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ICU Topicsendocrine

ICU · endocrine

Acute Severe DKA and HHS — Comprehensive Integrated Diabetic Emergencies

Also known as Diabetic ketoacidosis (DKA) · Hyperosmolar hyperglycaemic state (HHS) · Hyperglycaemic emergencies · Diabetic coma · Diabetic ketoacidosis · Fixed-rate intravenous insulin infusion (FRIII) · Beta-hydroxybutyrate · Cerebral oedema in DKA · Hyperosmolar non-ketotic coma (HONK) · Euglycaemic DKA (SGLT2 inhibitor)

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are the two life-threatening hyperglycaemic emergencies of diabetes, lying on a spectrum of insulin deficiency. DKA = absolute insulin deficiency → hyperglycaemia (over 250 mg/dL (about fourteen mmol/L)), metabolic acidosis (arterial pH under 7.30, bicarbonate under 18 mEq/L), and ketosis (serum ketones positive, anion gap over 10); occurs mainly in type 1 diabetes. HHS = relative insulin deficiency with enough residual insulin to suppress ketogenesis but not hyperglycaemia → extreme hyperglycaemia (over 33.3 mmol/L by ADA, over 30 by JBDS), hyperosmolality (320 mOsm/kg or more), profound dehydration (100-220 mL/kg), and NO significant ketoacidosis (pH over 7.3, bicarbonate 15 or more, ketonaemia 3.0 mmol/L or less); occurs mainly in elderly type 2 diabetics. Precipitants are shared — infection is the single commonest. Management is fluids first (0.9% saline 15-20 mL/kg/h), potassium addressed before insulin (delay insulin if K+ under 3.3 mmol/L), fixed-rate insulin 0.1 units/kg/h (JBDS de-escalates to 0.05 once glucose is under 14 mmol/L; HHS 0.05 units/kg/h per JBDS, 0.1 per ADA), bicarbonate only if pH under 6.9, and treatment of the precipitant.

high21 referencesUpdated 26 July 202620 min readSource-verified · Oct 2026

Checked against its sources on 13 Oct 2026

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Red flags

  • ALWAYS check serum potassium BEFORE giving insulin. If K+ <3.3 mEq/L, delay insulin and begin potassium replacement with the fluids (20-30 mEq per litre of fluid; treatment goal 4-5 mEq/L) — insulin drives K+ intracellularly and risks life-threatening arrhythmia. This is the single most examined DKA principle.
  • Use a weight-based fixed-rate intravenous insulin infusion (FRIII) at 0.1 units/kg/h. Guidelines that use a loading bolus give 0.1 units/kg IV followed by the same infusion rate — or 0.14 units/kg/h with no bolus. The infusion continues until ketonaemia resolves, not until glucose normalises.
  • When glucose falls below 14 mmol/L, do NOT stop insulin — ADD a 5% or 10% glucose infusion and consider de-escalating the FRIII from 0.1 to 0.05 units/kg/h (JBDS). Insulin must continue to suppress ketogenesis; stopping it leaves the ketoacidosis untreated.
  • Bicarbonate ONLY if arterial pH <6.9 (100 mmol NaHCO3 in 400 mL sterile water with 20 mEq KCl at 200 mL/h for 2 h until pH >7.0), or peri-intubation when pH <7.2 and/or bicarbonate <10 mEq/L. Randomised data from pH 6.9-7.1 show no benefit; reported harms include hypokalaemia, reduced tissue oxygen uptake, paradoxical CNS acidosis and cerebral oedema (RR 4.2 in children).
  • Cerebral oedema is the leading cause of DKA death in children (mortality 20-40%; it accounts for 57-87% of DKA deaths in children; 1-5% of episodes). Signs: headache, deteriorating consciousness, seizures, sphincter incontinence, pupillary changes, bradycardia, rising blood pressure, respiratory arrest. Treat with mannitol infusion and mechanical ventilation (3% hypertonic saline is an accepted alternative). Correct slowly — no more than 3 mOsm/kg/h in children.
  • HHS mortality (10-20%, about ten times DKA's under 1%) is driven by age, comorbidity and dehydration. FLUIDS are the primary treatment: JBDS estimates losses of 100-220 mL/kg and starts insulin (0.05 units/kg/h) only once osmolality stops falling with fluid replacement alone — unless there is significant ketonaemia.
  • Do not lower osmolality too fast in HHS — JBDS aims for a decline of 3.0-8.0 mOsm/kg/h (ADA/Diabetes Canada under 3). Named harms to prevent include osmotic demyelination, fluid overload and VTE.
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Target exams

CICMFFICMEDIC

Red flags

  • ALWAYS check serum potassium BEFORE giving insulin. If K+ <3.3 mEq/L, delay insulin and begin potassium replacement with the fluids (20-30 mEq per litre of fluid; treatment goal 4-5 mEq/L) — insulin drives K+ intracellularly and risks life-threatening arrhythmia. This is the single most examined DKA principle.
  • Use a weight-based fixed-rate intravenous insulin infusion (FRIII) at 0.1 units/kg/h. Guidelines that use a loading bolus give 0.1 units/kg IV followed by the same infusion rate — or 0.14 units/kg/h with no bolus. The infusion continues until ketonaemia resolves, not until glucose normalises.
  • When glucose falls below 14 mmol/L, do NOT stop insulin — ADD a 5% or 10% glucose infusion and consider de-escalating the FRIII from 0.1 to 0.05 units/kg/h (JBDS). Insulin must continue to suppress ketogenesis; stopping it leaves the ketoacidosis untreated.
  • Bicarbonate ONLY if arterial pH <6.9 (100 mmol NaHCO3 in 400 mL sterile water with 20 mEq KCl at 200 mL/h for 2 h until pH >7.0), or peri-intubation when pH <7.2 and/or bicarbonate <10 mEq/L. Randomised data from pH 6.9-7.1 show no benefit; reported harms include hypokalaemia, reduced tissue oxygen uptake, paradoxical CNS acidosis and cerebral oedema (RR 4.2 in children).
  • Cerebral oedema is the leading cause of DKA death in children (mortality 20-40%; it accounts for 57-87% of DKA deaths in children; 1-5% of episodes). Signs: headache, deteriorating consciousness, seizures, sphincter incontinence, pupillary changes, bradycardia, rising blood pressure, respiratory arrest. Treat with mannitol infusion and mechanical ventilation (3% hypertonic saline is an accepted alternative). Correct slowly — no more than 3 mOsm/kg/h in children.
  • HHS mortality (10-20%, about ten times DKA's under 1%) is driven by age, comorbidity and dehydration. FLUIDS are the primary treatment: JBDS estimates losses of 100-220 mL/kg and starts insulin (0.05 units/kg/h) only once osmolality stops falling with fluid replacement alone — unless there is significant ketonaemia.
  • Do not lower osmolality too fast in HHS — JBDS aims for a decline of 3.0-8.0 mOsm/kg/h (ADA/Diabetes Canada under 3). Named harms to prevent include osmotic demyelination, fluid overload and VTE.
The one-paragraph exam answer

DKA and HHS are the two life-threatening hyperglycaemic emergencies — two ends of one spectrum of insulin deficiency. DKA is the absolute-deficiency end: glucose over 250 mg/dL (about fourteen mmol/L), arterial pH under 7.30, bicarbonate under 18 mEq/L in mild DKA and under 10 when severe, ketones positive, anion gap over 10. HHS is the relative-deficiency end: glucose over 33.3 mmol/L (ADA) or over 30 (JBDS), osmolality 320 mOsm/kg or more, fluid losses of 100-220 mL/kg, pH over 7.3 with ketonaemia 3.0 mmol/L or less. The pillars are identical for both — fluids first, potassium addressed before insulin, fixed-rate insulin, treat the precipitant — and the order never changes.[1][2][3][4][5]

Meet the patient

A young man is wheeled in drowsy, breathing deep and fast, breath thick with pear-drops. Glucose very high, venous pH under 7.0, bicarbonate single digits, beta-hydroxybutyrate high, potassium under 3.3. New type 1 diabetes — eight kilograms gone in a fortnight. On the next trolley an elderly woman, found unresponsive at home: glucose markedly raised, osmolality above 320, pH normal, only trace ketones, right lower lobe pneumonia on the film.[1][5]

Two patients, one disease spectrum — the admission biochemistry of the first (glucose about 40 mmol/L, bicarbonate about 7, pH about 7.1) is exactly the order seen in published DKA cohorts. The registrar question on the round is always the same: "What is your first move, and in what order?" This topic is the ordered answer — and the single rule that fails more candidates than any other is buried inside it.[1][2][11]

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References21ShowHide
  1. [1]Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes Diabetes Care, 2009.PMID 19564476
  2. [2]Dhatariya KK The management of diabetic ketoacidosis in adults-An updated guideline from the Joint British Diabetes Society for Inpatient Care Diabet Med, 2022.PMID 35224769
  3. [3]Mustafa OG, Haq M, Dashora U, et al. Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults: An updated guideline from the Joint British Diabetes Societies (JBDS) for Inpatient Care Group Diabet Med, 2023.PMID 36370077
  4. [4]Lin R, Wootton E, Gaca M, Venkatesh B, Bellomo R, Ekinci E. Hyperosmolar hyperglycaemic state: A systematic review of management guidelines and their evidence Diabet Med, 2026.PMID 41587208
  5. [5]Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment Diabetes Care, 2014.PMID 25342831
  6. [6]Long B, Lentz S, Koyfman A, Gottlieb M. Euglycemic diabetic ketoacidosis: Etiologies, evaluation, and management Am J Emerg Med, 2021.PMID 33626481
  7. [7]Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics N Engl J Med, 2001.PMID 11172153
  8. [8]Decourcey DD, Steil GM, Wypij D, et al. Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year retrospective analysis of mortality Pediatr Crit Care Med, 2013.PMID 23863818
  9. [9]Glaser N Cerebral edema in children with diabetic ketoacidosis Curr Diabetes Rep, 2001.PMID 12762956
  10. [10]Curtis JR, Bohn D, Daneman D. Use of hypertonic saline in the treatment of cerebral edema in diabetic ketoacidosis (DKA) Pediatr Diabetes, 2001.PMID 15016186
  11. [11]Umpierrez GE, Cuervo R, Karabell A, et al. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart Diabetes Care, 2004.PMID 15277410
  12. [12]El Feky AY, Abdou MS, Naguib R, et al. Effectiveness and Safety of Early Insulin Glargine U100 and Glargine U300 Administration in the Management of Diabetic Ketoacidosis in Adults With Type 1 Diabetes Mellitus: A Randomized Clinical Trial Endocr Pract, 2025.PMID 40840711
  13. [13]Karslioglu French E, Donihi AC, Korytkowski MT. Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients BMJ, 2019.PMID 31142480
  14. [14]Dunn BK, Coore H, Bongu N, et al. Treatment Challenges and Controversies in the Management of Critically Ill Diabetic Ketoacidosis (DKA) Patients in Intensive Care Units Cureus, 2024.PMID 39360087
  15. [15]Basnet S, Musaitif R, Khanal A, et al. Effect of Potassium Infusions on Serum Levels in Children during Treatment of Diabetic Ketoacidosis J Pediatr Intensive Care, 2020.PMID 32351765
  16. [16]Miyazaki R, Okano H, Goto S, Tanaka H, Okamoto H. Severity and Clinical Outcomes Among ICU Patients With Diabetic Ketoacidosis: An Analysis of the Japanese Intensive Care Patient Database Crit Care Explor, 2026.PMID 42545873
  17. [17]Umpierrez G, Korytkowski M. Diabetic emergencies - ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia Nat Rev Endocrinol, 2016.PMID 26893262
  18. [18]Dhatariya K, Mustafa O, Stathi D Hyperglycemic Crises Endotext, 2000.PMID 25905280
  19. [19]Stoner GD. Hyperosmolar Hyperglycemic State Am Fam Physician, 2017.PMID 29431405
  20. [20]Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia The American Journal of Medicine, 1999.PMID 10225241
  21. [21]Dhatariya KK, Glaser NS, Codner E, Umpierrez GE. Diabetic ketoacidosis Nat Rev Dis Primers, 2020.PMID 32409703
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