Young man with vomiting, drowsiness and severe dehydration
A 22-year-old male university student is brought to the emergency department of a district hospital at 2 a.m. after two days of vomiting and increasing drowsiness. He has had polyuria and polydipsia for three weeks and was diagnosed with type 1 diabetes eight months ago but stopped insulin four days ago because he ran out and could not afford more. On examination he is drowsy but arousable, with deep sighing respirations, dry mucous membranes, and capillary refill of 4 seconds. Pulse 118/min, BP 92/60 mmHg, temperature 37.1°C, weight 55 kg. Bedside glucose is 486 mg/dL; urine ketones are 4+. Venous blood gas: pH 7.10, pCO2 22 mmHg, bicarbonate 8 mmol/L. Sodium 131 mmol/L, potassium 5.6 mmol/L, chloride 98 mmol/L, creatinine 1.5 mg/dL. The hospital has no intensive care unit and only one functioning infusion pump.
1. Outline your first two hours of fluid and electrolyte management, including the volume and type of fluid and how you will handle the serum potassium of 5.6 mmol/L. Explain the reasoning behind each step.
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Fluids. Start 0.9% sodium chloride 1 L (about 15–20 mL/kg) over the first hour, because this patient is hypotensive and significantly volume-depleted. Reassess pulse, BP, capillary refill, and urine output after each litre rather than following a fixed total; in a 55-kg adult, give a second litre over the next 1–2 hours if he remains tachycardic or oliguric. Avoid rapid bicarbonate-containing fluids.
Potassium. The serum potassium is 5.6 mmol/L, so do not add potassium yet. Hyperkalaemia in DKA reflects insulin deficiency and extracellular shift, not total-body excess; total-body potassium is almost certainly low. Recheck potassium hourly. Once it falls below 5.2 mmol/L, add 20–40 mmol/L of potassium chloride to the maintenance fluid. If it falls below 3.3 mmol/L, hold insulin and give potassium more aggressively before restarting.
Reasoning. Insulin drives potassium into cells, so starting insulin without a potassium plan can cause fatal hypokalaemia; waiting for potassium to normalise before giving any insulin, however, prolongs acidosis. Fluids first, insulin second, potassium replacement as soon as the level allows is the safe sequence.
2. When and how will you start insulin, and how will you adjust the regimen when the glucose falls to 220 mg/dL? What monitoring is essential in a ward without intensive care?
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Start a fixed-rate intravenous insulin infusion of 0.1 units/kg/hour (5.5 units/hour) after the first litre of fluid and after confirming potassium is not below 3.3 mmol/L. Do not give a bolus. The aim is a fall in glucose of 50–75 mg/dL/hour; faster falls risk osmotic shifts and cerebral oedema.
When glucose reaches about 250 mg/dL, do not stop insulin. Add 5% dextrose to the intravenous fluid - for example, alternate 0.9% saline with 5% dextrose - and continue insulin at 0.05–0.1 units/kg/hour until the acidosis resolves (pH above 7.30, bicarbonate above 15 mmol/L, anion gap closed). Insulin is needed to switch off ketogenesis, not just to lower glucose.
Ward monitoring: hourly capillary glucose, hourly potassium for the first 6 hours, venous pH and bicarbonate every 2–4 hours, strict fluid balance and urine output, neurological checks for headache or drowsiness, and cardiac rhythm if potassium is abnormal. Without intensive care, write the monitoring on a chart and assign a named nurse; the commonest error is stopping insulin when glucose normalises while acidosis persists.
3. Name two interventions that are often done incorrectly in DKA and explain the harm they can cause.
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Routine intravenous bicarbonate. It is often given for a low pH, but in DKA the acidosis is due to ketones and will correct with fluids and insulin. Bicarbonate can cause paradoxical intracellular acidosis, worsen hypokalaemia, shift the oxygen dissociation curve, and provoke cerebral oedema; it is generally reserved for pH below 6.9 with haemodynamic compromise.
Rapid large-volume fluid resuscitation or stopping insulin too early. Giving several litres quickly, especially to a young patient, can produce rapid osmotic shifts and cerebral oedema. Stopping the insulin infusion when glucose reaches normal leaves ketogenesis untreated and causes rebound acidosis. A third common error is giving potassium too early when the serum level is still high, which risks hyperkalaemic arrhythmia; equally, failing to add potassium once insulin has been started risks dangerous hypokalaemia. The safe approach is protocol-driven, reassessed hourly, with glucose and potassium checked together.