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Level 2 of 6Must-remember

Hyperosmolar hyperglycaemic state

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Recognise the constellation, not one threshold: hypovolaemia with volume depletion of 10–20% of body weight, severe hyperglycaemia with glucose above 30 mmol/L (above 540 mg/dL), and hyperosmolality with serum osmolality above 320 mOsmol/kg — occurring without significant ketonaemia (blood ketones below 3.0 mmol/L) and without significant acidosis (pH above 7.3, H+ below 50 nmol/L, bicarbonate above 15 mmol/L).Not available at your setup — Serum electrolytes.
  • Secure the diagnosis at the bedside in minutes with three tests and one calculation: glucose, blood ketones and a venous blood gas, plus a calculated osmolality — venous is sufficient, arterial puncture adds nothing, and the gas delivers sodium, potassium, chloride, lactate and glucose within minutes.Not available at your setup — Arterial blood gas.
  • Calculate the osmolarity and state which formula you used: Davidson's (2 x sodium) + glucose + urea, all in mmol/L, is tied to the above-320 diagnostic threshold and the above-340 and above-360 decision points; Kumar & Clark use 2(sodium + potassium) + glucose + urea which reads roughly 8–10 mOsmol/kg higher; effective osmolality is (2 x sodium) + glucose. Normal osmolality is 285–300 mOsmol/kg.Not available at your setup — Serum electrolytes.
  • History of gradual decline over a fortnight, not acute collapse: polyuria, nocturia, thirst and polydipsia, weight loss, weakness, blurred vision, leg cramps, and increasing drowsiness or confusion, sometimes preceded by recurrent genital candidiasis or urinary infection.
  • Signs are dominated by the depth of volume depletion: sunken eyes, dry mucous membranes and dry axillae, reduced skin turgor (best assessed at the subclavicular area rather than the dorsum of an elderly hand), low jugular venous pressure, tachycardia, hypotension initially postural and later supine, cold peripheries with delayed capillary refill, and oliguria.
  • In contrast to DKA there is no Kussmaul breathing and no ketotic fetor, because there is no significant acidosis; and abdominal pain is uncommon in HHS, so its presence should prompt a search for a surgical cause or a mixed HHS/DKA picture.
  • Impaired consciousness tracks the osmolality: drowsiness, delirium, stupor and coma are usual once osmolality exceeds 340 mOsmol/kg, and a drowsy patient whose calculated osmolality is only 310 has a second diagnosis.Not available at your setup — Serum electrolytes.
  • HHS may produce focal signs — hemiparesis, visual field defects, aphasia — and seizures, all of which may resolve as the osmolality is corrected, but because the hyperosmolar state genuinely predisposes to stroke as well as mimicking it, focal deficits must not be attributed to metabolic derangement without imaging.
  • Poor prognostic signs to record on arrival: hypothermia (measure rectally if peripherally shut down), systolic blood pressure below 90 mmHg, tachycardia or bradycardia, sodium above 160 mmol/L, osmolality above 360 mOsmol/kg, and multiple comorbidities.Not available at your setup — Serum electrolytes.
  • Add as practical markers of severity: osmolality above 340 mOsmol/kg, Glasgow Coma Scale below 12, oliguria below 0.5 mL/kg/hr, hypokalaemia below 3.5 mmol/L, a coexisting acute vascular event, and ketonaemia or bicarbonate below 15 mmol/L.Not available at your setup — Serum electrolytes.
  • Record the ketone number, not the word negative: below 3.0 mmol/L supports HHS, above 1.0 mmol/L changes the insulin decision, and 3.0 mmol/L or more with bicarbonate below 15 or pH below 7.3 means a mixed HHS/DKA picture — which occurs in up to one-third of hyperglycaemic crises.Not available at your setup — Arterial blood gas.
  • Interpret the sodium correctly: hypernatraemia is common because water is lost in excess of sodium and potassium; a high sodium is the disease, not an artefact, while hyperglycaemia is simultaneously lowering the measured value — corrected sodium = measured sodium + 1.6 mmol/L for every 5.55 mmol/L (100 mg/dL) of glucose above normal.Not available at your setup — Serum electrolytes.
  • Whatever the potassium reads, total body stores are markedly depleted and the value will fall with treatment; check magnesium and phosphate too, since both are often low and fall further.Not available at your setup — Serum electrolytes.
  • Hunt the precipitant, because it usually determines survival: infection (pneumonia and urinary tract infection are the single most frequent), acute myocardial infarction and cerebrovascular events (both may be silent and will not be volunteered by a confused patient), pancreatitis, trauma, gastrointestinal haemorrhage, the postoperative period, glucose-rich drinks or intravenous fluids, glucocorticoids, thiazide diuretics, atypical antipsychotics and calcineurin inhibitors, and reduced access to water.
  • Danger signs during treatment matter as much, because in HHS deterioration usually happens after treatment begins: a falling conscious level while the biochemistry improves (exclude hypoglycaemia, then consider cerebral oedema, osmotic demyelination, stroke or haemorrhage, sepsis and hypoxia — not more fluid); osmolality falling faster than 8 mOsmol/kg/hr, sodium faster than 10 mmol/L in 24 hours, or glucose faster than 5 mmol/L/hr; persistent hypotension despite adequate fluid; new hypoxaemia or basal crackles indicating overload; and new or worsening ketonaemia.Not available at your setup — Serum electrolytes.
  • Take a baseline ECG, chest radiograph, full blood count, cultures, CRP, urine dipstick, creatine kinase, troponin, amylase, lactate, urea and creatinine, magnesium, phosphate and HbA1c, remembering that a raised white cell count is frequently a stress response and not proof of infection, that a high creatine kinase means rhabdomyolysis which worsens acute kidney injury, and that HbA1c establishes chronicity and identifies undiagnosed diabetes.Not available at your setup — Blood culture, Cardiac troponin, Serum electrolytes, Renal function (creatinine/urea).

Management— do this, in order

  • Go slowly — this is the first and most important principle. Outcomes are better with a slower approach to correcting the metabolic abnormality: there is no ketoacidosis demanding urgent reversal, and HHS occurs in people whose brains are already at higher risk of injury, so rapid shifts in osmolality must be avoided through less aggressive fluid replacement and glucose lowering guided by serial calculation of serum osmolality.Not available at your setup — Serum electrolytes.
  • Fluid is the treatment: 0.9% sodium chloride alone is used initially, and it is often enough to lower the glucose substantially.
  • First hour: 1 litre of 0.9% sodium chloride over 1 hour, given more rapidly if the systolic blood pressure is below 90 mmHg; persistent hypotension after adequate volume implies another shock state.
  • After the first hour: normally 0.5–1.0 litre per hour, adjusted to clinical status and calculated osmolality, prescribed in millilitres per hour with a start and finish time — the deficit may be 10–22 litres but it is replaced over days, not in one night.Not available at your setup — Infusion pump.
  • Aim for a positive fluid balance of 2–3 litres at 6 hours and 3–6 litres at 12 hours, with urine output at least 0.5 mL/kg/hr, reassessing for pulmonary oedema (basal crackles, rising respiratory rate, falling saturations) before each bag.
  • Give fluid more cautiously in coronary artery disease, heart failure or chronic kidney disease and in the very elderly, since rapid fluid replacement may precipitate cardiac failure in patients with coronary artery disease — stay at the lower end of the range with closer monitoring, but do not under-fill a patient who is 10–20% volume depleted, since under-resuscitation is equally lethal.
  • Hold the rates of correction: osmolality falling 3–8 mOsmol/kg per hour, sodium falling no more than 10 mmol/L in 24 hours, glucose falling no more than 5 mmol/L (90 mg/dL) per hour, and a glucose target after 6 hours of 10–15 mmol/L (180–270 mg/dL) — not normoglycaemia.Not available at your setup — Serum electrolytes.
  • Potassium above 5.5 mmol/L: add no potassium, continue saline, recheck in 1 hour, continuous cardiac monitoring.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, using premixed bags, aiming to maintain potassium at 4.0–5.0 mmol/L.Doctor / NurseNot available at your setup — Serum electrolytes.
  • Potassium below 3.5 mmol/L: cardiac monitoring, critical care input, and more than 40 mmol/L through an appropriate line — and do not start insulin until potassium replacement is running; add none to an oliguric patient until urine is flowing and a current value is available.Doctor / NurseNot available at your setup — ICU / HDU bed, Central venous access, Serum electrolytes.
  • Insulin is not first-line and should not be started in the first hour unless there is significant ketonaemia: in the first 0–60 minutes start a fixed-rate intravenous insulin infusion at 0.05 units/kg/hr ONLY IF blood ketones are above 1.0 mmol/L, and only after fluid has started; otherwise give no insulin.Doctor / NurseNot available at your setup — Infusion pump.
  • Between 1 and 6 hours: if glucose is falling by less than 5 mmol/L/hr AND the positive fluid balance is adequate (2–3 litres by 6 hours), increase the infusion to 0.1 units/kg/hr if it is running, or start at 0.05 units/kg/hr if it is not.Doctor / NurseNot available at your setup — Infusion pump.
  • After 6 hours: increase or decrease the infusion by 1 unit/hour to hold glucose at 10–15 mmol/L and ensure any ketones are clearing; use soluble human insulin (or a rapid-acting analogue intravenously by the same method) made up as 50 units in 50 mL of 0.9% sodium chloride equalling 1 unit/mL by syringe pump, so a 70 kg patient receives 3.5 units/hour at 0.05 units/kg/hr and 7 units/hour at 0.1 units/kg/hr.Doctor / NurseNot available at your setup — Infusion pump.
  • When blood glucose falls below 14 mmol/L, add 10% glucose at 125 mL/hour alongside the continuing saline — this prevents hypoglycaemia and lets a low-dose infusion keep running, holding the glucose in the target range and clearing ketones without dropping it too fast.
  • Thromboprophylaxis is a therapeutic intervention here, not a routine: prophylactic low-molecular-weight heparin should be given — enoxaparin 40 mg subcutaneously once daily, reduced to 20 mg once daily if the estimated glomerular filtration rate is below 30 mL/min — with mechanical prophylaxis where heparin is contraindicated.Doctor / NurseNot available at your setup — Renal function (creatinine/urea).
  • Protect the feet, a stated aim of HHS management: inspect heels, soles and interdigital spaces, keep heels off the mattress and reposition regularly, because 10–15% of people with diabetes develop foot ulcers and foot infections take hold rapidly and should be treated as medical emergencies with early broad-spectrum antibiotics.
  • Catheterise and monitor by the clock: hourly capillary glucose; sodium, potassium, urea and recalculated osmolality hourly for 6 hours then two-hourly while osmolality falls; hourly conscious level, urine output and cumulative balance; repeat ketones if the patient deteriorates or the glucose plateaus — and every value must carry a clock time.Doctor / NurseNot available at your setup — Serum electrolytes.
  • Treat the precipitant concurrently: cultures then early empirical antibiotics if sepsis is suspected, and stop the thiazide, SGLT2 inhibitors and nephrotoxins and withhold metformin while the patient is dehydrated or has acute kidney injury; consider a nasogastric tube in the obtunded or vomiting patient and give oxygen to conventional targets.Doctor / NurseNot available at your setup — Blood culture.

Caution— what harms

  • Never manage HHS as though it were DKA — the commonest serious error. There is no ketoacidosis to reverse, so there is no urgency to give insulin, and the brain has adapted over weeks to a very high osmolality, so there is a strong imperative not to correct it quickly.
  • Never give an intravenous insulin bolus in HHS, and never start insulin in the first hour unless blood ketones are above 1.0 mmol/L.Doctor / Nurse
  • Many patients with HHS are extremely sensitive to insulin and glucose may fall very rapidly once the infusion starts: to prevent cerebral damage the fall should be no more than 5 mmol/L (90 mg/dL) per hour, and if it is faster, reduce or stop the infusion.
  • Never let the osmolality fall faster than 8 mOsmol/kg per hour — that risks cerebral oedema and osmotic demyelination (central pontine myelinolysis) — and remember that the change in osmolality produced by a sodium falling faster than 10 mmol/L in 24 hours may cause cerebral damage.Not available at your setup — Serum electrolytes.
  • Do not aim for a normal glucose: the target after 6 hours is 10–15 mmol/L (180–270 mg/dL).
  • Do not reach for 0.45% sodium chloride because the sodium looks high — the measured sodium normally rises as the glucose falls, and that rise is expected, not a treatment failure; giving hypotonic fluid to a patient whose osmolality is already falling appropriately is a mechanism for causing cerebral oedema.Not available at your setup — Serum electrolytes.
  • Do not give intravenous sodium bicarbonate: there is no ketoacidosis to correct, and even in a mixed picture it is not generally recommended, being considered only below pH 6.9 and having been implicated in cerebral oedema.Not available at your setup — Arterial blood gas.
  • Do not use glucose-containing solutions as resuscitation fluid — 10% glucose has one defined role, at 125 mL/hour once the glucose falls below 14 mmol/L.
  • Do not reflexively sedate the agitated patient: delirium commonly occurs in older patients with HHS, so look first for hypoxia, hypoglycaemia, sepsis, pain and urinary retention, because sedation and restraint both increase the risk of aspiration and pressure damage.
  • Do not change the osmolality formula between calculations: choose one, state it, use it for every subsequent calculation — a trend computed two ways by two clinicians is precisely how a patient comes to be corrected too fast.Not available at your setup — Serum electrolytes.
  • Do not treat a raised anion gap as proof of ketoacidosis: the normal gap is below 17 mmol/L calculated as (sodium + potassium) − (chloride + bicarbonate), and in HHS a raised gap with a normal pH and bicarbonate reflects uraemia, lactate and the hyperosmolar state, not ketoacidosis.Not available at your setup — Serum electrolytes, Arterial blood gas.
  • Do not mistake the mild hyperchloraemic acidosis of large-volume saline for treatment failure: a rising plasma chloride with a persistently low bicarbonate even though the anion gap has returned to normal is neither treatment failure nor recurrent ketoacidosis and needs no bicarbonate.Not available at your setup — Serum electrolytes, Arterial blood gas.
  • Do not attribute focal deficits or a persisting reduced conscious level to the metabolic derangement without imaging — CT of the head is indicated for any focal sign, seizure, head injury from a collapse, or a conscious level that fails to improve as the osmolality falls.Not available at your setup — CT scan.
  • Do not be reassured by an absent fever or by hypothermia: fever is often absent despite infection, hypothermia is a poor prognostic sign rather than reassurance, and a raised white cell count is frequently a stress response rather than proof of infection — culture widely and treat on clinical grounds.Not available at your setup — Blood culture.

Refer / escalate

Seek specialist and critical care input early for the poor prognostic features (hypothermia, systolic below 90 mmHg, tachycardia or bradycardia, sodium above 160 mmol/L, osmolality above 360 mOsmol/kg, multiple comorbidities), for GCS below 12, oliguria below 0.5 mL/kg/hr, potassium below 3.5 mmol/L, a coexisting acute vascular event, a falling conscious level while the biochemistry improves, or an unclear predominant diagnosis in a mixed HHS/DKA picture — and consider renal replacement therapy for oliguria persisting despite adequate volume replacement, hyperkalaemia unresponsive to medical treatment, refractory acidosis, fluid overload or uraemic complications.

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