Hyperosmolar Hyperglycaemic State


  • Hyperosmolar hyperglycaemic state (HHS) = Hyperosmotic Hyperglycaemic Syndrome (HHS)
  • three times less frequent than DKA
  • deaths often due to co-morbid conditions (MI)
  • higher mortality rate than DKA
  • part of a continuum with DKA, with insulin resistance predominant over insulin deficiency


  • triggers: infection, MI, surgery, omission of normal medications
  • decreased insulin or resistance -> decreased glucose utilisation in skeletal muscle, increased fat and muscle breakdown
    -> increased hepatic gluconeogenesis
    -> increase in glucagon, cortisol, catecholamines
    -> increased BSL
    -> glycosuria + osmotic diuresis
    -> just enough insulin to prevent lipolysis and ketone production


  • polydipsia
  • polyuria
  • weight loss
  • weakness
  • slow onset
  • progressive dehydration
  • coma
  • causes: MI, infection, diuretics, CVA, PE


  • elderly
  • type II DM
  • mental obtundation/dementia
  • physical impairment limiting access to H2O
  • renal dysfunction
  • inappropriate diuretic use
  • steroids
  • beta-blockers
  • phenytoin


  • CVS – tachycardia, decreased skin turgor, sunken eyes, dry mouth
  • RESP – tachypnoea
  • CNS – drowsy, delirium, coma, focal or generalised seizures, visual changes, hemiparesis


  • very high osmolarity (> 320mosmol/kg)
  • very high glucose
  • little or no ketonuria (beta-hydroxybutyrate)
  • hyponatraemia (or pseudohyponatraemia -> hyperglycaemia draws water out of cells) or hypernatraemia
  • hypokalaemia
  • hypomagnesaemia
  • normal anion gap
  • ABG: pH normally > 7.3 (metabolic acidosis is not severe)
  • normal level of ketones
  • renal dysfunction commonly present

Diagnostic Criteria

  • serum osmolarity > 320mosmol/L
  • serum glucose > 33mmol/L
  • profound dehydration (elevated urea:creatinine ratio)
  • no ketoacidosis

Investigations for cause

  • CXR: chest infection
  • compliance with medication
  • ECG + TNT: MI
  • FBC
  • CRP
  • blood cultures
  • urine



(1) correct dehydration (often 6-9 L of H2O loss)
(2) provide insulin
(3) replace electrolytes
(4) correct metabolic acidosis


A – may require intubation if coma and not protecting airway
B – mechanical ventilation can minimise WOB and manage possible metabolic acidosis
C – resuscitate with isotonic fluid until patient has a normal heart rate and BP (see below for H2O replacement) or can use colloids.



(1) Calculate corrected Na+

  • if hypernatraemic, the corrected Na+ = measured Na+ + glucose/3
  • monitor this as Na+ changes for glucose

(2) Calculate H2O deficit

  • H2O deficit = 0.6 x premorbid weight x (1 – 140/corrected Na+)

(3) Fluid management in first 24 hours

  • maintenance as D5W at standard rate
  • if hypernatraemic: replace half the H2O deficit over 24 hours using ½ normal saline.

(4) Monitor Na+ closely – should not change more than 10mmol in 24 hours

(5) Replace other electrolytes as required

  • K+ (often require aggressive replacement – 10-20mmol/hr, make sure not anuric)
  • Mg2+
  • PO43
  • Ca2+

(6) Fluid management in second 24 hours

  • when glucose < 15mmol/L -> use D5W @ 100-250mL/hr AND saline
  • keep Na+ between 140-150mmol/L
  • the metabolic acidosis rarely requires specific treatment as responds to volume expansion and insulin therapy.


  • insulin at 0.05 U/kg/h
  • do not allow blood glucose to drop by more than 3 mmol/L/h
  • once glucose <15mmol/L and corrected Na+ 10% dextrose
  • thromboprophylaxis (SCD’s, clexane, TEDS) -> high risk of VTE
  • diagnose cause and treat: infection, compliance, MI, CVA


  • needs management in ICU
  • endocrine/general medical referral
  • family informed

Complication Management

  • delirium -> coma
  • cerebral oedema (prevent by resuscitation with isotonic fluid and slow correction of glucose)
  • seizures (focal and generalized)
  • severe dehydration and shock
  • renal failure
  • thrombotic complications: VTE, stroke, AMI
  • intercurrent events: sepsis, MI, aspiration
  • occlusive events: focal CNS signs, chorea, DIC, leg ischaemia, rhabdomyolysis
  • fluid overload and congestive heart failure
  • metabolic derangement: hypokalaemia, hypophosphataemia, hypomagnesaemia, hypoglycaemia, hyperchloraemia with NAGMA

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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