Medicine — Endocrine Emergencies, NMC MBBS licence examination syllabus (Nepal Medical Council).
Diabetic emergencies: DKA and the hyperosmolar state
The potassium result that looks normal is the one that kills the patient.
Diabetic ketoacidosis is one of the few emergencies where a competent, well-intentioned doctor can kill a patient by doing the obviously right thing in the wrong order. The patient is hyperglycaemic and acidotic, so insulin is clearly needed. Give it before checking the potassium and you can precipitate a fatal arrhythmia in a patient who was about to recover.
That is what this chapter is really about. The diagnosis is not difficult — three numbers and you have it. The physiology is a short chain you can derive. What has to be learned properly is the sequence of treatment, and why each step comes where it does.
🩺 Where this lives: A patient arrives in DKA with a potassium of 4.2 — squarely normal. It is tempting to read that as one less thing to worry about. It is the opposite: after hours of osmotic diuresis their total body potassium is severely depleted, and it only looks normal because acidosis has shifted potassium out of cells into the blood. Start insulin and that potassium moves back inside, the serum level falls, and the patient can arrest. The normal-looking number is the warning.
How DKA develops
Everything follows from an absolute lack of insulin, which produces two problems in parallel.
Notice that dehydration and acidosis have different causes — one from the osmotic diuresis, one from ketogenesis. That is why treatment has to address both, and why fluid alone will not clear the ketones while insulin alone will not fix a patient who is five litres down.
Insulin deficiency is usually not spontaneous. Something precipitated it, and finding that is part of the treatment rather than an afterthought.
COMMON PRECIPITANTS — mnemonic: the five I's
INFECTION the commonest — chest, urine, skin
INSULIN omitted missed doses, pump failure, or
deliberate omission
INFARCTION myocardial infarction, which may be
SILENT in a diabetic patient
INITIAL presentation DKA can be the first sign of type 1
IATROGENIC steroids, and SGLT2 inhibitors
(euglycaemic DKA)
A patient in DKA with no obvious cause needs an ECG and a
septic screen, not just an insulin infusion.
Recognising it
SYMPTOMS AND SIGNS
From the hyperglycaemia and dehydration
Polyuria, polydipsia, weight loss
Dry mucous membranes, tachycardia, hypotension
Reduced skin turgor, oliguria
From the ketoacidosis
KUSSMAUL BREATHING — deep, sighing hyperventilation.
This IS the respiratory compensation for the metabolic
acidosis, visible at the bedside.
Ketotic breath — described as pear-drops or acetone
Nausea, vomiting, ABDOMINAL PAIN — which can be severe
enough to mimic a surgical abdomen
From the whole picture
Drowsiness, confusion, and in severe cases coma
💡 Exam angle: abdominal pain in DKA is a favourite because it cuts both ways. The ketoacidosis itself causes pain severe enough to look surgical — so operating on it would be a serious error. But intra-abdominal sepsis is also a common precipitant of DKA. The safe approach is to treat the DKA and reassess the abdomen as the metabolic state corrects: pain from ketoacidosis resolves with treatment, pain from an underlying surgical problem does not.
The potassium trap
This is the single most examined point in the topic, and the mechanism is worth being able to state precisely. Two forces move potassium out of cells in DKA — the acidosis itself, and the absence of insulin, which normally drives potassium inward. So the serum reading is buoyed up while the body as a whole is being emptied through the urine. Insulin reverses both forces at once.
POTASSIUM RULES IN DKA
K⁺ < 3.5 REPLACE POTASSIUM FIRST.
Do not start insulin yet — it will drive
potassium lower and can cause arrhythmia.
K⁺ 3.5–5.5 Start insulin, and add potassium to the
replacement fluid once the patient is
passing urine.
K⁺ > 5.5 Start insulin without added potassium, and
recheck frequently — it will fall.
Monitor potassium HOURLY at first. It moves fast.
Managing it
💡 Exam angle: two ordering points are asked repeatedly. Fluid comes before insulin — the patient's circulation is the immediate threat, and rehydration alone lowers glucose substantially. And when the glucose falls you add dextrose rather than stopping the insulin, because the insulin is there to clear ketones, not merely to lower glucose. Stopping it early leaves the acidosis untreated and the patient relapses. The endpoint of treatment is ketone clearance and resolution of the acidosis, not a normal glucose.
COMPLICATIONS TO ANTICIPATE
HYPOKALAEMIA the commonest serious complication;
prevented by the rules above
HYPOGLYCAEMIA from insulin continued without added
dextrose
CEREBRAL OEDEMA rare but often fatal; the major risk
is in CHILDREN and young people, and
it is associated with rapid osmolar
shifts. Correct fluid deficits
cautiously in this group. Suspect it
if consciousness deteriorates during
apparently successful treatment.
ASPIRATION in a vomiting, drowsy patient —
consider a nasogastric tube
THROMBOSIS dehydration plus immobility; more
pronounced in HHS
The hyperosmolar hyperglycaemic state
HHS is the type 2 counterpart, and the difference comes entirely from residual insulin. A type 2 patient retains enough insulin to suppress lipolysis — so no significant ketones and no acidosis — but nowhere near enough to control glucose. The result is a slower, more profound dehydration.
The dangerous asymmetry is that HHS carries a higher mortality than DKA, despite lacking the acidosis that makes DKA look dramatic. It develops over days rather than hours, so the fluid deficit is far larger by the time the patient presents, and the patients are typically older with more comorbidity. Treating HHS as "DKA without the acid" is a mistake — the fluid and osmolality must be corrected more slowly, not less carefully.
Clinical reasoning: four presentations
🔍 Case 1 — the sequence question
PresentationA 22-year-old with type 1 diabetes: vomiting, drowsy, Kussmaul breathing. Glucose 29, ketones 5.4, pH 7.06, K⁺ 3.1.
Key clueThe potassium is 3.1 — already low before treatment has begun.
ReasoningInsulin will drive potassium further into cells. Starting it now risks a fatal arrhythmia in a patient whose whole-body potassium is profoundly depleted.
AnswerFluid resuscitation and potassium replacement first; withhold insulin until the potassium is above 3.5. Then start the fixed-rate infusion. The order is the entire answer.
🔍 Case 2 — the premature stop
PresentationFour hours into DKA treatment the glucose has fallen from 32 to 12 mmol/L. Ketones remain 3.8, pH 7.19. A colleague proposes stopping the insulin infusion.
TrapTreating glucose as the endpoint.
ReasoningThe insulin is there to switch off ketogenesis. Ketones are still high and the patient is still acidotic — stopping now allows the ketoacidosis to continue and the patient to relapse.
AnswerContinue the insulin and add intravenous dextrose to support the glucose while it runs. The endpoint is ketone clearance and resolution of the acidosis.
🔍 Case 3 — which emergency?
PresentationAn 80-year-old with type 2 diabetes, unwell for five days, now confused. Glucose 41, ketones 0.6, pH 7.36, osmolality 348, sodium 152.
Key cluesVery high glucose, minimal ketones, no acidosis, markedly raised osmolality, and a several-day history.
ReasoningResidual insulin has suppressed ketogenesis, so this is the hyperosmolar state rather than DKA. The slow onset means a very large fluid deficit.
AnswerHHS. Careful, gradual fluid replacement with close monitoring of osmolality and sodium; insulin at a lower rate or after fluid alone; thromboprophylaxis; treat the precipitant. Correct slowly — this is where HHS differs most from DKA.
🔍 Case 4 — deterioration during recovery
PresentationA 12-year-old in DKA is improving: glucose falling, acidosis correcting. Six hours in, she develops headache and becomes progressively drowsy.
Key clueNeurological deterioration while the biochemistry improves — the opposite of what the numbers predict.
ReasoningCerebral oedema is a rare but often fatal complication, predominantly in children and young people, associated with rapid osmolar shifts during treatment.
AnswerSuspect cerebral oedema. Urgent senior and critical care involvement. This is why fluid correction in children is deliberately more cautious — and why a patient getting sleepier as their gas improves must never be dismissed.
Commonly confused
Confusion
The distinction
Why it matters
Normal K⁺ vs normal potassium stores
Serum K⁺ is buoyed by acidosis and insulin lack
A "normal" K⁺ in DKA hides a large deficit that insulin will unmask.
Insulin first vs fluid first
Fluid comes first; insulin waits on the potassium
Getting this backwards can cause a fatal arrhythmia.
Glucose endpoint vs ketone endpoint
Treatment ends when ketones clear and acidosis resolves
Stopping insulin at a normal glucose leaves the DKA untreated.
DKA vs HHS
Ketones and acidosis present versus absent
HHS needs slower correction and carries higher mortality.
DKA abdominal pain vs surgical abdomen
Ketoacidotic pain resolves as the DKA is treated
Prevents both unnecessary surgery and missed sepsis.
Normal glucose vs no DKA
SGLT2 inhibitors permit euglycaemic DKA
Check ketones regardless of the glucose.
Rapid revision
MUST-KNOW FACTS
1. DKA triad: glucose > 11 (or known DM), ketones ≥ 3, pH < 7.3 or HCO₃⁻ < 15.
2. Cause: insulin deficiency → hyperglycaemia + unopposed lipolysis.
3. Dehydration comes from the osmotic diuresis; acidosis from ketones.
4. Kussmaul breathing IS the respiratory compensation.
5. Abdominal pain is common — and can mimic a surgical abdomen.
6. Precipitants: infection, insulin omission, infarction, initial
presentation, iatrogenic (steroids, SGLT2 inhibitors).
7. Total body potassium is ALWAYS depleted in DKA.
8. Serum K⁺ looks normal or high because acidosis shifts it out of cells.
9. Insulin drives K⁺ back INTO cells → serum potassium falls fast.
10. If K⁺ < 3.5, replace potassium BEFORE starting insulin.
11. Fluid first. Then potassium. Then insulin.
12. Fixed-rate insulin infusion; no bolus in standard adult protocols.
13. Add dextrose when glucose falls below ~14 — do NOT stop the insulin.
14. Endpoint is ketone clearance and resolution of acidosis, not glucose.
15. Monitor potassium hourly at first.
16. Cerebral oedema: rare, often fatal, mainly children — suspect if
consciousness falls while the biochemistry improves.
17. HHS: type 2, older, days of onset, glucose often > 30.
18. HHS has minimal ketones and no significant acidosis.
19. HHS osmolality is markedly raised (> 320).
20. HHS mortality is HIGHER than DKA.
21. Correct HHS fluid and osmolality SLOWLY; give thromboprophylaxis.
22. Always find and treat the precipitant — ECG and septic screen.
💡 Exam angle: almost every DKA question is really a sequencing question. Fluid before insulin; potassium before insulin if it is low; dextrose added rather than insulin stopped; ketones rather than glucose as the endpoint. If you can state that order and the reason for each step, you can answer most of what is asked — including the ones dressed up as something else.
Syllabus points
Pathophysiology: the two arms of insulin deficiency
The three diagnostic criteria
Precipitants and why finding them matters
Clinical features including Kussmaul breathing
Abdominal pain: ketoacidosis or surgical abdomen
The potassium trap and the rules that follow from it
Management sequence: fluid, potassium, insulin
Why dextrose is added rather than insulin stopped
Complications including cerebral oedema
The hyperosmolar hyperglycaemic state and how it differs
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