Clinical Presentation

The clinical manifestations of DKA are directly related to the three primary metabolic derangements—hyperglycemia, volume depletion, and acidosis. Hyperglycemia causes an increased osmotic load with movement of intracellular water into the vascular compartment. The ensuing osmotic diuresis gradually leads to volume loss in addition to renal losses of sodium, chloride, potassium, phosphorous, calcium, and magnesium. Initially, patients may compensate by increasing their fluid intake. In this initial period, polyuria and polydipsia are usually the only symptoms until ketonemia and acidosis develop. As the acidosis progresses, the patient develops a compensatory augmented ventilatory response. Increased ventilation is physiologically stimulated by acidemia to diminish the P co2 and thus counter the metabolic acidosis. The acidosis combined with the effects of prostaglandin 12 and E2 lead to the peripheral vasodilation despite profound levels of volume depletion. Prostaglandin release is also felt to play a role in the often unexplained nausea, vomiting, and abdominal pain that are frequently seen at presentation, especially in children. Vomiting, which may be a maladaptive physiologic response to diminish the acid load, unfortunately exacerbates the renal potassium losses and contributes to rapidly progressive volume loss, weakness, and weight loss. As volume depletion progresses, poor absorption of subcutaneous insulin renders it ineffective. Mental confusion or coma may be present at the time of presentation; these symptoms are much more likely with serum osmolarity >340 mOsm/L. If the serum osmolarity is <340 mOsm/L in a comatose patient, another cause of the coma should be sought.

Abnormal vital signs may be the only significant physical findings at the time of presentation. Tachycardia and either significant orthostasis or hypotension are usually present. Poor skin turgor denotes significant volume depletion. With severe acidemia, both the rate and depth of respirations are elevated secondary to compensatory hyperventilation (Kussmaul respirations). Acetone produces the characteristic fruity odor on the breath found in some patients. The absence of fever does not exclude infection as a source of the patient's ketoacidosis. Hypothermia is occasionally present.

Abdominal pain and tenderness can be due to gastric dilatation, ileus, or pancreatitis. Due to the frequency of abdominal pain and the presence of an elevated serum amylase in both DKA and pancreatitis, distinguishing the diagnoses may be difficult. Elevated serum lipase is more specific to pancreatitis and should be used to differentiate the two conditions.

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