Diabetic Emergencies: Hypoglycaemia and DKA
Diabetes has two emergencies that pull in opposite directions. One is glucose crashing too low — fast, frightening, and reversible in minutes with sugar. The other is glucose soaring while the body drowns in acid — slower to build but deadly if missed. Knowing how to recognise each, and the one first move that treats it, is genuinely life-saving knowledge.
The two great emergencies of diabetes are mirror images. Hypoglycaemia is too little glucose in the blood — usually because a dose of insulin or a sulfonylurea outweighed the food eaten. The brain, which runs almost entirely on glucose, is starved within minutes: sweating, trembling, confusion, and — if untreated — seizures and coma. Diabetic ketoacidosis (DKA) is the opposite: a severe lack of insulin lets glucose climb sky-high while the body, unable to use that glucose, burns fat instead and floods itself with acidic ketones. One is a crisis of minutes and low sugar; the other a crisis of hours and high sugar plus acid. Recognising which you're facing points straight at the treatment.
Hypoglycaemia — the crisis of minutes
Low glucose starves the brain — treat it the instant you suspect it. Hypoglycaemia is the commonest serious side effect of diabetes treatment, and its golden rule is speed: it is far safer to treat a suspected low immediately than to wait for confirmation, because the brain tolerates low glucose for only minutes. The early warning symptoms come from adrenaline (sweating, shaking, palpitations, hunger); if glucose keeps falling, the brain itself falters (confusion, slurred speech, odd behaviour, then seizures and coma). Treatment depends only on whether the patient can safely swallow. If conscious and able: give fast oral sugar — glucose tablets, juice, or sweets. If unconscious or unable to swallow: this is an emergency — give intramuscular glucagon (a hormone that rapidly releases glucose from the liver) or intravenous glucose if a line is available. A vital catch: patients on beta-blockers may lose the adrenaline warning symptoms (the shaking and palpitations are blunted), so a hypo can strike without warning — a direct link back to the cardiovascular chapter.
DKA — the crisis of hours
Diabetic ketoacidosis is what happens when insulin runs out completely — classically in type 1 diabetes, often triggered by an infection, a missed insulin dose, or a new diagnosis. Without insulin, cells can't take in glucose, so it piles up in the blood (very high sugar) and spills into the urine, dragging water with it and causing heavy dehydration. Meanwhile the starving cells burn fat for fuel, producing acidic ketones that turn the blood dangerously acidic. The picture is a triad: high glucose, ketones, and acidosis. The patient is dehydrated, breathing deeply and rapidly to blow off acid (Kussmaul breathing), often with a fruity smell on the breath, abdominal pain and vomiting. The treatment follows the problems in order, and the order matters: first and most important, aggressive intravenous FLUIDS to rehydrate; then an INSULIN infusion to switch off ketone production and lower glucose; and careful replacement of POTASSIUM, because insulin drives potassium into cells and levels can crash dangerously. Fluids first, then insulin, and watch the potassium — that sequence is the heart of DKA management.
- Hypoglycaemia = too little glucose; brain starves in minutes — treat on suspicion, fast.
- Conscious hypo → oral sugar; unconscious → IM glucagon or IV glucose.
- Beta-blockers can mask the adrenaline warning symptoms of a hypo.
- DKA = the triad of high glucose + ketones + acidosis; classically type 1, often infection-triggered.
- DKA treatment order: FLUIDS first → INSULIN infusion → replace POTASSIUM (insulin lowers it).
The most dangerous, easily-missed point in DKA is the potassium. When DKA begins, blood potassium often reads normal or even high — but the body is actually massively depleted of it, and the moment you start insulin, potassium pours into the cells and the blood level can plummet into a range that stops the heart. That's why insulin is never given blindly: potassium is checked and replaced alongside it. It's a perfect example of a treatment creating its own new danger — and of why the order and the monitoring, not just the drugs, are what keep the patient alive.
- Waiting to confirm a hypo before treating — treat immediately; the brain can't wait.
- Giving oral sugar to an unconscious patient — aspiration risk; use glucagon or IV glucose.
- Starting insulin in DKA before fluids and before checking potassium — dangerous hypokalaemia.
- Missing that a beta-blocked patient can have a hypo without the usual warning signs.
What is the correct first step in treating diabetic ketoacidosis (DKA)?
- Hypoglycaemia (low sugar) starves the brain in minutes — treat on suspicion.
- Conscious → oral sugar; unconscious → IM glucagon / IV glucose. Beta-blockers mask the warning.
- DKA = high glucose + ketones + acidosis; treat fluids → insulin → potassium.
- Insulin drives potassium into cells — check and replace it, or it can crash.
- Katzung BG. Basic & Clinical Pharmacology — Pancreatic Hormones & Antidiabetic Drugs (complications).
- Brunton LL, et al. Goodman & Gilman's The Pharmacological Basis of Therapeutics — Insulin & glucagon.
- ADA — Standards of Care in Diabetes (hyperglycaemic crises & hypoglycaemia).
- Joint British Diabetes Societies — Management of DKA guidelines.
