Diabetic Ketoacidosis is an acute life threatening complication of diabetes, it occurs in type 1 DM more than type 2.
Incidence
DKA accounts for 14 % of all hospital admissions of patients with diabetes and 16% of all diabetes related fatalities. DKA is often the first presentation in type 1 DM.
Pathophysiology
DKA is a state of absolute or relative insulin deficiency, so the counter –regulatory hormones increase (glucagon, growth hormone, cortisol, epinephrine). As a result of this hormonal imbalance, hepatic gluconeogenesis, glycogenolysis, and lipolysis ensue
Hepatic gluconeogenesis and glycogenolysis lead to severe hyperglycemia, while lipolysis leads to increase serum free fatty acids which metabolized in the liver and results in accumulation of ketone bodies (acetone, acetoacetate, and beta-hydroxybutyrate)
We need to know that only acetone is a true ketone, while acetoacetate is a true ketoacid and beta-hydroxybutyrate is a hydroxy acid. Progressive rise of blood concentration of these acidic substances leads to a state of ketonemia, although intracellular and extracellular body buffers can limit ketonemia in its early stage as we notice by normal arterial ph with a base deficit and a mild anion gap. when the the accumulated ketones exceeds the body capacity to rid off them, they execreted in the urine. If this situation is not treated immediately, more accumulation of ketone bodies leads to overt metabolic acidosis with a significant drop in serum PHand bicarbonate levels. Respiratory compensation for this acidotic problem leads to rapid, shallow breathing (kussmaul respiration).
Ketone bodies, especially beta-hydroxybutyrate induce nausea and vomiting that lead to fluid and electrolytes imbalance. Moreover, acetone is responsible for the fruity breath odor that characterize DKA patients. Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity.
Etiology
- In 25% of patients, DKA is present at diagnosis of type 1 DM due to acute insulin deficiency.
- Poor compliance with insulin.
- Forgotten doses due to illness.
- Bacterial infection.
- Klebsiella pneumonia.
- Medical, surgical, or emotional stress.
- Idiopathic.
Presentation
- The most common early symptoms of DKA are polydipsia and polyuria. Malaise and generalized fatigue can present as symptoms of DKA.
- Nausea and vomiting associated with diffuse abdominal pain and anorexia also occur in DKA.
- Altered consciousness can occur.
- Fruity smell of the breath.
Investigations
- Blood tests for glucose every 1-2 h until patient is stable, then every 4-6 h.
- serum electrolyte every 1-2 h until patient is stable, then every 4-6h
- Blood urea nitrogen (BUN)
- Arterial blood gas measurements (ABG)
According to the investigations DKA is divided into three types:
Management
It is advisable to manage DKA in ICU in the first 24-48 hours.
During treating patients with DKA, We should put some points in consideration.
- Correction of fluid loss.
- Correction of hyperglysemia.
- Correction of electrolytes disturbances.
- Correction of acid – base balance.
- Treatment of infection if present.
Correction of fluid loss
Fluid resuscitation is an essential point in managing DKA patients. IV fluids replaces intravascular and extravascular fluids and electrolyte losses. They also dilute glucose and circulating counterregulatory hormones levels. Correction of fluid is either by sodium chloride or ringer lactate solution.
Correction of fluid is as follow:
- Administration of 1-3 l during the first hour
- Administration of 1 l during the second hour
- Administration of 1l during the following 2 hours
- Administer 1l every 4 hours according to dehydration state and central venous pressure readings.
- When blood sugar decreases to less than 180 mg / dl, we start to give 5-10% dextrose with half isotonic sodium chloride solution.
Insulin Threapy
Insulin should be started 1 hour after fluid resuscitation. Only short acting insulin is used for correction of hyperglycemia. Subcutaneous absorption of insulin is reduced in DKA patients due yo dehydration, so IV route is preferred.
The initial insulin dose is a continuous IV insulin infusion by infusion pump at a rate of 0.1 U/ Kg / h. A mix of 24 units of regular in 60 ml of isotonic sodium chloride solution is infused at a rate of 15ml / h (6 U/ h) until the blood glucose level drops to less than 180 mg / dl, then the rate decreases to 5-7.5 ml/h (2-3U/H) until the ketoacidotic state ends. The optimal rate of glucose decline is 100mg /dl/h. Do not let the blood glucose level to fall below 200mg / dl during the first 4-5 hours of treatment. hypoglycemia may develop rapidly with correction of ketoacidosis due to improved insulin sensitivity.
Electrolyte correction
If the potassium level is 4.5 – 6 mEq/l, administer 10 mEq/h of potassium chloride. If the potassium level is 3 – 4.5 mEq/l, administer 20 mEq/h of potassium chloride. Monitor serum potassium hourly and stop infusion if potassium level is greater than 5 mEq/l. Serum potassium monitoring must continue even after potassium infusion is stopped.
Potassium replacement should be started with initial fluid replacement if potassium level is normal or low.
Correction of Acid – Balance
Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patients life. If it is indicated, 100 – 150 ml of 1.4 % concentration is infused initially. This may be repeated every half hour if necessary.
Treatment of concurrent infection
If infection is present, administer aspropriate antibiotic according to culture and sensitivity results.
At the end, DKA treatment should aim to correct dehydration reverse the acidosis and ketosis, reduce plasma glucose concentration to normal, replenish electrolyte loss and identify the underlying cause.
Review By: Dr. Hanan Anwar Abdel Ghafour
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