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Diabetic Ketoacidosis Bicarbonate Levels

Bicarbonate Therapy In Severe Diabetic Ketoacidosis

Bicarbonate Therapy In Severe Diabetic Ketoacidosis

Twenty-one adult patients with severe diabetic ketoacidosis entered a randomized prospective protocol in which variable doses of sodium bicarbonate, based on initial arterial pH (6.9 to 7.14), were administered to 10 patients (treatment group) and were withheld from 11 patients (control group). During treatment, there were no significant differences in the rate of decline of glucose or ketone levels or in the rate of increase in pH or bicarbonate levels in the blood or cerebrospinal fluid in either group. Similarly, there were no significant differences in the time required for the plasma glucose level to reach 250 mg/dL, blood pH to reach 7.3, or bicarbonate level to reach 15 meq/L. We conclude that in severe diabetic ketoacidosis (arterial pH 6.9 to 7.14), the administration of bicarbonate does not affect recovery outcome variables as compared with those in a control group. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: 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 gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Severe Ketoacidosis (ph ≤ 6.9) In Type 2 Diabetes: More Frequent And Less Ominous Than Previously Thought

Severe Ketoacidosis (ph ≤ 6.9) In Type 2 Diabetes: More Frequent And Less Ominous Than Previously Thought

BioMed Research International Volume 2015 (2015), Article ID 134780, 5 pages 1Division of Endocrinology, Internal Medicine Department, University Hospital “Dr. José E. González”, Autonomous University of Nuevo León, 64460 Monterrey, NL, Mexico 2Knowledge and Evaluation Research Unit, Division of Endocrinology, Diabetes, Metabolism and Nutrition, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA 3Department of Internal Medicine, University Hospital “Dr. José E. González”, Autonomous University of Nuevo León, 64460 Monterrey, NL, Mexico 4Latino Diabetes Initiative, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA Academic Editor: Gianluca Bardini Copyright © 2015 René Rodríguez-Gutiérrez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Diabetic ketoacidosis is a life-threatening acute metabolic complication of uncontrolled diabetes. Severe cases of DKA (pH ≤ 7.00, bicarbonate level ≤ 10.0, anion gap > 12, positive ketones, and altered mental status) are commonly encountered in patients with type 1 diabetes and are thought to carry an ominous prognosis. There is not enough information on the clinical course of severely acidotic type 2 diabetes (pH ≤ 6.9) patients with DKA, possibly because this condition is rarely seen in developed countries. In this series, we present 18 patients with type 2 diabetes, DKA, and a pH ≤ 6.9 that presented to a tertiary university hospital over the past 11 years. The objective was to describe their clinical characteristics, the triggering cause, and emphasis on treatment, evolution, and outcomes. The majority of Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

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 consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious, life-threatening complication of diabetes mellitus. DKA is characterized by the triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. It is part of a spectrum of hyperglycemia on which lies hyperosmolar hyperglycemic state (HHS). Though the two are distinct entities, they do share some commonalities. DKA is caused by the reduced effect of insulin, either due to deficit or reduction of levels, with concomitant elevation of counter regulatory hormones (glucagon, catecholamines, cortisol, and growth hormones), generally due to a precipitating stress. Increased gluconeogenesis, glycogenolysis, and decreased glucose uptake by cells leads to hyperglycemia, while insulin deficiency leads to mobilization and oxidization of fatty acids leading to ketogenesis. Although DKA may be the initial manifestation of diabetes, it is typically precipitated by other factors. It is critical for a clinician to identify and treat these factors. Infection can be found in 40-50% of patients with hyperglycemic crisis, with urinary tract infection and pneumonia accounting for the majority of cases. DKA is a life-threatening medical emergency with a mortality rate just under 5% in individuals under 40 years of age, but with a more serious prognosis in the elderly, who have mortality rates over 20%. Deaths may also occur as a result of hypokalemia induced arrhythmias and cerebral edema (more common in children). II. Diagnostic confirmation: are you sure your patient has diabetic ketoacidosis? Although the diagnosis of DKA can be suspected on clinical grounds, confirmation is based on laboratory tests including potential hydrogen (pH) level, urinalysis, and basic metabolic profile. summarizes the biochemical criteria for the diagnosis and asse Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

Bicarbonate In Diabetic Ketoacidosis - A Systematic Review

Bicarbonate In Diabetic Ketoacidosis - A Systematic Review

Objective: This study was designed to examine the efficacy and risk of bicarbonate administration in the emergent treatment of severe acidemia in diabetic ketoacidosis (DKA). Methods: PUBMED database was used to identify potentially relevant articles in the pediatric and adult DKA populations. DKA intervention studies on bicarbonate administration versus no bicarbonate in the emergent therapy, acid-base studies, studies on risk association with cerebral edema, and related case reports, were selected for review. Two reviewers independently conducted data extraction and assessed the citation relevance for Results: From 508 potentially relevant articles, 44 were included in the systematic review, including three adult randomized controlled trials (RCT) on bicarbonate administration versus no bicarbonate in DKA. We observed a marked heterogeneity in pH threshold, concentration, amount, and timing for bicarbonate administration in various studies. Two RCTs demonstrated transient improvement in metabolic acidosis with bicarbonate treatment within the initial 2 hours. There was no evidence of improved glycemic control or clinical efficacy. There was retrospective evidence of increased risk for cerebral edema and prolonged hospitalization in children who received bicarbonate, and weak evidence of transient paradoxical worsening of ketosis, and increased need for potassium supplementation. No studies involved patients with an initial pH < 6.85. Conclusions: The evidence to date does not justify the administration of bicarbonate for the emergent treatment of DKA, especially in the pediatric population, in view of possible clinical harm and lack of sustained benefits. Diabetic ketoacidosis (DKA) is a serious medical emer- gency resulting from relative or absolute insulin defi- ci Continue reading >>

Acid–base Problems In Diabetic Ketoacidosis

Acid–base Problems In Diabetic Ketoacidosis

Disorders of Fluids and Electrolytes The case description below highlights issues raised in an upcoming article about acid–base disturbance and its clinical implications in patients with diabetic ketoacidosis in the series “Disorders of Fluids and Electrolytes.” A 15-year-old boy with nephrotic syndrome presented with abdominal pain and vomiting. Lab data include: blood glucose 849 mg/dL, blood pH 7.19, PCO2 18 mm Hg, PO2 40 mm Hg, bicarbonate 7 mmol/L, sodium 125 mmol/L, potassium 6.2 mmol/L, chloride 81 mmol/L, and total carbon dioxide 8 mmol/L. What is the best strategy to support this patient? Polling and commenting are now closed. The editor’s recommendations appear below. The next challenge appears on March 5. Share: A 15-year-old boy with a history of glucocorticoid-dependent nephrotic syndrome since 5 years of age arrives in a community emergency department because of chest pain and nausea that has progressed to abdominal pain over the preceding 16 hours. The nephrotic syndrome was in remission while the patient was receiving glucocorticoids and cyclosporine. The patient and his mother stated that he had become very thirsty and had been drinking huge amounts of water over the past week. On the day of admission, he had several episodes of vomiting. There was no fever, cough, rhinorrhea, or diarrhea, and no family member, friend, or associate had been ill. The patient’s usual medications at the time of presentation included prednisone (at a dose of 50 mg daily), cyclosporine (125 mg twice daily), enalapril (10 mg daily), and ranitidine (75 mg daily). In addition, treatment with recombinant human growth hormone had been initiated for glucocorticoid-induced short stature. The patient and his family said that the urinary albumin level had been negative on a Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Bicarbonate In Diabetic Ketoacidosis - A Systematic Review

Bicarbonate In Diabetic Ketoacidosis - A Systematic Review

Abstract This study was designed to examine the efficacy and risk of bicarbonate administration in the emergent treatment of severe acidemia in diabetic ketoacidosis (DKA). PUBMED database was used to identify potentially relevant articles in the pediatric and adult DKA populations. DKA intervention studies on bicarbonate administration versus no bicarbonate in the emergent therapy, acid-base studies, studies on risk association with cerebral edema, and related case reports, were selected for review. Two reviewers independently conducted data extraction and assessed the citation relevance for inclusion. From 508 potentially relevant articles, 44 were included in the systematic review, including three adult randomized controlled trials (RCT) on bicarbonate administration versus no bicarbonate in DKA. We observed a marked heterogeneity in pH threshold, concentration, amount, and timing for bicarbonate administration in various studies. Two RCTs demonstrated transient improvement in metabolic acidosis with bicarbonate treatment within the initial 2 hours. There was no evidence of improved glycemic control or clinical efficacy. There was retrospective evidence of increased risk for cerebral edema and prolonged hospitalization in children who received bicarbonate, and weak evidence of transient paradoxical worsening of ketosis, and increased need for potassium supplementation. No studies involved patients with an initial pH < 6.85. The evidence to date does not justify the administration of bicarbonate for the emergent treatment of DKA, especially in the pediatric population, in view of possible clinical harm and lack of sustained benefits. Introduction Diabetic ketoacidosis (DKA) is a serious medical emergency resulting from relative or absolute insulin deficiency and the u Continue reading >>

Sodium Bicarbonate And Diabetic Ketoacidosis

Sodium Bicarbonate And Diabetic Ketoacidosis

OVERVIEW The correction of the acidaemia in DKA is achieved by correcting the underlying pathophysiology with fluid replacement and insulin The role of sodium bicarbonate (NaHCO3) as a therapy for diabetic ketoacidosis (DKA) is controversial Different sources have different values for the cut off pH which requires treatment, and other sources advise against NaHCO3 use in DKA completely — there is no consensus RATIONALE Reasons proposed for use of sodium bicarbonate in DKA: treatment of severe acidaemia, which causes catecholamine resistance and myocardial depression treatment of severe hyperkalemia replacement of bicarbonate loss from Renal or GI tract — theoretical potential for giving HCO3- with renal wasting of HCO3- or GI loss if delta ratio is <1 (as is usual for DKA) ketoacids lost in urine (hence delta ratio <1) cannot be converted into HCO3- DISADVANTAGES Side effects of sodium bicarbonate Worsening of intracellular acidaemia hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) volume overload rebound or ‘overshoot’ alkalosis hypokalaemia ionised hypocalcaemia impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK CSF acidosis hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: — increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis — shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues EVIDENCE A 2011 systematic review by C Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

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