Abdominal pain and vomiting is very common in childhood, and is often due to benign conditions such as gastroenteritis or food poisoning. However, this child looks ill, and is markedly dehydrated - warning signs that a more severe pathology may be present. At this point, the most important etiologies to consider are gastrointestinal conditions such as acute appendicitis and acute hepatitis; genitourinary conditions such as acute pyelopnephritis; and metabolic conditions such as diabetic ketoacidosis (DKA) or an adrenal (Addisonian) crisis. Acute hepatitis is unlikely in the absence of anorexia, jaundice or right hypochondriac tenderness. While the absence of fever, periumbilical pain, and tenderness or guarding in the right iliac fossa does not exclude acute appendicitis, it does make it less likely. The absence of renal angle tenderness is against the diagnosis of acute pyelonephritis. Note also the presence of dry mucous membranes, sunken eyes, reduced skin turgor, a prolonged capillary refill time (CRT) and tachycardia. When considered together, these features are suggestive of 10% dehydration. While appendicitis, hepatitis and pyelonephritis may cause dehydration due to vomiting, such a degree of dehydration over a short time would be rather unusual. However, metabolic diseases can easily cause rapid volume depletion. In addition, her rapid and shallow breathing is suspicious of metabolic acidosis. This is well known to occur in DKA, and less often, in an adrenal crisis. The venous blood gas assay confirms this. The diagnosis is clinched by the investigations showing marked hyperglycemia and ketonemia - this is DKA indeed. As DKA is often precipitated by infection, a full blood count is important. Note that the increased WBC count (in the range of 10,000-15,000/mm3) in this patient is characteristic of DKA and is not indicative of infection. In addition, estimation of renal functions and electrolytes is also important as renal impairment and electrolyte abnormalities may occur. Her management should commence with volume resuscitation via IV 0.9% saline. Insulin should NOT be given as a bolus dose, as this may precipitate cerebral edema. In addition, sodium bicarbonate should not be administered, as the acidosis in DKA corrects spontaneously after fluid and insulin replacement. Unnecessary bicarbonate therapy may cause paradoxical CNS acidosis and hypokalemia. It is unnecessary to keep her nil orally unless she is severely confused or drowsy, and aspiration is feared.
DKA is the leading cause of morbidity and mortality in children diagnosed with diabetes. Children with both type 1 and type 2 diabetes are affected, although the incidence is higher in those with type 1 diabetes. DKA may also be the initial presentation of diabetes, especially in younger children, with children below the age of 5 years at the highest risk. In DKA, the absolute or relative deficiency of insulin results in impaired glucose uptake by the peripheral tissues and liver, resulting in intracellular "starvation". To offset this, the body secretes counter-regulatory hormones (such as glucagon), which stimulate hepatic oxidation of fatty acids to ketones (which act as an alternative source of energy). These hormones also have the ancillary effect of increasing gluconeogenesis and glycogenolysis, resulting in hyperglycemia. This gives rise to an osmotic diuresis, resulting in hypovolemia and subsequent underperfusion of the tissues. The underperfused tissues start producing lactic acid (due to anaerobic metabolism). These along with the keto-acids create a metabolic acidosis (with a high anion gap). Simultaneously, serum potassium is lost via the osmotic diuresis, and replaced via migration of intracellular potassium. Thus total body potassium is often low. As mentioned earlier, DKA may occur in the setting of established disease, or may be the initial manifestation of diabetes. Young children may not demonstrate the classic history of polydipsia, polyuria and weight loss. The presentation may mimic an acute abdomen, with abdominal pain, nausea and vomiting. In addition, fatigue, thirst, polyuria, hyperventilation with kussmaul breathing and signs of dehydration may be noted. The breath may have a characteristic fruity smell (ketotic breath). Children are particularly prone to developing cerebral edema. Affected patients may complain of a headache, while loss of pupillary light reflexes and frank coma may occur. The diagnosis requires biochemical evidence of hyperglycemia, acidosis and ketonemia. Arterial or venous blood gases should be performed to demonstrate an acidic pH (note that venous blood pH closely mirrors that of arterial blood) and a low bicarbonate level. Ketones can be detected in the blood or on urinalysis. The management of DKA is conducted in a stepwise fashion, and is based on progressively reversing the underlying pathophysiology. The first principle is to replace lost fluids and electrolytes. The initial volume replacement should be with an isotonic fluid (such as 0.9% saline or lactated Ringer's solution). Once the patient is euvolemic, this can be changed to 0.45% saline (as it roughly matches the losses occurring due to osmotic diuresis). The second principle is administration of insulin to suppress the hyperglycemia and ketogenesis. This should be commenced after the initial volume resuscitation is complete. Administration of insulin prior to this (i.e. while the patient is dehydrated) is risky, as potassium level estimations may be inaccurate, and the action of insulin may be unpredictable. A short-acting insulin should be administered as a low-dose continuous infusion. High doses should be avoided, as over-rapid lowering of the hyperglycemia will reduce the serum osmolality, resulting in shifting of water into the intracellular space and potentially causing cerebral edema. Note also that over-aggressive insulin therapy may cause hypoglycemia, and then "rebound" hyperglycemia (as the body fights back by releasing a wash of counterregulatory hormones). Thus, once the serum glucose level reaches around 200 mg/dL, dextrose should be added to the IV fluids in order to maintain the glucose level above this limit. Potassium supplementation should be commenced along with insulin (or even earlier if the patient is hypokalemic). However, if the patient is hyperkalemic, potassium should be deferred until urine output is documented. The metabolic acidosis resolves spontaneously as the dehydration, ketosis and hyperglycemia is corrected. In addition to the above, monitoring of vital signs, mental status, fluid balance and capillary blood glucose is very important. Electrolytes, glucose and blood gases should be repeated every 2 to 4 hours, or more frequently if necessary. Urea, creatinine, and hematocrit should be assayed at 6 to 8 hour intervals until normal. While complete recovery is usual, DKA carries a significant risk of complications including cerebral edema, hypoglycemia and cardiac arrhythmias due to hyperkalemia, hypokalemia, and hypocalcemia. Cerebral edema (which occurs in 1% of all pediatric DKA episodes), is the commonest cause of mortality in children with DKA, accounting for 60% to 90% of all pediatric DKA deaths. Overall, the prognosis of DKA is excellent when diagnosed and treated early.