Patients with DKA present initially with polyuria, polydipsia, nausea, and vomiting. Abdominal pain occurs frequently and can mimic an acute abdomen. The abdomen may be tender from vomiting or distended secondary to a paralytic ileus. The presence of polyuria, despite a state of clinical dehydration, indicates osmotic diuresis and differentiates patients with DKA from patients with gastroenteritis or other gastrointestinal disorders. Respiratory compensation for acidosis results in tachypnea with deep (Küssmaul) respirations. The fruity odor of acetone frequently can be detected on the patient’s breath. An altered mental status can occur, ranging from disorientation to coma.
Laboratory studies reveal hyperglycemia (serum glucose concentrations ranging from 200 mg/dL to >1000 mg/dL).Arterial pH is below 7.30, and the serum bicarbonate concentration is less than 15 mEq/L. Serum sodium concentrationsmay be elevated, normal, or low, depending on the balance ofsodium and free water losses. The measured serum sodium concentration is artificially low, however, because of hyperglycemia. Hyperlipidemia also contributes to the decrease inmeasured serum sodium. The level of blood urea nitrogen(BUN) can be elevated with prerenal azotemia secondary todehydration. The white blood cell count is usually elevatedand can be left-shifted without implying the presence ofinfection. Fever is unusual and should prompt a search forinfectious sources that may have triggered the episode ofDKA.
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Therapy for patients with DKA involves careful replacement of fluid deficits, correction of acidosis and hyperglycemia via insulin administration, correction of electrolyte imbalances, and monitoring for complications of treatment. The optimal approach to management of DKA must strike a balance between adequate correction of fluid losses and avoidance of rapid shifts in osmolality and fluid balance. The most serious complication of DKA and its treatment is cerebral edema and cerebral herniation.
A patient with severe DKA is assumed to be approximately 10% dehydrated. If a recent weight measurement is available, the precise extent of dehydration can be calculated. An initial intravenous (IV) fluid bolus of a glucose-free isotonic solution (normal saline, lactated Ringer solution) at 10 to 20 mL/kg should be given to restore intravascular volume and renal perfusion. The remaining fluid deficit after the initial bolus should be added to maintenance fluid requirements, and the total should be replaced slowly over 36 to 48 hours. Ongoing losses resulting from osmotic diuresis usually do not need to be replaced unless urine output is large or signs of poor perfusion are present. Osmotic diuresis is usually minimal when the serum glucose concentration decreases to less than 300 mg/dL. To avoid rapid shifts in serum osmolality, 0.9% sodium chloride can be used as the replacement fluid for the initial 4 to 6 hours, followed by 0.45% sodium chloride.
Hyperglycemia. Fast-acting soluble insulin should be administered as a continuous IV infusion (0.1 U/kg/hour). Serum glucose concentrations should decrease at a rate no
Figure 171-2 Pathophysiology of diabetic ketoacidosis.
faster than 100 mg/dL/hour. When serum glucose concentrations decrease to less than 250 to 300 mg/dL, glucose should be added to the IV fluids. If serum glucose concentrations decrease to less than 200 mg/dL before correction of acidosis, the glucose concentration of the IV fluids should be increased, but the insulin infusion should not be decreased by more than half, and it should never be discontinued before resolution of acidosis.