Dka jason
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This document discusses the diagnosis and management of diabetic ketoacidosis (DKA). It outlines the signs and symptoms that suggest DKA including altered mental status, nausea/vomiting, and fruity breath odor. Key lab findings include hyperglycemia, hyperketonemia, and metabolic acidosis. Treatment involves monitoring glucose, electrolytes, and acid-base status while providing insulin and fluid resuscitation. Differential diagnoses that can mimic DKA's presentation are also reviewed.
Dka jason
- 1. DIABETIC KETOACIDOSIS- DIAGNOSIS AND MANAGEMENT jason zachariah
- 2. WHEN TO SUSPECT DKA? Altered consciousness is the most common cause for seeking medical attention. It may range from mild disorientation to frank coma. Insidious increased thirst and urination are common early symptoms. Nausea and vomiting, diffuse abdominal pain. Generalized weakness and fatiguability.
- 3. Symptoms of possible intercurrent infection- fever, dysuria, malaise and arthralgia History of rapid weight loss is a symptom in patients who are newly diagnosed with type 1 diabetes
- 4. PHYSICAL FINDINGS Signs of dehydration- weak and rapid pulse, dry tongue and skin, hypotension, and increased capillary filling time. Odour of breath: characteristic acetone odour Signs of acidosis: kussmaul or sighing respiration, abdominal tenderness, and altered sensorium
- 5. Signs of intercurrent illnesses: MI, UTI, pneumonia and perinephric abscess.
- 7. CARDINAL BIOCHEMICAL FEATURES Hyperglycemia >250mg/dl Hyperketonemia Metabolic acidosis- pH<7.3, HCO3 <15meq/L
- 8. INVESTIGATIONS: Venous blood: glucose, urea, electrolytes- (Na,K,HCO3) Arterial blood gases Urine-ketone bodies Infection screen- CBP, blood and urine culture, C-reactive protein, Chest Xray
- 9. URINE Highly positive for glucose and ketones. Rarely ketones may test negative in urine, because laboratory tests can detect only acetoacetate, while predominant ketone in severe untreated DKA is beta hydroxybutyrate. As clinical condition improves, it tests positive because of its breakdown to acetoacetate.
- 10. BLOOD AND PLASMA Glucose: may be as low as 250 mg/dL to as high as more than 800 mg/DL Sodium: The osmotic effect of hyperglycemia moves extracellular water to intravascular space. For each 100mg/dL of glucose over 100mg/dL, the serum sodium is lowered by approximately 1.6 mEq/L. When the glucose level falls, serum sodium will rise.- pseudohyponatremia
- 11. BLOOD (CONT’D) Potassium: elevated H+ drives the intracellular potassium to extracellular compartment and secondary aldosteronism drives the K+ cells from the kidney into urine. Serum potassium levels do not reflect the state of total body potassium.
- 12. BLOOD (CONT’D) Bicarbonate: used in conjunction with anion gap to assess degree of acidosis CBC- high WBC counts>15000 or marked left shift suggests underlying bacterial infection ABG: pH<7.3
- 13. BLOOD (CONT’D) Osmolarity: =2(Na+)meq/L + glucose mg/dL +BUN mg/dL by 4 Usually >330 mOsm/kg H20. If osmolarity is less than this in a comatose patient, search for another cause of obtundation Phosphorus: phosphate levels High anion gap a usual finding. Anion gap= Na-(Cl+HCO3)
- 14. OTHER TESTS Ecg- DKA maybe precipitated by a cardiac event Chest Xray- to rule out pulmonary infection
- 15. MONITORING Repeated monitoring of biochemistry is critical. Potassium needs to be checked every 1 to 2 hours during initial treatment. Glucose and other electrolytes should be checked every 2 hours or so.
- 17. DIFFERENTIAL DIAGNOSIS Lactic acidosis- serum glucose,ketones nl, lactate>5mm Saturation ketosis: urine ketone +ve, blood ketone –ve, arterial pH usually normal Alcoholic ketoacidosis: history of alcohol being main energy source for few days, strip test often -ve, normoglycemia or hypoglycemia common
- 18. DIFFERENTIAL DIAGNOSIS Uremic acidosis- normoglycemia Rhabdomyolysis: increased CPK Salicylate toxicity: normoglycemia, ketones negative