Diabetic Ketoacidosis

DKA is a medical emergency that requires prompt recognition and systematic management. It often occurs as the first presentation of T1DM or is precipitated by illness (infection), non-compliance with insulin, or physiological stress (e.g., MI or surgery). The diagnostic criteria in the UK (JBDS guidelines) are: 1. Blood glucose > 11.0 mmol/L (or known DM); 2. Capillary ketones > 3.0 mmol/L (or urinary ketones ++ or more); 3. Venous pH < 7.3 or bicarbonate < 15.0 mmol/L. DKA represents a profound catabolic state. The absolute lack of insulin leads to unrestrained lipolysis and fatty acid oxidation, generating acidic ketone bodies (beta-hydroxybutyrate and acetoacetate). Management follows a protocol-driven approach (A-E assessment). The primary goals are volume restoration, suppression of ketogenesis via insulin, and correction of electrolyte imbalances. A major risk during treatment, particularly in children and young adults, is cerebral oedema, which can occur with over-rapid fluid administration or rapid drops in plasma osmolality. Mortality remains roughly 2-5% in the UK, often due to the precipitating cause or complications of treatment.

The core pathology is insulin deficiency combined with an increase in counter-regulatory hormones: glucagon, catecholamines, cortisol, and growth hormone. In the liver, glucagon stimulates glycogenolysis and gluconeogenesis, while insulin normally suppresses these. Absence of insulin prevents glucose entry into peripheral tissues (GLUT4), exacerbating hyperglycaemia. Hyperglycaemia causes an osmotic diuresis, leading to severe dehydration and loss of sodium, potassium, and phosphate. Simultaneously, the lack of insulin allows Hormone-Sensitive Lipase (HSL) to break down triglycerides into glycerol and free fatty acids (FFAs). FFAs are taken up by the liver and enter the mitochondria via the carnitine shuttle. In the absence of insulin, these FFAs are shunted into ketogenesis rather than being resynthesised into triglycerides. The ketones produced are organic acids. As they accumulate, the blood pH falls (metabolic acidosis), and the anion gap increases.

Patients typically present within 24 hours of onset. Clinical features include polyuria, polydipsia, nausea, and vomiting. Abdominal pain is common and can mimic an acute abdomen. On examination, patients are dehydrated (tachycardia, hypotension, dry mucous membranes, reduced skin turgor). A characteristic sign is 'Kussmaul respiration'—deep, sighing breaths representing a compensatory respiratory alkalosis to counter metabolic acidosis. The breath may smell of 'pear drops' (acetone). Confusion or reduced GCS suggests severe acidosis or incipient cerebral oedema. Complications of DKA include severe hypokalaemia (as insulin shifts potassium into cells), aspiration pneumonia, and venous thromboembolism (VTE).

Bedside: Capillary blood glucose and ketones. Observations (BP, HR, RR, SpO2, Temp). Bloods: Venous Blood Gas (VBG) for pH/HCO3-/Lactate/K+. Formal lab glucose and ketones. U&Es (Creatinine, baseline Potassium). Full Blood Count (FBC) - often shows a 'stress' leucocytosis. CRP/Septic screen if infection suspected. Urine: Dipstick (ketones/nitrites) and MCS. Imaging: CXR to look for pneumonia. ECG to check for signs of hyper- or hypokalaemia (peaked T-waves or U-waves/flat T-waves).

1. Fluid Resuscitation: 1L 0.9% normal saline over 1 hour initially, then slower (typical 6L over 24h). 2. Fixed-Rate Insulin: 0.1 units/kg/hour (FRIII). Continue long-acting basal insulin. 3. Potassium Replacement: Even if K+ is normal, it will drop when insulin starts; add KCl to bags (except if K+ >5.5). 4. Monitoring: Hourly glucose/ketones, 2-hourly VBG. 5. Glucose Management: Once blood glucose < 14 mmol/L, start 10% dextrose to prevent hypoglycaemia while keeping the insulin infusion running to clear ketones. 6. Recovery: Switch to subcutaneous insulin once pH > 7.3, ketones < 0.6, and patient is eating. 7. VTE Prophylaxis: Low Molecular Weight Heparin (LMWH).