Diabetic ketoacidosis and hyperosmolar hyperglycaemic state

• Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycaemic state (HHS) are the two serious, acute, life-threatening hyperglycaemic emergencies of diabetes. Both arise from insulin deficiency plus a surge of stress hormones, but DKA adds ketone-driven metabolic acidosis, while HHS adds extreme hyperglycaemia and hyperosmolality without significant ketosis.
• DKA is more common in younger people with type 1 diabetes; HHS in older people with type 2 diabetes. They share precipitants: infection, missed or insufficient insulin, myocardial infarction, stroke, pancreatitis, and several drugs (SGLT2 inhibitors, corticosteroids, antipsychotics).
• DKA is diagnosed by glucose at or above 200 mg/dL (11.1 mmol/L) or a known history of diabetes, together with ketonaemia (beta-hydroxybutyrate at least 3.0 mmol/L) and metabolic acidosis (pH under 7.3 and/or bicarbonate under 18 mmol/L). ^[1]
• HHS is diagnosed by plasma glucose at or above 600 mg/dL (33.3 mmol/L), calculated osmolality above 300 mOsm/kg (or total osmolality above 320 mOsm/kg), and only minimal ketones and acidosis. ^[1][2]
• Treatment of both is the same spine: aggressive isotonic fluids first, then a fixed-rate intravenous insulin infusion once potassium has been assessed (and not if potassium is under 3.3 mmol/L), aggressive potassium replacement guided by frequent checks, a search for the trigger, and a careful overlap of 1 to 2 hours when switching to subcutaneous insulin.
• With treatment, DKA mortality is under 1% in high-income settings, but 5- to 10-fold higher in HHS, and much higher in low- and middle-income settings because of delayed diagnosis. ^[1]

By the end of this page you should be able to:

1. Define DKA and HHS and explain why DKA acidifies while HHS dehydrates.
2. List the major precipitants and name the drug classes that favour each.
3. State the 2024 ADA consensus diagnostic criteria and severity bands for DKA, and the diagnostic criteria for HHS.
4. Design an initial investigation panel and recognise the differential diagnoses of ketosis (starvation, alcoholic ketoacidosis) and of hyperosmolality.
5. Outline the management sequence — fluids, insulin, potassium, bicarbonate — including doses, rates, overlap and resolution criteria.
6. Identify treatment complications (hypoglycaemia, hypokalaemia, thrombosis, cerebral oedema in children) and how to mitigate them.
7. Adapt management when resources are scarce: no osmolality, no ketone meter, no intensive care.
8. State the concrete steps that prevent recurrence.

The two are not mutually exclusive. Mixed DKA–HHS occurs in more than one third of people presenting with a hyperglycaemic crisis, and the mixture carries a higher mortality than either alone (8% versus 5% for HHS and 3% for DKA in one cohort). ^[1] DKA also presents with euglycaemia in about 10% of cases (plasma glucose under 200 mg/dL [11.1 mmol/L]) when low insulin levels coexist with low carbohydrate intake, pregnancy, alcohol use, liver failure or SGLT2 inhibitor therapy — so a normal glucose does not exclude it. ^[1][2]

Severity of DKA (using the 2024 ADA consensus categories, of which not all variables need to be satisfied) guides where care is given: ^[1]

Nearly 1% of all hospitalisations in people with diabetes are for a hyperglycaemic crisis. In US data, 38% of these admissions are for DKA, 35% for HHS and 27% for mixed DKA–HHS. DKA is commonest in young adults aged 18 to 44 years (61.7%) with type 1 diabetes (70.6%); HHS is commonest in middle-aged adults 45 to 64 years (47.5%) with type 2 diabetes (88.1%). Between 6% and 21% of adults present with DKA as their initial diagnosis of type 1 diabetes, and more than half of adults with newly diagnosed diabetes presenting with unprovoked DKA in some series are Black/African American or Hispanic/Latino adults with type 2 diabetes (so-called ketosis-prone type 2 diabetes). ^[1]

Mortality has fallen: inpatient mortality is now about 0.20% in type 1 diabetes DKA and 1.04% in type 2 diabetes DKA, and about 0.77% for HHS in one US series, and mixed crises carry the highest inpatient mortality (8%). But deaths in type 1 diabetes in the year after a DKA episode are far above the population rate (13-fold, and 49-fold in those aged 15 to 39 years), reflecting both recurrence and the burden of premature disease. Mortality in low- and middle-income settings is starkly higher — 26% to 41.3% for DKA in sub-Saharan Africa, 30% in India, 23.6% in Pakistan — mostly from delayed diagnosis and treatment. ^[1]

The most common precipitants are infection (especially urinary tract infection and pneumonia, 14% to 58% of DKA cases and 30% to 60% of HHS cases) and omission or insufficient use of insulin. Stress from any acute illness, psychological stress and socioeconomic deprivation all raise risk; recurrent DKA is driven most strongly by mental health conditions and social determinants. ^[1]

Other acute conditions that can precipitate DKA include stroke, alcohol and substance use, pancreatitis, pulmonary embolism, myocardial infarction and trauma. Volume depletion is the primary driver of HHS, particularly in older adults with thirst impairment and limited access to fluids. ^[1]

Drugs that precipitate hyperglycaemic crises: ^[1]

The omission of insulin, often driven by cost, mental health, eating disorders or food insecurity, accounts for more than two thirds of DKA admissions in urban disadvantaged populations. Mental health screening, including depression screening with validated tools, and assessment of social determinants, are part of good care before discharge. ^[1]

The key difference between the two crises is the severity of insulin insufficiency. ^[1]

In DKA, severe (absolute or relative) insulin deficiency coincides with high counter-regulatory hormones. The low insulin-to-glucagon ratio raises hepatic glucose production (gluconeogenesis and glycogenolysis) and reduces peripheral glucose use, so hyperglycaemia worsens. Fat is mobilised (lipolysis), delivered to the liver, oxidised, and converted to ketone bodies (acetoacetate and beta-hydroxybutyrate), producing a high anion gap metabolic acidosis. Acetone, a breakdown product, gives the breath a fruity odour and Kussmaul (deep, rapid) breathing compensates for the acidosis. ^[1]

In HHS, there is enough residual insulin to suppress ketogenesis, but not enough to control hyperglycaemia. The resulting osmotic diuresis loses water and solutes; without adequate fluid intake, volume depletion, haemoconcentration, rising osmolality, renal impairment and finally altered cognition follow. Whole-body potassium is depleted by 3 to 6 mmol/kg in both conditions through osmotic diuresis, emesis and secondary hyperaldosteronism. ^[1]

Hyperglycaemia itself drives a pro-inflammatory state (raised TNF-alpha, interleukins, CRP, reactive oxygen species), which settles within 24 hours of insulin and hydration. ^[1]

DKA evolves over hours to a few days; HHS over days to weeks. Both cause polyuria, polydipsia, weight loss, dehydration and altered cognition. DKA adds nausea, vomiting and abdominal pain (in over 50% of cases), which may be due to the ketoacidosis or to its trigger (for example, appendicitis or pancreatitis), and Kussmaul breathing. Caution is needed when abdominal pain persists after dehydration and acidosis resolve. ^[1]

On examination, look for signs of volume depletion (tachycardia, hypotension, dry mucosa), Kussmaul respiration and ketotic breath, abdominal tenderness without guarding (attributable to the ketoacidosis), and evidence of infection or ischaemia. Mental state change is expected in severe DKA and in HHS. An ECG screens for ischaemia and hyperkalaemic peaked T waves. ^[1]

Differential diagnoses of ketonaemia are starvation ketosis (intake under 500 kcal [2090 kJ] daily), alcoholic ketoacidosis (binge drinking plus starvation and vomiting, with or without hyperglycaemia), and pregnancy ketosis (hyperemesis gravidarum). Hypothesis-generating clues are a low or normal glucose, a history of fasting or alcohol, and pregnancy. ^[1]

• Plasma glucose (capillary only for monitoring; venous glucose for decisions).
• Serum electrolytes and creatinine (sodium, chloride, bicarbonate, urea).
• Venous blood gas for pH and bicarbonate (arterial only if pulmonary pathology is suspected).
• Blood or urine ketones; prefer direct venous or capillary beta-hydroxybutyrate, the main ketoacid in DKA, because urine testing lags and can under- or over-estimate severity. ^[1]
• Full blood count and a screen for infection as clinically indicated (cultures, chest X-ray, urinalysis).
• ECG for ischaemia and hyperkalaemia.
• Serum osmolality in HHS or when the boundary is unclear.
• HbA1c, to assess pre-morbid control and to guide discharge dosing.
• Lipids if HHS is severe (some patients have pseudohyponatraemia from hyperlipidaemia). ^[1]

Beta-hydroxybutyrate at least 3.0 mmol/L picks up DKA with high sensitivity and specificity (over 90%) and correlates well with acid-base change. Nitroprusside urine tests measure acetoacetate, lag behind early in the illness and can give false positives with certain sulfhydryl drugs. An anion gap above 12 mmol/L indicates high anion gap acidosis; mixed acid-base disorders are present in about one third of cases (hyperchloraemic natriuresis, vomiting, compensatory hyperventilation), so the gap alone neither diagnoses nor excludes DKA and should not be used for resolution. ^[1]

Brain imaging only with a neurological indication. In HHS, serum osmolality calculation/estimation is central. Active screening for the trigger: ECG and cardiac enzymes when chest pain, sepsis work-up, amylase/lipase if abdominal pain persists, lumbar puncture if infection is suspected, head CT if focal neurology. Renal function daily; acute kidney injury (RIFLE criteria) affects 50% of adults admitted with DKA or HHS. ^[1]

All criteria must be met for each diagnosis, although the mixture is common (over one third). Severity of DKA follows the table above. ^[1][2]

1. Treat the patient, not the glucose: volume first, then insulin, with potassium guarded throughout.
2. Find and treat the trigger from the moment of admission.
3. Use an institutional protocol with validated insulin infusion guidance, frequent glucose and electrolyte monitoring, and pharmacy support.
4. Consider level of care by severity: mild DKA can be treated in the emergency department or step-down unit with close nursing supervision; severe DKA, HHS, critical illness, or altered mental status need intensive care. ^[1]

Fluid is the first and single most effective intervention: it restores perfusion, promotes renal glucose and ketone clearance, corrects electrolytes and lowers osmolality, and hyperglycaemia falls by roughly 50 to 70 mg/dL (2.8 to 3.9 mmol/L) per hour from saline alone. ^[1]

• In adults without renal or cardiac compromise, give 0.9% sodium chloride (or a balanced crystalloid such as Ringer's lactate or PlasmaLyte-148) at 500 to 1000 mL per hour for the first 2 to 4 hours. Balanced crystalloids resolve DKA faster with less hyperchloraemic acidosis; isotonic saline is cheaper and more widely available. ^[1]
• Correct estimated deficits over 24 to 48 hours; use smaller boluses (250 mL) and frequent reassessment in older adults, pregnancy, and heart or kidney disease. ^[1]
• When plasma glucose falls below 250 mg/dL (13.9 mmol/L), add 5% to 10% dextrose to the 0.9% saline to prevent hypoglycaemia while insulin continues. This is mandatory in euglycaemic DKA and in SGLT2 inhibitor-associated DKA. ^[1]
• In HHS, correct over 24 to 48 hours: glucose should not fall by more than 90 to 120 mg/dL per hour (5 to 6.7 mmol/L per hour), serum sodium should not fall by more than 10 mmol/L in 24 hours, and osmolality by no more than 3 to 8 mOsm/kg per hour. A 100 mg/dL (5.6 mmol/L) fall in glucose raises serum sodium by about 1.6 mmol/L, so an initial rise in sodium with fluids is expected and not a reason to use hypotonic saline unless osmolality is not falling despite adequate fluid balance. Insulin may be withheld with initial fluid administration alone to avoid a rapid drop in osmolality. ^[1]

Short-acting insulin by continuous intravenous infusion is preferred. Start the fixed-rate infusion at 0.1 units/kg/h as soon as venous access is available (a 0.1 units/kg intravenous or intramuscular bolus is reasonable if access is delayed). Once glucose is below 250 mg/dL (13.9 mmol/L), add 5% to 10% dextrose and reduce the insulin infusion to 0.05 units/kg/h, thereafter titrating to keep glucose around 200 mg/dL (11.1 mmol/L) until the ketoacidosis has resolved. ^[1]

Patients already using basal insulin should continue it during infusion; many protocols add a low dose of long-acting insulin (0.15 to 0.3 units/kg subcutaneously) early, which shortens time to resolution, duration of infusion and length of stay and prevents rebound hyperglycaemia. ^[1]

Mild, uncomplicated DKA (pH over 7.25, bicarbonate over 15 mmol/L, ketonaemia under 6.0 mmol/L) can be treated with subcutaneous rapid-acting insulin analogues 0.1 units/kg (or a weight-based rapid-acting dose) every 1 to 2 hours, in the emergency department or step-down unit instead of an infusion. ^[1]

In HHS, if there is no clinically significant ketonaemia (beta-hydroxybutyrate 1.0 to under 3.0 mmol/L, urine ketones under 2+, pH at least 7.3 and bicarbonate at least 18 mmol/L), start insulin at 0.05 units/kg/h; if there is mixed DKA/HHS (beta-hydroxybutyrate at least 3.0 mmol/L, ketonuria 2+ or greater, pH under 7.3, bicarbonate under 18 mmol/L), use 0.1 units/kg/h. ^[1]

Total body potassium is depleted 3 to 6 mmol/kg, yet most patients present with normal or high serum potassium because acidosis and insulin deficiency shift potassium out of cells. Insulin, correction of acidosis and fluid resuscitation all drive potassium back into cells, so serum levels fall by 1 to 2 mmol/L within 48 hours. ^[1]

• Replacement should start once serum potassium falls below 5.0 mmol/L, aiming to maintain 4 to 5 mmol/L. For most patients 20 to 30 mmol of potassium per litre of intravenous fluid suffices. ^[1]
• If potassium is already under 3.5 mmol/L on admission (about 5 to 10% of DKA cases), give potassium at 10 mmol/h and delay insulin until the level rises above 3.5 mmol/L, to avoid life-threatening arrhythmia and respiratory muscle weakness. ^[1]
• Severe hypokalaemia at or below 2.5 mmol/L during treatment is associated with a threefold increase in mortality. ^[1]
• Measure potassium 2 hours after starting insulin and every 4 hours until resolution. ^[1]
• Insulin and potassium are the main avoidable causes of sudden collapse in the first 12 hours.

Routine intravenous bicarbonate is not recommended: insulin and fluids resolve the acidosis, and bicarbonate may worsen hypokalaemia, reduce tissue oxygen uptake, predispose to cerebral oedema and cause paradoxical central nervous system acidosis. Consider it only if acidosis is severe, pH under 7.0; then give 100 mmol of 8.4% sodium bicarbonate in 400 mL sterile water every 2 hours to raise pH above 7.0. ^[1]

Whole-body phosphate is lost but serum phosphate is usually normal or high on admission. Unless there is muscle weakness with phosphate under 1.0 mmol/L (and the patient is not severely acidotic, where replacement risks hypocalcaemia), routine replacement is not indicated. Where needed, add 20 to 30 mmol of potassium phosphate to replacement fluids. ^[1]

This is the most commonly mishandled step. To prevent rebound hyperglycaemia or ketoacidosis while intravenous insulin washes out, give subcutaneous basal (or basal-bolus) insulin 1 to 2 hours before stopping the infusion, and overlap the two by 1 to 2 hours. ^[1][2]

Estimation of the total daily insulin dose: 0.5 to 0.6 units/kg/day in insulin-naive patients (about 0.3 units/kg/day if hypoglycaemia risk is high, for example in kidney failure or frailty); or from the existing regimen adjusted for the precipitating illness; or 80% of the home dose if stable. Give half as basal and half as prandial rapid-acting. Rapid-acting boluses 5 to 15 minutes before meals. ^[1][2]

Mixed DKA/HHS patients especially need close attention to overlap, because any lapse in insulin promptly rekindles ketogenesis.

Infusion rates, potassium thresholds, bicarbonate indication and resolution criteria are from reference 1. ^[1]

Capillary glucose every 1 to 2 hours. Venous blood gas, electrolytes, creatinine and beta-hydroxybutyrate every 4 hours until DKA resolves. Serum osmolality every 4 hours in HHS. Hourly fluid balance. Avoid using anion gap or urinary ketones as resolution criteria: hyperchloraemic normal-anion-gap acidosis is common during recovery and urinary ketone strips rise as beta-hydroxybutyrate is converted to acetoacetate. ^[1]

Resolution of DKA is a plasma beta-hydroxybutyrate under 0.6 mmol/L plus venous pH at least 7.3 or bicarbonate at least 18 mmol/L (and ideally glucose under 200 mg/dL [11.1 mmol/L]); for HHS, an osmolality under 300 mOsm/kg, corrected hyperglycaemia, urine output over 0.5 mL/kg/h, and cognitive recovery (glucose under 250 mg/dL [13.9 mmol/L]). ^[1]

Complications are common and are the main cause of death once the diagnosis is made. ^[1]

• Hypoglycaemia. Occurs in 16% to 28% of DKA treatments (severe hypoglycaemia under 40 mg/dL [2.2 mmol/L] in 2%) and carries a 4.8-fold rise in mortality. Mitigation: glucose monitoring every 1 to 2 hours, a reduction in insulin infusion to 0.05 units/kg/h once glucose is under 250 mg/dL, 5% to 10% dextrose in fluids, and clear hypoglycaemia rescue protocols. ^[1]
• Hypokalaemia. Occurs in approximately 55% of DKA and 51% of HHS; severe hypokalaemia under 2.5 mmol/L in 16% and 9% respectively. Severe hypokalaemia at or under 2.5 mmol/L increases inpatient mortality roughly fivefold. The rise and fall of potassium is the reason both infusion and replacement must be nurse-led with clear thresholds. ^[1]
• Hyperchloraemic non-anion-gap acidosis. Common during recovery; usually self-limiting, less frequent with balanced crystalloids and slower saline. Do not mistake it for unresolved DKA and delay transition to subcutaneous insulin. ^[1]
• Thrombosis. Both DKA and HHS, especially HHS, are pro-thrombotic. Clot structure is altered by acidosis and dehydration and reversible. Prophylactic low-molecular-weight heparin is recommended unless contraindicated, even though nationwide data have not always shown an excess of venous thromboembolism in HHS. ^[1]
• Cerebral oedema. Rare in adults (under 0.1% of events) but clinically devastating: mortality of about 30% against those without oedema. Risk comes from rapid osmotic shifts; treat adults with a slow osmolality correction, a low threshold for brain imaging and change in mental status as the trigger for mannitol and, if needed, mechanical ventilation. ^[1] In children it is the dominant lethal complication of DKA: an estimated frequency of 0.7 to 1 per 100 episodes, responsible for 60% to 90% of deaths in childhood DKA, usually within 12 hours of starting intravenous insulin, with subclinical swelling demonstrable in most. Risk factors are age under 5 years, new-onset diabetes, prolonged hyperglycaemia, high blood urea nitrogen, severe acidosis with low pCO2, and therapeutic errors (bicarbonate administration, excess fluid in the first 4 hours, insulin in the first hour of fluid therapy). Treatment is urgent: reduce fluid rate by one third, mannitol 0.5 to 1 g/kg over 10 to 15 minutes (repeat in 30 to 120 minutes if needed), with 3% hypertonic saline 2.5 to 5 mL/kg as an alternative, head elevated 30 degrees, with readiness to intubate. ^[3]
• Osmotic demyelination syndrome. Rare; from rapid correction of hyponatraemia in hyperosmolar patients. Keep the rate of change in osmolality within 3 to 8 mOsm/kg per hour. ^[1]
• Acute kidney injury. Affects about half of adults admitted with DKA or HHS, usually recovers with rehydration; daily renal monitoring is recommended. ^[1]

Special populations: frail older adults more often have HHS or mixed crises with very high morbidity; in SGLT2 inhibitor therapy, expect euglycaemic DKA and stop the drug on admission; in end-stage kidney disease the risk is about 4% with fluid overload and hyperkalaemia; in pregnancy, up to 2% of pregestational diabetes develops DKA, often euglycaemic, requiring senior obstetric and medical care. ^[1]

Most patients recover fully with timely treatment; in-hospital mortality in adults is now around 1% (DKA) and under 1% (HHS in series from high-income settings). Outcomes are driven far more by the trigger (myocardial infarction, sepsis, stroke) than by the metabolic disturbance itself. Poor prognostic markers are older age, HHS or mixed patterns, and serious concurrent illness. People discharged after DKA have a one-year age-corrected mortality rate 13 times that of the general population, which underlines that every admission is a chance to reset the patient's insulin, education and social supports. ^[1]

Prevention is where the real mortality gap closes. Up to 22% of those admitted with DKA are readmitted within 30 days, 40.8% of 30-day readmissions are for recurrent DKA, and close to 90% of same-year readmissions are 1 to 3 episodes. Follow-up within 2 to 4 weeks of discharge and structured patient education both reduce recurrence. ^[1]

Concrete steps before discharge: ^[1]

• Review the trigger (insulin omission, mental health, social barriers, drug initiation).
• Reinforce sick-day rules: never stop insulin during illness; increase monitoring; use ketone strips or a meter when glucose is above 13 mmol/L (234 mg/dL) or when unwell.
• Confirm glucose and ketone monitoring technique; offer CGM (associated with a 53% fall in DKA hospitalisations in type 1 diabetes and 47% in type 2 diabetes).
• Provide adequate insulin supply, needles, glucagon and contact numbers, and involve social services where access is a problem.
• Screen for mental health and disordered eating, including with a validated depression tool.
• Address food insecurity, housing and insurance barriers where possible; these are major drivers of recurrent crises.
• Arrange follow-up within 2 to 4 weeks, ideally with specialist review for anyone with recurrent crises, who can benefit from peer support, behavioural family therapy and 24-hour advice lines.

The high mortality in low- and middle-income countries (26% to 41.3% for DKA in sub-Saharan Africa) is not from a different disease but from late diagnosis and missing tools. Adapting safely: ^[1]

• When there are no ketone strips or meters, use an anion gap above 12 mmol/L plus clinical picture (type 1 diabetes, acidosis, Kussmaul breathing, acetone) for DKA; treat empirically if unsure, since fluids and a low-dose insulin infusion are safe.
• When osmolality is unavailable, estimate it (2 x sodium + glucose in mmol/L + urea) and follow serum sodium and mental status; use fluids guided by perfusion and urine output.
• A bedside clock, a basic chemistry panel, normal saline and an insulin infusion set with a predictable pump or drip rate save more lives than any advanced test.
• Weigh fluids by clinical assessment and urine output (aim more than 0.5 mL/kg/h); avoid rapid osmolality falls.
• Reserve bicarbonate strictly for pH under 7.0; avoid it in children and wherever monitoring is limited.
• Use low-dose insulin correctly: 0.1 units/kg/h fixed-rate, then halve and add dextrose below 250 mg/dL (13.9 mmol/L).
• Protect the airway and circulation. Many centres cannot intubate or provide central lines; use the smallest fluid boluses that restore perfusion, especially in children and older adults, and refer early.
• Therapy must include the trigger: treat malaria, pneumonia, urinary infection and surgical abdomen on their own standing protocols; in low-resource settings these are the real killers and the reason for most late deaths.
• Cerebral oedema must be recognised clinically (headache, vomiting, bradycardia, hypertension, falling oxygen saturation, neurological change) and treated at the bedside with fluid reduction, mannitol and head elevation while arranging transfer. ^[1][3]

• DKA is hyperglycaemia plus ketonaemia (beta-hydroxybutyrate at least 3.0 mmol/L) plus acidosis (pH under 7.3, bicarbonate under 18 mmol/L); HHS is severe hyperglycaemia (at least 600 mg/dL [33.3 mmol/L]), hyperosmolality (over 300 calculated, 320 total mOsm/kg), and only minimal ketones, with pH at least 7.3. Mixed is common and worse.
• Infection and missed insulin top the precipitant list in both; SGLT2 inhibitors, steroids and antipsychotics are drug triggers, SGLT2 inhibitors often producing euglycaemic DKA.
• Fluids first: 500 to 1000 mL/h of 0.9% saline or balanced crystalloid for 2 to 4 hours; glucose falls roughly 50 to 70 mg/dL per hour from fluids alone.
• Insulin: 0.1 units/kg/h intravenous, fall to 0.05 units/kg/h with 5% to 10% dextrose below 250 mg/dL (13.9 mmol/L); aim for about 200 mg/dL (11.1 mmol/L) until resolution.
• HHS uses lower insulin (0.05 units/kg/h, or 0.1 if mixed) and slower correction: no more than 90 to 120 mg/dL per hour glucose fall, osmolality 3 to 8 mOsm/kg per hour.
• Potassium: total body deficit 3 to 6 mmol/kg; replace to 4 to 5 mmol/L, 20 to 30 mmol per litre; if K under 3.5, give 10 mmol/h and hold insulin until it exceeds 3.5 mmol/L; check 2 hours after starting insulin and every 4 hours thereafter.
• Bicarbonate only if pH is below 7.0; then 100 mmol of 8.4% over 2 hours.
• Resolution: DKA on ketones under 0.6 mmol/L plus pH at least 7.3 or bicarbonate at least 18 mmol/L; HHS on osmolality under 300 plus glucose under 250 plus urine output over 0.5 mL/kg/h plus cognitive recovery.
• Transition safely: overlap of 1 to 2 hours and subcutaneous basal given 1 to 2 hours before stopping the infusion.
• Complications: hypoglycaemia (16% to 28%), hypokalaemia (about 55% DKA, 51% HHS), thrombosis (prophylactic low-molecular-weight heparin), cerebral oedema (rare in adults; in children the killer — 0.7 to 1 in 100, mannitol 0.5 to 1 g/kg), osmotic demyelination, acute kidney injury (50%).
• Prevention and social work reduce recurrence far more than any drug change.

Related topics (plain text, linked once the discipline is complete): acid-base disorders; diabetes mellitus type 1 and type 2; diabetic nephropathy; glycaemic targets in adults; hypokalaemia; lactic acidosis; osmolality and sodium disorders; stroke and acute brain injury in infection; SGLT2 inhibitors.