ICU · Endocrine
Hypoglycaemia in the ICU
Also known as Hypoglycaemia · Hypoglycaemic coma · Insulin overdose · Neuroglycopenia · Whipple triad · Sulfonylurea overdose · Octreotide · Insulinoma · Hypoglycaemia-associated autonomic failure · Insulin autoimmunity (Hirata syndrome)
Hypoglycaemia is a frequent and serious adverse effect of antidiabetic therapy; inpatients who develop it have longer stays and increased mortality. In ICU trials moderate hypoglycaemia spans 2.3–3.9 mmol/L (41–70 mg/dL) and severe hypoglycaemia means glucose at or under 2.2 mmol/L (40 mg/dL) — severe episodes carried an adjusted hazard ratio for death of 2.10 in the NICE-SUGAR cohort. Profound hypoglycaemia — typically under 1 mmol/L (18 mg/dL) with a flat EEG — causes neuronal death (hippocampal dentate gyrus and superficial cortex vulnerable; cerebellum and brainstem spared). Causes: insulin or insulin secretagogue treatment (the most common cause), sulfonylurea poisoning (sustained hypoglycaemia refractory to IV dextrose — add octreotide), critical illnesses, hormone deficiencies such as adrenal crisis, non-islet cell tumours, and accidental/surreptitious insulin. Management: check glucose in any unconscious or seizing patient (ICU point-of-care meters read higher than laboratory values, under-detecting hypoglycaemia); oral carbohydrate if conscious; IV dextrose if not (25 g of 50% dextrose is the conventional ampule; 10% dextrose resolves symptoms with fewer adverse events); IM glucagon 1 mg if there is no IV access (intranasal glucagon 3 mg is non-inferior); octreotide 50 µg SC/IV followed by three 50 µg doses every 6 hours for sulfonylurea poisoning; thiamine 200 mg IV three times daily given before any carbohydrate in the malnourished or alcoholic patient; hydrocortisone 100 mg IV bolus then 200 mg/24 h for adrenal crisis. Document Whipple's triad, then take the critical sample (insulin, C-peptide, proinsulin, beta-hydroxybutyrate, oral hypoglycaemic agents, insulin antibodies) to find the cause.
Checked against its sources on 3 Sept 2026
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Red flags
- Severe hypoglycaemia (glucose at or under 2.2 mmol/L / 40 mg/dL) carried an adjusted hazard ratio for death of 2.10 in the NICE-SUGAR cohort — treat immediately, do not wait for laboratory confirmation
- Check glucose in ANY unconscious, seizing, collapsed, or bizarre-behaviour patient — ICU point-of-care meters read higher than laboratory values (mean difference ~24 mg/dL, ~37 mg/dL in shock) and can under-detect hypoglycaemia
- Recurrent hypoglycaemia with shock: consider adrenal crisis — rapid IV hydrocortisone (100 mg bolus, then 200 mg/24 h) plus 0.9% saline
- Sulfonylurea poisoning: glucose AND glucagon exacerbate insulin release and lead only to temporary benefit with later relapse — add octreotide 50 µg SC/IV followed by three 50 µg doses every 6 hours
- Give thiamine 200 mg IV three times daily BEFORE any carbohydrate in the alcoholic or malnourished patient (EFNS recommendation)
- Hypoglycaemia mimics stroke, seizure, intoxication and psychiatric illness — never assume intoxication without a glucose check
Meet the patient
A 34-year-old woman with type 1 diabetes is brought by ambulance after a generalised tonic-clonic seizure at home. Her partner reports she skipped dinner after a busy shift; her insulin pump was found disconnected. GCS 9, fingerprick glucose reads LOW (below 1.1 mmol/L); laboratory glucose confirms 1.0 mmol/L — a reminder that unexpected point-of-care readings in ICU patients deserve laboratory confirmation, because POC meters can under-detect hypoglycaemia.[15]
This is severe hypoglycaemia — a medical emergency. In the NICE-SUGAR cohort, severe hypoglycaemia (blood glucose at or under 40 mg/dL [2.2 mmol/L]) carried an adjusted hazard ratio for death of 2.10 (95% CI 1.59–2.77), and 35.4% of those patients died within 90 days versus 23.5% of patients without hypoglycaemia.[5] Neuronal death occurs only when profound hypoglycaemia drives the EEG flat — usually after glucose has fallen below 1 mM (18 mg/dL) for some period — so a laboratory glucose of 1.0 mmol/L is a true neurological emergency.[11] The first move is a fingerprick in ANY patient with altered mental status or a seizure; the second is treatment; the third is finding the cause. Hold the rule — check, treat, explain — and every hypoglycaemia stem answers itself.
References17ShowHide
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- [2]Cryer PE. Individualized glycemic goals and an expanded classification of severe hypoglycemia in diabetes. Diabetes Care, 2017.PMID 29162584
- [3]van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. New England Journal of Medicine, 2001.PMID 11794168
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- [13]Matsuhisa M, Takita Y, Nasu R, et al. Nasal glucagon as a viable alternative for treating insulin-induced hypoglycaemia in Japanese patients with type 1 or type 2 diabetes — a phase 3 randomized crossover study. Diabetes Obesity and Metabolism, 2020.PMID 32115879
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- [15]Mishra K, Mishra S, Katial T. Accuracy of point-of-care capillary blood sugar measurements in critically ill patients — an observational study. International Journal of Critical Illness and Injury Science, 2024.PMID 39005980
- [16]Martel-Duguech L, Poirier J, Bourdeau I, Lacroix A. Diagnosis and management of secondary adrenal crisis. Reviews in Endocrine and Metabolic Disorders, 2024.PMID 38411891
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