الفهرس 
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Abstract
Diabetic ketoacidosis (DKA) is a metabolic derangement characterized by the triad of hyperglycemia, acidosis and ketosis that occurs in the presence of very low levels of effective insulin action. It is the leading cause of mortality in children with type 1 diabetes.
Hyperglycemia that exceeds the usual renal threshold of approximately 10 mmol/L (180 mg/dL) together with hyperketonemia cause osmotic diuresis, dehydration and obligatory loss of electrolytes which is often aggravated by vomiting associated with severe ketosis. These changes stimulate further stress hormone production, which induces more severe insulin resistance and worsening hyperglycemia and hyperketonemia.
Diabetic ketoacidosis is biochemically defined as the presence of:
• Hyperglycemia with blood glucose higher than 250 mg/dl.
• Venous pH <7.3 and/or bicarbonate <15 mmol/L.
• Ketonemia (concentration of total ketone bodies >5 mmol/L) and ketonuria.
Evaluation of a patient with diabetic ketoacidosis include:
Assessment of severity of dehydration.
Assessment of level of consciousness
Assessment of severity of acid base and electrolyte disturbance by laboratory findings
In children with diabetic ketoacidosis (DKA), abdominal pain and vomiting occasionally prompt the measurement of pancreatic enzymes.
Elevated pancreatic enzymes can occur due to Acute Pancreatitis (AP) or numerous non-specific reasons. Non-specific enzyme elevation can be seen in patients with head injury, acute renal failure or patients on hemodialysis.
Acute, clinically apparent pancreatitis during DKA has been documented previously, mainly in adults and rarely in children. Elevated pancreatic enzymes without clinical signs or symptoms and without radiographic evidence of pancreatitis, however, have been documented with much greater frequency.
Elevated serum pancreatic enzyme levels in DKA could result from mild pancreatic injury caused by decreased intravascular volume and poor splanchnic perfusion during DKA and/or by injury resulting from reperfusion of previously ischemic tissues.
Another possibility of the cause of elevated amylase level in DKA is an extra pancreatic origin triggered by the dysmetabolic state, like release of salivary gland amylase or its accumulation secondary to suboptimal excretion in the urine.
In acute pancreatitis, serum lipase rises by 4-8hrs, peaks at 24-48hrs, remains elevated for 8-14 days and its Concentration often remains elevated longer than serum amylase. The serum amylase level is typically elevated for up to 4 days.
The present study was designed to study serum amylase and lipase levels in pediatric patients with diabetic ketoacidosis and exclude pancreatitis as a cause of enzyme elevation even in presence of abdominal pain. It was conducted on 65 children aged >18year between May 2016 and March 2017.