Diabetic Ketoacidosis
QUICK LOOK AT THE CHAPTER AHEAD
Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus where the patient manifests a blood glucose > 250 mg/dL, serum pH < 7.3, serum HCO3 < 15 mEq/L, and ketonemia or ketonuria. DKA results from too little insulin in relation to an increased caloric intake or increased bodily stress. In this chapter we identify how DKA occurs, the clinical manifestations, and treatment and nursing implications.
 Figure 47-1 Diabetic ketoacidosis. |
Diabetes mellitus is a group of heterogeneous disorders that affect carbohydrate metabolism and glucose homeostasis. There are two classifications of diabetes: type 1, characterized by pancreatic B-cell destruction requiring insulin replacement, and type 2, characterized by a secretory defect in insulin production and a resistance to the action of insulin on peripheral tissues. Type 2 diabetes can be controlled with diet and exercise. Under normal conditions, insulin is released into the bloodstream continuously and increases with demands such as snacks and meals. Acute and chronic complications can happen with abnormal insulin release. Hyperglycemia and hypoglycemia are two extremes of blood glucose imbalance. Diabetic ketoacidosis (DKA), discussed in this chapter, and hyperosmolar hyperglycemic nonketotic syndrome, discussed in Chapter 48, are two critical hyperglycemic states.
DKA is a serious complication of diabetes mellitus where the patient manifests a blood glucose > 250 mg/dL, serum pH < 7.3, serum HCO3 < 15 mEq/L, and ketonemia or ketonuria. DKA results from too little insulin in relation to an increased caloric intake or increased bodily stress. It
primarily occurs with type 1 diabetes but can also take place with type 2 diabetes during times of severe illness or trauma that cause an increased demand for insulin that cannot be met. When insufficient insulin is not available for glucose metabolism or carbohydrate metabolism, the liver metabolizes fats (lipolysis) to supply the body’s energy needs. Ketoacids are the product of this fat metabolism, and large quantities are released when carbohydrate stores are limited or cannot be accessed. An increased H+ load develops as more ketones are produced than can be used, resulting in metabolic acidosis. With an altered pH, the body attempts to eliminate the ketones via urine, resulting in ketonuria. In an attempt to correct the state of acidosis, buffering cations, such as bicarbonate and potassium, are depleted with the excretion of ketoacids, and the acidotic state worsens.
primarily occurs with type 1 diabetes but can also take place with type 2 diabetes during times of severe illness or trauma that cause an increased demand for insulin that cannot be met. When insufficient insulin is not available for glucose metabolism or carbohydrate metabolism, the liver metabolizes fats (lipolysis) to supply the body’s energy needs. Ketoacids are the product of this fat metabolism, and large quantities are released when carbohydrate stores are limited or cannot be accessed. An increased H+ load develops as more ketones are produced than can be used, resulting in metabolic acidosis. With an altered pH, the body attempts to eliminate the ketones via urine, resulting in ketonuria. In an attempt to correct the state of acidosis, buffering cations, such as bicarbonate and potassium, are depleted with the excretion of ketoacids, and the acidotic state worsens.
Diabetic ketoacidosis results from too little insulin in relation to an increased caloric intake or increased bodily stress. When sufficient insulin is not available for glucose metabolism or carbohydrate metabolism, the liver metabolizes fats (lipolysis) to supply the body’s energy needs. Ketoacids are the product of this fat metabolism, and large quantities are released when carbohydrate stores are limited or cannot be accessed.
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