DKA and HHS

Both are hyperglycaemic crises driven by insufficient insulin. The difference is whether there is enough insulin to prevent fat breakdown.

DKA — typically type 1. Insulin is essentially absent, so the body burns fat, producing ketones, producing acidosis. Glucose is high but often under 600.

HHS — typically type 2. There is some residual insulin: enough to suppress ketone production, but not enough to control glucose. Glucose climbs extremely high, dragging enormous volumes of water into the urine. No significant acidosis, but profound dehydration.

HHS develops slowly over days and carries the higher mortality, largely because it is caught later and the patient is often older with less reserve.

The DKA-specific findings all trace back to acid:

• Kussmaul respirations — deep, rapid, laboured breathing as the lungs blow off CO₂ to compensate
• Fruity or acetone breath from exhaled ketones
• Abdominal pain, nausea, and vomiting, which can mimic a surgical abdomen

The findings shared by both are dehydration findings: extreme thirst, polyuria progressing to oliguria, dry mucous membranes, tachycardia, hypotension, and declining mental status. Neurological changes are generally more pronounced in HHS because the osmolarity is higher.

Both conditions follow the same sequence, and the order is the point.

Fluids first. These patients are litres down. Isotonic crystalloid restores circulating volume and by itself lowers glucose substantially through dilution and improved renal clearance.

Then insulin, as a regular insulin infusion. Only regular insulin is given IV.

Then dextrose, added once glucose approaches roughly 250 mg/dL — while the insulin infusion continues. This surprises people, but the insulin is still needed to clear ketones and close the acidosis. Dextrose prevents hypoglycaemia in the meantime.

This is the highest-yield idea in the entire topic.

On arrival, serum potassium often reads normal or high — acidosis has driven potassium out of the cells and into the serum. But total body potassium is severely depleted, because it has been pouring out through the kidneys for days.

The moment insulin starts, potassium moves back into cells and the serum level falls fast. A patient who looked fine on arrival can drop into dangerous hypokalemia within an hour or two.

So: check potassium before starting insulin, and monitor it closely throughout. If potassium is already low, it is replaced before insulin begins. Continuous cardiac monitoring is standard throughout.