Hyperglycemia in the critically ill

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Hyperglycemia can be either the primary problem, as in diabetic emergencies, or a result of other processes, such as hyperglycemia secondary to sepsis. Diabetic emergencies Diabetic ketoacidosis

Diabetic ketoacidosis is the most common form of diabetic emergency. It is part of the spectrum of diabetic emergencies (Table 1) which have varying degrees of hyperglycemia, acidosis, and ketosis.

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Table 1 A comparison of clinical and biochemical indices in the spectrum of diabetic emergencies

Diabetic ketoacidosis typically occurs in type I or insulin-dependent diabetics. The main problem is an absolute or relative lack of insulin, leading to unrestrained oversecretion of glucagon (Fig 1). This process will not be turned off until insulin inhibits the secretion of glucagon. Most tissues do not starve as they are able to use fuel other than glucose.

glucose and ketone bodies.

As the blood glucose increases, changes occur in body fluid compartments and in the renal handling of sodium and water ( F2sieL.a.Dd.M.£G§[ry...1989). Initially, extracellular glucose causes water to move out of cells into the extracellular fluid to maintain osmotic equilibrium. The renal threshold for glucose is exceeded, and glucose spills into the urine causing an osmotic diuresis. Typically, more water than sodium is lost, with varying potassium, phosphate, and magnesium losses.

The intracellular fluid volume becomes depleted because water moves into the extracellular fluid, which in turn becomes depleted as a result of the osmotic diuresis. Eventually this process can lead to severe hypovolemia and shock. Organ perfusion may be compromised, resulting in impaired function such as oliguria and decreased level of consciousness. Poor tissue perfusion and oxygen delivery may cause lactic acidosis.

The level of dehydration, hypovolemia, and electrolyte loss is also influenced by oral fluid intake, the presence of vomiting, diarrhea, fever, and pre-existing renal function.

Glucagon stimulates the production of ketone bodies which are utilized for energy by the brain and by skeletal and cardiac muscle. The hydrogen ion produced with each ketone body soon overwhelms the acid-base buffering capacity and leads to a high-anion-gap metabolic acidosis. Ketone body production far outweighs the peripheral utilization of ketone bodies as fuel.

The pathophysiology results in the clinical picture of hyperglycemia, acidosis, dehydration, polyuria, polydipsia, and electrolyte disturbance. Hyperosmolar non-ketotic coma

Patients with hyperosmolar non-ketotic coma are hyperglycemic, hyperosmolar, and severely dehydrated by the same mechanisms as patients with diabetic ketoacidosis.

The major difference is that, unlike in patients with ketoacidosis, ketone bodies are either not produced or produced in small amounts. Classically, patients with hyperosmolar non-ketotic coma are undiagnosed type II or non-insulin-dependent diabetics and, as such, may have enough residual insulin to inhibit lipolysis, and hence ketone body production, but not enough to prevent hyperglycemia ( Cefaju 1991). Hyperosmolarity may also inhibit lipolysis. Patients with hyperosmolar non-ketotic coma are often profoundly dehydrated because of prolonged glycosuria and polyuria. Their ability to take oral fluids to correct the dehydration may be limited because of their age and coexisting dementia or the diabetic process itself, producing confusion and coma. Patients with hyperosmolar non-ketotic coma often have coexisting illness such as myocardial ischemia or decreased renal function. When hypovolemia supervenes on this background, decreased organ perfusion, ischemia, and lactic acidosis may result.

Patients with hyperosmolar non-ketotic coma are often very hyperglycemic. The osmotic diuresis produces severe hypovolemia and urine output falls, secondary to decreased renal blood flow. Glucose is no longer lost in the urine at the same rate, resulting in a sharp increase in the serum levels.

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