DKA is a well-known cause of hypokalemia caused by osmotic diuresis leading to a total body potassium deficiency of 3 to 6 mEq/kg. At presentation, potassium levels are typically “normal†due to the extracellular shift of potassium (K+) from insulin deficiency and acidosis.
Laboratory findings consistent with the diagnosis of diabetic ketoacidosis (DKA) include blood pH < 7.3, serum bicarbonate < 18 mEq/L, anion gap > 10 mEq/L and increased serum osmolarity.
Suspect diabetic ketoacidosis (DKA) in a person with known diabetes or significant hyperglycaemia (finger-prick blood glucose level greater than 11 mmol/L) and the following clinical features: Increased thirst and urinary frequency. Weight loss. Inability to tolerate fluids.
During diabetic ketoacidosis, there may be rapid shifts in the plasma concentration of potassium ions. Although diabetic ketoacidosis leads to a deficit in total-body stores of potassium ion, the plasma concentration is usually normal or elevated, since the acidemia leads to the exit of potassium ions from cells.
If you detect ketones in your blood or urine, general treatment guidelines include drinking plenty of water or other calorie-free fluids to help flush ketones out of the body, taking insulin to bring your blood glucose level down, and rechecking both your blood glucose level and ketone level every three to four hours.
Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor.
Hyperosmolar hyperglycemic state (HHS) is one of two serious metabolic derangements that occur in patients with diabetes mellitus (DM). It is a life-threatening emergency that, although less common than its counterpart, diabetic ketoacidosis (DKA), has a much higher mortality rate, reaching up to 5-10%.
DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia. The precipitating factors, clinical features, evaluation, and diagnosis of DKA and HHS in adults will be reviewed here.
About two-thirds of patients will develop hypokalemia in the course of treatment for DKA. Potassium repletion should commence once the serum potassium falls below 5.3 mEq/L if patients have normal renal function. Twenty to 30 mEq of potassium may be supplemented to each liter of fluids.
Fluid resuscitation is a critical part of treating patients with DKA. Intravenous solutions replace extravascular and intravascular fluids and electrolyte losses. They also dilute both the glucose level and the levels of circulating counterregulatory hormones.
DKA is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism. The most common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes.
Serum ketones are not present because the amounts of insulin present in most patients with type 2 diabetes are adequate to suppress ketogenesis.
Insulin is known to decrease the catecholamine-induced production of these 2 potent vasodilators. Severe insulin deficiency as seen in DKA thus leads to increased production of PGI2 and PGE2, which leads to vasodilation and hypotension.
Hypovolemia shock with hypotension should be treated by rapid restoration of intravascular volume using isotonic crystalloid solutions such as 0.9% saline. In the first two hours 1-2 L of fluid may be required to correct hypovolemia.
In a person without diabetes, insulin, glucagon, and other hormones prevent ketone levels in the blood from getting too high.
What do my results mean?
| normal/negative | less than 0.6 millimoles per liter (mmol/L) |
|---|
| high | 1.6 to 3.0 mmol/L |
| very high | greater than 3.0 mmol/L |
The optimal rate of glucose decline is 100 mg/dL/h. Do not allow the blood glucose level to fall below 200 mg/dL during the first 4-5 hours of treatment. Hypoglycemia may develop rapidly with correction of ketoacidosis due to improved insulin sensitivity.
Fluid loss from DKA can lead to kidney and organ damage, brain swelling that can eventually cause a coma, and fluid buildup in your lungs.
Diabetic ketoacidosis (DKA) is the most common hyperglycemic emergency in patients with diabetes mellitus. DKA most often occurs in patients with type 1 diabetes, but patients with type 2 diabetes are susceptible to DKA under stressful conditions, such as trauma, surgery, or infections.
Among the symptoms of DKA associated with possible intercurrent infection are fever, dysuria, coughing, malaise, chills, chest pain, shortness of breath, and arthralgia.
The most common precipitating factor in the development of DKA or HHS is infection. Other precipitating factors include cerebrovascular accident, alcohol abuse, pancreatitis, myocardial infarction, trauma, and drugs.
Differences between ketosis and ketoacidosis. Ketosis and ketoacidosis both involve the production of ketones in the body. However, while ketosis is generally safe, ketoacidosis can be life-threatening. Nutritional ketosis occurs when the body starts burning fat instead of glucose.
In most cases, ketoacidosis in people with diabetes will be accompanied by high sugar levels. However, ketoacidosis can also occur at low or normal blood glucose levels.
While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L.
In most cases, ketoacidosis in people with diabetes will be accompanied by high sugar levels. However, ketoacidosis can also occur at low or normal blood glucose levels.
HYPERGLYCEMIA. The hyperglycemia in DKA is the result of three events: (a) increased gluconeogenesis; (b) increased glycogenolysis, and (c) decreased glucose utilization by liver, muscle, and fat.
Very rarely, DKA can occur in people without diabetes. In this case, insulin levels fall enough to induce diabetic ketoacidosis, even though blood glucose levels are not elevated.
When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2. Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly.
Treatment usually involves:
- Fluid replacement. You'll receive fluids — either by mouth or through a vein — until you're rehydrated.
- Electrolyte replacement. Electrolytes are minerals in your blood that carry an electric charge, such as sodium, potassium and chloride.
- Insulin therapy.
