ESSENTIALS OF DIAGNOSIS
Hyperglycemia > 600 mg/dL (33.3 mmol/L).
Serum osmolality > 310 mOsm/kg.
No acidosis; blood pH > 7.3.
Serum bicarbonate > 15 mEq/L.
Normal anion gap (< 14 mEq/L).
This second most common form of hyperglycemic coma is characterized by severe hyperglycemia in the absence of significant ketosis, with hyperosmolality and dehydration. It occurs in patients with mild or occult diabetes, and most patients are typically middle-aged to elderly. Accurate figures are not available as to its true incidence, but from data on hospital discharges it is rarer than DKA even in older age groups. Underlying chronic kidney disease or heart failure is common, and the presence of either worsens the prognosis. A precipitating event such as infection, myocardial infarction, stroke, or recent operation is often present. Certain medications such as phenytoin, diazoxide, corticosteroids, and diuretics have been implicated in its pathogenesis, as have procedures associated with glucose loading such as peritoneal dialysis.
A partial or relative insulin deficiency may initiate the syndrome by reducing glucose utilization of muscle, fat, and liver while inducing hyperglucagonemia and increasing hepatic glucose output. With massive glycosuria, obligatory water loss ensues. If a patient is unable to maintain adequate fluid intake because of an associated acute or chronic illness or has suffered excessive fluid loss, marked dehydration results. As the plasma volume contracts, kidney function becomes impaired, limiting the urinary glucose losses and exacerbating the hyperglycemia. Severe hyperosmolality develops that causes mental confusion and finally coma. It is not clear why ketosis is virtually absent under these conditions of insulin insufficiency, although reduced levels of growth hormone may be a factor, along with portal vein insulin concentrations sufficient to restrain ketogenesis.
Onset may be insidious over a period of days or weeks, with weakness, polyuria, and polydipsia. The lack of features of DKA (eg, vomiting, rapid deep breathing, acetone odor) may retard recognition of the syndrome and delay therapy until dehydration becomes more profound than in ketoacidosis. Reduced intake of fluid is not an uncommon historical feature, due to either inappropriate lack of thirst, nausea, or inaccessibility of fluids to elderly, bedridden patients. A history of ingestion of large quantities of glucose-containing fluids, such as soft drinks or orange juice, can occasionally be obtained. Lethargy and confusion develop as serum osmolality exceeds 310 mOsm/kg, and convulsions and coma can occur if osmolality exceeds 320–330 mOsm/kg. Physical examination confirms the presence of profound dehydration in a lethargic or comatose patient without Kussmaul respirations.
Severe hyperglycemia is present, with blood glucose values ranging from 800 mg/dL to 2400 mg/dL (44.4 mmol/L to 133.2 mmol/L) (Table 27–10). In mild cases, where dehydration is less severe, dilutional hyponatremia as well as urinary sodium losses may reduce ...