Dka In Hypoglycemia
#2 0 They are two different entities. While they will both cause acidosis the mechanism of acidosis is different. DKA is from ketosis and acidosis from Hypoglycamia is lactic acid. Is this what you are asking? 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. 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. Diabetic Ketoacidosis Causes, Symptoms, and Treatment by eMedicineHealth.com An insulin reaction occurs when a person with diabetes becomes confused or even unconscious because of hypoglycemia (hypo=low + glycol = sug Continue reading >>
Prevalence And Significance Of Lactic Acidosis In Diabetic Ketoacidosis
Abstract The prevalence and clinical significance of lactic acidosis in diabetic ketoacidosis (DKA) are understudied. The objective of this study was to determine the prevalence of lactic acidosis in DKA and its association with intensive care unit (ICU) length of stay (LOS) and mortality. Retrospective, observational study of patients with DKA presenting to the emergency department of an urban tertiary care hospital between January 2004 and June 2008. Results Sixty-eight patients with DKA who presented to the emergency department were included in the analysis. Of 68 patients, 46 (68%) had lactic acidosis (lactate, >2.5 mmol/L), and 27 (40%) of 68 had a high lactate (>4 mmol/L). The median lactate was 3.5 mmol/L (interquartile range, 3.32-4.12). There was no association between lactate and ICU LOS in a multivariable model controlling for Acute Physiology and Chronic Health Evaluation II, glucose, and creatinine. Lactate correlated negatively with blood pressure (r = −0.44; P < .001) and positively with glucose (r = 0.34; P = .004). Lactic acidosis is more common in DKA than traditionally appreciated and is not associated with increased ICU LOS or mortality. The positive correlation of lactate with glucose raises the possibility that lactic acidosis in DKA may be due not only to hypoperfusion but also to altered glucose metabolism. Continue reading >>
Any Benefit To Sodium Bicarbonate In Dka?
In a prior post, we discussed the use of an initial insulin bolus in the management of diabetic ketoacidosis (DKA). Today we will address another facet of DKA management, for which there is less than optimal evidence and that is: Any benefit to sodium bicarbonate in DKA? Consensus guidelines for the management of DKA recommended administering sodium bicarbonate to DKA patients who present with an initial blood gas pH of < 7.0. That recommendation was updated and changed in 2009 to limit sodium bicarbonate use to DKA patients with blood gas pH of < 6.9. More recently, Chua et al. published a systematic review of 44 articles discussing bicarbonate administration and Duhon et al. published the largest retrospective review of DKA patient with presenting pH of < 7.0. What are the most recent studies evaluating: Any benefit to sodium bicarbonate in DKA? Chua et al (21906367) Duhon et al (23737516) Objective Efficacy and risk of bicarb administration in severe acidemia in DKA Determine whether bicarb therapy is associated with reduced time to resolution of acidemia Methods Systematic review of pubmed database Retrospective cohort of DKA pts with initial pH < 7.0 who did vs did not receive bicarb Results 44 articles included -Heterogeneity in pH threshold, concentration, amount, & timing of bicarb administration -Transient improvement in metabolic acidosis -No improved glycemic control -Associated risk of cerebral edema in pediatric pts No study involved patients with a pH < 6.85 86 patients -No difference found in: 1. Time to resolution of acidemia 2. Time to hospital discharge 3. Time on IV insulin 4. Potassium requirement in 1st 24 hrs -Subgroup analysis of pH <6.9 (n=20) showed no statistical diff in time to resolution of acidemia Conclusion Evidence does not justify the ad Continue reading >>
Metabolic Acidosis
Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>
Diabetic Ketoacidosis
4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the Continue reading >>
Acid–base Problems In Diabetic Ketoacidosis
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. Dr. Halperin reports holding a patent on the use of sodium-linked glucose transporter 2 inhibitors to increase the excretion of water in patients with hyponatremia (US 8,518,895,B2) and a pending patent application on the use of sodium-linked glucose transporter 2 inhibitors to increase urine volume and lower solute concentration in the urine (08578 11286 PSP). No other potential conflict of interest relevant to this article was reported. We thank Drs. Arlan Rosenbloom, Brian Robinson, and Robert Jungas for their critique and helpful suggestions in the preparation of an earlier version of the manuscript, and S.Y. Lee for secretarial assistance. From the Renal Division, St. Michael’s Hospital and University of Toronto, and Keenan Research Center, Li Ka Shing Knowledge Institute of St. Michael’s Hospital, University of Toronto, Toronto. Address reprint requests to Dr. Halperin at the Department of Medicine, University of Toronto Keenan Research Center, Li Ka Shing Knowledge Institute of St. Michael’s Hospital, 30 Bond St., Rm. 408, Toronto, ON M5B 1W8, Canada, or at [email protected] Continue reading >>
Diabetic Ketoacidosis
Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>
Haemofiltration As A Treatment Option In Refractory Life-threatening Diabetic Ketoacidosis
Background: Treating life-threatening diabetic ketoacidosis (DKA) with a pH of <6.9 is extremely challenging and often refractory to treatment using standard fixed dose insulin DKA management protocols which may not work effectively at this low pH because of increased insulin resistance. I.v. bicarbonate (HCO3) use in this situation can be considered but remains controversial due to the risk of significant side effects as well as limited evidence in literature. Here we attempt to describe a case of fulminant DKA without renal failure, where treatment with haemofiltration (HF) for severe metabolic acidosis was successful. Case history: A 23-year-old female with history of recurrent episodes of DKA and poor diabetes control secondary to non-compliance, presented to the emergency department via ambulance after being found collapsed and had successful cardiopulmonary resuscitation for pulseless electrical activity and was subsequently treated with standard DKA protocol. Investigations on admission: pH 6.752, HCO3 1.3, lactate 3.1, base excess −30, blood glucose 45 mmol/l, blood ketones 6 mmol/l, creatinine 133 mmol, urea 10.8 mmol, and eGFR 43. Treatment: Despite maximal DKA treatment over three hours, including 5 l of i.v. fluid, and maximum fixed rate i.v. insulin at 15 units/h, she continued to be in severe metabolic acidosis with pH 6.772, HCO3 1.7, ketones 5, and blood glucose 40.1, without any improvement in her Glasgow coma scale of 8. Options were discussed at length with critical care and endocrine teams regarding use of i.v. bicarbonate therapy vs HF. She was then put on HF which resolved the metabolic acidosis completely within 12 h. Discussion: Our patient responded to HF with resolution of severe metabolic acidosis. There are no guidelines at present that com Continue reading >>
Acidosis
The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis. Respiratory acidosis develops when there is too much carbon dioxide (an acid) in the body. This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include: Chest deformities, such as kyphosis Chest injuries Chest muscle weakness Chronic lung disease Overuse of sedative drugs Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis: Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by: Cancer Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar (hypoglycemia) Medications, such as salicylates MELAS (a very rare genetic mitochondrial disorder that affects energy production) Prolonged lack of oxygen from shock, heart failure, or seve Continue reading >>
Management Of Diabetic Ketoacidosis In Children And Adolescents
Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>
Diabetic Ketoacidosis And Cerebral Edema
Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti Continue reading >>
Understanding The Presentation Of Diabetic Ketoacidosis
Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>
1685: Type B Lactic Acidosis In Diabetic Ketoacidosis Responding To Thiamine Therapy
Prescribing InformationImportant Safety Information Patients being treated with Vitamin K antagonist therapy have underlying disease states that predispose them to thromboembolic events. Potential benefits of reversing VKA should be weighed against the risk of thromboembolic events, especially in patients with history of such events. Resumption of anticoagulation therapy should be carefully considered once the risk of thromboembolic events outweighs the risk of acute bleeding. Both fatal and nonfatal arterial and venous thromboembolic complications have been reported in clinical trials and postmarketing surveillance. Monitor patients receiving Kcentra, and inform them of signs and symptoms of thromboembolic events. Kcentra was not studied in subjects who had a thromboembolic event, myocardial infarction, disseminated intravascular coagulation, cerebral vascular accident, transient ischemic attack, unstable angina pectoris, or severe peripheral vascular disease within the prior 3 months. Kcentra might not be suitable for patients with thromboembolic events in the prior 3 months. Kcentra is contraindicated in patients with known anaphylactic or severe systemic reactions to Kcentra or any of its components (including heparin, Factors II, VII, IX, X, Proteins C and S, Antithrombin III and human albumin). Kcentra is also contraindicated in patients with disseminated intravascular coagulation. Because Kcentra contains heparin, it is contraindicated in patients with heparin-induced thrombocytopenia (HIT). Indications Kcentra®, Prothrombin Complex Concentrate (Human), is a blood coagulation factor replacement product indicated for the urgent reversal of acquired coagulation factor deficiency induced by Vitamin K antagonist (VKA—eg, warfarin) therapy in adult patients with ac Continue reading >>
Potassium Balance In Acid-base Disorders
INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>
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 >>
