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DKA is an ACUTE, MAJOR, LIFE-THREATENING complication of diabetes. Is consequence of absolute or relative insulin deficiency with increase in counter-regulatory hormones. Characterized by hyperglycemia, acidosis, and ketonuria.
DKA is an ACUTE, MAJOR, LIFE-THREATENING complication of diabetes. Is consequence of absolute or relative insulin deficiency with increase in counter-regulatory hormones. Characterized by hyperglycemia, acidosis, and ketonuria.
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DKA is an ACUTE, MAJOR, LIFE-THREATENING complication of diabetes. Is consequence of absolute or relative insulin deficiency with increase in counter-regulatory hormones. Characterized by hyperglycemia, acidosis, and ketonuria.
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Objectives Definition of DKA and its Pathophysiology Causes and precipitating factors Clinical features by history and physical examination Investigations for DKA (Diagnosis & Monitoring) Management Complications Prognosis. Introduction Diabetic ketoacidosis (DKA) is an ACUTE, MAJOR, LIFE-THREATENING complication of diabetes. DKA is defined: o Clinically as an acute state of severe uncontrolled diabetes that requires emergency treatment with insulin and intravenous fluids. o 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. Pathophysiology DKA is characterized by hyperglycemia, acidosis, and ketonuria. DKA is consequence of absolute or relative insulin deficiency with increase in counter-regulatory hormones . ↓Insulin and ↑counter-regulatory hormone→ 1. Gluconeogenesis and glycogenolysis → Hyperglycemia . 2. Lipolysis → Free Fatty Acids → Ketogenesis → Ketonemia and ketonuria→ ↓ pH and bicarbonate serum levels→ Metabolic acidosis → Ketoacidosis. Pathophysiology cont. Hyperglycemia→ Glycosuria→ Osmotic diuresis→ dehydration and tissue hypoperfusion. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis→ concentration disturbance. Osmotic diuresis→ Potassium Sodium loss in the urine. High serum osmolarity→ Dilutional hyponatremia. Causes and Precipitating Factors The most common Other precipitants precipitants 2.CVA 3.Intracranial bleeding 2.Infections (30–50%): 4.Acute pulmonary embolism pneumonia, urinary tract 5.Intestinal or mesenteric thrombosis 6.Intestinal obstruction infections, sepsis, 7.Acute pancreatitis gastroenteritis 8.Alcohol intoxication or abuse 3.Inadequate insulin treatment 9.Severe burns, hyperthermia or hypothermia (20–40%): includes 10.Endocrine disorders: Cushing's noncompliance, insulin pump syndrome, thyrotoxicosis, failure acromegaly 11.Total parenteral nutrition 4.Myocardial ischemia or 12.Drugs: β-blockers, diuretics, infarction (3–6%): often corticosteroids, antipsychotics Clinical Features Symptoms: Signs: 2.Polydypsia. 2.Dehydration: 3.Polyuria. o Dry skin and mucous . 4.Hyperglycemia. o Orthostatic 5.Nausea, lethargy, hypotension. anorexia, weakness. o Tachycardia. 6.Abdominal pain. o Reduced JVP. 7.Reduced motility of GI. o Reduced mental 8.Vomiting. function 3.Ketosis: Diagnosis Table -1 Diagnostic criteria for diabetic ketoacidosis and the hyperosmolar hyperglycemic state Mild DKA Moderate DKA Severe DKA Plasma glucose (mg/dL) >250 >250 >250 Effective serum osmolality (mOsm/kg) Variable Variable Variable Urine or serum ketones (NP reaction) Positive Positive Positive Arterial pH 7.25–7.30 7.00–7.24 <7.00 Serum bicarbonate (mEq/L) 15–18 10–15 <10 Anion gap (mEq/L) >10 >12 >12 Typical mental status Alert Drowsy Stupor or coma Investigations Glucose level. Serum Ketones. Acid-base status: pH, Serum bicarbonate and Anion gap. Electrolytes: Na +K+ Cl - Mg +2 ECG CBC, WBC. Urinalysis. Cardiac markers, Liver enzymes and Amylase. Chest X-Ray. Blood and urine culture. Management Confirm diagnosis and admit to hospital or ICU. Assess: o Serum electrolytes, Acid-base status and Renal function. Replace fluids: o 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour); o subsequently, 0.45% saline at 150–300 mL/h; o change to 5% glucose and 0.45% saline at 100– Management cont. 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. Assess patient: What precipitated the episode (noncompliance, infection, trauma, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG). Measure capillary glucose every 1–2 h; measure electrolytes (especially K+, bicarbonate, Management cont. Monitor vital signs, mental status, fluid intake and output every 1–4 h. 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. 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. Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in Complications Cerebral edema Cardiac dysrhythmia Pulmonary edema Nonspecific myocardial injury may occur in severe DKA. Microvascular changes consistent with diabetic retinopathy. Prognosis Excellent: especially in younger patients if intercurrent infections are absent. 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. signs of poor prognosis: deep coma at the time of diagnosis, hypothermia, and oliguria. References Cecil Medicine, 23rd Ed Harrison's Principles of Internal Medicine, 17th Edition, 2008 eMedicine.com Specialties > Endocrinology > Diabetes Mellitus Thank You Any Questions ?