Bibliography Of The Diabetes Mellitus

Cryer PE, Fisher JN, Shamoon H. Hypoglycemia. Diabetes Care 1994; 17: 734-55

Frier BM, Fisher BM, eds. Hypoglycemia and Diabetes. London: Edward Arnold, 1993

Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycaemic crises in patients with diabetes. Diabetes Care 2GG1; 24: 131-53

Schade DS, Eaton RP, Alberti KGGM, Johnston DG. Diabetic Coma, Ketoacidotic and Hyperosmolar. Albuquerque: University of New Mexico Press, 1981

Small M, Alzaid A, MacCuish AC. Diabetic hyperosmolar non-ketoacidotic decompensation. Q J Med 1988; 66: 251-7

Diabetes Care Hypoglycemia

Figure 76 Hypoglycemia is a major problem for insulin-treated diabetic patients; over 30% of such patients experience hypoglycemic coma at least once. Around 10% experience coma in any given year and around 3% are incapacitated by frequent severe episodes. Hypoglycemia is usually due to an excessive dose of insulin, reduced or delayed ingestion of food, or increased energy expenditure owing to exercise. Identification of the cause, and appropriate remedial action and education, are mandatory. Patients treated with sulfonylureas frequently experience hypoglycemia

Figure 76 Hypoglycemia is a major problem for insulin-treated diabetic patients; over 30% of such patients experience hypoglycemic coma at least once. Around 10% experience coma in any given year and around 3% are incapacitated by frequent severe episodes. Hypoglycemia is usually due to an excessive dose of insulin, reduced or delayed ingestion of food, or increased energy expenditure owing to exercise. Identification of the cause, and appropriate remedial action and education, are mandatory. Patients treated with sulfonylureas frequently experience hypoglycemia

Patient Activation Measure

Figure 77 Hypoglycemia is associated with regional brain activation. Here CMG positron emission tomography (PET) has been used to measure changes in global and regional brain glucose metabolism. Hypoglycemia has been shown to be associated with activation of the brain stem, prefrontal cortex and anterior cingulate (yellow/orange indicates regions of increased glucose uptake and metabolism) and with reduced neuronal activation in the midline occipital cortex and cerebellar vermis (blue)

Death From Diabetes Mellitus

Figure 78 Diabetic ketoacidosis remains a significant cause of death in patients with type 1 diabetes mellitus and is characterized by marked hyperglycemia, hyperketonemia (usually detected by the presence of ketonuria), a low arterial pH, and fluid and electrolyte depletion with prerenal uremia. Treatment involves rehydration with saline, low-dose intravenous insulin infusion, potassium replacement, bicarbonate if arterial pH is < 7.0 and therapy directed at the underlying cause, if apparent

Figure 78 Diabetic ketoacidosis remains a significant cause of death in patients with type 1 diabetes mellitus and is characterized by marked hyperglycemia, hyperketonemia (usually detected by the presence of ketonuria), a low arterial pH, and fluid and electrolyte depletion with prerenal uremia. Treatment involves rehydration with saline, low-dose intravenous insulin infusion, potassium replacement, bicarbonate if arterial pH is < 7.0 and therapy directed at the underlying cause, if apparent

Death From Diabetes Mellitus

Causes of death in diabetic ketoacidosis

Cerebral edema

Causes of death in diabetic ketoacidosis

m Hypovolemic M shock (arterial V I thrombosis may I ^ ^^^^^

follow correction %of DKA) M Ë Mesenteric % arterial ® occlusion M

Acute pancreatitis

Cerebrovascular accident

Figure 79 Myocardial infarction and infection are the most common causes of death in diabetic ketoacidosis. Cerebral edema is an uncommon and poorly understood cause of death, and appears to have a predilection for younger patients. Thromboembolic complications are an important cause of mortality. DKA, diabetic ketoacidosis

Cerebral Edema Dka

Figure 80 Hyperosmolar non-ketoacidotic coma usually affects middle-aged or elderly patients with previously undiagnosed type 2 diabetes mellitus. It is characterized by marked hyperglycemia (usually > 50 mmol/l; 900 mg/dl) and prerenal uremia without significant hyperketonemia and acidosis. Treatment is by fluid replacement, attention to electrolyte balance and insulin therapy as for diabetic ketoacidosis, and most patients will not ultimately require permanent insulin therapy. The condition has a high mortality owing to a high incidence of serious associated disorders and complications

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