DKA

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DKA

  1. 1. إعداد و تقديم طلاب سنة سادسة سمهر العلي – معاذ عيّاد – يزيد جبريل
  2. 2. Objectives <ul><li>Definition of DKA and its Pathophysiology </li></ul><ul><li>Causes and precipitating factors </li></ul><ul><li>Clinical features by history and physical examination </li></ul><ul><li>Investigations for DKA (Diagnosis & Monitoring) </li></ul><ul><li>Management </li></ul><ul><li>Complications </li></ul><ul><li>Prognosis. </li></ul>
  3. 3. Introduction <ul><li>Diabetic ketoacidosis (DKA) is an ACUTE, MAJOR, LIFE-THREATENING complication of diabetes. </li></ul><ul><li>DKA is defined: </li></ul><ul><ul><li>Clinically as an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids. </li></ul></ul><ul><ul><li>Biochemically as an increase in the serum concentration of ketones greater than 5 mEq/L, a blood glucose level of greater than 250 mg/dL (although it is usually much higher), blood pH of less than 7.2, and a bicarbonate level of 18 mEq/L or less. </li></ul></ul>
  4. 4. Pathophysiology <ul><li>DKA is characterized by hyperglycemia, acidosis, and ketonuria. </li></ul><ul><li>DKA is consequence of absolute or relative insulin deficiency with increase in counter-regulatory hormones . </li></ul><ul><li>↓ Insulin and ↑ counter-regulatory hormone -> </li></ul><ul><ul><li>Gluconeogenesis and glycogenolysis -> Hyperglycemia . </li></ul></ul><ul><ul><li>Lipolysis -> Free Fatty Acids -> Ketogenesis -> Ketonemia and ketonuria -> ↓ pH and bicarbonate serum levels -> Metabolic acidosis -> Ketoacidosis. </li></ul></ul>
  5. 5. Pathophysiology cont. <ul><li>Hyperglycemia -> Glycosuria -> Osmotic diuresis -> dehydration and tissue hypoperfusion. </li></ul><ul><li>Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis -> concentration disturbance. </li></ul><ul><li>Osmotic diuresis -> Potassium Sodium loss in the urine. </li></ul><ul><li>High serum osmolarity -> Dilutional hyponatremia. </li></ul>
  6. 6. Causes and Precipitating Factors <ul><li>The most common precipitants </li></ul><ul><li>Infections (30–50%): pneumonia, urinary tract infections, sepsis, gastroenteritis </li></ul><ul><li>Inadequate insulin treatment (20–40%): includes noncompliance, insulin pump failure </li></ul><ul><li>Myocardial ischemia or infarction (3–6%): often clinically “silent” in diabetic patients </li></ul><ul><li>Other precipitants </li></ul><ul><li>CVA </li></ul><ul><li>Intracranial bleeding </li></ul><ul><li>Acute pulmonary embolism </li></ul><ul><li>Intestinal or mesenteric thrombosis </li></ul><ul><li>Intestinal obstruction </li></ul><ul><li>Acute pancreatitis </li></ul><ul><li>Alcohol intoxication or abuse </li></ul><ul><li>Severe burns, hyperthermia or hypothermia </li></ul><ul><li>Endocrine disorders: Cushing's syndrome, thyrotoxicosis, acromegaly </li></ul><ul><li>Total parenteral nutrition </li></ul><ul><li>Drugs: β-blockers, diuretics, corticosteroids, antipsychotics </li></ul>
  7. 7. Clinical Features <ul><li>Symptoms: </li></ul><ul><li>Polydypsia. </li></ul><ul><li>Polyuria. </li></ul><ul><li>Hyperglycemia. </li></ul><ul><li>Nausea, lethargy, anorexia, weakness. </li></ul><ul><li>Abdominal pain. </li></ul><ul><li>Reduced motility of GI. </li></ul><ul><li>Vomiting. </li></ul><ul><li>Signs: </li></ul><ul><li>Dehydration: </li></ul><ul><ul><li>Dry skin and mucous . </li></ul></ul><ul><ul><li>Orthostatic hypotension. </li></ul></ul><ul><ul><li>Tachycardia. </li></ul></ul><ul><ul><li>Reduced JVP. </li></ul></ul><ul><ul><li>Reduced mental function </li></ul></ul><ul><li>Ketosis: </li></ul><ul><ul><li>Sweet odor </li></ul></ul><ul><ul><li>Kussmaul breathing </li></ul></ul>
  8. 8. Diagnosis
  9. 9. Investigations <ul><li>Glucose level. </li></ul><ul><li>Serum Ketones. </li></ul><ul><li>Acid-base status: pH, Serum bicarbonate and Anion gap. </li></ul><ul><li>Electrolytes: Na + K + Cl - Mg +2 </li></ul><ul><li>ECG </li></ul><ul><li>CBC, WBC. </li></ul><ul><li>Urinalysis. </li></ul><ul><li>Cardiac markers, Liver enzymes and Amylase. </li></ul><ul><li>Chest X-Ray. </li></ul><ul><li>Blood and urine culture. </li></ul>
  10. 10. Management <ul><li>Confirm diagnosis and admit to hospital or ICU. </li></ul><ul><li>Assess: </li></ul><ul><ul><li>Serum electrolytes, Acid-base status and Renal function. </li></ul></ul><ul><li>Replace fluids: </li></ul><ul><ul><li>2–3 L of 0.9% saline over first 1–3 h ( 10–15 mL/kg per hour ); </li></ul></ul><ul><ul><li>subsequently, 0.45% saline at 150–300 mL/h ; </li></ul></ul><ul><ul><li>change to 5% glucose and 0.45% saline at 100–200 mL/h when plasma glucose reaches 250 mg/dL ( 14 mmol/L ). </li></ul></ul>
  11. 11. Management cont. <ul><li>Administer short acting insulin : IV ( 0.1 units/kg ) or IM ( 0.3 units/kg ), then 0.1 units/kg/hour by continuous IV infusion; increase 2- to 3-fold if no response by 2–4 h. If initial serum K + is < 3.3 mmol/L ,do not administer insulin until the potassium is corrected to > 3.3 mmol/L . </li></ul><ul><li>Assess patient : What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG). </li></ul><ul><li>Measure capillary glucose every 1–2 h ; measure electrolytes (especially K + , bicarbonate, phosphate) and anion gap every 4 h for first 24 h. </li></ul>
  12. 12. <ul><li>Monitor vital signs, mental status, fluid intake and output every 1–4 h. </li></ul><ul><li>Replace K + : 10 mEq/h when plasma K + < 5.5 mEq/L , ECG normal, urine flow and normal creatinine documented; administer 40–80 mEq/h when plasma K + < 3.5 mEq/L or if bicarbonate is given. </li></ul><ul><li>Continue above until patient is stable, glucose goal is 150–250 mg / dL , and acidosis is resolved. Insulin infusion may be decreased to 0.05–0.1 units/kg per hour. </li></ul><ul><li>Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous insulin injection. </li></ul>Management cont.
  13. 13. Complications <ul><li>Cerebral edema </li></ul><ul><li>Cardiac dysrhythmia </li></ul><ul><li>Pulmonary edema </li></ul><ul><li>Nonspecific myocardial injury may occur in severe DKA. </li></ul><ul><li>Microvascular changes consistent with diabetic retinopathy. </li></ul>
  14. 14. Prognosis <ul><li>Excellent: especially in younger patients if intercurrent infections are absent. </li></ul><ul><li>The worst prognosis: is usually observed in patients who are older with severe intercurrent illnesses, eg, myocardial infarction, sepsis, or pneumonia, especially when they are treated outside an ICU. </li></ul><ul><li>signs of poor prognosis: deep coma at the time of diagnosis, hypothermia, and oliguria. </li></ul>
  15. 15. References <ul><li>Cecil Medicine, 23rd Ed </li></ul><ul><li>Harrison's Principles of Internal Medicine, 17th Edition, 2008 </li></ul><ul><li>eMedicine.com Specialties > Endocrinology > Diabetes Mellitus </li></ul>
  16. 16. <ul><li>Thank You </li></ul><ul><li>Any Questions ? </li></ul>

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