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Why Is There Acidosis In Dka?

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Management Of A Dka Patient With Severe Metabolic And Ketoacidosis With Chronic Renal Insufficiency Brian Albany Otterbein University, Boomer.albany@otterbein.edu

Management Of A Dka Patient With Severe Metabolic And Ketoacidosis With Chronic Renal Insufficiency Brian Albany Otterbein University, [email protected]

Otterbein University Digital Commons @ Otterbein MSN Student Scholarship Student Research & Creative Work Fall 2014 Follow this and additional works at: Part of the Endocrine System Diseases Commons, Medical Pathology Commons, and the Nursing Commons This Project is brought to you for free and open access by the Student Research & Creative Work at Digital Commons @ Otterbein. It has been accepted for inclusion in MSN Student Scholarship by an authorized administrator of Digital Commons @ Otterbein. For more information, please contact [email protected] Recommended Citation Albany, Brian, "Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency" (2014). MSN Student Scholarship. Paper 6. Implications for nursing care Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency Brian Albany BSN, CCRN Introduction Case Study References Underlying Pathophysiology Diabetic ketoacidosis (DKA) serves as one the leading causes of mortality in diabetic patients [14]. The mortality has decreased over the past several decades due to the rapid recognition of the disease state and the improvement of management of DKA [14]. Despite a decline in mortality rates over the past twenty years from 7.96% to 0.67%, errors in management of the disease state are associated with significant morbidity and mortality [2]. Utilization of DKA protocols in the acute care setting have allowed congruency in care and delivery of effective lifesaving treatment. Despite advances in standardized DKA protocols, there still remains a gap in how to manage specific patient populations with end stage renal disease. Understanding the pathophysiology behind these patient populations will yield better outcomes with the ultimate Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

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 >>

A Rare Cause Of Metabolic Acidosis: Ketoacidosis In A Non-diabetic Lactating Woman

A Rare Cause Of Metabolic Acidosis: Ketoacidosis In A Non-diabetic Lactating Woman

Gordon Sloan1, Amjad Ali1 and Jonathan Webster1[1] Department of Diabetes and Endocrinology, Sheffield Teaching Hospital, Sheffield, UK Summary Ketoacidosis occurring during lactation has been described infrequently. The condition is incompletely understood, but it appears to be associated with a combination of increased metabolic demands during lactation, reduction in carbohydrate intake and acute illness. We present a case of a 27-year-old woman, 8 weeks post-partum, who was exclusively breastfeeding her child whilst following a low carbohydrate diet. She developed gastroenteritis and was unable to tolerate an oral diet for several days. She presented with severe metabolic acidosis on admission with a blood 3-hydroxybutyrate of 5.4 mmol/L. She was treated with intravenous dextrose and intravenous sodium bicarbonate, and given dietary advice to increase her carbohydrate intake. She made a rapid and full recovery. We provide a summary of the common causes of ketoacidosis and compare our case with other presentations of lactation ketoacidosis. Learning points: Ketoacidosis in the lactating woman is a rare cause of raised anion gap metabolic acidosis. Low carbohydrate intake, starvation, intercurrent illness or a combination of these factors could put breastfeeding women at risk of ketoacidosis. Ketoacidosis in the lactating woman has been shown to resolve rapidly with sufficient carbohydrate intake and intravenous dextrose. Early diagnosis and prompt treatment are essential because the condition is reported to be reversible with a low chance of recurrence with appropriate dietary advice. Background Ketoacidosis is a common cause of raised anion gap metabolic acidosis. It most frequently occurs in individuals with type 1 diabetes. Starvation commonly causes ketosis but ra Continue reading >>

Electrolyte Imbalance In Diabetic Ketoacidosis

Electrolyte Imbalance In Diabetic Ketoacidosis

If you have diabetes, it's important to be familiar with diabetic ketoacidosis (DKA). DKA is a serious complication of diabetes that occurs when lack of insulin and high blood sugar lead to potentially life-threatening chemical imbalances. The good news is DKA is largely preventable. Although DKA is more common with type 1 diabetes, it can also occur with type 2 diabetes. High blood sugar causes excessive urination and spillage of sugar into the urine. This leads to loss of body water and dehydration as well as loss of important electrolytes, including sodium and potassium. The level of another electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood. Video of the Day Insulin helps blood sugar move into cells, where it is used for energy production. When insulin is lacking, cells must harness alternative energy by breaking down fat. Byproducts of this alternative process are called ketones. High concentrations of ketones acidify the blood, hence the term "ketoacidosis." Acidosis causes unpleasant symptoms like nausea, vomiting and rapid breathing. Bicarbonate is an electrolyte that normally counteracts blood acidity. In DKA, the bicarbonate level falls as ketone production increases and acidosis progresses. Treatment of DKA includes prompt insulin supplementation to lower blood sugar, which leads to gradual restoration of the bicarbonate level. Potassium may be low in DKA because this electrolyte is lost due to excessive urination or vomiting. When insulin is used to treat DKA, it can further lower the blood potassium by pushing it into cells. Symptoms associated with low potassium include fatigue, muscle weakness, muscle cramps and an irregular heart rhythm. Severely low potassium can lead to life-threatening heart rhythm abnorm Continue reading >>

Any Benefit To Sodium Bicarbonate In Dka?

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 >>

Acid–base Problems In Diabetic Ketoacidosis

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 >>

Lactic Acidosis Associated With Ketoacidosis

Lactic Acidosis Associated With Ketoacidosis

Surely there are enough reasons to have a nice acidosis when you are full of ketones. But on top of all that, you can also get a lactic acidosis. There is an association of diabetic ketoacidosis and lactic acidosis that goes beyond the tendency of diabetics to be on metformin. Indeed, in one case series there was “significant” lactate levels (i.e. over 4.0 mmol/L) in 40% of the patients. Glucose levels tended to correlated with lactate levels, suggesting that the lactate here is being produced as a result of some sort of abnormal cellular carbohydrate handing. The authors of this recent paper have admitted that this association is poorly researched. There does not seem to be a good mechanism worked out at this stage. Again, endogenous catecholamine excess is implicated. It is known that adrenaline levels correlate with DKA severity. D-lactate production may also play a role. A 2011 study has correlated D-lactate levels to the size of the anion gap in diabetic ketoacidosis; the article also ventures a hypothetical mechanism as to how this comes about. In any case, a much earlier study has demonstrated that whereas the ketone body levels correlated well with pH, the lactate did not, which suggests that lactate plays a fairly minor role in the actual acidosis. Additionally, Kerry Brandis reports on the interaction of lactate and ketoacids (specifically, on how lactate production tends to reduce the concentration of acetoacetate, thus fooling the most common ketone tests Continue reading >>

Diabetic Ketoacidosis: A Serious Complication

Diabetic Ketoacidosis: A Serious Complication

A balanced body chemistry is crucial for a healthy human body. A sudden drop in pH can cause significant damage to organ systems and even death. This lesson takes a closer look at a condition in which the pH of the body is severely compromised called diabetic ketoacidosis. Definition Diabetic ketoacidosis, sometimes abbreviated as DKA, is a condition in which a high amount of acid in the body is caused by a high concentration of ketone bodies. That definition might sound complicated, but it's really not. Acidosis itself is the state of too many hydrogen ions, and therefore too much acid, in the blood. A pH in the blood leaving the heart of 7.35 or less indicates acidosis. Ketones are the biochemicals produced when fat is broken down and used for energy. While a healthy body makes a very low level of ketones and is able to use them for energy, when ketone levels become too high, they make the body's fluids very acidic. Let's talk about the three Ws of ketoacidosis: who, when, and why. Type one diabetics are the group at the greatest risk for ketoacidosis, although the condition can occur in other groups of people, such as alcoholics. Ketoacidosis usually occurs in type one diabetics either before diagnosis or when they are subjected to a metabolic stress, such as a severe infection. Although it is possible for type two diabetics to develop ketoacidosis, it doesn't happen as frequently. To understand why diabetic ketoacidosis occurs, let's quickly review what causes diabetes. Diabetics suffer from a lack of insulin, the protein hormone responsible for enabling glucose to get into cells. This inability to get glucose into cells means that the body is forced to turn elsewhere to get energy, and that source is fat. As anyone who exercises or eats a low-calorie diet knows, fa Continue reading >>

Compensatory Hypochloraemic Alkalosis In Diabetic Ketoacidosis

Compensatory Hypochloraemic Alkalosis In Diabetic Ketoacidosis

Diabetic ketoacidosis acid-base imbalance hypochloraemia DKA Diabetic ketoacidosis [HCO3−] concentration of bicarbonate in arterial plasma [Na+] concentration of sodium in arterial plasma [Cl−] concentration of chloride in arterial plasma [Na+]/[Cl−] ratio sodium/chloride ratio in arterial plasma [XA−] concentration of unmeasured anions in arterial plasma [A−] sum of negative charged albumin and phosphate in arterial plasma [K+] concentration of potassium in arterial plasma Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus. Metabolic acidosis caused by ketoacids is an essential component of DKA and can have detrimental effects on cardiac, respiratory and metabolic function [1]. The only known compensatory response to metabolic acidosis in DKA is hyperventilation with consecutive respiratory alkalosis [1]. The effect of chloride on acid-base state has been known for many years. Hyperchloraemia and hypochloraemia cause metabolic acidosis and metabolic alkalosis, respectively [2, 3]. Recent research indicates that changes in chloride play an important role in the compensation of lactic acidosis [4]. Although chloride concentrations are frequently decreased in DKA, it is not known, whether these changes play a role in the acid-base state in this entity. The aim of this study was to investigate the effect of hypochloraemic alkalosis on acid-base state of patients with DKA. A total of 21 patients with DKA (11 women, 10 men, 44±16 years) admitted to the emergency department of a primary care hospital were studied. Fluid, insulin or bicarbonate had not been administered before the investigation. Of these patients, four had new onset diabetes and 17 patients had known insulin-dependent diabetes. DKA was triggered by inadequate insulin Continue reading >>

Diabetic Ketoacidosis And Cerebral Edema

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 >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Copyright © 2014 Nupur Sinha 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. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>

Review Of Evidence For Adult Diabetic Ketoacidosis Management Protocols

Review Of Evidence For Adult Diabetic Ketoacidosis Management Protocols

1Department of Endocrinology, Austin Health, Melbourne, VIC, Australia 2Department of Medicine, Austin Health, University of Melbourne, Melbourne, VIC, Australia 3Department of Intensive Care, Austin Health, Melbourne, VIC, Australia 4Menzies School of Health Research, Darwin, NT, Australia Background: Diabetic ketoacidosis (DKA) is an endocrine emergency with associated risk of morbidity and mortality. Despite this, DKA management lacks strong evidence due to the absence of large randomised controlled trials (RCTs). Objective: To review existing studies investigating inpatient DKA management in adults, focusing on intravenous (IV) fluids; insulin administration; potassium, bicarbonate, and phosphate replacement; and DKA management protocols and impact of DKA resolution rates on outcomes. Methods: Ovid Medline searches were conducted with limits “all adult” and published between “1973 to current” applied. National consensus statements were also reviewed. Eligibility was determined by two reviewers’ assessment of title, abstract, and availability. Results: A total of 85 eligible articles published between 1973 and 2016 were reviewed. The salient findings were (i) Crystalloids are favoured over colloids though evidence is lacking. The preferred crystalloid and hydration rates remain contentious. (ii) IV infusion of regular human insulin is preferred over the subcutaneous route or rapid acting insulin analogues. Administering an initial IV insulin bolus before low-dose insulin infusions obviates the need for supplemental insulin. Consensus-statements recommend fixed weight-based over “sliding scale” insulin infusions although evidence is weak. (iii) Potassium replacement is imperative although no trials compare replacement rates. (iv) Bicarbonate replacement Continue reading >>

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