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Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome

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Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a conse- quence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment proto- cols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome The two most common life-threaten- having type 2 diabetes because 29% ing complications of diabetes mellitus of patients were obese, had measur- include diabetic ketoacidosis (DKA) able insulin secretion, and had a low Guillermo E. Umpierrez, MD, FACP; and hyperglycemic hyperosmolar syn- prevalence of autoimmune markers of Mary Beth Murphy, RN, MS, CDE, drome (HHS). Although there are ␤-cell destruction.4 MBA; and Abbas E. Kitabchi, PhD, important differences in their patho- Treatment of patients with DKA MD, FACP, FACE genesis, the basic underlying mecha- and HHS utilizes significant health nism for both disorders is a reduction care resources. Recently, it was esti- in the net effective concentration of mated that treatment of DKA episodes circulating insulin coupled with a accounts for more than one of every concomitant elevation of counterreg- four health care dollars spent on direct ulatory hormones (glucagon, cate- medical care for adults with type 1 cholamines, cortisol, and growth hor- diabetes, and for one of every two dol- mone). lars for those patients experiencing These hyperglycemic emergencies multiple episodes of DKA.5 continue to be important causes of Despite major advances in their morbidity and mortality among management, recent series have patients with diabetes. DKA is report- reported a mortality rate of 2–5% for ed to be responsible for more than DKA, and ~15% for HHS.1,2 DKA is 100,000 hospital admissions per year the most common cause of death in in the United States1 and accounts for children and adolescents with type 1 4–9% of all hospital discharge sum- diabetes and accounts for half of all maries among patients with diabetes.1 deaths in diabetic patients <24 years The incidence of HHS is lower than of age.6 DKA and accounts for <1% of all pri- The cause of death in patients with mary diabetic admissions.1 DKA and HHS rarely results from the Most patients with DKA have type metabolic complications of hyper- 1 diabetes; however, patients with glycemia or metabolic acidosis but type 2 diabetes are also at risk during rather relates to the underlying med- the catabolic stress of acute illness.2 ical illness that precipitated the meta- Contrary to popular belief, DKA is bolic decompensation. Thus, success- more common in adults than in chil- ful treatment requires a prompt and dren.1 In community-based studies, careful search for the precipitating more than 40% of African-American cause(s). patients with DKA were >40 years of This review discusses the pathogen- age and more than 20% were >55 esis, clinical presentation, complica- years of age.3 Many of these adult tions, and recommendations for treat- patients with DKA were classified as ment of DKA and HHS. 28 Diabetes Spectrum Volume 15, Number 1, 2002 PATHOGENESIS synthesis. Malonyl CoA inhibits carni- reported that psychological problems to Practice Research From / With Diabetes Acute Care of Patients DKA is characterized by hyper- tine palmitoyl-transferase I (CPT I), complicated by eating disorders were glycemia, metabolic acidosis, and the rate-limiting enzyme for transester- a contributing factor in 20% of recur- increased circulating total body ification of fatty acyl CoA to fatty acyl rent ketoacidosis in young women. ketone concentration. Ketoacidosis carnitine, allowing oxidation of fatty More recently, it was reported that up results from the lack of, or ineffective- acids to ketone bodies. CPT I is to one-third of young women with ness of, insulin with concomitant ele- required for movement of FFA into the type 1 diabetes have eating distur- vation of counterregulatory hormones mitochondria where fatty acid oxida- bances,18 which affect the manage- (glucagon, catecholamines, cortisol, tion takes place. The increased activity ment of diabetes and increase the risk and growth hormone).7,8 The associa- of fatty acyl CoA and CPT I in DKA of microvascular complications. tion of insulin deficiency and leads to accelerated ketogenesis.8 Factors that may lead to insulin omis- increased counterregulatory hormones Studies in animals and humans sion in young subjects included fear of leads to altered glucose production with diabetes have shown that lower gaining weight with good metabolic and disposal and to increased lipolysis insulin levels are needed for antilipoly- control, fear of hypoglycemia, rebel- and production of ketone bodies. sis than for peripheral glucose lion from authority, and diabetes- Hyperglycemia results from increased uptake.10,11 HHS is characterized by a related stress. Noncompliance with hepatic and renal glucose production relative deficiency of insulin concen- therapy has also been reported to be a (gluconeogenesis and glycogenolysis) tration to maintain normoglycemia major precipitating cause for DKA in and impaired glucose utilization in but adequate levels to prevent lipolysis urban black and medically indigent peripheral tissues.7 Increased gluco- and ketogenesis.11 To date, very few patients. A recent study reported that neogenesis results from the high avail- studies have been performed compar- in urban black patients, poor compli- ability of noncarbohydrate substrates ing differences in counterregulatory ance with insulin accounted for more (alanine, lactate, and glycerol in the response in DKA versus HHS. than 50% of DKA cases admitted to a liver and glutamine in the kidney)9 Patients with HHS have been reported major urban hospital.3 and from the increased activity of glu- to have higher insulin concentration Most patients with HHS have type coneogenic enzymes (phosphoenol (demonstrated by basal and stimulat- 2 diabetes. HHS is the initial manifes- pyruvate carboxykinase [PEPCK], ed C-peptide levels),12 and reduced tation of diabetes in 7–17% of fructose-1,6-bisphosphatase, and concentrations of FFA, cortisol, patients.1,3 Infection is the major pre- pyruvate carboxylase). From a quanti- growth hormone, and glucagon com- cipitating factor, occurring in tative standpoint, increased hepatic pared to patients with DKA.12–14 30–60% of patients, with urinary glucose production represents the However, one study reported similar tract infections and pneumonia being major pathogenic disturbance respon- levels of FFA in patients with DKA the most common infections.19 In sible for hyperglycemia in patients and HHS,12 indicating that further many instances, an acute illness, such with DKA.7 In addition, both hyper- studies are needed to characterize as cerebrovascular accident or glycemia and high ketone levels cause metabolic responses in such patients. myocardial infarction, provokes the osmotic diuresis that leads to hypo- release of counterregulatory hor- volemia and decreased glomerular fil- PRECIPITATING CAUSES mones, resulting in hyperglycemia. tration rate. The latter further aggra- DKA is the initial manifestation of dia- Furthermore, in many cases, the vates hyperglycemia. betes in 20% of adult patients1 and patient or caregiver is unaware of the The mechanisms that underlie the 30–40% of children15,16 with type 1 signs and symptoms of decompensat- increased production of ketones have diabetes. In patients with established ed diabetes, or the patient is unable to recently been reviewed.8 The combina- diabetes, precipitating factors for DKA treat the progressive dehydration. tion of insulin deficiency and increased include infections, intercurrent illness- Certain medications that cause DKA concentration of counterregulatory es, psychological stress, and poor com- may also precipitate the development hormones causes the activation of hor- pliance with therapy. Infection is the of HHS, including glucocorticoids, mone-sensitive lipase in adipose tissue. most common precipitating factor for thiazide diuretics, dilantin, and ␤- The increased activity of tissue lipase DKA, occurring in 30–50% of cases. blockers. causes breakdown of triglyceride into Urinary tract infection and pneumonia glycerol and free fatty acids (FFA). account for the majority of infections. DIAGNOSIS While glycerol becomes an important Other acute conditions that may pre- Symptoms and Signs substrate for gluconeogenesis in the cipitate DKA include cerebrovascular The clinical presentation of DKA usu- liver, the massive release of FFA accident, alcohol/drug abuse, pancre- ally develops rapidly, over a period of assumes pathophysiological predomi- atitis, pulmonary embolism, myocar- <24 hours. Polyuria, polydipsia, and nance, as they are the hepatic precur- dial infarction, and trauma. Drugs that weight loss may be present for several sors of the ketoacids. In the liver, FFA affect carbohydrate metabolism, such days before the development of are oxidized to ketone bodies, a as corticosteroids, thiazides, sympath- ketoacidosis, and vomiting and process predominantly stimulated by omimetic agents, and pentamidine, abdominal pain are frequently the glucagon. Increased concentration of may also precipitate the development
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