Explain the acute complications of DM

Explain the acute complications of DM.

The acute complications of DM are metabolic in nature with extension to other systems secondarily. In the absence of adequate amounts of insulin, IDDM patients develop hyperglycemia, osmotic diuresis, and acidosis. Surgery, trauma, or infection frequently precipitates such episodes. Ketoacidosis may coexist with hyperglycemia of 1000 mg/dL or more. The various ketone bodies produce acidosis with a wide anion gap, as demonstrated in the case presented here. Ketones may rise to 30 mM/L from a normal level of 0.15 mM/L. Kussmaul’s respirations develop in severe cases and are due to significant metabolic acidosis. Expired tidal volumes often emit an acetone odor. In the case of severe osmotic diuresis, lactic acidosis may exist on the basis of hypoperfusion. Acidosis from any source predisposes to depressed myocardial contractility and poor periph-eral perfusion, thereby exacerbating lactic acidosis. Dehydration frequently results from osmotic diuresis and vomiting. Despite dehydration, oliguria generally does not manifest until late in the course of disease. Acidosis drives potassium extracellularly into the vascular space, where it is eliminated through the kidneys. As acidosis resolves and potassium moves intracellularly, serum hypokalemia manifests. Unless renal failure or anuria coexist, potassium replacement should start early. Hyponatremic sodium determinations are frequently found during periods of hyperglycemia, due to the increased serum osmolality. Hypothermia and mental status compromise may accom-pany DKA.

Treatment includes a bolus dose of 10 U of intravenous regular insulin, to rapidly suppress lipolysis and drive glu-cose intracellularly, followed by an infusion of regular insulin, 1–4 U/hr. Large amounts of normal saline will be needed for intravascular volume replacement. If there is adequate urine output and normal renal function, potas-sium supplementation should be administered to avoid the development of hypokalemia as the DKA resolves. Bicarbonate should be administered if the pH is less than 7.1 and there is hemodynamic instability.

NIDDM patients exposed to infection, surgery, or dehy-dration may develop hyperosmolar nonketotic states. Endogenous circulating insulin generally prevents ketosis but remains insufficient to avert hyperglycemia. Hyperglycemia in excess of 600 mg/dL results in extreme hyperosmolarity, producing osmotic diuresis, hypotension, acidosis, and mental status changes progressing to coma. Osmolarities of hyperglycemic nonketotic states may exceed 330 mOsm/L. Approximate serum osmolarity may be calculated from the following formula:

Osmolarity = 2[Na⁺ + K⁺] + glucose/18 + BUN/2.8

Hyperosmolar nonketotic states respond well to rehy-dration with normal saline and small doses of insulin. However, rapid correction of hyperosmolarity risks cere-bral edema and worsening of mental processes.