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1 Aggravating factors Angina may be aggravated by hypertension, LV failure, arrhythmia (usually tachycardias), strenuous activity, cold temperatures, and emotional states These factors should be identified and treated when possible 2 Nitroglycerin Nitroglycerin, 03 06 mg sublingually or 04 08 mg translingually by spray, should be taken 5 minutes before any activity likely to precipitate angina Sublingual isosorbide dinitrate (25 10 mg) is only slightly longer-acting than sublingual nitroglycerin 3 Long-acting nitrates Longer-acting nitrate preparations include isosorbide dinitrate, 10 40 mg orally three times daily; isosorbide mononitrate, 10 40 mg orally twice daily or 60 120 mg once daily in a sustained-release preparation; oral sustained-release nitroglycerin preparations, 625 125 mg two to four times daily; nitroglycerin

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 at least middle-aged to elderly Accurate figures are not available as to its true incidence, but from data on hospital discharges it is rarer than diabetic ketoacidosis even in older age groups Lethargy and confusion develop as serum osmolality exceeds 310 mosm/kg, and coma can occur if osmolality exceeds 320 330 mosm/kg A committee of the ADA has recommended replacing the previous name of this disorder (hyperglycemic, hyperosmolar, nonketotic coma) with the consensus term hyperglycemic hyperosmolar state Underlying renal insufficiency or congestive 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 drugs such as phenytoin, diazoxide, corticosteroids, and diuretics have been implicated in its pathogenesis, as have procedures associated with glucose loading such as peritoneal dialysis

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Fluid replacement is of paramount importance in treating nonketotic hyperglycemic coma The onset of hyperosmolarity is more insidious in elderly people without ketosis than in younger individuals with high serum ketone levels, which provide earlier indicators of severe illness (vomiting, rapid deep breathing, acetone odor, etc) Consequently, diagnosis and treatment are often delayed until fluid deficit has reached levels of 6 10 L If hypovolemia is present as evidenced by hypotension and oliguria, fluid therapy should be initiated with 09% saline In all other cases, 045% saline appears to be preferable as the initial replacement solution because the body fluids of these patients are markedly hyperosmolar As much as 4 6 L of fluid may be required in the first 8 10 hours Careful monitoring of the patient is required for proper sodium and water replacement Once blood glucose reaches 250 mg/dL, fluid replacement should include 5% dextrose in either water, 045% saline solution, or 09% saline solution The rate of dextrose infusion should be adjusted to maintain glycemic levels of 250 300 mg/dL in order to reduce the risk of cerebral edema An important end point of fluid therapy is to restore urinary output to 50 mL/h or more

FIGURE 3-18

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 plasma volume contracts, renal insufficiency develops, and the resultant limitation of renal glucose loss leads to increasingly higher blood glucose concentrations 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

Less insulin may be required to reduce the hyperglycemia in nonketotic patients as compared to those with diabetic ketoacidotic coma In fact, fluid replacement alone can reduce hyperglycemia considerably by correcting the hypovolemia, which then increases both glomerular filtration and renal excretion of glucose An initial dose of 015 unit/kg is followed by an insulin infusion of 1 2 units/h, which is titrated to lower blood glucose levels by 50 70 mg/dL per hour

Onset may be insidious over a period of days or weeks, with weakness, polyuria, and polydipsia The lack of features of

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