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Is Ketoacidosis Reversible

[alcoholic Ketoacidosis And Reversible Neurological Complications Due To Hypophosphataemia].

[alcoholic Ketoacidosis And Reversible Neurological Complications Due To Hypophosphataemia].

Abstract A 57-year-old man with chronic alcoholism was admitted to our hospital due to disturbance of consciousness and polyradiculitis. Laboratory examination revealed metabolic acidosis, hypokalemia and hypophosphataemia. Alcoholic ketoacidosis is a common disorder in alcoholic patients. All patients present with a history of heavy alcohol misuse, preceding a bout of particularly excesive intake, which had been terminated by nausea, vomiting and abdominal pain. The most important laboratory results are: normal or low glucose level, metabolic acidosis with a raised anion GAP, low or absent blood alcohol level and urinary ketones. The greatest threats to patients are: hypovolemia, hypokaliemia, hypoglucemia and acidosis. Alcohol abuse may result in a wide range of electrolyte and acid-base disorders including hypophosphataemia, hypomagnesemia, hypocalcemia, hypokalemia, metabolic acidosis and respiratory alkalosis. Disturbance of consciousness in alcoholic patients is observed in several disorders, such drunkenness, Wernicke encephalopathy, alcohol withdrawal syndrome, central pontine myelinolysis, hepatic encephalopathy, hypoglucemia and electrolyte disorders. Continue reading >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>

How Can Diabetic Ketoacidosis Cause Cerebral Edema In Infants?

How Can Diabetic Ketoacidosis Cause Cerebral Edema In Infants?

Diabetic Ketoacidosis (DKA) in and of itself does not cause cranial edema. What happens with DKA is the excess glucose in the blood changes the osmolarity of the blood, and causes fluid shift from intracelluar to extracellular. This causes the cells to shrink somewhat. Upon finding the patient in the DKA state, the teatment is insulin and IV fluids. Insulin and the hydration IV fluids reverse the DKA state, and also the osmolarity of the extracellular fluid, causing a fluid shift back into the cell. With the osmolarity reversed, the cells begin swelling—sometimes sometimes larger than before: this is what causes the edema in the cerebrum. This is particularly dangerous because the brain cells have nowhere to go, being encased within the skull. Even though infants have fontanelles and the skull has not fused solid, the extra fluid causes compression within the brain, which in turn can adversely affect the brain function. Continue reading >>

Diabetic Coma

Diabetic Coma

Diabetic coma is a reversible form of coma found in people with diabetes mellitus. It is a medical emergency.[1] Three different types of diabetic coma are identified: Severe low blood sugar in a diabetic person Diabetic ketoacidosis (usually type 1) advanced enough to result in unconsciousness from a combination of a severely increased blood sugar level, dehydration and shock, and exhaustion Hyperosmolar nonketotic coma (usually type 2) in which an extremely high blood sugar level and dehydration alone are sufficient to cause unconsciousness. In most medical contexts, the term diabetic coma refers to the diagnostical dilemma posed when a physician is confronted with an unconscious patient about whom nothing is known except that they have diabetes. An example might be a physician working in an emergency department who receives an unconscious patient wearing a medical identification tag saying DIABETIC. Paramedics may be called to rescue an unconscious person by friends who identify them as diabetic. Brief descriptions of the three major conditions are followed by a discussion of the diagnostic process used to distinguish among them, as well as a few other conditions which must be considered. An estimated 2 to 15 percent of diabetics will suffer from at least one episode of diabetic coma in their lifetimes as a result of severe hypoglycemia. Types[edit] Severe hypoglycemia[edit] People with type 1 diabetes mellitus who must take insulin in full replacement doses are most vulnerable to episodes of hypoglycemia. It is usually mild enough to reverse by eating or drinking carbohydrates, but blood glucose occasionally can fall fast enough and low enough to produce unconsciousness before hypoglycemia can be recognized and reversed. Hypoglycemia can be severe enough to cause un Continue reading >>

Reversible Myocardial Dysfunction In A Patient With Alcoholic Ketoacidosis: A Role For Hypophosphatemia

Reversible Myocardial Dysfunction In A Patient With Alcoholic Ketoacidosis: A Role For Hypophosphatemia

Abstract A 39-year-old-woman had alcoholic ketoacidosis complicated by reversible life-threatening myocardial dysfunction. This complication occurred a few hours after correction of acidosis in association with severe hypophosphatemia. A marked improvement in clinical, echocardiographic, and hemodynamic features was associated with the normalization of the serum phosphorus level. This case illustrates a rare complication of hypophosphatemia, emphasizing the need for emergency physicians to consider this metabolic disorder in the treatment of patients with alcoholic ketoacidosis. The pathogenesis of hypophosphatemia in alcoholic ketoacidosis, its potential role in myocardial dysfunction, and its therapeutic implications in emergencies are discussed. To access this article, please choose from the options below Continue reading >>

The Metabolic Derangements And Treatment Of Diabetic Ketoacidosis

The Metabolic Derangements And Treatment Of Diabetic Ketoacidosis

This article has no abstract; the first 100 words appear below. Diabetic ketoacidosis is a common illness among patients with diabetes. The exact prevalence is unknown, but in one community the rate was estimated to be 13.4 episodes per 1000 patient-years in young persons with diabetes.1 It remains a serious event, with mortality rates as high as 6 to 10 per cent.2 , 3 In children under 10 years of age, diabetic ketoacidosis accounts for 70 per cent of diabetes-related deaths.4 Death may be due to derangements that are directly attributable to ketoacidosis, to complications associated with the illness itself, or to abnormalities induced by treatment. Because a substantial percentage of deaths is . . . Supported by a grant (AM 18573) from the U.S. Public Health Service. From the Departments of Internal Medicine and Biochemistry, Southwestern Medical School, the University of Texas Health Science Center at Dallas. Address reprint requests to Dr. Foster at the University of Texas Health Science Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75235. Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Severe Diabetic Ketoacidosis Associated With Acute Myocardial Necrosis

Severe Diabetic Ketoacidosis Associated With Acute Myocardial Necrosis

We describe a case of a 28-year-old woman who was admitted to our hospital with severe diabetic ketoacidosis. She was known to have had type 1 diabetes for 10 years. During the previous 2 days, she had gone to a party, drank a considerable amount of alcohol, and did not administer her regular dose of insulin. On admission, she was semicomatose and tachypnoic, her blood pressure was 90/70 mmHg, and her heart rate 80 bpm. Laboratory tests showed severe metabolic acidosis (pH 6.92, bicarbonate 2.2 mmol/l, pCO2 1.49 kPa), very high blood glucose (75 mmol/l), hyponatremia (104.3 mmol/l), hypochloremia (70 mmol/l), severe hyperkalemia (8.5 mmol/l), and elevated blood urea (20.3 mmol/l) and creatinine (317 μmol/l). Blood ethanol level was 0.2 g/l. Screening for possible intoxication, including cocaine, opiates, and amphetamines, was negative. Electrocardiogram (ECG) showed sinus rhythm with wide QRS complexes and diffuse nonspecific ST changes. The patient was treated with continuous intravenous saline and insulin infusion. After 12 h, her blood glucose decreased to 17.5 mmol/l (pH 7.23, bicarbonate 12.0 mmol/l, potassium 5.12 mmol/l, and sodium 127.8 mmol/l). Blood urea decreased to 14.6 mmol/l and creatinine to 154 μmol/l. ECG was also normalized. After 36 h, the patient experienced transient stabbing chest pain, which was partially relieved by the change of body position. Complex ventricular arrhythmias, including short runs of ventricular tachycardia, were noticed. Repeat ECG revealed mild ST elevations in leads II, III, and aVF with negative T-waves in leads V2–V4. Echocardiography revealed somewhat depressed left ventricular systolic function (LVEF 45%) with hypokinesis of the posterior and inferior walls. Serum troponin I increased to 343 ng/ml (normal value ≤0.4 Continue reading >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

A Preventable Crisis People who have had diabetic ketoacidosis, or DKA, will tell you it’s worse than any flu they’ve ever had, describing an overwhelming feeling of lethargy, unquenchable thirst, and unrelenting vomiting. “It’s sort of like having molasses for blood,” says George. “Everything moves so slow, the mouth can feel so dry, and there is a cloud over your head. Just before diagnosis, when I was in high school, I would get out of a class and go to the bathroom to pee for about 10–12 minutes. Then I would head to the water fountain and begin drinking water for minutes at a time, usually until well after the next class had begun.” George, generally an upbeat person, said that while he has experienced varying degrees of DKA in his 40 years or so of having diabetes, “…at its worst, there is one reprieve from its ill feeling: Unfortunately, that is a coma.” But DKA can be more than a feeling of extreme discomfort, and it can result in more than a coma. “It has the potential to kill,” says Richard Hellman, MD, past president of the American Association of Clinical Endocrinologists. “DKA is a medical emergency. It’s the biggest medical emergency related to diabetes. It’s also the most likely time for a child with diabetes to die.” DKA occurs when there is not enough insulin in the body, resulting in high blood glucose; the person is dehydrated; and too many ketones are present in the bloodstream, making it acidic. The initial insulin deficit is most often caused by the onset of diabetes, by an illness or infection, or by not taking insulin when it is needed. Ketones are your brain’s “second-best fuel,” Hellman says, with glucose being number one. If you don’t have enough glucose in your cells to supply energy to your brain, yo Continue reading >>

Treatment Of Diabetic Ketoacidosis Associated With Antipsychotic Medication: Literature Review

Treatment Of Diabetic Ketoacidosis Associated With Antipsychotic Medication: Literature Review

Background The second-generation antipsychotics (SGAs) are associated with metabolic disturbances. Diabetic ketoacidosis (DKA) is a rare, but potentially fatal sign of acute glucose metabolism dysregulation, which may be associated with the use of SGAs. This study aims to review published reports of patients with schizophrenia and antipsychotic drug–associated DKA, focusing on the effective management of both conditions. Methods Using a predefined search strategy, we searched PubMed and EMBASE from their inception to July 2016. The search terms were related to “diabetic ketoacidosis” and “antipsychotic medication.” Case reports, case series, and reviews of case series written in English language were included in the review. Results Sixty-five reports were analyzed. In most patients who developed antipsychotic-associated DKA, 1 or more suspected antipsychotic medications were discontinued. In 5 cases, a rechallenge test was trialed, and in only 1 case, it resulted in the elevation of blood glucose. The majority was subsequently treated with a different SGA in combination with insulin/oral hypoglycemic agents; although approximately a third of patients had a complete resolution of symptoms or could control diabetes with diet only at the point of discharge. Conclusions Patients taking antipsychotic medications should be regularly screened for insulin resistance and educated about potential complications of antipsychotic medications. This will allow clinicians to individualize treatment decisions and reduce iatrogenic contribution to morbidity and mortality. To achieve best treatment outcomes, antipsychotic-induced DKA should be treated jointly by psychiatry and endocrinology teams. Continue reading >>

Posterior Reversible Encephalopathy Syndrome Complicating Diabetic Ketoacidosis; An Important Treatable Complication

Posterior Reversible Encephalopathy Syndrome Complicating Diabetic Ketoacidosis; An Important Treatable Complication

Abstract Development of acute neurological symptoms secondary to cerebral oedema is well described in diabetic ketoacidosis (DKA) and often has a poor prognosis. We present the clinical and radiological data of a 17-yr-old girl who developed cortical blindness, progressive encephalopathy, and seizures caused by posterior reversible encephalopathy syndrome (PRES) that developed after her DKA had resolved. Vasogenic oedema in PRES resolves if the underlying trigger is identified and eliminated. In this case, hypertension was identified as the likely precipitating factor and following treatment her vision and neurological symptoms rapidly improved. We suggest how recent DKA may have contributed to the development of PRES in this patient. Continue reading >>

Why Can't Animals Turn Fatty Acids Into Glucose?

Why Can't Animals Turn Fatty Acids Into Glucose?

Animals can’t turn fatty acids into glucose because fatty acids are metabolized 2 carbons at a time into the acetyl units of acetyl-CoA, and we have no enzymes to convert acetyl-CoA into pyruvate or any other metabolite in the gluconeogenesis pathway. Essentially, as I tell my students, the pyruvate dehydrogenase reaction is crossing the Rubicon: once it’s done, you can’t go back. The oxidative decarboxylation of pyruvate is irreversible, and there is no reverse bypass in animal cells. Acetyl-CoA of course enters the Krebs cycle, which ends with oxaloacetate, which is on the gluconeogenic pathway, but the Krebs cycle starts by reacting acetyl-CoA with OAA, and thus OAA production is balanced by OAA consumption: there is no net conversion of acetyl-CoA into OAA. Plants, fungi, and some microbes do have a way to do this: a bypass in the Krebs cycle called the glyoxylate cycle. Isocitrate, instead of being oxidized to alpha-ketoglutarate, is split into succinate and glyoxylate (HC(O)-COO), by an enzyme called isocitrate lyase. The glyoxylate reacts with another acetyl-CoA to form malate, in a reaction catalyzed by malate synthase. The succinate and malate both undergo their usual reactions in the Krebs cycle, resulting in the formation of two oxaloacetates. Thus the cell achieves a net conversion of two acetyl-CoA into OAA, and the OAA can be used for gluconeogenesis. This allows, among other things, plant seeds to store energy and carbon in the form of fats, but use them to create glucose and thus cellulose for cell walls when the seed germinates into a sprout. If we had isocitrate lyase and malate synthase, we could do this trick to, and diabetics wouldn’t have to worry about ketoacidosis. But, we don’t. Edit: for the sake of accuracy, I should mention that fat Continue reading >>

Reversible Hyperinsulinuria In Diabetic Ketoacidosis In Man

Reversible Hyperinsulinuria In Diabetic Ketoacidosis In Man

Urinary clearance and fractional urinary clearance of immunoreactive insulin (IRI) and beta 2-microglobulin (I beta 2M) were studied in patients with diabetic ketoacidosis (DKA) before, during, and after treatment. Our results indicate that in DKA in man a) there is an approximate 250-fold increase in urinary and fractional urinary clearance of IRI and a 600-fold increase in urinary and fractional urinary I beta 2M clearance, which suggests that the hyperinsulinuria is secondary to a nonspecific defect in tubular luminal uptake of low-molecular-weight proteins, although decreased IRI degradation cannot be excluded; b) because increased IRI clearance is not changed by the pharmacologic plasma IRI levels achieved, the residual tubular absorptive capacity is not saturable; c) I beta 2M clearance but not IRI clearance is significantly improved by the time metabolic control is attained, suggesting separate tubular transport systems; d) a small, therapeutically insignificant fraction of the infused insulin is lost in the urine during therapy of DKA; and e) defective renal tubular luminal uptake (and possibly degradation) of IRI is reversible. Adrenal enucleation is followed by a period of increased sodium reabsorption thought to be due to excess mineralocorticoid activity. However, it has not been demonstrated that increased production of any known mineralocorticoid accounts for this antinatriuresis. Recently, 19-hydroxydeoxycorticosterone (19-OH-DOC) was found in incubates of regenerating adrenal capsules 3-4 days postenucleation and 19-nordeoxycorticosterone (19-nor-DOC) was identified in the urine of rats with regenerating adrenals. Because it was possible that these hormones might play a role in the sodium retention after adrenal enucleation, we compared the mineralocorti Continue reading >>

What Is The Treatments For Ketoacidosis?

What Is The Treatments For Ketoacidosis?

Management of diabetic ketoacidos Time: 0–60 mins 1. Commence 0.9% sodium chloride If systolic BP > 90 mmHg, give 1 L over 60 mins If systolic BP < 90 mmHg, give 500 mL over 10–15 mins, then re-assess. If BP remains < 90 mmHg, seek senior review 2. Commence insulin treatment 50 U human soluble insulin in 50 mL 0.9% sodium chloride infused intravenously at 0.1 U/kg body weight/hr Continue with SC basal insulin analogue if usually taken by patient 3. Perform further investigations: see text 4. Establish monitoring schedule Hourly capillary blood glucose and ketone testing Venous bicarbonate and potassium after 1 and 2 hrs, then every 2 hrs Plasma electrolytes every 4 hrs Clinical monitoring of O2 saturation, pulse, BP, respiratory rate and urine output every hour 5. Treat any precipitating cause Time: 60 mins to 12 hrs • IV infusion of 0.9% sodium chloride with potassium chloride added as indicated below 1 L over 2 hrs 1 L over 2 hrs 1 L over 4 hrs 1 L over 4 hrs 1 L over 6 hrs • Add 10% glucose 125 mL/hr IV when glucose < 14 mmol/L • Be more cautious with fluid replacement in elderly, young people, pregnant patients and those with renal or heart failure. If plasma sodium is > 155 mmol/L, 0.45% sodium chloride may be used. • Adjust potassium chloride infusion Plasma potassium (mmol/L) Potassium replacement (mmol/L of infusion) > 5.5 Nil 3.5–5.5 40 < 3.5 Senior review – additional potassium required Time: 12–24 hrs • Ketonaemia and acidosis should have resolved (blood ketones < 0.3 mmol/L, venous bicarbonate > 18 mmol/L). Request senior review if not improving • If patient is not eating and drinking Continue IV insulin infusion at lower rate of 2–3 U/kg/hr Continue IV fluid replacement and biochemical monitoring • If ketoacidosis has resolved and Continue reading >>

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