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 With Diabetes Mellitus
Publication Date: 2004-05 Fourth quarter ICD 10 AM Edition: Fourth edition Query Number: 2125 30 year old patient with a PDx on discharge summary of metabolic acidosis. Patient is also an IDDM, with a history of a flu like illness for the past week, and noted to be dehydrated on admission. Patient stated BSL readings had been good. LOS 4 days. Following the Index Diabetes, acidosis, lactic - lactic is an essential modifier and there is no default or entry for metabolic or any of the other types of acidosis apart from ketoacidosis. 1. There is an excludes note under E87.2 Acidosis - Excludes: diabetic acidosis (E10- E14 with common 4th character .1). It would seem as though the classification is telling coders to code all types of acidosis to 'lactic acidosis' when in a diabetic patient. However the Index entry under Diabetes does not give this impression. Please could the committee confirm that the correct code/s would be E10.13 'Type 1 diabetes mellitus with lactic acidosis, without coma' for the diagnosis of metabolic acidosis in a diabetic patient. 2. Respiratory, lactic, and metabolic acidosis, ketoacidosis and acidosis NEC are all indexed to E87.2. Should coders code all the above conditions in a diabetic patient to E1x.1x 'Diabetes with lactic acidosis' (except of course ketoacidosis which has an index entry under diabetes)? Search Details: ACS 0401 Diabetes, NCCH database, Coding Matters, VICC newsletter Response Metabolic acidosis is not the same as ketoacidosis and lactic acidosis. As metabolic acidosis is not linked to Diabetes in the index, follow the index entry: Acidosis (lactic) (respiratory) E87.2 - metabolic NEC E87.2 Assign code E87.2 Acidosis. Continue reading >>
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What Alkalizes The Blood?
The therapeutic range is very narrow. As Mr. Stephenson and Mr. Seidman have noted, the body fights to maintain a very narrow range of pH. That said, our traditional understanding of acid/base balance in the body may be incomplete ([The Stewart model. "Modern" approach to the interpretation of the acid-base metabolism].) What you may be referring to is the use of exercise to increase alertness. This is certainly effective, increasing blood flow and the transport of nutrients. It may not clinically alter your blood pH, but the products of breaking down muscle and ligament groups to repair would be mildly acidifying. Overdo the exercise, and you risk damaging your tissues ([Blood acid-base balance of sportsmen during physical activity].) Despite the narrow balance of pH, it is possible to generate metabolic (as opposed to respiratory) acidosis through diet, Again, this is very mild compared to emergency room states, but can have long term negative effects. Elderly individuals seem more susceptible to abnormalities, but the solution is to increase fruits and vegetables. (Effect of diet composition on acid-base balance in adolescents, young adults and elderly at rest and during exercise.) Is this a negative situation or one that is fringe of the mainstream. No, it's a healthy, mainstream idea that too many people ignore. (Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysi... - PubMed - NCBI) Continue reading >>
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Metabolic Acidosis
Metabolic acidosis is the most common acid–base disorder and can be life threatening. It results from excessive cellular acid production, reduced acid secretion, or loss of body alkali. The body has two buffering mechanisms to counteract an increase in acid. The initial response is to increase carbon dioxide excretion by increasing ventilation. The second response is increased renal excretion of acids and renal regeneration of bicarbonate. The adequacy of compensation can be assessed by the quick check method or the Winter formula (Table 2). Metabolic acidosis can be classified into two categories using the anion gap. Each category has a distinct differential diagnosis. Anion gap = [Sodium] – ([Chloride] + [Bicarbonate]) Normally, the anion gap is approximately 12 ± 2 meq/L (12 ± 2 mmol/L). Most unmeasured anions consist of albumin. Therefore, the presence of either a low albumin level or an unmeasured cationic light chain, which occurs in multiple myeloma, results in a low anion gap. Increased hydrogen ion concentration or decreased bicarbonate concentration will increase the gap. When the primary disturbance is a metabolic acidosis, the anion gap helps to narrow the diagnostic possibilities to an increased anion gap acidosis or a normal anion gap acidosis. Increased Anion Gap Metabolic Acidosis Common causes include ketoacidosis (diabetes mellitus, alcohol abuse, starvation), lactic acidosis, chronic kidney disease, salicylate toxicity, and ethylene glycol and methanol poisoning. Diabetic ketoacidosis is the most common cause of an increased anion gap acidosis, but a normal anion gap acidosis may be present early in the disease course when the extracellular fluid (ECF) volume is nearly normal. Ketoacidosis also may develop in patients with a histor Continue reading >>
Relationship Between Severity Of Hyperglycemia And Metabolic Acidosis In Diabetic Ketoacidosis
We evaluated 114 hospital admissions for diabetic ketoacidosis (occurring in 78 patients) retrospectively by using the Mayo Clinic medical records system. Initial plasma glucose and serum bicarbonate values were examined by using regression analysis. No correlation was found between these two measurements (r = −0.03). The reason for this dissociation between hyperglycemia and hyperketonemia needs further elucidation, but it may be related to impaired hepatic glucose production in some patients. Copyright © 1988 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved. Continue reading >>
Metabolic Acidosis
Acidosis - metabolic Metabolic acidosis is a condition in which there is too much acid in the body fluids. Causes 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: Other causes of metabolic acidosis include: Symptoms Most symptoms are caused by the underlying disease or condition that is causing the metabolic acidosis. Metabolic acidosis itself most often causes rapid breathing. Acting confused or very tired may also occur. Severe metabolic acidosis can lead to shock or death. In some situations, metabolic acidosis can be a mild, ongoing (chronic) condition. Exams and Tests These tests can help diagnose acidosis. They can also determine whether the cause is a breathing problem or a metabolic problem. Tests may include: Arterial blood gas Basic metabolic panel, (a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and functions) Urine pH Lactic acid test Arterial blood gas analysis Other tests may be needed to determine the cause of the acidosis. Treatment Treatment is aimed at the health problem causing the acidosis. In some cases, sodium bicarbonate (the chemical in baking soda) may be given to reduce the acidity of the blood. Often, you will receive lots of fluids through your ve Continue reading >>
Metabolic Acidosis
Metabolic Acidosis Definition Metabolic acidosis is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid. Description Metabolic acidosis, as a disruption of the body's acid/base balance, can be a mild symptom brought on by a lack of insulin, a starvation diet, or a gastrointestinal disorder like vomiting and diarrhea. Metabolic acidosis can indicate a more serious problem with a major organ like the liver, heart, or kidneys. It can also be one of the first signs of drug overdose or poisoning. Causes and symptoms Metabolic acidosis occurs when the body has more acid than base in it. Chemists use the term "pH" to describe how acidic or basic a substance is. Based on a scale of 14, a pH of 7.0 is neutral. A pH below 7.0 is an acid; the lower the number, the stronger the acid. A pH above 7.0 is a base; the higher the number, the stronger the base. Blood pH is slightly basic (alkaline), with a normal range of 7.36-7.44. Acid is a natural by-product of the breakdown of fats and other processes in the body; however, in some conditions, the body does not have enough bicarbonate, an acid neutralizer, to balance the acids produced. This can occur when the body uses fats for energy instead of carbohydrates. Conditions where metabolic acidosis can occur include chronic alcoholism, malnutrition, and diabetic ketoacidosis. Consuming a diet low in carbohydrates and high in fats can also produce metabolic acidosis. The disorder may also be a symptom of another condition like kidney failure, liver failure, or severe diarrhea. The build up of lactic acid in the blood due to such conditions as heart failure, shock, or cancer, induces metabolic acidosis. Some poisonings and overdoses (aspirin, Continue reading >>
What Chemical Processes Or Reactions Contribute To Metabolic Acidosis?
There are three primary states metabolic acidosis. Their underlying physiological causes are from diabetes (ketoacidosis), normal anion gap acidosis from ailments such as kidney malfunction (renal tubular acidosis or more specifically hyperchloremic acidosis), and rare congenital mitochondrial disorders (lactic acidosis). More common causes of metabolic acidosis may come from liver disease or damage or from the ingestion of certain anti-retroviral drugs and poisons such as arsenic. In ketoacidosis, the body does not have enough insulin which allows glucose to be transported across the cell membranes. The body's response is to try to compensate for the supposed lack of energy source (starvation defense, even though there is plenty in the blood) by digesting fat which is converted by the liver into alternative energy sources, i.e. ketones such as acetoacetate and the carboxylic acid β-hydroxybutyrate. These byproducts are acidic and lower the pH of the blood. In renal tubular acidosis (RTA) the kidneys are not acidifying the urine as efficiently as they should which allows acid in the blood to accumulate. RTA is a normal anion gap acidosis during which the alpha intercalated cells fail to secret acid. This can be caused by toxin damage from toluene or lithium carbonate among others, or by mutations. Two well known genetic causes of RTA are a mutation in the anion exchanger AE1 (Band 3) transport protein that controls chloride and bicarbonate exchange across the plasma membrane, and mutations to the apical proton pump vH+-ATPase. A reduction in plasma bicarb concentration and increased chloride prevents pH buffering and reduces the pH. Lesser known mutations that have the same effect are in the family of serine-threonine protein kinases WNK1 or WNK4, specifically, the min Continue reading >>
Bicarbonate Therapy In Severe Metabolic Acidosis
Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>
D-lactate: A Novel Contributor To Metabolic Acidosis And High Anion Gap In Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA),the most common and serious acute complication of diabetes, is characterized by hyperglycemia and severe high–anion-gap metabolic acidosis with ketonemia (1). In DKA, the high anion gap is attributed largely to excessive production of blood ketone bodies, and serum β-hydroxybutyrate quantification is recommended for the diagnosis and monitoring of DKA (2). However, even counting of all the ketone bodies, including β-hydroxybutyrate, does not account for the entire anion gap, suggesting that there are additional sources of anion production in DKA. We recently demonstrated that plasma d-lactate concentrations were greatly increased in DKA compared with the concentrations in diabetic patients or a healthy control group (3). Nevertheless, the clinical value of d-lactate measurement in metabolic acidosis, especially the contribution of d-lactate to the metabolic acidosis and high anion gap in DKA, is not well appreciated. We report here that decreasing d-lactate concentrations are associated with improved clinical situations, whereas increased lactate concentrations are associated with the severity of metabolic acidosis and high anion gap in patients with DKA. The study included 38 diabetic patients with DKA, 42 diabetic patients without DKA, and 40 healthy controls. The institutional ethics review board of the First Affiliated Hospital of Wenzhou Medical College approved the study, and written informed consent was obtained from all study participants. For patients with DKA, blood samples were collected at the time of admission to the emergency room and following medical treatment after admission, when the patient's condition became stabilized. Plasma methylglyoxal was assayed by LC-MS (3). Plasma d-lactate concentration was determined by an e Continue reading >>
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Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>
Metabolic Acidosis
Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>
How Does Diabetic Ketoacidosis Cause Vomiting?
DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body’s cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can’t get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn’t available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body’s metabolic processes aren’t able to function as well. A higher level of ketones also affects levels of sugar and electrolytes in the body. As ketones accumulate in the blood, more ketones will be passed in the urine, taking sodium and potassium salts out with them. Over time, levels of sodium and potassium salts in the body become depleted, which can cause nausea and vomiting. The result is a vicious cycle. The most important prevention strategies are to monitor blood glucose levels routinely, keep blood glucose levels controlled (e.g., Continue reading >>
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 >>
Diabetic Ketoacidosis: Evaluation And Treatment
Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>
