Ihe laboratory parameters used to define HHNS—glucose >400, osmolarity >315, ph >7.3, and negative serum ketones—are fairly arbitrary. Ihose values are found in the American Diabetes Association position statement for Hospital Admission Guidelines for Diabetes Mellitus. 9 Depending on concurrent illness and duration of disease, a "mixed disorder" with metabolic acidosis may be found. Essential laboratory tests should include serum glucose, electrolytes, calculated and measured serum osmolality, blood urea nitrogen (BUN), ketones, and creatinine, as well as cell blood count. In view of the frequency of precipitating causes and underlying medical conditions associated with HHNS, a broad range of ancillary studies should be considered. Ihese should include blood cultures, sputum collection, urinalysis and culture, liver and pancreatic enzyme determinations, cardiac enzymes, thyroid function, and coagulation profiles. Other ancillary studies such as chest x-ray, electrocardiogram, computed tomography, and lumbar puncture and toxicologic studies should be considered. Arterial blood-gas determination is of added value only if there is suspicion of a respiratory component to the acid-base abnormality, as both P co2 and pH can be predicted from HCO3- concentration obtained in venous electrolytes (see Chap, 21, "Acid-Base Disorders").
In general, electrolyte abnormalities reflect a contraction alkalosis with varying degrees of wide-anion-gap metabolic acidosis. Initial serum electrolyte determinations can be reported as seemingly normal because the metabolic alkalosis and acidosis may largely cancel out each other's effect. A lack of careful analysis of serum chemistries may lead to a delayed appreciation of the severity of the underlying abnormalities, including volume loss. Ihe only clue to a serious derangement may be the widened anion gap. Serum sodium is suggestive but not a reliable indicator of degree of volume contraction. Although the patient is certainly total body sodium depleted, the serum sodium (even corrected for the glucose elevation) may be low, normal, or elevated. Measured serum sodium, however, is often reported as low due to the dilutional effect of hyperglycemia. It is important to correct for this effect. Serum sodium decreases by approximately 1.6 meq per every 100 mg/dL increase in serum glucose above 100 mg/dL or corrected [N»*J ■ mcuutd (N.I 4 ' * * if"^'~ "»)
Elevated corrected serum sodium during severe hyperglycemia is usually explainable only by significant volume contraction. Normal sodium level or hyponatremia usually (but not invariably) suggests modest dehydration.
Serum osmolality has also been shown to correlate with severity of disease as well as neurologic impairment and coma. A calculated effective serum osmolality excludes osmotically inactive urea, which is usually included in laboratory measures of osmolarity. The formula for calculated effective osmolality is
Normal serum osmolality range is approximately 275 to 295 mosm/kg. Values above 300 mosm are usually clinically indicative of significant hyperosmolality.
Hypokalemia probably poses the most immediate electrolyte-based risk and should be anticipated. Losses of 300 to 600 meq are not uncommon. Initial values may be reported as normal during a period of severe volume contraction. Again, the patient is surely total body potassium depleted, but acid-base abnormalities may conspire to mask or augment the deficit. As intravascular volume is replaced, potassium losses become more apparent. Patients who have low serum K+ during the period of severe volume contraction are at greatest risk for dysrhythmia. The importance of K + replacement during periods of rehydration and insulin therapy cannot be overemphasized.
Both prerenal azotemia and renal azotemia are common with plasma BUN-creatinine ratios often exceeding 30:1. Leukocytosis is variable and, when present, is usually due to infection or hemoconcentration. Hypophosphatemia may occur during periods of prolonged hyperglycemia. Acute consequences such as CNS abnormalities, cardiac dysfunction, and rhabdomyolysis are rare and usually associated with serum phosphate levels below 1.0 mg/dL. Routine replacement of phosphate or magnesium, unless severe, is usually unnecessary. Both electrolytes tend to normalize as the metabolic derangement is addressed. When necessary, gradual replacement minimizes the risks of complications such as renal failure. Metabolic acidosis is a wide-anion-gap type often due to poor tissue perfusion resulting in lactic acidosis, uremia, mild starvation ketosis, or all three.
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