Diabetic Ketoacidosis

Introduction

Diabetic Ketoacidosis (DKA) is the most severe acute complication of type 1 diabetes. About 30-40% of freshly diagnosed type 1 diabetes patients present with DKA. This condition is also the commonest cause of death in these children.

Categorization Of Severity

Table 1: Severity of DKA

Criteria for Diagnosis

Hyperglycemia: blood glucose >200 mg/dl (11.1 mmol/L)

Metabolic acidosis: pH <7.3; serum bicarbonate <15 mmol/L

Ketosis: Ketonemia >3 mmol/l, ketonuria >2+

Management guidelines

Emergency assessment & monitoring

Secure the airway and empty the stomach if the child is drowsy or unconscious .Give Oxygen if there is severe circulatory impairment or shock. A peripheral IV line should be secured at the earliest. Connect to a cardiac monitor for continuous ECG monitoring. Measure blood glucose and blood/urine ketones with bedside meters. The level of consciousness should be assessed using the Glasgow Coma Scale. The degree of dehydration should be assessed based on Table 2.

Table 2: Degree of dehydration

Obtain samples for lab measurements

Plasma glucose, electrolytes (Na, K), pH, HCO3, blood urea, creatinine, Hb, CBC, and hematocrit should be done in all cases. Serum osmolality, Albumin, PO4, Mg, and HbA1C are optional. Urine examination for microscopy and ketone bodies should be done. Specimens (blood, urine, and throat swab) are sent for culture and sensitivity. Antibiotics should be given for febrile patients. Urine catheterization is done in unconscious children

Monitoring

The cornerstone of successful management of DKA is meticulous monitoring. Hourly monitoring of vital signs: HR, RR, BP, SPO2, neurological signs (GCS), fluid input and output, capillary glucose level (bedside) 4 hourly monitoring of pH, HCO3, electrolytes, ketones. Always watch for warning signals of cerebral edema (headache, vomiting, bradycardia, irritability, rising BP, low SPO2).

Fluid Therapy

Fluid bolus:

• Child in shock or severe circulatory collapse (rare): Infusions of N. Saline 20 ml/kg bolus as quickly as possible .Carefully reassess and repeat if necessary
• Severely volume depleted but not in shock: Volume expansion (resuscitation) with 0.9% saline 10- 20 ml/kg over 1-2 hours, may be repeated if necessary
• Patients with mild DKA: do not require a fluid bolus

Subsequent fluid management:

Deficit replacement plus maintenance therapy: Fluid management (deficit replacement) should be with 0.9% saline for at least 4-6 hours. The rate of fluid (IV and oral) should be calculated to rehydrate evenly over 48 hours. The infusion rate should not exceed 1.5-2 times the usual daily maintenance requirement .Urinary losses need not routinely be added to the calculation of replacement fluid .When oral fluid is tolerated, IV fluid should be reduced accordingly. After 4-6 hours, deficit replacement should be with a solution that has a tonicity equal to or greater than 0.45% saline. If serum sodium is low at 4-6 hours, the sodium content of the fluid should not be reduced

Insulin therapy

Start insulin infusion 1-2 hours after starting fluid replacement therapy; i.e. after the patient has received initial volume expansion. Dose: 0.1 unit/kg/hour (e.g. dilute 50 units Regular [soluble] insulin in 50 ml normal saline, 1 unit = 1 ml).The route of administration is intravenous, using an infusion pump. An IV bolus should not be used at the start of therapy. The dose of insulin should usually remain at 0.1 unit/kg/h at least until resolution of DKA (pH >7.30, bicarbonate >15 mmol/l), which invariably takes longer than the normalization of blood glucose concentrations. 5% glucose should be added to the IV fluid (e.g. 5% glucose in 0.45% saline) when the plasma glucose falls to 250 mg/dl.

Potassium replacement

Replacement therapy is required even if the potassium levels are normal. The trans-cellular shift to ECF due to hypertonicity causes ECF potassium levels almost normal initially even if the child is having hypokalemia. If the patient is having hypokalemia, start potassium replacement at the time of initial volume expansion and before starting insulin therapy. Otherwise, start replacing potassium after initial volume expansion and concurrent with starting insulin therapy. If the patient is hyperkalemic defer potassium replacement therapy until urine output is documented. Continuous ECG monitoring will help in assessing the status of serum K.The starting potassium concentration in the infusate should be 40 mmol/l. Subsequent potassium replacement therapy should be based on serum potassium measurements. Potassium replacement should continue throughout IV fluid therapy. Potassium chloride is less preferred (to reduce risk of hyperchloremic acidosis)

Bicarbonate and phosphate therapy

Bicarbonate therapy is not needed except in a critical child with severe academia and shock. Dose: 1-2 mmol/kg over 60 minutes. Phosphate supplementation is not needed

Management of cerebral edema

Reduce the rate of fluid administration by one-third. Elevate the head end of the bed. Give mannitol 0.5-1 g/kg IV over 20 minutes and repeat if there is no initial response in 30 minutes. Hypertonic saline (3%), 5 ml/kg over 30 minutes, maybe an alternative to mannitol, especially if there is no initial response to mannitol. Mannitol should be readily available at the bedside. Intubation may be necessary for the patient with impending respiratory failure. After initial treatment has been started, a cranial CT scan should be obtained to rule out other possibilities especially thrombosis or hemorrhage.

Changing to subcutaneous insulin

When oral fluid is tolerated, IV fluid should be reduced. Change to subcutaneous insulin is planned, only when acidosis has resolved. The first SC injection should be given 15-30 minutes (with rapid-acting insulin) or 1-2 hours (with Regular insulin) before stopping the insulin infusion and given preferably, just before mealtime. Directly change over to split mix or basal-bolus régime. Frequent blood sugar monitoring is needed for titrating the dose

Conclusion

DKA is a possibility in any child who presents with altered sensorium, abdominal pain, rapid breathing, and dehydration. Fluid management is the cornerstone of DKA management. Cerebral edema is the commonest life-threatening complication of DKA; early diagnosis and treatment are life-saving.