DKA and HHS — Written Clinical Reasoning

SAQ 1 — Severe DKA: Diagnosis, Protocol, and Complications (20 marks, 30 minutes)

Prompt: Establish the diagnosis with severity grading, calculate the anion gap and corrected sodium, construct a complete management plan following the JBDS protocol with drug doses and monitoring targets, and discuss the complications you must anticipate with their prevention and recognition. [1]

Model Answer

Diagnosis and severity (3 marks): [1]

This is severe diabetic ketoacidosis. The diagnosis is confirmed by all four criteria: glucose above 11 (31 mmol/L), ketones above 3 (beta-hydroxybutyrate 7.8), venous pH below 7.3 (6.98), and bicarbonate below 15 (6 mmol/L). The precipitant is insulin omission — he stopped his insulin two days ago. The severity grade is severe because the pH is below 7.0 and the bicarbonate is below 10. This warrants ICU admission. [1]

Anion gap and corrected sodium (2 marks): [1]

Anion gap = sodium minus chloride minus bicarbonate = 130 minus 92 minus 6 = 32 (markedly elevated; normal 8-12). This confirms a high-anion-gap metabolic acidosis, consistent with ketoacidosis. [1]

Corrected sodium = measured sodium + 0.4 x (glucose minus 5.5) = 130 + 0.4 x (31 minus 5.5) = 130 + 0.4 x 25.5 = 130 + 10.2 = about 140 mmol/L. The corrected sodium is normal, which means 0.9% saline is the appropriate fluid choice (not 0.45%, which would be used if the corrected sodium were high). [1]

Management plan — the JBDS protocol (12 marks): [1]

1. Resuscitate and monitor (2 marks): ABCDE, oxygen, two large-bore cannulae, continuous cardiac monitoring, hourly glucose and potassium, two-hourly ketones and venous gas. A urinary catheter if the patient is oliguric or unable to pass urine. Move to ICU given the severe grade. [1]

2. Fluid resuscitation (3 marks): Start 0.9% saline immediately — 1 litre in the first hour, then 1 litre over 2 hours, then 1 litre over 2 hours, then 1 litre over 4 hours, with reassessment at each stage. Fluid is the first and most important intervention; it lowers glucose by restoring perfusion and switching off the osmotic diuresis before insulin is even started. [1]

3. Fixed-rate intravenous insulin infusion (3 marks): Start after the first litre of fluid and once potassium is confirmed safe (it is 5.8, so safe to proceed). FRIII at 0.1 units/kg/hour of soluble human insulin (Actrapid). Make up 50 units in 50 mL of 0.9% saline. For a 70 kg patient, this is 7 units/hour. The goal is ketogenesis suppression — target a fall in ketones of at least 0.5 mmol/L/hour and a rise in bicarbonate of 3 mmol/L/hour. No loading bolus. [1]

4. Potassium management (2 marks): The potassium is 5.8, which is above 5.5, so no potassium is added to the first bag. However, insulin will drive potassium into cells and the level will fall rapidly — check hourly. Once the potassium drops below 5.5, switch to 0.9% saline with 40 mmol/L potassium. Target range 4-5.5 mmol/L. [1]

5. Dextrose switch (1 mark): When the glucose falls below 14 mmol/L, switch the fluid to 10% dextrose at 125 mL/hour while continuing the FRIII unchanged. Consider reducing the FRIII to 0.05 units/kg/hour if the glucose is falling faster than 3 mmol/L/hour. [1]

6. Investigate and treat the precipitant (1 mark): Insulin omission is the precipitant here, but I would still screen for an intercurrent infection (blood cultures, urine culture, chest X-ray) and do an ECG and troponin. The diabetes and mental health team should review to address the reasons for insulin omission and to prevent recurrence. [1]

Complications to anticipate (3 marks): [1]

1. Cerebral oedema: He is 19, within the higher-risk age group. Watch for headache, vomiting, drowsiness, bradycardia, rising blood pressure. The Glaser study identified low initial PaCO2 (he has 14, very low), high urea (he has 12), and bicarbonate administration as risk factors [2]. I will NOT give bicarbonate. If cerebral oedema is suspected, reduce fluids, give mannitol 0.5-1 g/kg or 3% saline, and move to ICU.

2. Hypokalaemia: The potassium is currently 5.8 but will fall. I will check hourly and replace aggressively. This is the most dangerous metabolic complication — hypokalaemic arrhythmia is a leading cause of death during treatment. [1]

3. Hypoglycaemia: I will switch to dextrose at glucose below 14 and reduce the FRIII if the fall is too rapid. Hourly glucose monitoring is mandatory. [1]

Communication (1 mark): I will explain to the patient and his mother that this is a life-threatening condition caused by stopping insulin, that the treatment takes about 24 hours with close monitoring in ICU, and that the diabetes team will work with him on sick-day rules (never stop insulin during illness — you often need more) and on the reasons for the omission. [1]

SAQ 2 — Differentiating DKA from HHS and Euglycaemic DKA (10 marks, 20 minutes)

Prompt: Compare and contrast the diagnostic criteria, pathophysiology, and management principles of (a) classic DKA, (b) hyperosmolar hyperglycaemic state, and (c) euglycaemic DKA. Explain how the pathophysiology of each dictates the management. [1]

Model Answer

Classic DKA (3 marks): [1]

Diagnostic criteria: glucose above 11 mmol/L, ketones above 3 mmol/L, pH below 7.3, bicarbonate below 15, elevated anion gap. Pathophysiology: absolute insulin deficiency (type 1) causes unchecked lipolysis and hepatic ketogenesis, producing ketoacidosis. The osmotic diuresis causes dehydration. Management: fluid resuscitation (0.9% saline protocol), fixed-rate insulin at 0.1 units/kg/hour to suppress ketogenesis, potassium replacement (target 4-5.5), dextrose at glucose below 14, resolution by ketones below 0.6. The key principle is that insulin suppresses ketogenesis — the ketone level drives the duration of therapy [4].

HHS (3 marks): [1]

Diagnostic criteria: glucose above 33 mmol/L, osmolality above 320 mOsm/kg, ketones below 3 mmol/L, pH above 7.3, bicarbonate above 15. Pathophysiology: relative insulin deficiency (type 2) — there is enough insulin to suppress lipolysis and ketogenesis (so no significant ketoacidosis) but not enough to prevent marked hyperglycaemia, which develops over days to weeks, causing profound dehydration (6-9 litres) and hyperosmolality. Management differences: fluid is even more critical and more cautious (elderly patients, cardiac and renal comorbidity); insulin is at lower doses (0.05 units/kg/hour or fluid alone initially); there is no ketone target (resolution is glucose and osmolality-driven); prophylactic low-molecular-weight heparin is routine (high thrombotic risk); and the precipitant (usually infection or infarction) is the primary determinant of survival [1]. Mortality is 10-20%, much higher than DKA.

Euglycaemic DKA (3 marks): [1]

Diagnostic criteria: DKA with a glucose below 11 mmol/L — all other criteria (ketones above 3, pH below 7.3, bicarbonate below 15) are met, but the glucose is deceptively normal. Pathophysiology: classically seen with SGLT2 inhibitors, which cause glucosuria that lowers glucose (preventing the usual hyperglycaemia), while the resulting low insulin-to-glucagon ratio drives ketogenesis. Also seen in pregnancy, starvation, and alcohol misuse [3]. Management: identical to classic DKA — FRIII at 0.1 units/kg/hour with fluid, but dextrose is started from the outset (because the glucose is already below 14). The trap is missing the diagnosis because the glucose is reassuring; the defence is to check ketones in any acidotic diabetic, especially on an SGLT2 inhibitor.

How pathophysiology dictates management (1 mark): [1]

In all three, the common thread is insulin deficiency. But the degree of residual insulin determines the phenotype: none (DKA — ketosis), some (HHS — no ketosis but severe hyperglycaemia), or SGLT2-modulated (euglycaemic DKA — ketosis without hyperglycaemia). The management principle flows from this: the DKA protocol targets ketogenesis (insulin until ketones clear), the HHS protocol targets hyperosmolality (fluid-dominant, cautious insulin), and the euglycaemic DKA protocol is the DKA protocol with early dextrose. [1]

SAQ 3 — Precipitant Recognition and Sick-Day Education (8 marks, 15 minutes)

Prompt: A 62-year-old woman with type 2 diabetes (metformin, empagliflozin, gliclazide) is admitted with a pneumonia. Three days into admission, she develops euglycaemic DKA (glucose 10, ketones 4.2, pH 7.14). Explain the mechanism, the immediate and longer-term management of the SGLT2 inhibitor, and the sick-day rule education you will provide. [1]

Model Answer

Mechanism (2 marks): The empagliflozin caused glucosuria, lowering her glucose. The low glucose suppressed endogenous insulin secretion and raised glucagon. The high glucagon-to-insulin ratio, amplified by the stress of pneumonia (counter-regulatory hormones), drove hepatic ketogenesis. The glucose stayed near-normal because the drug kept excreting it, masking the ketoacidosis — euglycaemic DKA. The metformin was held on admission (standard sick-day rule), so it is not the cause [3].

Immediate management (2 marks): Cease the empagliflozin immediately. Start the DKA protocol: FRIII at 0.1 units/kg/hour, fluid resuscitation with 0.9% saline, dextrose from the outset (glucose is already below 14), potassium replacement. Treat the pneumonia. The DKA will not resolve until the infection is controlled. [1]

Longer-term management of the SGLT2 inhibitor (2 marks): The cardiovascular and renoprotective benefits of SGLT2 inhibitors are substantial and proven. I would NOT stop the empagliflozin permanently. I would resume it once the patient is fully recovered, eating and drinking normally, and the DKA has resolved — but with clear education about the sick-day rule and the warning symptoms of DKA (nausea, vomiting, abdominal pain). If she has recurrent euglycaemic DKA on the SGLT2 inhibitor despite adherence to sick-day rules, I would reconsider the drug with the diabetes team. [1]

Sick-day rule education (2 marks): I would teach the patient that during any acute illness with vomiting, diarrhoea, fever, or reduced oral intake, she should hold the empagliflozin and the metformin (but never stop her insulin or sulfonylurea without advice), maintain hydration, check glucose and ketones if unwell, and seek medical help if ketones are above 1.5 or she cannot keep fluids down. I would provide this in writing and involve the diabetes educator. The principle is that the drugs that can cause dehydration or acidosis (SGLT2 inhibitors, metformin, ACE inhibitors, diuretics, NSAIDs) should be held during acute illness, while insulin must continue. [1]