Diabetic ketoacidosis DKA
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Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two serious acute complications of diabetes characterized by high blood sugar levels. DKA involves ketones in the blood while HHS does not. Treatment for DKA involves rehydration with saline, potassium replacement, low-dose insulin therapy, monitoring blood sugars and electrolytes closely. The goals are to lower blood sugars and acid levels while replenishing fluids and salts. Complications can include low blood sugar, low potassium, or brain swelling.
![Fluid replacement
• Fluid repletion is usually initiated with isotonic
saline (0.9 percent sodium chloride [NaCl]).
• The optimal rate of isotonic saline infusion is
dependent upon the clinical state of the patient.
• Adequate rehydration with correction of the
hyperosmolar state may enhance the response to
low-dose insulin therapy.](https://image.slidesharecdn.com/dka-190524110920/85/Diabetic-ketoacidosis-DKA-13-320.jpg)
Diabetic ketoacidosis DKA
- 1. DIABETIC KETOACIDOSIS (DKA) Ayeshe Abu Hussein
- 2. Introduction • Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most serious acute complications of diabetes. • DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis.
- 3. Diabetic ketoacidosis VS hyperosmolar hyperglycemic state
- 4. PRECIPITATING FACTORS • Infection (often pneumonia or UTI). • Discontinuation of or inadequate insulin therapy. • Acute major illnesses. • New onset type 1 diabetes. • Drugs
- 5. CLINICAL PRESENTATION • Diabetic ketoacidosis (DKA) usually evolves rapidly, over a 24-hour period. • The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss. • Patients with DKA may present with nausea, vomiting, and abdominal pain.
- 6. Initial evaluation • The initial evaluation of patients with hyperglycemic crises should include assessment of cardiorespiratory status, volume status, and mental status. • The initial history and rapid but careful physical examination should focus on: • Airway, breathing, and circulation (ABC) status • Mental status • Possible precipitating events (eg, source of infection, myocardial infarction) • Volume status
- 7. Laboratory evaluation • Serum glucose • Serum electrolytes (with calculation of the anion gap), blood urea nitrogen (BUN), and plasma creatinine • Complete blood count (CBC) with differential • Urinalysis and urine ketones by dipstick • Plasma osmolality • Serum ketones (if urine ketones are present) • Arterial blood gas if the serum bicarbonate is substantially reduced or hypoxia is suspected • Electrocardiogram
- 8. Laboratory findings • Serum glucose: Euglycemic DKA has been described, particularly in patients with poor oral intake, treatment with insulin prior to arrival in the emergency department, or in pregnant women . • Serum ketones: Three ketone bodies are produced and accumulate in DKA: acetoacetic acid, beta- hydroxybutyric acid and acetone.
- 9. • Serum potassium: Patients presenting with DKA or HHS have a potassium deficit that averages 300 to 600 mEq . • Insulin therapy shifts potassium into cells and lowers the potassium concentration. Careful monitoring and timely administration of potassium supplementation are essential. • Serum creatinine: Most patients with uncontrolled hyperglycemia have acute elevations in the BUN and serum creatinine concentration.
- 10. • Serum amylase and lipase: These enzymes are often elevated in patients with DKA who do not have any other clinical or radiological evidence of pancreatitis. • Leukocytosis: The majority of patients with hyperglycemic emergencies present with leukocytosis. • Lipids: Patients with DKA or HHS may present with marked hyperlipidemia.
- 11. DIFFERENTIAL DIAGNOSIS • Alcoholic and fasting ketoacidosis. • Anion gap acidosis. • Metabolic encephalopathy.
- 12. Treatment • The first step in the treatment of DKA is infusion of isotonic saline to expand extracellular volume and stabilize cardiovascular status. • The next step is correction of the potassium deficit. • Low-dose intravenous (IV) insulin should be administered to all patients with moderate to severe DKA who have a serum potassium ≥3.3 mEq/L
- 13. Fluid replacement • Fluid repletion is usually initiated with isotonic saline (0.9 percent sodium chloride [NaCl]). • The optimal rate of isotonic saline infusion is dependent upon the clinical state of the patient. • Adequate rehydration with correction of the hyperosmolar state may enhance the response to low-dose insulin therapy.
- 15. Potassium replacement • If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride (KCl 20 to 40 mEq/hour, which usually requires 20 to 40 mEq/L added to saline) should be given. • If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV KCl (20 to 30 mEq) is added to each liter of IV replacement fluid. • If the initial serum potassium concentration is greater than 5.3 mEq/L, then potassium replacement should be delayed until its concentration has fallen below this level.
- 17. Insulin • Initiate treatment with low-dose IV insulin in all patients with moderate to severe DKA who have a serum potassium ≥3.3 mEq/L. • IV regular insulin and rapid-acting insulin analogs are equally effective in treating DKA . The choice of IV insulin is based upon institutional preferences, clinician experience, and cost concerns
- 19. Bicarbonate and metabolic acidosis • The venous pH and bicarbonate concentration should be monitored every two hours, and bicarbonate doses can be repeated until the pH rises above 7.00 . • When the bicarbonate concentration increases, the serum potassium may fall, and more aggressive KCl replacement may be required.
- 20. Phosphate depletion • The routine use of phosphate replacement in the treatment of DKA is not recommend. • However, phosphate replacement should be strongly considered if severe hypophosphatemia occurs.
- 21. MONITORING • The serum glucose should initially be measured every hour until stable. • While serum electrolytes, blood urea nitrogen (BUN), creatinine, and venous pH should be measured every (2-4) hours, depending upon disease severity and the clinical response.
- 22. Converting to subcutaneous insulin • The American Diabetes Association (ADA) guidelines for DKA recommend that IV insulin infusion be tapered and a multiple- dose, subcutaneous insulin schedule be started when the blood glucose is <200 mg/dL (11.1 mmol/L) and at least two of the following goals are met : • Serum anion gap <12 mEq/L (or at the upper limit of normal for the local laboratory) • Serum bicarbonate ≥15 mEq/L • Venous pH >7.30
- 23. COMPLICATIONS • Hypoglycemia and hypokalemia are the most common complications of the treatment of DKA. • Cerebral edema • Noncardiogenic pulmonary edema
Editor's Notes
- #5: Acute major illnesses such as myocardial infarction, cerebrovascular accident, sepsis, or pancreatitis. Drugs that affect carbohydrate metabolism, including glucocorticoids, higher-dose thiazide diuretics, sympathomimetic agents (eg, dobutamineand terbutaline) , and second-generation “atypical” antipsychotic agents .
- #6: symptoms of hyperosmolar hyperglycemic state (HHS) develop more insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission. As the degree or duration of hyperglycemia progresses, neurologic symptoms, including lethargy, focal signs, and obtundation, can develop. Neurologic symptoms are most common in HHS, while hyperventilation and abdominal pain are primarily limited to patients with DKA. Possible causes of abdominal pain include delayed gastric emptying and ileus induced by the metabolic acidosis and associated electrolyte abnormalities .
- #8: Additional testing, such as cultures of urine, sputum, and blood, serum lipase and amylase, and chest radiograph should be performed on a case-by-case basis. Measurement of glycated hemoglobin (A1C) may be useful in determining whether the acute episode is the culmination of an evolutionary process in previously undiagnosed or poorly controlled diabetes or a truly acute episode in an otherwise well-controlled patient.
- #9: acetoacetic acid, which is the only one that is a true ketoacid; beta-hydroxybutyric acid (a hydroxyacid formed by the reduction of acetoacetic acid); and acetone, which is derived from the decarboxylation of acetoacetic acid. Acetone is a true ketone, not an acid. Urine ketone bodies are detected with nitroprusside tests, while serum ketones can be detected with either a nitroprusside test or by direct assay of beta-hydroxybutyrate levels. Direct assay of beta-hydroxybutyrate levels is preferred, particularly for monitoring response to therapy.
- #14: Na+ should be corrected for hyperglycemia (for each 100 mg/dL glucose >100 mg/dL, add 2.0 mEq to sodium value for corrected serum sodium value
- #16: The choice of replacement fluid (isotonic or one-half isotonic saline) depends upon the state of hydration, corrected sodium concentration, dose of KCl, blood pressure, and a clinical assessment of overall volume status.
- #22: Repeat arterial blood gases are unnecessary during the treatment of DKA; venous pH, which is approximately 0.03 units lower than arterial pH , is adequate to assess the response to therapy and avoids the pain and potential complications associated with repeated arterial punctures.