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Diabetic ketoacidosis; presentation, treatment, outcome:Louisiana State University Medical Center :"Presentation: DKA often presents as anorexia, N/V, and abdominal pain. a. Abdominal pain be sufficiently severe to suggest an acute surgical abdomen. b. Abdominal tenderness, guarding, decreased bowel sounds, and increased WBC may be present. c. Abdominal pain 2o DKA almost always subsides in 6-8 hours after institution of therapy. DKA is often preceeded by a period of polvdipsia, polyphagia, polyuria, weight loss, increasing weakness, and mental obtundation. The onset is usually gradual over several days. Hypothermia is the rule and does not preclude infection."
http://lib-sh.lsumc.edu/fammed/intern/dka.html

Diagnosis of Ketoacidosis:Robin R. Hemphill, MD:"History and Physical: Patients with DKA usually present with complaint of fatigue, malaise, thirst, and polyuria. Depending on the length of symptoms the patient may be able to report weight loss. As the patient becomes increasingly ill they may begin to vomit and complain of abdominal pain. The exact cause of abdominal pain that is associated with DKA is not known. The abdominal pain is disturbing since it may be secondary to the DKA, or be from the pathologic process that initiated the crisis, such as pyelonephritis, pancreatitis, etc. Usually, abdominal pain secondary to DKA will begin to resolve with treatment. The physical signs of DKA can be variable. Most patients will have some degree of tachycardia, but the blood pressure is often normal. Evidence of dehydration, such as loss of skin turgor, and dry mucus membranes may be present. The patient may be febrile, and extreme elevations of temperature should not be assumed to be the result of dehydration. Hypothermia may also be seen. The respiratory rate may be normal or somewhat rapid, but if the patient is examined closely the deep breathing typical of “Kussmaul” respirations may be noted."
http://www.embbs.com/cr/dka/dkankh.html

Diabetic ketoacidosis a comprehensive review:Merk:"Diabetic ketoacidosis (DKA) results from grossly deficient insulin availability, causing a transition from glucose to lipid oxidation and metabolism (see below). In type I DM patients, DKA is commonly precipitated by a lapse in insulin treatment or by an acute infection, trauma, or infarction that makes usual insulin treatment inadequate. Although type II DM patients rarely have DKA, many may have ketone formation and acidosis (usually mild) because of a decrease in food intake and a marked decrease in insulin secretion due to severe and chronic hyperglycemia (glucose toxicity). These patients usually do not require insulin after the acute metabolic event is corrected"
http://www.merck.com/pubs/mmanual/section2/chapter13/13b.htm

Pathophysiology of diabetic ketoacidosis:emedicine:"Many of the underlying pathophysiologic disturbances in DKA are directly measurable by the clinician and need to be followed throughout the course of treatment. Close attention to clinical lab data allows the emergency physician not only to track the underlying acidosis and hyperglycemia but also to prevent common potentially lethal complications such as hypoglycemia, hyponatremia, and hypokalemia. The absence of insulin, the primary anabolic hormone, means that tissues such as muscle, fat, and liver do not take up glucose. Counterregulatory hormones, such as glucagon, growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty acids and gluconeogenesis, which is the main cause for the elevation in serum glucose in DKA. Beta-oxidation of these free fatty acids leads to increased formation of ketone bodies. Overall, metabolism in DKA shifts from the normal fed state characterized by carbohydrate metabolism to a fasting state characterized by fat metabolism."
http://www.emedicine.com/emerg/topic135.htm

Management of diabetic ketoacidosis:American Academy of Family Physicians:"Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non≠insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults."
http://www.aafp.org/afp/990800ap/455.html

Causes and risks of diabetic ketoacidosis:Medline plus:"In a person with diabetes, if insulin is not present for the body to use glucose as a fuel source, body fat is used as fuel. The by-products of fat metabolism are ketones. Ketones build up in the blood and "spill" over into the urine. A condition called ketoacidosis develops when the blood is more acidic than body tissues. Blood-glucose levels become elevated (above 300 mg/dL) because of increased production of glucose in the liver and decreased glucose uptake by the cells. Diabetic ketoacidosis may be the first symptom of a person with Type I diabetes; or it may be the result of increased insulin needs in Type I diabetes because of infection, trauma, heart attack, or surgery. People with Type II diabetes usually develop ketoacidosis only under conditions of severe stress. Poor compliance with diet and treatment is usually the cause when episodes are recurrent.Diabetics should learn to recognize the early warning signs and symptoms of ketoacidosis. Measurement of urine ketones in people with infections or people on insulin pump therapy can give more information than glucose measurements alone"
http://www.nlm.nih.gov/medlineplus/ency/article/000320.htm#causesAndRisk

What Are The Warning Signs Of Ketoacidosis?:diabetes.org:"Ketoacidosis usually develops slowly. But when vomiting occurs, this life-threatening condition can develop in a few hours. The first symptoms are: Thirst or a very dry mouth. Frequent urination. High blood-sugar levels. High levels of ketones in the urine. Next, other symptoms appear: Constantly feeling tired. Dry or flushed skin. Nausea, vomiting, or abdominal pain (Vomiting can be caused by many illnesses, not just ketoacidosis. If vomiting continues for more than 2 hours, contact your health care practitioner.) A hard time breathing (short, deep breaths). Fruity odor on breath. A hard time paying attention, or confusion"
http://www.diabetes.org/main/application/commercewf?origin=*.jsp&event=link(C4_7)

Treatment of diabetic ketoacidosis:childhooddiabetes.com:"The treatment of a child with DKA should be initiated without delay-The most important components of the treatment are fluids, insulin and electrolytes and venous access must be secured immediately after admission. If the child is in a state of shock (hypotension, poor peripheral circulation, semi-comatose) resuscitation should be initiated with boluses of 10-15 ml/kg of 0.9% isotonic saline plus 5 % human albumin and repeated until an adequate circulation is achieved. If ventilation is inadequate, assisted ventilation or intubation should be considered If the child is unconscious or vomits repeatedly, a nasogastric tube should be inserted If the child is unconscious, has a palpable bladder or not has passed urine for 3-4 hours the bladder should be catheterised"
http://www.childhooddiabetes.com/view.asp?documentID=94

Ketosis-Ketoacidosis, what is it; is it safe?:Lindora, Inc:"Being in ketosis means your body has burned a large amount of fat in response to the fact that it didn't have sufficient glucose available for energy needs. Under everyday conditions, the carbohydrates you eat are converted to glucose, which is the body's primary source of energy. Whenever your intake of carbohydrates is limited to a certain range, for a long enough period of time, you'll reach a point where your body draws on its alternate energy system, fat stores, for fuel. This condition called dietary ketosis, means your body burns fat and turns it into a source of fuel called ketones. Ketones are produced whenever body fat is burned. When you burn a larger amount of fat than is immediately needed for energy, the excess ketones are discarded in the urine. Dietary ketosis is among the most maligned and misunderstood concepts in nutrition because it is often confused with ketoacidosis, which is a life-threatening condition most often associated with uncontrolled insulin-deficient Type 1 diabetes. In the Type 1 diabetic, the absence of insulin leads to a toxic build-up of blood glucose and an extreme break-down of fat and muscle tissue. This condition doesn't occur in individuals who have even a small amount of insulin, whether from natural production or artificially administered"
http://www.ketosis-ketoacidosis-difference.com/

CEREBRAL EDEMA IN DIABETIC KETOACIDOSIS :Vanderbilt Medical Center:"In spite of advances over the past several decades in the understanding and treatment of diabetes mellitus, the incidence of DKA has not decreased. Ketoacidosis is the leading cause of death in young patients with diabetes. Death is usually due to electrolyte abnormalities, shock, aspiration pneumonitis, or myocardial infarction. Fatal cerebral edema has been recognized with increasing frequency since the earliest reports in the 1960's. The development of cerebral edema in patients with DKA is not heralded by any warning signs, nor are there any predictive indicators. Paradoxically, cerebral edema becomes clinically apparent 6- 10 hours after therapy has begun, at a time when severe acidosis has been partially corrected, the blood glucose level is falling, adequate circulation has been restored, and all indications suggest that the patient is recovering"
http://www.mc.vanderbilt.edu/peds/pidl/acute/cerebr.htm



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Last updated by Andrew Lopez, RN on Wednesday, September 29, 2010


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