An alcoholic vagrant was admitted to the Accident and Emergency Department after being found collapsed on the street


An alcoholic vagrant was admitted to the Accident and Emergency Department after being found collapsed on the street. Four hours previously he had been spotted wandering outside the hospital and appeared well. On examination he had a Glasgow coma scale of 5. His heart rate was 120 beats/min and regular. The blood
pressure measured 80/50 mmHg. The respiratory rate was 24/min. The patient was apyrexial. The pupils were dilated. Neurological examination revealed blurred disk margins and depressed reflexes. Investigations are shown.
What is the diagnosis?

a. Euglycaemic ketoacidosis.
b. Methanol toxicity.
c. Ethylene glycol poisoning.
d. Tricyclic antidepressant overdose.
e. Hepatic encephalopathy.
Sodium 131 mmol/l Potassium 5.4 mmol/l Urea 5 mmol/l Creatinine 110 mol/l Bicarbonate 12 mmol/l Chloride 96 mmol/l Glucose 6 mmo/l Amylase 120 iu/l (NR <220 iu/l) Plasma osmolality 320 mOsm/l ECG Sinus tachycardia, left axis deviation Arterial blood gases: pH 7.21 PaO2 9 kPa PaCO2 2.1 kPa Bicarbonate 12 mmol/l Blood lactate 6 mmol/l Urinalysis Protein 0 Glucose 0 Ketones +


The main differential diagnoses of severe metabolic acidosis and collapse specific to an individual who abuses alcohol includes methanol toxicity, ethylene glycol poisoning, acute severe pancreatitis and acute hepatic failure. The patient has a normal amylase therefore acute pancreatitis is unlikely. The actual plasma osmolality is higher than the calculated plasma osmolality (approximately 284 mOsm/l) suggesting the presence of a large concentration of an osmotically active substance. The most probable candidates include methanol or ethylene glycol (anti-freeze). Both conditions present with drunkenness, acidosis and coma and in untreated cases the mortality is high. Methanol and ethylene glycol are relatively toxic; however, once ingested they are metabolized to formic acid (methanoic acid) and glycolic acid, respectively, by the enzyme alcohol dehydrogenase, both of which are very toxic. Patients with methanol toxicity may complain of headache, nausea, fatigue or reduced visual acuity if not
comatosed. Reduced visual acuity is due to optic nerve damage resulting from increased concentrations of formic acid, the oxidized metabolite of methanol. Mydriasis, reduced visual reflexes to light and hyperaemia of the optic disc are early features of methanol toxicity. Untreated patients may develop blindness. Patients with ethylene glycol poisoning may present in a similar fashion; however, reduced visual acuity is not a classical feature whereas flank pain and renal failure due to crystallization of oxalic acid in the renal tubules is common. Urinalysis under Wood’s light in patients with ethylene glycol poisoning may reveal oxalate crystals in the urine but an absence does not exclude the diagnosis. Patients with ethylene glycol poisoning also develop severe cardiac failure if untreated. The presence of visual symptoms favour methanol intoxication in this case. The management of methanol toxicity and ethylene glycol toxicity is the same, as tabulated below. Tricyclic anti-depressant overdose can also present with acidosis and dilated pupils; however, one would have expected brisk reflexes and possible wide QRS complexes on the 12-lead ECG