Hepatic Failure/GI/Endocrine Emergencies

Patients with HHS do not normally develop ketoacidosis. Although there is an overall insulin

deficiency in both DKA and HHS, there is enough insulin secretion to prevent ketogenesis in

patients with HHS.

Lack of access to water, either because of the illness itself or because of an altered thirst response

in older adult patients, can worsen the severity of dehydration in the setting of hyperglycemia.

Typically, DKA and HHS are caused by an insufficiency of insulin in patients with diabetes combined

with another potential trigger such as infection, medication nonadherence, myocardial infarction,

cerebrovascular accident, pancreatitis, and certain drugs (i.e., steroids, diuretics, vasopressors,

antipsychotics, cocaine, sodium-glucose cotransporter 2 inhibitors).

Management

Primarily involves fluid resuscitation, correction of hyperglycemia, and electrolyte (mainly

potassium) replacement. Correction of acidemia may also be indicated.

Patients are often profoundly hypovolemic. Total body water deficits may be as high as 10–12 L and

should be replaced within the first 24 hours.

In the absence of concomitant cardiogenic shock, 0.9% sodium chloride should be administered

at a rate of 15–20 mL/kg (typically 1–1.5 L) for the first hour. Thereafter, fluid administration

is titrated to hemodynamic parameters and urine output (i.e., fluid infusion rates typically

250–500 mL/hour).

ii.

Patients with mild dehydration and normal or high sodium concentrations can be changed to

0.45% sodium chloride infused at a rate of 250–500 mL/hour.

iii.

Maintenance fluids can be switched to a dextrose-containing fluid (often 5% dextrose with

0.45% sodium chloride) once BG concentrations have dropped to less than 200 mg/dL in DKA

and less than 300 mg/dL in HHS.

iv.

Serum sodium concentration should be considered when choosing resuscitation fluid because

rapid correction of hypernatremia may have severe consequences.

Recent studies suggest that time to DKA resolution may be shorter when balanced crystalloids

are used for resuscitation in place of saline, but further studies are needed to confirm benefit.

Insulin therapy is the main treatment modality of DKA and HHS.

Insulin corrects hyperglycemia and inhibits the release of free fatty acids, which decreases

ketone formation and corrects acidosis.

ii.

Intravenous regular insulin is preferred to subcutaneous insulin because of its short half-life

and ease of titration.

iii.

Initiate with a 0.1-unit/kg intravenous bolus, followed by a 0.1-unit/kg/hour continuous

infusion. Bolus dosing may vary by patient and institution; if bolus is given, BG should be

monitored closely to avoid hypoglycemia. An alternative approach, without an initial bolus

but initiated at a higher continuous infusion rate (0.14 unit/kg/hour), provides a time similar

to DKA resolution.

iv.

The insulin infusion should subsequently be titrated on an hourly basis to decrease BG

concentrations by 50–75 mg/dL/hour.

DKA: Decrease dose to 0.02–0.05 unit/kg/hour once BG concentrations drop to 200 mg/dL,

and maintain a BG of 150–200 mg/dL until ketoacidosis has resolved.

vi.

HHS: Decrease dose to 0.02–0.05 unit/kg/hour once BG concentrations drop to 300 mg/dL,

and maintain a BG of 200–300 mg/dL until mental status changes have resolved.