Friday, February 22, 2008

Diabetic Ketoacidosis and its complications

Diabetic Ketoacidosis is the most severe form of dehydration for an insulin dependent diabetic (Type I) but also in the non-insulin dependent diabetic (Type II experience HHS). Also know as DKA (Diabetic Ketoacidosis) it can occur from a relative or absolute deficiency of insulin; demonstrated by hyperglycemia, dehydration, and acid producing derangements of metabolism; acidosis. This condition can present as a true emergency in the insulin dependent diabetic or to the person that did not know they had diabetes; only signs and symptoms of dehydration or malaise. The causes of DKA and hyperglycemia can result from infection, disruption of treatment, and as a result of new onset; typically characterized by having a blood sugar (BS) above 300mg/dL, low bicarbonate (<15mEq/L), and acidosis with a pH less than 7.30 and associated ketonemia and ketonuria. Some of the complications from DKA can be cerebral edema (the major cause of mortality and morbidity in DKA), renal failure, cardiac disturbances, pulmonary edema, or even acute gastric dilation. In order to understand how some of the signs and symptoms occur you need to look into a basic physiological process. The body uses many mechanisms to balance acid levels, energy levels, energy sources, and function which is termed maintaining homeostasis. When homeostasis is jeopardized the body tries to counteract and protect itself. However, when our internal mechanisms cannot maintain homeostasis any longer it requires medical treatment and intervention based on clinical (lab and diagnostic) studies. In the diabetic, more specifically DKA, conditions such as a silent MI, CVA, or thrombosis may contribute to the evolvement of DKA.

The primary mechanism behind DKA occurs when insulin is deficient, levels of glucagons elevate, catecholamines are stimulated and hepatic glucose production is increased. The response to this is a decrease in the uptake of insulin from the peripheral tissues. The bottom line is that there is elevated production of glucose and non-usage of the circulating peripheral glucose.

Insulin is the primary anabolic hormone which means that muscle, fat and the liver do not take up glucose. There are other hormones (counter regulatory) such as glucagon, growth hormone, and catecholamines which accelerate the triglyceride breakdown into free roaming fatty acids and stimulate gluconeogenesis. This causes an elevation in the blood glucose levels in DKA. A result of the oxidation of free fatty acids (in the liver) is the production of ketone bodies, the two primaries are beta hydroxybutyrate and acetoacetic acid, hence the term switching metabolism; changing from carbohydrate metabolism to fat metabolism.

During the metabolic mayhem, a metabolic acidosis prevails. This condition of acidosis depletes the fluid between and inside the cells of its acid buffers. As the body begins to lose its ability to buffer acidic conditions adequately it finds an alternate route to eliminate the ketones; via the urine (ketonuria). Subsequently when blood concentrations of glucose are exceedingly high, the ability of the kidney to absorb glucose is exceeded and the glucose begins to spill into urine waste (glycosuria). The resulting complication here is free water loss because of a condition known as osmotic diuresis which results in dehydration, thirst, low perfusion to tissues, and quite possibly lactic acidosis. This would explain a common set of symptoms called Poly, Poly, Poly…..Polyuria, Polydipsia, and Polyphagia.

Polydipsia comes from dehydration that is sensed by the hypothalamus because you are thirsty from the loss of water. Polyuria occurs because you are urinating so much from the body’s attempt to rid itself of the excess glucose and buffer the acidity of the blood. Polyphagia comes from the switching of metabolism, the body is requiring carbohydrates for energy and you just cannot use the energy source; a lack of insulin.

With the loss of free water and the existence of changes in the osmotic gradient the patient is at severe risk for a severe electrolyte imbalance. The primary electrolyte concerns are sodium, potassium, magnesium, and phosphate. Potassium loss occurs as a result of extraction from intracellular fluid to exchange for the hydrogen ion build up in the extracellular areas in order to help with the buffering process. The potassium loss continues through the urine because of the change in the osmotic gradient. Sodium is lost in a similar fashion but the initial hyponatremia present in evaluation is related to a dilutional process. Water is extracted into the extracellular space as well, creating the dilution and is lost via urinary excretion due to the osmotic gradient change. Magnesium and phosphorous are lost similarly. The most important of the mentioned electrolytes is potassium. The production of the ketone bodies, in abundance, will lead to general abdominal pain with nausea and vomiting contributing to further loss of sodium and potassium.

The goals of treatment are to reverse the rehydrate the body, correct the hyperglycemia, and replenish the loss of electrolytes. After initial identification and treatment you must find the underlying cause and further treat any of the potential complications; MI, CVA, cardiogenic shock, sepsis, and thrombus. IV fluid regimens will vary upon diagnostic and lab evaluation and ensure proper renal function. This would also be true for the levels of electrolyte losses. Additional complications will be treated as they are discovered.

In conclusion the patient with Type I diabetes or new onset of diabetes can be life threatening and is considered a true medical emergency. Early identification and intervention are necessary to prevent complications. Early identification consists of not only correcting the condition of hyperglycemia, hypovolemic, and electrolyte imbalances but more importantly the underlying cause. These causes can range from infection to organ dysfunction. Close monitoring of treatment effectiveness can reduce or eliminate the long term complications of cardiac disruption, sepsis, hypovolemic shock, and renal damage; consequences of cerebral edema also need to be considered.

Check for further details.