Diabetic Ketoacidosis DKA)

DKA is caused by an absence or markedly inadequate amount of insulin DKA is caused by an absence or markedly inadequate amount of insulin. This deficit in available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. The three main clinical features of DKA are Hyperglycemia Dehydration and electrolyte loss Acidosis

Clinical Features Clinical Features The hallmark of DKA is the combination of hyperglycemia, a serum bicarbonate below 15mEq/L, and an elevated anion gap. The blood glucose is usually above 250 mg/dL, Arterial PH below 7.3 and ,moderat or sever ketonemia or ketouria

PATHOPHYSIOLOGY Diabetic ketoacidosis (DKA) is a critical illness that manifests with severe hyperglycemia, metabolic acidosis, and fluid and electrolyte imbalances. DKA results from severe insulin deficiency that leads ; the release of glucagon from the liver (glycolylsis) disordered metabolism of proteins, carbohydrates, and fats(gluconeogeneses ) the condition, leading to further hyperglycemia and hyperosmolality, ketoacidosis, and volume depletion

DKA) Diabetic ketoacidosis (DKA) is usually seen in insulin-dependent diabetic patients TYPE 1 but in 20% of cases, there is no previous history of diabetes mellitus. DKA is most often the result of inappropriate insulin dosing, but some patients have a concurrent illness, most commonly an infection. Non diabetic causes of DKA Starvation ketoacidosis alcoholic ketoacidosis

CAUSES pancreatitis , alcohol abuse, trauma, and drugs. In addition, many people with type 1 diabetes present with DKA on initial diagnosis. Also, many patients with type 1 diabetes suddenly discontinue their insulin and deteriorate

The hyperglycemia of DKA leads to polyuria and polydipsia, the patient may experience blurred vision, weakness, and headache. The ketosis and acidosis of DKA lead to gastrointestinal symptoms such as anorexia, nausea, vomiting, and abdominal pain.

Signs of Diabetic sign of d(DKA) ■ Hyperventilation ■ Kussmaul’s respirations and “fruity” breath ■ Lethargy, stupor, coma ■ Hyperglycemia ■ Glycosuria ■ Volume depletion ■ Hyperosmolality ■ Decreased bicarbonate (15 mEq/L) ■ Decreased pH (<7.3

LABORATORY STUDIES Urin ketones , hyperglycemia , acid -base imbalance, metabolic acidosis, high anion gap , serum Na may be low ,serum K normal creatinine, and BUN are all elevated.

Management Reserve hydration Replace insulin Reserve ketoacidosis Replenish electrolyte

Rehydration In dehydrated patients, rehydration is important for maintaining tissue perfusion. In addition, fluid replacement enhances the excretion of excessive glucose by the kidneys. The patient may need as much as 6 to 10 L of IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, and vomiting

Initially, 0.9% sodium chloride (normal saline) solution is administered at a rapid rate, usually 0.5 to 1 L/hour for 2 to 3 hours. Half-strength normal saline (0.45%) solution (also known as hypotonic saline solution) may be used for patients with hypertension or hypernatremia and those at risk for heart failure.

After the first few hours, half-strength normal saline solution is the fluid of choice for continued rehydration, provided the blood pressure is stable and the sodium level is not low. Moderate to high rates of infusion (200 to 500 mL/hour) may continue for several more hours. When the blood glucose level reaches 300 mg/dL (16.6 mmol/L) or less, the IV solution may be changed to dextrose 5% in water (D5W) to prevent a precipitous decline in the blood glucose level

Insulin is usually infused intravenously at a slow, continuous rate (eg, 5 units/hour). Hourly blood glucose values must be measured. IV fluid solutions with higher concentrations of glucose, such as normal saline (NS) solution (eg, D5NS, D5.45NS), are administered when blood glucose levels reach 250 to 300 mg/dL (13.8 to 16.6 mmol/L), to avoid too rapid a drop in the blood glucose level (ie, hypoglycemia) during treatment.

Restoring Electrolytes the serum level of potassium decreases as potassium reenters the cells during the course of treatment of DKA; therefore, the serum potassium level must be monitored frequently.

Some of the factors related to treating DKA that reduce the serum potassium concentration include : Rehydration, which leads to increased plasma volume and subsequent decreases in the concentration of serum potassium. Rehydration also leads to increased urinary excretion of potassium. Insulin administration, which enhances the movement of potassium from the extracellular

Bicarbonate Bicarbonate therapy does not improve the outcome in DKA, and is not recommended, regardless of the severity of the acidemia PH below7.0