Hepatic Failure/GI/Endocrine Emergencies

Adrenal crisis (i.e., acute adrenal insufficiency or Addisonian crisis) is a life-threatening disorder

caused by glucocorticoid (and possibly mineralocorticoid) deficiency.

Adrenal crisis necessitating hospital admission has an incidence of 3.3 per 100 patient-years in

those with chronic adrenal insufficiency.

Critical illness–related corticosteroid insufficiency (CIRCI) is a separate entity from adrenal crisis.

The prevalence of CIRCI is about 10%–20% but depends on the definition used and the population

evaluated. Prevalence rates as high as 60% for patients with septic shock have been reported.

Clinical presentation of DKA

Current guidelines define DKA as a combination of hyperglycemia (BG greater than 200 mg/dL

or prior history of diabetes), ketosis (positive urine or serum ketones), and acidosis (pH less than

7.30 and/or bicarbonate concentration less than 18 mmol/L). Patients with severe DKA present with

severe acidemia (pH less than 7), a serum bicarbonate less than 10 mmol/L, and depressed mental

status (stupor or coma).

Guidelines were updated with a new definition of hyperglycemia in 2024 to reflect the increasing

percentage of patients who present with euglycemic DKA.

Serum glucose concentrations are usually less than 800 mg/dL but may be more elevated in

patients who are comatose. In the setting of starvation, pregnancy, treatment with insulin prior to

presentation, or use of sodium-glucose- cotransporter 2 inhibitors, glucose may be normal or only

mildly elevated.

A lack of insulin leads to reduced glucose uptake, which, together with increased counterregulatory

hormone (catecholamines, cortisol, glucagon, and growth hormone) release, leads to increased

lipolysis. The released free fatty acids are metabolized in the liver to ketone bodies (β-hydroxybutyrate

and acetoacetate), resulting in ketonemia and elevated anion gap metabolic acidosis.

deteriorate rapidly.

Typically occurs in young, leaner patients with type 1 diabetes

Patients may present with symptoms of nausea and vomiting (80% of patients; more indicative of

DKA than of HHS), polyuria, polydipsia, weight loss, abdominal pain (30% of patients), and fruity

breath from acetone in the blood. Signs of DKA include tachycardia, poor skin turgor, hypotension

(because of intravascular volume loss from osmotic diuresis), and Kussmaul respirations (due to

severe acidemia).

Measured serum potassium may be high because hyperosmolality, and lack of endogenous insulin

causes intracellular potassium ions to shift into the extracellular space. However, patients typically

have a relative deficiency of total body potassium, which can be worsened with insulin treatment.

HHS is defined as BG greater than 600 mg/dL and elevated serum osmolarity (calculated effective

serum osmolality greater than 300 mOsm/kg or total serum osmolality greater than 320 mOsm/kg)

with pH greater than 7.3 and serum bicarbonate greater than or equal to 15 mmol/L. Ketones are

not present or only measured in small amounts.

HHS presentation is often later in the disease course than DKA (because of the lack of ketosis),

and symptoms evolve over days to weeks. Patients also have higher degrees of dehydration owing

to osmotic diuresis.

More common in older patients with obesity with type 2 diabetes

confusion is much more apparent in HHS and is directly related to the serum osmolality.