time? (2 marks)[1]
Ethylene glycol itself is an osmotically active alcohol — it contributes to the measured osmolality (high osmolar gap) but is not charged (does not affect the anion gap). It is metabolised by alcohol dehydrogenase (rate-limiting) to glycoaldehyde, then glycolic acid (main cause of the high anion gap acidosis), glyoxylic acid and oxalic acid, which precipitates with calcium to form calcium oxalate crystals in the renal tubules, causing acute kidney injury.[1]
So as metabolism proceeds: the parent alcohol is consumed (osmolar gap falls) and acid metabolites accumulate (anion gap rises) — the two gaps move in opposite directions, and a late presentation may have a near-normal osmolar gap but a very high anion gap with renal failure.[1]
c) Outline the immediate management, including specific antidote and indications for haemodialysis. (3 marks)[1]
- Resuscitation — ABCDE, IV access, treat shock (balanced crystalloid), airway protection if GCS under 8.[1]
- Block alcohol dehydrogenase — Fomepizole 15 mg/kg IV loading then 10 mg/kg every 12 h for 4 doses, then 15 mg/kg q12h until ethylene glycol level under 20 mg/dL and acidosis resolved. (If fomepizole unavailable, an ethanol infusion to maintain blood ethanol 100 to 150 mg/dL.)[1]
- Cofactors — thiamine 100 mg IV and pyridoxine 50 mg IV daily, which divert metabolism away from oxalate towards less toxic metabolites.[1]
- Haemodialysis — indications: severe acidosis (pH under 7.25 to 7.30), renal failure, ethylene glycol level over 50 mg/dL, or visual/cerebral involvement (more relevant to methanol). Dialysis removes the parent alcohol and metabolites and corrects the acidosis.[1]
- Supportive — correct hypocalcaemia only if symptomatic (avoid over-replacement as it drives oxalate precipitation); treat hyperkalaemia; do not give bicarbonate routinely (only for pH under 7.1 with instability).[1]
d) Two hours into treatment he becomes confused and restless; repeat gas shows pH 7.05, HCO3 5. The team asks whether to give IV sodium bicarbonate. State the indications for bicarbonate in metabolic acidosis and the reasons it is not routine. (2 marks)[1]
Indications for sodium bicarbonate (narrow):
- pH under 7.1 to 7.15 WITH haemodynamic instability (catecholamines are less effective at extreme acidosis).
- Hyperkalaemia with ECG changes (shifts K+ into cells).
- Tricyclic antidepressant overdose with QRS widening (the sodium load more than the alkalaemia stabilises the myocardium).
- Severe renal acidosis not yet dialysed.
Not routine because: bicarbonate buffers H+ by generating CO2 (HCO3 + H+ to H2O + CO2), which diffuses into cells faster than bicarbonate and can worsen intracellular and CNS acidosis if ventilation is inadequate; it also causes hypernatraemia, volume overload, hypokalaemia, and overshoot alkalosis, and trials (e.g. BICAR-ICU) show no mortality benefit in lactic acidosis. The principle is always to treat the underlying cause (here: fomepizole + dialysis), not the number.[1]
References4ShowHide
- [1]Adrogué HJ, Madias NE Management of life-threatening acid-base disorders. First of two parts N Engl J Med, 1998.PMID 9414329
- [2]Wrenn K The delta (delta) gap: an approach to mixed acid-base disorders Ann Emerg Med, 1990.PMID 2240729
- [3]Figge J, Jabor A, Kazda A, et al. Anion gap and hypoalbuminemia Crit Care Med, 1998.PMID 9824071
- [4]Jaber S, Paugam C, Futier E, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial Lancet, 2018.PMID 29910040