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Severe Acidosis

An Unusual Case Of Severe (fatal) Metabolic Acidosis

An Unusual Case Of Severe (fatal) Metabolic Acidosis

An unusual case of severe (fatal) metabolic acidosis Summarized from Saidi H, Mani M. Severe metabolic acidosis secondary to coadministration of creatine and metformin, a case report. Amer J Emerg Med 2010; 28: 388. e5-388. e6. Metabolic acidosis, the most common disturbance of acid-base balance among the critically ill, is characterized by arterial blood gas results that reveal primary decrease in bicarbonate and compensatory decrease in pCO2(a). Blood pH is reduced unless respiratory compensation is complete. It is most often the result of lactic acid accumulation due to circulatory collapse but there are many other causes. A recently published case history describes metabolic (lactic) acidosis occurring in a 42-year-old man. The cause was attributed to the net effect of two drugs: creatine and metformin. The first is commonly self-prescribed by athletes and body builders to improve muscle capacity; and the second is a blood glucose-lowering agent prescribed for diabetes management. This previously healthy man was self-prescribing creatine (5 g/day), when he became ill and was admitted to hospital. Diabetes was diagnosed, stabilized and the patient was discharged in a healthy state with a prescription for metformin 500 mg twice daily. Three weeks later he was admitted emergently to hospital in a critically ill state. Blood gas results (reduced pH 7.25; reduced bicarbonate 12 mmol/L; reducedpCO2(a) 3.5 kPa; and markedly increased blood lactate 17.2 mmol/L) confirmed partially compensated metabolic (lactic) acidosis. He had no urine output, and raised serum creatinine (309 mmol/L) confirmed acute renal failure. Due to his deteriorating condition he was urgently transferred for dialysis with bicarbonate replacement, but suffered cardiac arrest and sadly died before comp Continue reading >>

Metabolic Acidosis In Emergency Medicinetreatment & Management

Metabolic Acidosis In Emergency Medicinetreatment & Management

Metabolic Acidosis in Emergency MedicineTreatment & Management Author: Antonia Quinn, DO; Chief Editor: Romesh Khardori, MD, PhD, FACP more... The initial therapeutic goal for patients with severe acidemia is to raise the systemic pH above 7.1-7.2, a level at which dysrhythmias become less likely and cardiac contractility and responsiveness to catecholamines will be restored. Metabolic acidosis can be reversed by treating the underlying condition or by replacing the bicarbonate. The decision to give bicarbonate should be based upon the pathophysiology of the specific acidosis, the clinical state of the patient, and the degree of acidosis. [ 10 ] Treating the underlying conditions in high AG states usually is sufficient in reversing the acidosis. Treatment with bicarbonate is unnecessary, except in extreme cases of acidosis when the pH is less than 7.1-7.2. For all cases of diabetic ketoacidosis, the role of bicarbonate is controversial, regardless of the pH or bicarbonate level. In hyperchloremic acidosis, the central problem is with the reabsorption or regeneration of bicarbonate. In these conditions, therapy with bicarbonate makes physiologic sense and is prudent in patients with severe acidosis. Caution with bicarbonate therapy is indicated because of its potential complications, including the following: Tissue hypoxia via leftward shift of hemoglobin-oxygen dissociation curve Alkali stimulation of organic acidosis (lactate) Metabolic acidosis secondary to ingestions (eg, salicylate, methanol, ethylene glycol) often requires dialysis therapy, and a nephrologist should be consulted early in the case management. Toxicologic consultation should also be considered in such cases. Dialysis is the preferred treatment for patients with significant metabolic acidosis in the Continue reading >>

Symptoms Of Acidosis And Their Affect On The Human Body

Symptoms Of Acidosis And Their Affect On The Human Body

Symptoms of acidosis can be alarming for any person who is unaware of its existence in their body or do not understand the disorder. The symptoms of acidosis can be different depend on its cause. Acidosis disrupts proper cellular function and activity, leading to various disease and sickness. Common causes of acidosis include an existence of an underlying illness, diabetes, smoking, poor diet, kidney disorders, genetic factors or excessive use of alcohol. Technically, acidosis is defined as an increase of hydrogen ion concentration at the cellular level. This in due course leads to acidity of blood plasma. Acidosis is usually diagnosed when the blood pH of an individual falls below 7.35. To determine the cause of acidosis, an arterial blood gas analysis is required. There are two types of acidosis- metabolic and respiratory. Respiratory acidosis is caused when the lungs become incapable of getting rid of carbon dioxide by themselves. Metabolic acidosis occurs due to the failure of the kidneys to eliminate enough acid from the body. Primary Symptoms of Acidosis Regardless of whether you are suffering from metabolic or respiratory acidosis, symptoms of acidosis are usually similar. Take a look at some of the primary signs and symptoms of acidosis listed below. • Fatigue • Confusion • Headaches • Shortness of breath • Bad breath • Lethargy • Body odor or excessive sweating • Sleepiness • Under- eye dark circles Acidosis causes the human cells to be exposed to acidic environment repeatedly, leading to a drop in oxygen levels. Lack of oxygen can sometimes lead to severe acidosis symptoms including shock or death. However, most symptoms listed above usually occur due to lack of oxygen in the body. Symptoms of Acidosis: Mental Symptoms One of the most common Continue reading >>

Severe Acidosis Caused By Starvation And Stress.

Severe Acidosis Caused By Starvation And Stress.

Severe acidosis caused by starvation and stress. Department of Pediatrics, Children's Hospital of Wisconsin, Milwauke, WI, USA. A 1-year-old boy had severe anoxic brain injury owing to a cardiorespiratory arrest. He had an initial metabolic acidosis, but this largely resolved by hospital day 2. He then had a persistent, profound metabolic acidosis. Evaluation on hospital day 6 found that the patient had ketonemia, ketonuria, and a normal serum glucose level; he had received no intravenous dextrose during his hospitalization. The dextrose-free fluids were given initially to protect his brain from the deleterious effects of hyperglycemia after brain injury. Continuation beyond 24 hours was inadvertent. The initiation of dextrose-containing intravenous fluids produced a rapid resolution of his metabolic acidosis. Starvation usually produces a mild metabolic acidosis, but when combined with physiologic stress, starvation may cause a severe metabolic acidosis. Among the few reports of severe starvation ketoacidosis, our case is unique because the patient was monitored closely in an intensive care unit, allowing us to describe the time course of the acidosis in detail. Continue reading >>

Acidosis

Acidosis

For acidosis referring to acidity of the urine, see renal tubular acidosis. "Acidemia" redirects here. It is not to be confused with Academia. Acidosis is a process causing increased acidity in the blood and other body tissues (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma. The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH. Acidosis is said to occur when arterial pH falls below 7.35 (except in the fetus – see below), while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes. The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g., healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.[1] Signs and symptoms[edit] General symptoms of acidosis.[2] These usually accompany symptoms of another primary defect (respiratory or metabolic). Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen i Continue reading >>

Acidosis

Acidosis

When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s processes produce acid. Your lungs and kidneys can usually compensate for slight pH imbalances, but problems with these organs can lead to excess acid accumulating in your body. The acidity of your blood is measured by determining its pH. A lower pH means that your blood is more acidic, while a higher pH means that your blood is more basic. The pH of your blood should be around 7.4. According to the American Association for Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight, these numerical differences can be serious. Acidosis can lead to numerous health issues, and it can even be life-threatening. There are two types of acidosis, each with various causes. The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, depending on the primary cause of your acidosis. Respiratory acidosis Respiratory acidosis occurs when too much CO2 builds up in the body. Normally, the lungs remove CO2 while you breathe. However, sometimes your body can’t get rid of enough CO2. This may happen due to: chronic airway conditions, like asthma injury to the chest obesity, which can make breathing difficult sedative misuse deformed chest structure Metabolic acidosis Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t eliminate enough acid or when they get rid of too much base. There are three major forms of metabolic acidosis: Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your body lacks enough insulin, keton Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

OVERVIEW a metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood -> resulting in a fall in arterial plasma bicarbonate CAUSES pathophysiological mechanism: (i) A gain of strong acid (ii) A loss of base the gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion). bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis). CLASSIFICATION high anion gap Lactate Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents Ketones Renal Normal anion gap Chloride Acetazolamide and Addisons GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies) Extras – RTA MAINTENANCE the disorder is maintained as long as the primary cause persists. in many cases the acid-base disturbance tends to increase in severity while the problem causing it persists though this is not absolute. EFFECTS Respiratory Effects hyperventilation (Kussmaul respirations) – this is the compensatory response shift of oxyhaemoglobin dissociation curve (ODC) to the right – due to the acidosis occurs rapidly decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) -> after 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Cardiovascular Effects depression of myocardial contractility sympathetic overactivity resistance to the effects of catecholamines peripheral arteriolar vasodilatation venoconstriction of peripheral veins vasoconstriction of pulmonary arteries (increased Continue reading >>

Merck And The Merck Manuals

Merck And The Merck Manuals

Acidosis is caused by an overproduction of acid in the blood or an excessive loss of bicarbonate from the blood (metabolic acidosis) or by a buildup of carbon dioxide in the blood that results from poor lung function or depressed breathing (respiratory acidosis). If an increase in acid overwhelms the body's acid-base control systems, the blood will become acidic. As blood pH drops (becomes more acidic), the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing (respiratory compensation). Breathing faster and deeper increases the amount of carbon dioxide exhaled. The kidneys also try to compensate by excreting more acid in the urine. However, both mechanisms can be overwhelmed if the body continues to produce too much acid, leading to severe acidosis and eventually heart problems and coma. The acidity or alkalinity of any solution, including blood, is indicated on the pH scale. Metabolic acidosis develops when the amount of acid in the body is increased through ingestion of a substance that is, or can be broken down (metabolized) to, an acid—such as wood alcohol (methanol), antifreeze (ethylene glycol), or large doses of aspirin (acetylsalicylic acid). Metabolic acidosis can also occur as a result of abnormal metabolism. The body produces excess acid in the advanced stages of shock and in poorly controlled type 1 diabetes mellitus (diabetic ketoacidosis). Even the production of normal amounts of acid may lead to acidosis when the kidneys are not functioning normally and are therefore not able to excrete sufficient amounts of acid in the urine. Major Causes of Metabolic Acidosis Diabetic ketoacidosis (buildup of ketoacids) Drugs and substances such as acetazolamide, alcohols, and aspirin Lactic acidosis (buildup of lactic acid Continue reading >>

Transient Vision Loss In A Patient With Severe Metforminassociated Lactic Acidosis

Transient Vision Loss In A Patient With Severe Metforminassociated Lactic Acidosis

Transient vision loss in a patient with severe metforminassociated lactic acidosis From the 1Nephrology Unit and 2Anaesthesia and Intensive Care Unit, Hospital Da Costa, Burela, Spain Search for other works by this author on: From the 1Nephrology Unit and 2Anaesthesia and Intensive Care Unit, Hospital Da Costa, Burela, Spain Search for other works by this author on: From the 1Nephrology Unit and 2Anaesthesia and Intensive Care Unit, Hospital Da Costa, Burela, Spain Search for other works by this author on: From the 1Nephrology Unit and 2Anaesthesia and Intensive Care Unit, Hospital Da Costa, Burela, Spain Search for other works by this author on: From the 1Nephrology Unit and 2Anaesthesia and Intensive Care Unit, Hospital Da Costa, Burela, Spain Search for other works by this author on: QJM: An International Journal of Medicine, Volume 105, Issue 8, 1 August 2012, Pages 781783, S. Cigarrn, M.L. Rodriguez, M. Pousa, H. Menndez, M.J. Mendez; Transient vision loss in a patient with severe metforminassociated lactic acidosis, QJM: An International Journal of Medicine, Volume 105, Issue 8, 1 August 2012, Pages 781783, A 54-year-old male, insulin-dependent diabetic and chronic kidney disease stage I, was brought to Emergency Department with a complaint of acute vision loss, severe hypoglycemia, hyperventilation, metabolic acidosis and acute renal failure. Five days prior to admission suffered diarrhea and vomiting with loss of vision at the last 12 h. Home medications included insulin lantus, valsartan 160 mg, amlodipine 5 mg and metformin 850 mg twice a day. There was not previous history of drinking alcohol, smoking or drugs abuse. In the emergency room, physical examination revealed an ill man with a Kussmaul respiratory pattern with 34 breaths/min, dry mucous membranes a Continue reading >>

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

Volume 147, Issue 5 , May 2014, Pages 1698-1705 Acidosis is a very common pathologic process in perioperative management. However, how to correct severe acidosis to improve the efficacy of vasoconstrictors in hemodynamically unstable patients is still debated. The present study investigated whether severe extracellular acidosis influences the vasoactive properties of vasoconstrictors on human isolated arteries. Segments of intact distal internal mammary arteries were removed from 41 patients undergoing artery bypass grafting. The arterial rings were washed in Krebs-Henseleit solution and suspended in an organ bath. The rings were set at a pretension equivalent of 100 mm Hg, and the relaxation response to 10 M acetylcholine was verified. Concentrationresponse curves for epinephrine, norepinephrine, methoxamine (1A/D-adrenoceptor agonist), phenylephrine (equipotent agonist of 1A/B-adrenoceptors), and clonidine (2-adrenoceptor agonist) were achieved under control conditions (pH 7.40) and under acidic conditions by substitution of the Krebs-Henseleit solution with a modified solution. Decreasing the pH from 7.40 to 7.20, 7.0, or 6.80 did not significantly alter the potency and efficacy of epinephrine and norepinephrine, although the standardized effect size was sometimes large. Severe acidosis (pH6.80) did not significantly change the potency and efficacy of phenylephrine and clonidine, although it increased the efficacy and potency of methoxamine (P<.001 and P=.04 vs paired control conditions, respectively). Extracellular acidosis did not impair the vasoactive properties of epinephrine and norepinephrine in human medium-size arteries until pH 6.80. The results of the present study also suggest that acidosis might potentiate arterial responsiveness to vasoconstrictors, mos Continue reading >>

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Antoine Kimmoun , Emmanuel Novy , Thomas Auchet , Nicolas Ducrocq , and Bruno Levy CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France Antoine Kimmoun, Email: [email protected] . Author information Copyright and License information Disclaimer Copyright Kimmoun et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution Continue reading >>

Acidosis

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 >>

Bicarbonate Therapy In Severe Metabolic Acidosis

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 >>

Common, Yet Elusive: A Case Of Severe Anion Gap Acidosis

Common, Yet Elusive: A Case Of Severe Anion Gap Acidosis

Common, yet elusive: a case of severe anion gap acidosis 1 Marina Kishlyansky ,1 Sylvia Biso ,1 Soumya Patnaik ,1 and Chitra Punjabi 1 1 Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA, USA 1 Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA, USA 1 Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA, USA 1 Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA, USA 1 Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA, USA 1 Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA, USA *Correspondence address. Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Suite 363, Philadelphia, PA 19118, USA. Tel: +1-973-874-3640; Fax: +1-215-456-7375; E-mail: [email protected] Received 2017 May 15; Accepted 2017 Jul 14. Copyright The Author 2017. Published by Oxford University Press. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected] Acidbase disturbances are common occurrence in hospitalized patients with life threatening complications. 5-oxoproline has been increasingly recognized as cause of high anion gap metabolic acidosis (AGMA) in association with chronic acetaminophen use. However, laboratory workup for it are Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

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