Severe diabetic ketoacidosis – a remarkable case study

Diabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of type 1 diabetes caused by insulin deficiency. It is characterized by raised blood glucose (hyperglycemia), metabolic acidosis, and increased blood/urine ketones.

Dehydration and electrolyte disturbance are common and affected patients may develop some degree of acute kidney injury (AKI) consequent on fluid loss (hypovolemia) due to osmotic diuresis associated with severe hyperglycemia. DKA evolves rapidly over a short time frame (hours rather than days) and can occur (rarely) in those with type 2 diabetes. 

This DKA case study is particularly noteworthy because of the severity of the hyperglycemia and acid-base disturbance, and the fact that the patient survived such profound metabolic disturbance and associated life-threatening hemodynamic changes.

The case concerns a 33-year-old woman with ”brittle” type 1 diabetes treated with continuous subcutaneous insulin infusion (insulin pump). She had, in common with many brittle diabetics, a history of gastroparesis (delayed stomach emptying). 

Some 36 hours prior to emergency hospital admission she complained of abdominal pain and vomiting after attending a party. Her condition deteriorated before transfer to hospital. The ambulance team reported a rapid decline in Glasgow Coma Score (GCS) from 13 to 3 in only 10 minutes, sinus tachycardia, undetectable peripheral pulse, and hypotension (BP 99/52 mmHg). 

Clinical examination revealed severe dehydration and respiratory distress (respiration rate 40 breaths/min). Urgent intubation was necessary and systolic blood pressure dropped further to 55 mmHg. Initial (fingerstick) blood glucose was above the upper detection limit of the analyzer and blood ketones were >8.0 mmol/L.

Blood gas analysis revealed severe metabolic acidosis (pH 6.74, bicarbonate 5 mmol/L, pCO₂ 39.9 mmHg (5.3 kPa) and hypoxemia (pO₂ 50.2 mmHg, 6.7 kPa). Among other abnormal laboratory test results, perhaps the most remarkable was serum glucose 107 mmol/L (1924 mg/dL). (Serum glucose >33 mmol/L (600 mg/dL) is rarely seen in patients with DKA.) 

White blood count (32.8x10⁹/L), C-reactive protein (789 nmol/L) and lactate (4.6 mmol/L) were also grossly elevated. Other laboratory testing revealed severe hyponatremia (sodium 113 mmol/L), severe hyperkalemia (6.7 mmol/L) and acute kidney failure (serum creatinine 332 µmol/L). 

Following presumptive diagnosis of DKA, sepsis and acute renal failure, the patient was treated with aggressive IV fluids, norepinephrine, bicarbonate, and insulin, IV bolus and drip. Intensive investigation for evidence of infection proved fruitless.

With treatment, the patient’s condition improved over the following days and she was extubated. Normal renal function was restored after 2 days. 

In discussion of this case history, the authors briefly review the pathogenesis and treatment of DKA in general terms. They also highlight some interesting features of this case. One aspect discussed relates to the blood gas results on admission, in particular the curiously normal pCO₂ (39.9 mmHg, 5.3kPa). 

Metabolic acidosis usually provokes compensatory hyperventilation and reduced pCO₂. The authors propose plausible theories to explain the much higher than expected pCO₂ in this case. They also propose that the remarkably high blood glucose in this case is the result of the combined effect of reduced glucose elimination consequent on renal failure and the presence of gastroparesis.