Laboratory Findings

The family physician should expect the hematocrit and hemoglobin to be elevated in these patients as a result of hemoconcentration. A low value with dehydration indicates a source of blood loss, such as a stress ulcer in the stomach. A white blood cell (WBC) count as high as 20,000 cells/ mm3 without other evidence of infection is not unusual but should trigger a thorough evaluation, especially of the chest, where the signs of pneumonia may be confounded by the dehydration. A reduction in oxygen partial pressure (Po2) with marked hyperventilation is an ominous sign of lung compromise. Antibiotic coverage after appropriate cultures is indicated until the clinical situation is better defined.

The diagnostic hyperglycemia associated with reduced bicarbonate (HCO3-, usually designated "CO2" on a basic metabolic profile [BMP]) is accompanied by hyperkalemia in approximately 30% of patients, normokalemia in 50%, and hypokalemia in 15% to 20%. To some extent, serum potassium depends on the severity of the acidosis and duration of the polyuria or vomiting. Hypokalemia is the most dangerous clinical scenario because insulin treatment can cause a precipitous decline in potassium, which may weaken the hyperventilatory effort, causing more profound acidosis and cardiopulmonary arrest. The finding of hypokalemia (and probably even normokalemia) on BMP or electrocardiogram (ECG) with good urine output indicates immediate potassium replacement. In general, hypokalemia on the initial BMP indicates a potassium deficit greater than 400 mEq. Hyperkalemia at the onset of DKA indicates a loss of about 200 mEq of potassium before presentation.

Serum sodium and chloride may also be affected by the extent of water depletion or urine losses caused by the osmotic diuresis or sodium bound to the ketonic anions. Thus, serum sodium of 145 mEq/L would indicate a predominant water deficiency, whereas 129 mEq/L suggests more significant sodium losses. In either case, water is always deficient despite dilutional changes in serum sodium caused by hyperglyce-mia, and patients require water and salt repletion therapies. Importantly, the anion gap indicates the severity of the acidosis. Values in the high 30s suggest tissue hypoxia and possible lactate production in addition to the ketonic anions. This could be a dangerous sign if no improvement is noted after fluid resuscitation and insulinization. Lactic acidosis accompanying DKA is rare unless there is an underlying serious diagnosis such as sepsis or a myocardial infarction. However, a patient who is near death before presenting may have perfusion failure initiating lactate production.

Other abnormalities in DKA include prerenal azotemia, although the serum creatinine can be elevated artifactually by ketones in the blood. If so, creatinine promptly normalizes as ketones are cleared with treatment. Phosphate may shift the same as potassium in metabolic acidosis. Total-body phosphate is depleted, but repletion is usually deferred to the subacute phase of treatment, unless extreme weakness does not improve and extremely low serum phosphates are found. If drawn, amylase may be elevated without specific signs of pancreatitis.

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