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Is Dka Metabolic Or Respiratory Acidosis?

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Abstract We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18–61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 ± 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios Δ anion gap/Δ bicarbonate () and sodium/chloride ()). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status. Continue reading >>

Respiratory Failure In Diabetic Ketoacidosis

Respiratory Failure In Diabetic Ketoacidosis

Go to: INTRODUCTION Ketoacidosis in subjects with type 1, or less frequently, type 2 diabetes mellitus remains a potentially life-threatening diabetic manifestation. The subject has justifiably attracted attention in the literature. Sequential reviews[1-9] have documented important changes in the clinical concepts that are related to diabetic ketoacidosis (DKA) and its management. A large number of case series of DKA have addressed various aspects of its clinical presentation and management. For this review, we selected representative studies focused on management, outcome, age differences, gender differences, associated morbid conditions, ethnicity and prominent clinical and laboratory features[10-35]. In recognition of the complexity of treatment, the recommendation to provide this care in intensive care units was made more than 50 years ago[36]. Severe DKA is treated in intensive care units today[31]. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe[39]. Losses of fluids and electrolytes, which are important causes of morbidity and mortality in DKA, vary greatly between patients. Quantitative methods estimating individual losses and guiding their replacement have also been reported[40,41]. The outcomes of DKA have improved with new methods of insulin administration[42] and adherence to guidelines[43-46]. The aim of treatment is to minimize mortality and prevent sequelae. One study documented that the target of zero mortality is feasible[42]. However, mortality from DKA, although reduced progressively in the early decades after the employment of insulin treatment[1], remains high. Up to fifty plus years ago, mortality from DKA was between 3% and 10%[1,16]. A recent review re Continue reading >>

An Exceptional Case Of Diabetic Ketoacidosis

An Exceptional Case Of Diabetic Ketoacidosis

Copyright © 2017 Celine Van de Vyver 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. Abstract We present a case of diabetic ketoacidosis, known as one of the most serious metabolic complications of diabetes. We were confronted with rapid neurological deterioration and unseen glycaemic values, which reached almost 110 mmol/L, subsequently resulting in hyperkalaemia and life-threatening dysrhythmias. This is the first reported live case with such high values of blood glucose and a favourable outcome. 1. Introduction Diabetic ketoacidosis (DKA) is known as one of the most serious complications of diabetes, besides hyperosmolar hyperglycaemic syndrome (HHS), and it is associated with significant morbidity and mortality. The symptoms are often nonspecific and there are many diseases that mimic the presentation. The clinical course usually evolves within a short time frame (<24 h). DKA exists of a triad of uncontrolled hyperglycaemia, metabolic acidosis, and increased total body ketone concentration [1]. These three criteria are needed for diagnosis. The most common precipitating factors of DKA are infections and discontinuation of or inadequate insulin therapy. Mainstays of treatment are correction of hypovolemia and hyperglycaemia, rapid administration of insulin, and electrolyte management. Glycaemic values in DKA normally do not exceed 33 mmol/L. In contrast, blood glucose in HHS is often higher [2, 3]. We present a case of severe diabetic ketoacidosis with glycaemic values of almost 110 mmol/L, leading to neurologic sequelae and requiring more aggressive treatment. A similar case report detailing th Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

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 >>

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

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... 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. The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia Rapid weight loss in patients newly diagnosed with type 1 diabetes 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: Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation 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 >>

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Introduction Recently there have been numerous publications and discussions about whether VBGs can replace ABGs in DKA. The growing consensus is that VBGs are indeed adequate. Eliminating painful, time-consuming arterial blood draws is a huge step in the right direction. However, the ABG vs. VBG debate overlooks a larger point: neither ABG nor VBG measurements are usually helpful. It is widely recommended to routinely obtain an ABG or VBG, for example by both American and British guidelines. Why? Is it helping our patients, or is it something that we do out of a sense of habit or obligation? Diagnosis of DKA: Blood gas doesn’t help These are the diagnostic criteria for DKA from the America Diabetes Association. They utilize either pH or bicarbonate in a redundant fashion to quantify the severity of acidosis. It is unclear what independent information the pH adds beyond what is provided by the bicarbonate. Practically speaking, the blood gas doesn’t help diagnose DKA. This diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level). The addition of a blood gas to serum chemistries only adds information about the respiratory status, which does not help determine if the patient has ketoacidosis. Management: Does the pH help? It is debatable whether knowing or attempting to directly “treat” the pH is helpful. The pH will often be very low, usually lower than would be expected by looking at the patient. This may induce panic. However, it is actually a useful reminder that acidemia itself doesn't necessarily cause instability (e.g. healthy young rowers may experience lactic acidosis with a pH <7 during athletic exertion; Volianitis 2001). A question often arises regarding whether bicarbonate Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

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 one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Acid-base And Electrolyte Disturbances In Patients With Diabetic Ketoacidosis

Volume 34, Issue 1 , September 1996, Pages 23-27 Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis Get rights and content We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 1861 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios anion gap/ bicarbonate ( )). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status. 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 >>

Kussmaul Breathing - An Overview | Sciencedirect Topics

Kussmaul Breathing - An Overview | Sciencedirect Topics

Nicholas J. White, in Manson's Tropical Infectious Diseases (Twenty-third Edition) , 2014 Hyperventilation or Kussmaul's breathing (sometimes termed respiratory distress) is a poor prognostic sign in malaria. In the tachypnoea associated with high fever, breathing is shallow compared with the ominous laboured hyperventilation associated with metabolic acidosis, pulmonary oedema or bronchopneumonia. Acute pulmonary oedema (acute respiratory distress syndrome) may develop at any time in severe falciparum malaria. It is particularly common in pregnant women, but rare in children. In some cases malaria ARDS may be difficult to distinguish clinically from pneumonia. The heart sounds are normal. The central venous pressure and pulmonary artery occlusion pressures are usually normal, the cardiac index is high and systemic vascular resistance is low. This points to an increase in capillary permeability (unless the patient has been overhydrated). The chest radiograph shows increased interstitial shadowing and a normal heart size. Julian L. Seifter, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 Symptoms include nausea, vomiting, anorexia, polydipsia, and polyuria. Patients often exhibit Kussmaul respirations and volume depletion. Neurologic symptoms include fatigue and lethargy with depression of the sensorium. CSF exhibits a change in acid-base status with treatment of diabetic ketoacidosis. Even without bicarbonate administration, CSF pH falls as a result of the ventilatory response to the correction of acidosis and the sudden rise in Pco2. However, no correlation between decreased CSF pH and depression of sensorium has been established. Ketoacidosis is also seen in cases of starvation, in which it is generally mild and not associated with hyperglycemia. Ketoacids 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 >>

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