DKA, HHS and complication monitoring

Diabetic ketoacidosis

Insulin deficiency permits lipolysis and ketogenesis; acidosis, osmotic diuresis and vomiting cause major fluid and electrolyte losses. The 2024 adult consensus requires diabetes/hyperglycaemia (glucose at least 11.1 mmol/L or known diabetes), ketosis (blood beta-hydroxybutyrate at least 3 mmol/L or significant urine ketones), and acidosis (pH below 7.3 or bicarbonate below 18 mmol/L). SGLT2-associated DKA may have little glucose elevation. Check ketones when an unwell patient taking an SGLT2 inhibitor has nausea, abdominal pain or tachypnoea.

Seek the precipitant: infection, insulin interruption, infarction, pregnancy, pancreatitis or medicines. Assess airway, perfusion, mental state, fluid deficit and ECG, with glucose, ketones, electrolytes, kidney function and venous blood gas. Potassium can be normal or high despite a substantial total-body deficit.

Treatment combines isotonic fluid, insulin and potassium monitoring under a validated hospital protocol. Rates must reflect age, cardiac and renal function. If potassium is below 3.5 mmol/L, replace it and defer insulin until it is above that level; insulin shifts potassium intracellularly and can provoke arrhythmia. Replacement rates require appropriate venous access, monitoring and local limits, not an unmonitored 20–40 mmol/h prescription.

For significant adult DKA, an insulin infusion is commonly started at 0.1 units/kg/h after potassium safety is established. Once glucose falls below 13.9 mmol/L, the consensus recommends adding dextrose and reducing insulin to about 0.05 units/kg/h. Continue insulin to suppress ketogenesis; do not stop simply because glucose normalises. Reassess glucose frequently and ketones, pH, potassium and fluid balance serially. Bicarbonate is not routine.

Resolution uses ketone clearance with correction of acidosis, not glucose alone. Hyperchloraemic acidosis during recovery can confuse anion-gap interpretation. Give subcutaneous basal insulin with the appropriate overlap before stopping an infusion, restore nutrition safely, and address education, sick-day rules and access to insulin.

Hyperglycaemic hyperosmolar state

HHS features severe hyperglycaemia, hyperosmolality and dehydration without the degree of ketosis/acidosis characteristic of DKA. The adult consensus includes glucose at least 33.3 mmol/L, effective osmolality above 300 mOsm/kg or total osmolality above 320, beta-hydroxybutyrate below 3 and no substantial acidosis (pH at least 7.3 and bicarbonate at least 15). Mixed DKA/HHS exists and needs a pathway addressing both.

Effective calculated osmolality in SI units is 2 × sodium + glucose; total calculated osmolality additionally includes urea. For sodium 152 and glucose 48.2, effective osmolality is 304 + 48.2 = 352.2 mOsm/kg. State which equation is being used rather than switching thresholds silently.

Restore circulation carefully, monitor glucose, sodium, potassium, urine output and osmolality, and identify the trigger. Older patients often have cardiac or renal disease, so a universal fluid timetable is unsafe. An osmolality decline of about 3–8 mOsm/kg/h is a consensus safety goal; avoid rapid shifts. Initial fluid itself lowers glucose. Insulin timing and dose differ from DKA when ketosis is absent; use the local protocol and obtain senior input. Assess thrombosis risk and give appropriate prophylaxis unless contraindicated.

DKA/HHS response example

In a patient whose glucose falls while ketones and acidosis persist, add the protocol dextrose and continue appropriately adjusted insulin rather than stopping because glucose is normal. Recheck potassium and the precipitating illness. A rising sodium during HHS treatment may reflect glucose correction rather than an automatic need for hypotonic fluid; interpret measured sodium with osmolality and volume response. If fluids worsen respiratory distress, reassess overload and obtain senior support. Resolution requires the specified biochemical/clinical criteria, not a single improved capillary glucose.

Chronic Microvascular & Macrovascular Complications

• Diabetic Retinopathy: Pathophysiological Manifestation: Non-proliferative (microaneurysms, dot-and-blot haemorrhages, cotton wool spots, hard exudates) vs Proliferative (neovascularisation, vitreous haemorrhage, retinal detachment); Screening Standard in Australia: Dilated fundoscopy or digital retinal photography every 2 years (annually if abnormalities identified); Evidence-Based Intervention: Glycaemic and BP control; pan-retinal photocoagulation (PRP); intravitreal anti-VEGF agents (aflibercept, ranibizumab) for macular oedema
• Diabetic Neuropathy: Pathophysiological Manifestation: Distal symmetrical sensorimotor polyneuropathy (glove-and-stocking pattern); autonomic neuropathy (gastroparesis, postural hypotension, cardiac denervation, erectile dysfunction); Screening Standard in Australia: Annual 10-g Semmes-Weinstein monofilament test and $128\text{ Hz}$ tuning fork vibration testing; structured foot inspection for ulcers/calluses; Evidence-Based Intervention: Glycaemic control; podiatry care; custom pressure-relieving footwear; symptomatic neuropathic pain management (duloxetine, pregabalin, amitriptyline)
• Macrovascular Disease: Pathophysiological Manifestation: Accelerated coronary artery disease, ischaemic stroke, and peripheral arterial disease driven by endothelial dysfunction and atheroma formation; Screening Standard in Australia: Use the current Australian CVD risk calculator in eligible primary-prevention patients, including people with diabetes aged 35–79; apply earlier First Nations assessment and recommended review intervals. Established CVD requires secondary prevention; Evidence-Based Intervention: Statin therapy (target LDL $< 1.8\text{ mmol/L}$, or $< 1.4\text{ mmol/L}$ in known ASCVD); blood pressure target $< 130/80\text{ mmHg}$; antiplatelet therapy (aspirin $100\text{ mg}$ secondary prevention)

Primary references (checked 7 October 2026): 2024 hyperglycaemic-crisis consensus.