The document discusses diabetic ketoacidosis (DKA), providing details on the pathophysiology, classification, epidemiology, etiology, clinical manifestations, diagnosis, and treatment of DKA and type 1 diabetes mellitus. DKA results from a lack of insulin leading to hyperglycemia, glucosuria, ketoacidosis, and potentially a life-threatening cerebral edema during treatment. Treatment involves fluid resuscitation, electrolyte replacement, insulin therapy, and careful monitoring to resolve acidosis and hyperglycemia while avoiding cerebral edema.
It is important to stress that IDDM is NOT just a disorder affecting glucose (carbohydrate) metabolism, but that ALL the body’s energy sources are affected.
As the population becomes increasingly obese, more and more adolescents are presenting with Type II diabetes, a disease rarely seen by pediatricians.
It should be emphasized that the dehydration in DKA is hypertonic dehydration, and therefore plasma volume is fairly well preserved. It is rare, even in severe DKA, that a patient will present shocky from hypovolemia and dehydration. Therefore, there is rarely a need for large volumes (> 40 cc/kg) of fluid in the acute setting
It is important to emphasize that the acidosis, NOT hyperglycemia is the metabolic derangement in DKA. Therefore, the provision of adequate insulin is key. It is only when the acidosis begins resolving that we are sure that the amount of insulin provided is adequate. Once we know we are providing adequate insulin, we use added glucose to the IVF to adjust the blood sugar between 100 and 200 mg/dL. We don’t alter the rate of the insulin infusion to maintain desired blood glucose levels.
10 - 20 cc/kg bolus of NS would be adequate. Though the patient is dehydrated (dry lips), his hemodynamics are good, with acceptable vitals and good perfusion. There would be no reason to administer more than 20 cc/kg fluids. While this patient is clearly acidemic, he is NOT in impending cardiovascular collapse and therefore there is no justification for the administration of bicarbonate. In fact, administration of bicarbonate has been associated with the development of cerebral edema. The “true” serum sodium is 143 133 + 0.016[700-100] Insulin is generally started at 0.1 u/kg/hr. Therefore, in this 30 kg patient, an insulin infusion of 3 u/hr of regular insulin should be initiated. IVF of 2/3 NS or NS should be started at ~ 2400 cc/m 2 /day, which is approximately 1.5 x maintenance
This patient is exhibiting cerebral edema, the most feared and lethal complication of DKA. Management at this point consists of securing the airway by endotracheal intubation and hyperventilating the patient. Mannitol 0.5 - 1 g/kg and or hypertonic saline (~5cc/kg 3% NaCl) should be administered as well. It would not be appropriate to stop the insulin infusion, or to bolus the patient with glucose. It should be noted that even patients receiving proper management for DKA (like this patient) may nonetheless develop cerebral edema.
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