Cetoacidosis Diabetica

Overview of the Diagnosis and Management of Diabetic Ketoacidosis
MOHSEN S. ELEDRISI, MD; MOHAMMED S. ALSHANTI, MD; M. FAIQ SHAH, MD; BASEM BROLOSY, MD; NERMEEN JAHA, MD

ABSTRACT: Diabetic ketoacidosis is an acute complication of diabetes mellitus that can be life-threatening if not treated properly. Once thought to occur only in patients with type 1 diabetes, diabetic ketoacidosis has beenalso observed in patients with type 2 diabetes under certain conditions. The basic underlying mechanism for diabetic ketoacidosis is insulin deficiency coupled with elevated levels of counter-regulatory hormones, such as glucagon, cortisol, catecholamines, and growth hormone. Diabetic ketoacidosis can be the initial presentation of diabetes mellitus or precipitated in known diabetic patients bymany factors, most com-

monly infection. The management of diabetic ketoacidosis involves careful clinical evaluation, correction of metabolic abnormalities, identification and treatment of precipitating and comorbid conditions, appropriate long-term treatment of diabetes, and plans to prevent recurrence. Certain areas need further research, such as indications for the use of bicarbonate andphosphates and the use of intravenous rapid-acting insulin. KEY INDEXING TERMS: Diabetes; Ketoacidosis; Insulin; Fluid management. [Am J Med Sci 2006;331(5):243– 251.]

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iabetic ketoacidosis (DKA) is a metabolic derangement that, as the name implies, consists of three concurrent abnormalities: high concentration of blood glucose, high levels of ketone bodies, and metabolic acidosis.1 The originaldescription of DKA dates to 1886, more than 3 decades before the discovery of insulin.2 It is estimated that 2% to 8% of hospital admissions for children with diabetes are due to DKA, with about 160,000 hospital admissions per year in the United States.3 The annual incidence rate for DKA in the pediatric population ranges from 4.6 to 8 episodes per 1000 patients with diabetes, with a trend towardan increased hospitalization rate in the past two decades.4 Before the discovery and use of insulin in 1922, the mortality rate in patients with DKA was almost 100%. By 1932, the mortality rate dropped to 29%,5 and the current mortality rate is less than 5% in

experienced centers.1 The prognosis of DKA is worsened at the extremes of age and in the presence of coma and hypotension.1Pathophysiology Diabetic ketoacidosis comprises three elements: marked hyperglycemia, ketosis, and acidosis. This clinical syndrome is accompanied by volume and electrolyte depletion. The main underlying pathophysiologic mechanism in DKA is insulin deficiency, either relative or absolute, combined with excess of insulin counter-regulatory hormones, including glucagon, catecholamines, cortisol, and growthhormone and elevation of proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-6, interleukin-1 , and interleukin-8), free fatty acids, and plasminogen activator inhibitor-1.6 These hormonal abnormalities lead to alterations in the metabolism of carbohydrates, proteins, and lipids. The following section briefly discusses those metabolic disturbances. Hyperglycemia In normal conditions,insulin suppresses hepatic glucose production and lipolysis. In DKA, insulin deficiency and high levels of counter-regulatory hormones lead to marked hyperglycemia and increased free fatty acids and amino acids. Insulin deficiency leads to hepatic glucose overproduction while elevated concentrations of glucagon and catecholamines result in in243

From the Department of Internal Medicine, KingAbdulaziz National Guard Medical Center (MSE) and the Department of Emergency Medicine, King Faisal Specialist Hospital (MSA, MFS, BB, NJ), Alahsa, Saudi Arabia. Submitted April 25, 2005; accepted in revised form September 27, 2005. Correspondence: Mohsen Eledrisi, MD, Department of Internal Medicine, Division of Endocrinology, King Abdulaziz National Guard Medical Center, P.O. Box 2477, Alahsa...