SMLE Clinical Reasoning Walkthrough: Differentiating DKA and HHS

Compare diabetic ketoacidosis (DKA) with hyperosmolar hyperglycemic state (HHS), then practise recognition, the initial management decision, and the mechanism of ketosis.

Clinical case: DKA or HHS?

A 68-year-old man with type 2 diabetes develops confusion and weakness after an infection and missed medication. He is dehydrated, with blood pressure 88/55 mmHg and pulse 122 beats/min. Glucose is 850 mg/dL, potassium 4.2 mmol/L, pH 7.34, bicarbonate 20 mmol/L, urine ketones trace, and serum osmolality 345 mOsm/kg.

Which diagnosis best explains the overall presentation?

1. Diabetic ketoacidosis
2. Hyperosmolar hyperglycemic state
3. Hypoglycemic encephalopathy
4. Lactic acidosis alone

Best answer: hyperosmolar hyperglycemic state. The marked hyperglycemia, hyperosmolality, dehydration, and altered mental status support HHS. The supplied results do not show the significant ketosis and acidosis required for DKA. Infection can precipitate a hyperglycemic crisis and can coexist with it; this vignette does not exclude concurrent infection or sepsis.

Distinguishing DKA and HHS

Do not diagnose either condition from glucose alone. Read the ketones and acid-base results, assess osmolality when HHS is suspected, and consider mixed DKA/HHS rather than forcing every patient into one category.

Why insulin deficiency produces ketosis

Insulin normally restrains adipose-tissue lipolysis. When that restraint is lost, stored triglycerides are broken down into fatty acids and glycerol. The liver uses fatty acids for ketone production; glycerol can contribute to gluconeogenesis. This connects insulin deficiency with hyperglycemia, ketogenesis, and metabolic acidosis.

Insulin deficiency can accompany type 1 diabetes and other forms of diabetes or pancreatic disease. Polyuria, polydipsia, and weight loss warrant assessment. Long-term insulin replacement, glucose monitoring, and education are distinct from the monitored emergency management of DKA or HHS.

DKA recognition and management

Diagnose DKA with diabetes or hyperglycemia, ketosis and metabolic acidosis; remember that SGLT2-associated DKA can occur without marked hyperglycemia. Start intravenous isotonic saline or balanced crystalloid, adapting the rate to hydration, cardiac and renal status. Check potassium before insulin: if potassium is below 3.5 mmol/L, replace it and delay insulin until potassium is above 3.5 mmol/L. Follow a monitored insulin and electrolyte protocol, adding dextrose as glucose falls so insulin can continue to clear ketones. Assess resolution using ketones and acid-base recovery rather than glucose or the anion gap alone. Treat the precipitant and overlap subcutaneous insulin before stopping the infusion.

Volume replacement restores perfusion, while insulin can lower potassium rapidly and cause dangerous hypokalemia. Total body potassium is depleted even when the initial measured concentration is normal or high. Frequent glucose, electrolyte, ketone and acid-base measurements guide treatment. Bicarbonate is not routine treatment and is considered only in severe acidosis under the local protocol. Hyperchloremic acidosis after treatment can make the anion gap misleading as a resolution criterion. Search for infection, missed insulin and other precipitants; consider euglycemic DKA when a patient taking an SGLT2 inhibitor has ketosis and acidosis.

Potassium before insulin

If potassium is below 3.5 mmol/L, begin replacement and delay insulin until potassium is above 3.5 mmol/L. Use a monitored local protocol and continue serial electrolyte measurements. The initial concentration can look normal or high despite total-body depletion.

Fluid replacement also requires reassessment. Older adults and people with cardiac or renal impairment need particular care to avoid overload. HHS requires controlled correction of glucose and osmolality; the fastest possible glucose reduction is not the goal.

Practice case: the first management step

A 19-year-old woman with type 1 diabetes presents with vomiting, deep rapid breathing, glucose 460 mg/dL, pH 7.18, and positive serum ketones. Serum potassium is 4.0 mmol/L. What is the most appropriate first step in management?

1. Intravenous isotonic saline infusion
2. Subcutaneous rapid-acting insulin
3. Intravenous sodium bicarbonate
4. Oral rehydration solution

Best answer among these options: intravenous isotonic saline. Initial isotonic fluid replacement addresses dehydration. Check potassium and follow a monitored insulin and electrolyte protocol. Bicarbonate is not routine at the pH supplied. Selected uncomplicated cases may receive subcutaneous insulin with appropriate monitoring, but oral fluids alone are inadequate for this presentation.

Practice question: lipolysis

Insulin deficiency leads to unchecked adipose tissue lipolysis, which results in an increased systemic production of:

1. Fatty acids
2. Triglycerides
3. Low-density lipoproteins
4. Amino acids

Best answer: fatty acids. Triglyceride breakdown releases fatty acids and glycerol. Amino acids arise from protein breakdown, while LDL is a lipoprotein particle rather than the direct product of adipose lipolysis. Fatty acids supply substrate for ketogenesis.

Monitoring recovery

Follow ketones and acid-base recovery, not glucose alone. The consensus defines DKA resolution using blood ketones below 0.6 mmol/L together with pH at least 7.3 or bicarbonate at least 18 mmol/L. Do not use the anion gap or urine ketones alone to decide that DKA has resolved. Treat the precipitating illness and plan the transition to subcutaneous insulin and ongoing diabetes care.

References

• ADA/EASD and partner societies: Hyperglycemic Crises in Adults With Diabetes, 2024 consensus report
• NICE NG17: Type 1 diabetes in adults