Results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids, ketones.
A process which is a condition where the body can’t utilize sugar as fuel due to the absence of insulin and starts burning fat.
This produces ketones, which are toxic for the body.
Typically characterized by hyperglycemia over 300 mg/dL, low bicarbonate level, and acidosis with ketonemia and ketonuria.
Moderate diabetic ketoacidosis can be categorized by pH <7.2 and serum bicarbonate <10 mEq/L, whereas severe disease has pH <7.1 and bicarbonate <5 mEq/L.
Diabetic ketoacidosis usually occurs in people with type 1 diabetes mellitus, but diabetic ketoacidosis can develop in any person with diabetes.
Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age.
As the body produces a stress response to dehydration, hormones glucagon, growth hormone and adrenaline break down muscle, fat, and liver cells into glucose and fatty acids.
Fatty acids that are formed are converted to ketones by a process called oxidation.
In diabetic ketoacidosis, the body shifts from using carbohydrates for fuel to a fasting state using fat.
Because insulin is unavailable to transport glucose into cells for use, glucose levels rise.
As blood sugar levels rise, the kidneys dump the glucose into the urine, increasing urination and causing dehydration.
Mental status changes can be seen with mild-to-moderate disease and more severe deterioration in mental status is typical with moderate-to-severe disease.
About 10% of total body fluids are lost as the patient enters into diabetic ketoacidosis.
Significant loss of potassium and other salts with excessive urination occurs.
The most common events that cause a person with diabetes to develop diabetic ketoacidosis are: infection or missed or inadequate administration of insulin, newly diagnosed patients, myocardial infarction, stroke, stress, alcohol, drug abuse and surgery.
Approximately 5% to 10% of cases have no identifiable cause.
Males and females are equally affected.
Incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with diabetic ketoacidosis.
Frequency 1 in 2000.
The high levels of glucose and ketones in the blood spill, passively, into the urine.
The resulting osmotic diuresis of glucose causes the removal of water and electrolytes from the blood resulting in potentially fatal dehydration.
Patients present with excessive thirst or drinking alot of fluids, frequent urination, weakness, vomiting, anorexia, impaired mental status,abdominal pain, shortness of breath, dry skin, dry mouth, tachycardia, hypotension, tachypnea, fruity odor on breath and appear acutely ill.
Mortality 2-5%.
Infection most common precipitating cause.
Management reqires close attention to tracking of the underlying acidosis and hyperglycemia as well as prevention of potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia.
Secondary consequences of the metabolic derangements in diabetic ketoacidosis include metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers.
Hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose.
Process may be associated with severe dehydration and significant hypokalemia with potassium loss as high as 5 mEq per kg of body weight.
The serum potassium concentration can drop precipitously once insulin treatment is started, and needs to be monitored closely.
Urinary loss of ketones with diuresis and intact renal function may also lead to hyperchloremic acidosis.
Hyperglycemia moves extravascular water to the intravascular space and for each 100 mg/dL of glucose over 100 mg/dL, the serum sodium level is lowered by approximately 1.6 mEq/L.
When glucose levels fall with insulin treatment, the serum sodium level rises by a corresponding amount.
ECGs may be used to assess the cardiac effects of extremes in potassium levels.
Bicarbonate levels in conjunction with the anion gap are used to assess degree of acidosis.
The presence of leucocytosis or a left shift in differential may suggest the presence of infection.
pH on a venous blood gas level in patients with DKA was 0.03 lower than pH on an arterial blood gas in diabetic ketoacidosis, making arterial blood gas analysis unnecessary.
Measuring blood and urine acetone and acetoacetic acid are helpful to evaluate acidosis.
Patients with diabetic ketoacidosis who are in a coma typically have osmolalities >330 mOsm/kg H2 O.
Hyperamylasemia may be seen.
BUN level is increased and the anion gap is higher than normal.
Potassium, glucose and other electrolyte levels should be checked every 2 hours or so during initial management.
Phosphorous levels may be low, and should be monitored every 4 hours during therapy.
High serum glucose levels may lead to dilutional hyponatremia.
High triglyceride levels may lead to factitious low glucose levels
High levels of ketone bodies may lead to factitious elevation of creatinine level.
Chest X-rays should be performed to rule out the presence of pneumonia.
Patients should be treated initially in an ICU setting.
Patients are monitored closely and are treated with intravenous fluids to correct dehydration, insulin to correct hyperglycemia, correction of electrolyte abnormalities, particularly hypokalemia, correction of acidosis and treat infection, if present.
Rapid correction of dehydration is required with isotonic sodium chloride or lactated Ringer’s solution.
Even with mild dehydration at least 3 liters of fluid has been lost.
Fluids should be given at a rate of 1000cc during the first 30 minutes, 1000cc over the second hour and 1000cc over the following two hours and 1000cc every 4 hours until normalization of hydration.
When hydration is normal isotonic sodium chloride should be utilized, especially if hypernatremia is present.
Hyperglycemia is corrected more slowly than dehydration ans is treated with a regular insulin drip at 0.1U/kg/hr.
Utilizing an insulin drip prevents high insulin induced severe hypoglycemia, and hypokalemia.
Because of dehydration and possible erratic absorption of insulin it should not be administered subcutaneously, in this clinical setting.