Code Ready
Log inSign up free

Level 2 of 6Must-remember

Diabetic ketoacidosis

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Diagnose on three bedside tests in ten minutes: capillary glucose, blood ketones and a venous blood gas — a venous sample suffices to diagnose and to manage DKA, arterial puncture is unnecessary, and the venous gas also returns a potassium within two minutes.Not available at your setup — Arterial blood gas.
  • The cardinal triad, all three limbs of which must be present: hyperglycaemia with blood glucose above 11.1 mmol/L (200 mg/dL) or a known diagnosis of diabetes whatever the glucose; hyperketonaemia with capillary or serum beta-hydroxybutyrate of 3.0 mmol/L or more, or more than 2+ ketonuria on dipstick if no ketone meter is available; and metabolic acidosis with venous bicarbonate below 15 mmol/L and/or venous pH below 7.3 (H+ above 50 nmol/L). Two limbs out of three is not DKA.Not available at your setup — Arterial blood gas. If no ketone meter is available, use more than 2+ ketonuria on urine dipstick.
  • Euglycaemic DKA is the trap: the full acidotic ketotic picture with a glucose below 11 mmol/L — fewer than 5% of cases overall but 70% of SGLT2-inhibitor-associated cases (Davidson's), around 10% overall (CMDT), and classically in type 1 diabetes in pregnancy; a person with diabetes who is ketotic and acidotic has DKA regardless of the glucose.
  • Do not exclude DKA because the patient has type 2 diabetes: 10–15% of episodes occur in type 2 diabetes, and 25–50% of children with new type 1 diabetes present in DKA.
  • Symptoms to ask for: polyuria including nocturia, thirst and polydipsia, weight loss, weakness and prostration, blurred vision, leg cramps, nausea and vomiting, and abdominal pain — evolving over several hours to a couple of days, considerably faster than the days-to-weeks course of the hyperosmolar hyperglycaemic state.
  • Signs of volume depletion: sunken eyes, dry mucous membranes, dry axillae, reduced skin turgor (best tested at the subclavicular area), reduced jugular venous pressure, tachycardia, hypotension postural or supine, and cold cyanosed peripheries.
  • Look for Kussmaul respiration and the acetone breath: deep sighing breathing and a sweet pear-drop odour make the diagnosis at the bedside for those able to detect it.
  • Assess conscious level: delirium, drowsiness or coma is present in around 10% of patients, with up to 5% presenting comatose.
  • Two counter-intuitive observations: disappearing hyperventilation is a bad sign — Kussmaul breathing becomes less marked in very severe acidosis owing to respiratory depression, so a patient whose deep breathing settles while the bicarbonate is still 5 mmol/L is decompensating, not improving; and temperature is unreliable, since fever is unusual even when infection is present and mild or even severe hypothermia may occur, easily overlooked unless a rectal temperature is taken with a low-reading thermometer.
  • Any one of these markers indicates severe DKA: blood ketones above 6 mmol/L; bicarbonate below 5 mmol/L; venous or arterial pH below 7.0 (H+ above 100 nmol/L); potassium on admission below 3.5 mmol/L; Glasgow Coma Scale below 12 or an abnormal AVPU score; oxygen saturation below 92% on air; systolic blood pressure below 90 mmHg; heart rate above 100 or below 60 beats/min; anion gap above 16 mmol/L; and persistent hypotension or oliguria below 0.5 mL/kg/hr.Not available at your setup — Arterial blood gas.
  • A simpler parallel grading uses pH alone: mild 7.26–7.30, moderate 7.0–7.25, severe below 7.0; CMDT characterises mild DKA as an alert patient with pH 7.25–7.30 or bicarbonate 15–18 mmol/L and beta-hydroxybutyrate 3–6 mmol/L.Not available at your setup — Arterial blood gas.
  • Potassium is the number that kills and it misleads twice: it may be normal or frankly high on arrival despite a whole-body deficit of 3–5 mmol/kg, then falls precipitously once fluid and insulin begin — read it before starting insulin and treat any value below 3.5 or above 6.5 mmol/L as an immediate arrhythmic emergency.Not available at your setup — Arterial blood gas, Serum electrolytes.
  • Search deliberately for the precipitant, because that is what kills the patient: infection (pneumonia and urinary tract infection above all), acute myocardial infarction which may be silent in diabetes, cerebrovascular disease, pancreatitis, surgery, trauma and pregnancy; intercurrent illness accounts for 30–40% of cases, interruption of insulin therapy 15–30%, and previously undiagnosed diabetes 10–20%.
  • Ask specifically about insulin omission: the commonest error is behavioural — the patient reduces or omits insulin because nausea or vomiting has made them unable to eat, a factor in at least 25% of all DKA admissions.
  • Ask about drugs: glucocorticoids, SGLT2 inhibitors, atypical antipsychotics (olanzapine and clozapine in particular), immune checkpoint inhibitors and recreational drugs.
  • Red flags that outrank any number: a falling conscious level while the biochemistry is improving is cerebral oedema until proven otherwise (particularly in a child or young adult, typically 4 to 12 hours into treatment); loss of Kussmaul breathing at an unchanged pH signals impending respiratory failure; falling oxygen saturation during treatment suggests pulmonary oedema or ARDS; hypotension persisting after 1000 mL of fluid is no longer simple hypovolaemia; and ketones failing to fall means the insulin is not reaching the patient or the precipitant is untreated.

Management— do this, in order

  • The order is fluid first, potassium second, insulin third, precipitant fourth — restore the circulating volume; replace potassium before insulin drives it into cells; run a fixed-rate insulin infusion until the ketones, not the glucose, have cleared; and identify and treat the precipitating illness — while measuring, charting and acting on the numbers hourly.
  • Airway and breathing take precedence where the conscious level is reduced, with oxygen to maintain saturations at or above 94%; sedation and unhurried intubation are hazardous in severe acidosis because the patient is hyperventilating to survive and even a short apnoeic period can produce a catastrophic fall in pH.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Fluid if systolic blood pressure is at least 90 mmHg: 0.9% sodium chloride 1 litre intravenously over 1 hour, with no potassium in this first litre.
  • Fluid if systolic blood pressure is below 90 mmHg: 0.9% sodium chloride 500 mL intravenously over 10–15 minutes, reassess, and repeat once if still below 90 mmHg; failure to respond to 1000 mL indicates a coexisting shock state.
  • Continuing replacement: 1 L over 2 hours, then 1 L over 2 hours, then 1 L over 4 hours, then 1 L over 4 hours, then 1 L over 6 hours, each with potassium chloride as below; Davidson's gives a slightly slower sequence of 1 L over 1 hour, then 1 L over 2 hours, then 1 L over 4 hours.
  • Be more cautious with fluid in young adults under about 25 years, in pregnancy, in older adults, and in anyone with a history of kidney or heart failure, because over-rapid replacement is implicated in cerebral oedema in the young and pulmonary oedema in the elderly; aim for a urine output of at least 0.5 mL/kg/hr and replace the residual deficit gradually over the following two days.
  • Potassium above 5.5 mmol/L: add no potassium, continue saline, continuous cardiac monitoring, recheck in 1 hour.Not available at your setup — Serum electrolytes.
  • Potassium 3.5–5.5 mmol/L: potassium chloride 40 mmol/L in each litre of 0.9% sodium chloride from the second litre onwards, using premixed bags, aiming to hold the potassium at 4.0–5.0 mmol/L.Not available at your setup — Serum electrolytes.
  • Potassium below 3.5 mmol/L: this is severe DKA — continuous cardiac monitoring and more than 40 mmol/L through a reliable line in a closely monitored setting, and insulin should be withheld or delayed until potassium replacement is running, because insulin will drive the level lower and can cause a fatal arrhythmia.Not available at your setup — Serum electrolytes, Infusion pump.
  • Insulin, first line: soluble human insulin as a fixed-rate intravenous infusion at 0.1 unit/kg body weight per hour — typically 6–10 units/hour in an adult — with no intravenous bolus; a rapid-acting analogue (aspart or lispro) may be substituted in the same units by the same route, and the rate may be reduced to 0.02–0.1 unit/kg/hour as acidosis and insulin resistance resolve.Doctor / NurseNot available at your setup — Infusion pump.
  • Continue the patient's usual long-acting subcutaneous basal insulin (glargine, detemir, degludec or isophane) at the usual dose and time throughout — the step most often omitted — and if newly diagnosed give a long-acting analogue in a dose equivalent to a usual regimen; do not stop the insulin because the glucose has normalised, because the insulin is treating the ketosis.Doctor / Nurse
  • Where no infusion pump is available, do not delay insulin: soluble human insulin 0.1 unit/kg intramuscularly hourly is accepted, though absorption is unreliable in a vasoconstricted patient, so restore volume first.Doctor / NurseNot available at your setup — Infusion pump. Give soluble human insulin 0.1 unit/kg intramuscularly hourly instead.
  • Subcutaneous rapid-acting analogue regimens are established in mild to moderate, uncomplicated DKA only — alert, pH at least 7.0, no severity marker, not shocked: aspart or lispro 0.1 unit/kg subcutaneously, then 0.1 unit/kg hourly, or 0.2 unit/kg two-hourly, with the same hourly monitoring; this route is not acceptable in severe DKA or shock.Doctor / Nurse
  • When the blood glucose falls below 14 mmol/L (250 mg/dL), start 10% glucose at 125 mL/hour intravenously alongside and in addition to the saline, continuing until the patient is eating and drinking normally; in euglycaemic DKA the glucose infusion starts at the same time as the insulin.
  • Treatment targets in descending order of usefulness: blood ketones falling by at least 0.5 mmol/L per hour (the primary target); venous bicarbonate rising by at least 3.0 mmol/L per hour (the substitute where ketone measurement is unavailable); capillary glucose falling by at least 3.0 mmol/L per hour (the least specific); and potassium held between 4.0 and 5.5 mmol/L.Not available at your setup — Arterial blood gas. If ketone measurement unavailable, track venous bicarbonate instead.
  • If the ketones are not falling, check the plumbing before the pharmacology: is the pump on, is the line connected unkinked and patent, has the cannula tissued, does the syringe contain insulin at the concentration assumed (U-100 and U-40 must never be confused) — then increase the fixed-rate infusion by 1.0 unit/hour increments hourly until ketones fall at target, then reconsider the precipitant and the diagnosis.Not available at your setup — Infusion pump.
  • Supportive care: a nasogastric tube if the patient is obtunded or persistently vomiting; a urinary catheter if no urine has been passed within 2–4 hours or if the patient is incontinent or anuric; thromboprophylaxis with low-molecular-weight heparin in older or high-risk individuals unless contraindicated; broad-spectrum antibiotics once cultures are taken if infection is suspected; and examine the chest, abdomen, skin and — taking the socks off — the feet for new ulceration or ischaemia.Not available at your setup — Blood culture.

Caution— what harms

  • Never start insulin before you know the potassium. The venous gas potassium must be known before the insulin infusion begins, and insulin must be withheld or delayed if the potassium is below 3.5 mmol/L until replacement is running.
  • Never give an intravenous insulin bolus. The fixed dose of 0.1 unit/kg/hour is sufficient to suppress ketogenesis, lower the glucose and correct the electrolyte disturbance; boluses add nothing and increase the risk of hypoglycaemia and rapid osmolar shift. Never bolus a child at all.
  • Never stop the insulin because the glucose has normalised — the insulin is treating the ketosis, and 10% glucose at 125 mL/hour is what allows it to keep running once the glucose falls below 14 mmol/L.
  • Never omit the usual long-acting basal subcutaneous insulin — stopping it causes rebound hyperglycaemia and recurrent ketoacidosis when the infusion stops.
  • Do not add potassium to the first litre, and do not add it in an oliguric patient until urine is flowing and the level is known — pre-renal acute kidney injury is common in DKA.
  • Never use urine ketone dipsticks to track response: nitroprusside strips detect acetoacetate and acetone and not 3-hydroxybutyrate, the dominant ketone in severe DKA, so they underestimate severity on admission and, as 3-hydroxybutyrate converts to acetoacetate during recovery, urinary ketones may rise while the patient improves.
  • Do not treat leucocytosis as proof of infection — polymorphonucleocytosis occurs as a stress response with no infection present — and do not treat a raised amylase or lipase as pancreatitis, since it is non-specifically raised in 16–25% of DKA.
  • Do not give intravenous bicarbonate: it is not generally recommended because there is no evidence of benefit, it can produce a paradoxical fall in cerebrospinal fluid pH implicated in cerebral oedema, and it drives potassium into cells; the threshold for even considering it is pH below 6.9 (Davidson's) or below 7.0 (Kumar & Clark), it should be an isotonic 1.26% solution if given at all, and it must never be given to a child.
  • A falling conscious level while the biochemistry improves is cerebral oedema until proven otherwise — treat it before imaging it, and never let a scan delay treatment.
  • Do not bolus a child who is not shocked, and never use a deficit estimate above 10% of body weight; over-rapid fluid, over-rapid correction of osmolality and bicarbonate are all implicated in cerebral oedema.
  • Do not sedate or intubate unhurriedly in severe acidosis: the patient is hyperventilating to survive and even a short apnoeic period can produce a catastrophic fall in pH.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Do not mistake hyperchloraemic acidosis for persisting DKA: if the ketones have cleared and the anion gap has normalised but the bicarbonate remains low, this is the predictable consequence of replacing lost organic anions with chloride from saline, it corrects spontaneously within days, and it must not be treated with more insulin or with bicarbonate.
  • Do not add potassium chloride to Hartmann's solution — it cannot be done, so if Hartmann's is used a separate arrangement for potassium is required.
  • Do not convert to subcutaneous insulin at the wrong moment: convert only when the patient is biochemically stable and able to eat and drink normally, give the short-acting or premixed subcutaneous insulin with a meal, and continue the intravenous infusion for a further 30 minutes afterwards — stopping at the moment of injection leaves an insulin gap and the patient re-ketoses.

Refer / escalate

Escalate to critical care or transfer for severe DKA (ketones above 6 mmol/L, bicarbonate below 5 mmol/L, pH below 7.0, potassium below 3.5 mmol/L, GCS below 12, SpO2 below 92% on air, systolic below 90 mmHg, heart rate above 100 or below 60/min, anion gap above 16 mmol/L, oliguria below 0.5 mL/kg/hr), for any child or young adult with suspected cerebral oedema, for hypotension persisting after 1000 mL of fluid, and for pregnancy — while continuing fluid, potassium and the fixed-rate insulin infusion throughout the journey.

PreviousNext

Read the full lesson free

Create a free account to unlock every page, the level exams, and progress tracking.

Sign up freeLog in