2.67 CME

Penatalaksanaan Ketoasidosis Diabetik

Pembicara: Dr. Dhanya Soodhana

Senior Specialist, Pediatric and Adolescent Endocrinology, Aster MIMS, Calicut, Kerala

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Keterangan

Pediatric diabetes, primarily type 1, is a condition in which a child’s pancreas produces little or no insulin. Early diagnosis is vital, as symptoms like frequent urination, excessive thirst, and weight loss can appear quickly. Managing pediatric diabetes involves consistent blood sugar monitoring, insulin therapy, and a well-balanced diet that supports growth and development. Education for both the child and family is essential to manage diabetes effectively and confidently. Regular physical activity is also recommended, as it helps enhance insulin sensitivity and supports overall health.

Ringkasan

  • Diabetic ketoacidosis (DKA) is a serious complication of insulin deficiency, primarily affecting type 1 diabetics but increasingly seen in type 2 as well. DKA is characterized by elevated blood glucose, acidosis, and ketosis. The diagnostic criteria include blood glucose above 200 mg/dL, pH less than 7.3 or bicarbonate less than 18 mEq/L, and elevated ketone levels. Blood beta-hydroxybutyrate measurement using a keto glucometer is recommended over urine dipsticks.
  • Risk factors for DKA development include young age at diagnosis, delayed diagnosis, lower socioeconomic status, and insulin omission. Pathophysiology involves either absolute or relative insulin deficiency, increased counter-regulatory hormones, lipolysis, and ketogenesis. Increased proteolysis leads to gluconeogenesis and hyperglycemia, causing osmotic diuresis, dehydration, and electrolyte loss.
  • Initial management of DKA involves addressing dehydration, acidosis, and ketosis, restoring blood glucose levels, identifying and treating precipitating events, monitoring complications, and counseling for recurrent DKA prevention. All newly diagnosed DKA patients should be admitted. Indications for PICU care include prolonged symptoms, compromised circulation, depressed consciousness, risk of cerebral edema, severe acidosis, and adrenal insufficiency.
  • Resuscitation includes airway management, 100% oxygen, and establishing two IV lines. Blood pressure may be normal or high initially due to counter-regulatory hormones and ADH release. Vital signs, GCS, weight, height, and dehydration percentage should be assessed. Labs to be drawn include RVs, blood ketones, venous blood gas, electrolytes, BUN, creatinine, CBC, anion gap, and corrected sodium.
  • Fluid therapy starts with 10 ml/kg NS bolus over 30 minutes, followed by calculating replacement fluids over 48 hours based on dehydration percentage. Normal saline is the initial fluid, possibly switching to half-normal saline based on sodium levels. Avoid bolus insulin and infuse insulin at 0.05-0.1 unit/kg/hour, titrating to maintain blood glucose between 100-150 mg/dL, adjusting dextrose as needed, and never stopping insulin unless resolved or below target range.
  • Potassium replacement should begin after initial volume expansion, starting with 40 mEq/L in maintenance fluids, monitoring ECG for tall T waves indicating hyperkalemia before potassium supplementation is initiated. Phosphate depletion can occur, leading to various symptoms, and phosphate administration requires monitoring for hypocalcemia. Bicarbonate therapy is avoided except in life-threatening hyperkalemia or severe acidosis compromising cardiac function.
  • Cerebral edema is a dreaded complication, with risk factors including young age, new onset, prolonged symptoms, severe acidosis, high fluid volume, and rapid decline in serum osmolarity. Diagnosis relies on diagnostic or major/minor criteria, with treatment including head elevation, fluid reduction, mannitol or hypertonic saline, and CT scan consideration. Counsel parents on the disease, insulin therapy, blood sugar checks, diet, exercise, sick day rules, and injection techniques for prevention of recurrent DKA.

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