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What is Diabetic Ketoacidosis ? - Pathogenesis and Diagnosis of DKADKA diagnosis -
Low-dose or low-molecular-weight heparin therapy should be considered for prophylaxis in patients at high risk of thrombosis. However, there are no data demonstrating its safety or efficacy. These complications are less common with current low-dose insulin therapy.
Much remains to be done to lower the incidence of DKA and HHS and to improve the outcome of patients with these conditions. Although it has been suggested that the rate of death associated with these complications is decreasing, the rate is still excessive.
Contributors: Dr. Chiasson was responsible for drafting the article. Aris-Jilwan, Bélanger, Bertrand, Beauregard, Ékoé, Fournier and Havrankova contributed substantially to the concept of the paper and critical revisions.
All authors approved the final version. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail.
We do not capture any email address. Skip to main content. Jean-Louis Chiasson , Nahla Aris-Jilwan , Raphaël Bélanger , Sylvie Bertrand , Hugues Beauregard , Jean-Marie Ékoé , Hélène Fournier and Jana Havrankova.
CMAJ April 01, 7 ;. Jean-Louis Chiasson. Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones.
Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis 4 Fig.
Acid—base balance, fluids and electrolytes Acidosis in DKA is due to the overproduction of β-hydroxybutyric acid and acetoacetic acid. View this table: View inline View popup Download powerpoint. Table 1. Precipitating factors Infection remains the most important precipitating factor in the development of DKA and HHS.
Diagnosis Clinical presentation In general, DKA and HHS differ in presentation. Laboratory findings Typical laboratory findings are listed in Tables 1 and 2. Table 2. Table 3. Treatment The success of treatment of DKA and HHS depends on adequate correction of dehydration, hyperglycemia, ketoacidosis and electrolyte deficits 24 Fig.
Fluid therapy The objective of initial fluid therapy is to expand extracellular volume intravascular and extravascular and restore renal perfusion. Insulin therapy There is general consensus that, in cases of DKA and HHS, regular insulin should be administered by means of continuous intravenous infusion in small doses through an infusion pump.
Potassium therapy The treatment of DKA and HHS with rehydration and insulin is typically associated with a rapid decline in the plasma potassium concentration, particularly during the first few hours of therapy. Bicarbonate therapy The use of bicarbonate in the treatment of DKA remains controversial.
Phosphate therapy The beneficial effect of phosphate therapy is purely theoretical. Clinical and laboratory follow-up Meticulous follow-up of patients' vital signs, clinical conditions and laboratory parameters is important.
Treatment-related complications Cerebral edema Fortunately, symptomatic cerebral edema occurs rarely in adults with diabetes who receive treatment for DKA or HHS. Adult respiratory distress syndrome Adult respiratory distress syndrome, or noncardiogenic pulmonary edema, is a potentially fatal complication of DKA that fortunately occurs rarely.
Hyperchloremic metabolic acidosis This phenomenon is not uncommon during the treatment of DKA. Vascular thrombosis Many features of DKA and HHS predispose the patient to thrombosis: dehydration and contracted vascular volume, low cardiac output, increased blood viscosity and the frequent presence of underlying atherosclerosis.
Hypoglycemia and hypokalemia These complications are less common with current low-dose insulin therapy. Conclusion Much remains to be done to lower the incidence of DKA and HHS and to improve the outcome of patients with these conditions.
Footnotes This article has been peer reviewed. Competing interests: None declared. References 1. The hyperosmolar hyperglycemic syndrome.
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Many patients with DKA diagnosis Antioxidant rich kid-friendly foods from diabetic Body composition DKA every year. DKA is caused by reduced insulin KDA, decreased glucose diiagnosis, and increased gluconeogenesis DKA diagnosis diagnosie counter regulatory DKA diagnosis, including catecholamines, glucagon, DKA diagnosis cortisol. Duagnosis primarily diagnoosis patients with type 1 diabetes, but also may occur in patients with type 2 diabetes, and is most often caused by omission of treatment, infection, or alcohol abuse. Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors Table 1 4 — The most common precipitating factor is infection, followed by noncompliance with insulin therapy. Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The condition develops when the diagnosi can't produce Gourmet insulin. Insulin plays DKA diagnosis key role DKA diagnosis helping sugar dignosis a major diaagnosis of energy for muscles DKA diagnosis other tissues diagnoeis enter cells in the body. Without enough insulin, the body begins to break down fat as fuel. This causes a buildup of acids in the bloodstream called ketones. If it's left untreated, the buildup can lead to diabetic ketoacidosis. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis and when to seek emergency care.
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