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Hyperchloremic Acidosis Symptoms

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Go to: Introduction Acute metabolic acidosis (defined temporally as lasting minutes to a few days) has traditionally been divided into two major categories based on the level of the serum anion gap: non-anion gap and high anion gap metabolic acidosis [1]. As implied, with the former acid–base disorder, the anion gap is within normal limits, whereas with the latter disorder it is increased. This categorization is primarily used to facilitate the differential diagnosis of metabolic acidosis. However, it also has relevance for predicting the clinical outcome and determining indications for treatment. Although many clinicians presume that acute metabolic acidosis in seriously ill patients will be due to a high anion gap acidosis, recent studies indicate that a non-anion gap metabolic acidosis or combination of non-anion gap and high anion gap metabolic acidosis might be more frequent [2, 3]. Based on these observations, it appears important to more clearly define the potential effects of non-anion gap metabolic acidoses on organ function as a basis for generating evidence-based guidelines for therapy. In the present review, we summarize our current understanding of the pathophysiology of acute non-anion gap acidosis, its clinical characteristics, its adverse effects on cellular function, and also the benefits and complications of therapy. Go to: Definition In non-anion gap or hyperchloremic metabolic acidosis, a reduction in serum [HCO3−] is matched by an approximately equivalent increase in the serum chloride concentration resulting in hypobicarbonatemia and hyperchloremia in the absence of an increase in the serum anion gap [4, 5]. In fact, since a decrease in blood pH alters the protonation of albumin (which normally makes up the majority of the anion gap), a slight Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Renal tubular acidosis (RTA) is a group of disorders affecting the renal tubular cells that result in hyperchloremic metabolic acidosis with a normal anion gap. Renal tubular acidosis (RTA) is a group of disorders affecting the renal tubular cells that result in hyperchloremic metabolic acidosis with a normal anion gap. Hyperchloremic metabolic acidosis with a normal anion gap Type I: Distal or classic RTA (H+ retention) Etiology: Underlying cause is usually undetermined, but is generally acquired Renal tubular toxins: Heavy metals, ethylene glycol, drugs (gentamicin, cephalosporins, tetracyclines, salicylate) Type I (distal or classic RTA) is caused by an inability of the distal tubule cells to secrete H+ or to produce acidic urine. There is excessive K+ secretion and severe hypokalemia. Type II (proximal RTA) is caused by a failure of HCO3 resorption in the proximal tubule with subsequent loss of HCO3 into urine. The proximal tubule is the site where the majority of filtered HCO3- is reabsorbed via Na+ and H+ exchange and the breakdown of carbonic acid to carbon dioxide and water under the influence of carbonic anhydrase. Hydrogen ions are usually secreted when HCO3 ion is reabsorbed. Failure to reabsorb HCO3 results in excessive urinary losses, basic urine pH, and systemic acidosis. Hyperchloremia develops because of renal conservation of chloride to maintain electroneutrality consequent to HCO3 loss. Christine E. Kurschat, Seth L. Alper, in Molecular and Genetic Basis of Renal Disease , 2008 Renal tubular acidosis (RTA) is a failure of renal regulatory mechanisms to maintain systemic pH homeostasis. Patients present with hyperchloremic metabolic acidosis in the setting of an inappropriate inability to acidify urine pH below 5.5. The associated clinical syndrome can Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Hyperchloremic acidosis is a known complication of intestinal bypass, due to both intestinal bicarbonate loss and renal tubular acidosis (RTA). Julian L. Seifter, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 Hyperchloremic Metabolic Acidosis of Nonrenal Origin Associated with Hypokalemia Hypokalemic, hyperchloremic acidosis may result from loss of a body fluid that is low in Cl relative to Na+ and K+ when compared with the ratio of Cl to Na+ in extracellular fluid. For example, stool losses of Na+, K+, and HCO3 in small bowel diarrhea or organic acid anions of bacterial origin in colonic diarrhea lead to hyperchloremic acidosis (Chapter 142). Pancreatic secretions (Chapter 201) or heavy losses from ileostomy sites may lead to loss of bicarbonate-containing fluids. Secretagogues such as vasoactive intestinal peptide (VIP), which is associated with neoplasms of the pancreas or sympathetic chain (Chapter 201), cause large losses of HCO3 in stool, with a resulting hypokalemic, hyperchloremic metabolic acidosis. Concomitant gastric achlorhydria is part of the syndrome known as watery diarrhea, hypokalemic, hypochlorhydric acidosis. Urinary diversions, such as ureterosigmoidostomies and ileal loops, may increase chloride absorption in exchange for bicarbonate in the intestinal segment and lead to hyperchloremic acidosis. Thomas D. DuBose, in Therapy in Nephrology & Hypertension (Third Edition) , 2008 Both uremic acidosis and hyperchloremic acidosis of renal insufficiency require oral alkali replacement to maintain [HCO3] between 20 and 24 mEq/L. This can usually be accomplished with relatively modest amounts of alkali (1-1.5 mEq/kg/day). Sodium citrate (Shohl's Solution or Bicitra) has been shown to enhance the absorption of aluminum from the gastrointestinal t Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi 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 >>

What Is Metabolic Acidosis?: Signs, Symptoms, Causes And Treatment

What Is Metabolic Acidosis?: Signs, Symptoms, Causes And Treatment

What is Metabolic Acidosis?: Signs, Symptoms, Causes and Treatment What is Metabolic Acidosis?: Signs, Symptoms, Causes and Treatment Itis a condition where your body is making too much acid than it is getting rid of. As a result, there is too much acid in the body. Metabolic acidosis usually occurs when your lungs and kidneys are unable to maintain your bodys normal pH balance. Your blood acidity is measured using pH level. If your pH level is low, you have more acid in the blood. The blood pH level in people who are healthy is between 7.35 and 7.45.MA occurs when the blood pH level falls below 7.35. In case your pH level is more than 7.45, then it means you have too many bases in the blood, a condition known as alkalosis. If not diagnosed, MA could result in a condition known as acidemia, where the pH level in the blood is low because the body is producing more hydrogen ions. Acidemia could also arise when the kidney fails to form bicarbonate. It is advisable to consider MA as a sign of underlying medical condition. For MA to be successfully treated, identification of the underlying medical condition is important. There are instances when MA could become serious and lead to coma or even death. However, some patients have mild MA that is not life threatening. There are certain risk factors which increases your chances of getting MA. If you are diabetic, have kidney failure, are obese, are suffering from dehydration, or are using aspirin, you have a higher risk of getting metabolic acidosis. The symptoms of metabolic acidosis usually differ depending on the cause. However, patients with this condition usually experience the following signs and symptoms of MA: If you are experiencing any of the above signs and symptoms of metabolic acidosis, you should book an appointme Continue reading >>

Is Correcting Hyperchloremic Acidosis Beneficial?

Is Correcting Hyperchloremic Acidosis Beneficial?

You are here: Home / PULMCrit / Is correcting hyperchloremic acidosis beneficial? Is correcting hyperchloremic acidosis beneficial? An elderly woman presents with renal failure due to severe dehydration from diarrhea. She has a hyperchloremic acidosis from diarrhea with a chloride of 115 mEq/L, bicarbonate of 15 mEq/L, and a normal anion gap. During her volume resuscitation, should isotonic bicarbonate be used to correct her hyperchloremic acidosis? Does correcting her hyperchloremic acidosis actually help her, or does this just make her numbers better? The use of bicarbonate for treatment of metabolic acidosis is controversial. However, this controversy centers primarily around use of bicarbonate for management of lactic acidosis or ketoacidosis.Treatment of these disorders requires reversing the underlying disease process, with bicarbonate offering little if any benefit.Hyperchloremic metabolic acidosis is different.Whether due to bicarbonate loss or volume repletion with normal saline, the primary problems is a bicarbonate deficiency.Treating this with bicarbonate is a logical and accepted approach: Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial. Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base, which, given time, can be converted back to bicarbonate However, clinicians are often reluctant to treat hyperchloremic metabolic acidosis with bicarbonate, since the benefits of treatment are unclear.This post will attempt to clarify the rationale for treatment. Resuscitation with balanced crystalloids improves renal function There is growing evidence that resuscitation with normal saline impairs renal blood flow and function ( Young 2014 ).For example, Chowdhury 2012 inve 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 >>

Sid Hyperchloremic Acidosis

Sid Hyperchloremic Acidosis

Strong ions are cations and anions that exist as charged particles dissociated from their partner ions at physiologic pH. The SID (Strong Ion Difference) is the difference between the positively- and negatively-charged strong ions in plasma. This method of evaluating acid-base disorders was developed to help determine the mechanism of the disorder rather than simply categorizing them into metabolic vs. respiratory acidosis/alkalosis as with the Henderson-Hasselbalch equation. Strong cations predominate in the plasma at physiologic pH leading to a net positive plasma charge of approximately +40: SID = [strong cations] [strong anions] = [Na+ + K+ + Ca2+ + Mg2+] [Cl- + lactate- + SO42-] Disturbances that increase the SID increase the blood pH while disorders that decrease the SID lower the plasma pH. According to the law of electroneutrality the sum of positive charges is equal to the sum of negative charges. Therefore the SID must be equal to the sum of weak anions in the body (such as bicarbonate, albumin, and phosphate). Hyperchloremic acidosis may result from chloride replacing lost bicarbonate. Such bicarbonate-wasting conditions may be seen in the kidneys (renal tubular acidosis) or the GI tract (diarrhea). This may also occur with aggressive volume resuscitation with normal saline (>30cc/kg/hr) due to excessive chloride administration impairing bicarbonate resorption in the kidneys. The strong ion difference of normal saline is 0 (Na+ = 154mEq/L and Cl- = 154mEq/L SID = 154 154 = 0). Therefore, aggressive administration of NS will decrease the plasma SID causing an acidosis. Administering a solution with a high SID such as sodium bicarbonate should be expected to treat this strong ion acidosis. Continue reading >>

Treating Intraoperative Hyperchloremic Acidosis With Sodium Bicarbonate Or Tris-hydroxymethyl Aminomethane: A Randomized Prospective Study

Treating Intraoperative Hyperchloremic Acidosis With Sodium Bicarbonate Or Tris-hydroxymethyl Aminomethane: A Randomized Prospective Study

We demonstrated that saline infusion of approximately 35 mL/kg within 2 h during anesthesia and surgery will inevitably lead to hyperchloremic acidosis in a dose-dependent manner (1) . Also, the infusion of saline-based colloid solutions will result in hyperchloremic acidosis (2) . In this context, the seemingly harmless and benign character of this acid-base disturbance was called into question (35) . Still, severe hyperchloremic acidosis should be avoided. One possibility to reach this target is the use of balanced solutions, such as lactated Ringers solution or Hextend (1,3,4) . The second possibility is correcting this acidosis at an early state. Until now, however, there was an open discussion as to the better concept for treating this kind of acidosis: with sodium bicarbonate (BIC) or tris-hydroxymethyl aminomethane (THAM) (6) . Undoubtedly, both drugs may lead to a correction of the acidosis; however, the respective effects on mechanical ventilation aiming at constant Paco2 and serum concentrations of electrolytes or unmeasured ions should be very different. By comparing two groups of patients with intraoperative hyperchloremic acidosis caused by 0.9% saline infusion and randomly assigned to receive equal doses of either BIC or THAM, we assessed the effect of both drugs on all important variables of acid-base chemistry at 0, 10, and 20 min after buffering. For evaluating the causes of the changes in pH after buffering, we planned to interpret the changes in serum bicarbonate concentration [Bic] and base excess [BE] as calculated by the Henderson-Hasselbalch equation and the Siggaard-Andersen nomogram (7) in the light of the Stewart (8) approach to acid-base chemistry. For more clarity of the following passage, all abbreviations (and calculations) are explained i Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Normal albumin-corrected anion gap acidosis Hyperchloremic acidosis is a common acid-base disturbance in critical illness, often mild (standard base excess >-10 mEq/L). Definitions of hyperchloremic acidosis vary. The best are not based on chloride concentrations, but on the presence of metabolic acidosis plus the absence of significant concentrations of lactate or other unmeasured anions. 2. standard base excess less than -3 mEq/L or bicarbonate less than 22 mmol/L, 3. Albumin corrected anion gap normal (5-15 mEq/L). A normal strong ion gap is an alternative indicator of the absence of unmeasured anions, although rarely used clinically and offering little advantage over the albumin corrected anion gap. The degree of respiratory compensation is relevant. It is appropriate if PaCO2 approximates the two numbers after arterial pH decimal point (e.g. pH=7.25, PaCO2=25 mm Hg; this rule applies to any primary metabolic acidosis down to a pH of 7.1). Acidosis is severe if standard base excess is less than -10 mEq/L, or pH is less than 7.3, or bicarbonate is less than 15 mmol/L. Common causes in critical illness are large volume saline administration, large volume colloid infusions (e.g. unbalanced gelatine or starch preparations) following resolution of diabetic keto-acidosis or of other raised anion gap acidosis, and post hypocarbia. Hyperchloremic acidosis often occurs on a background of renal impairment/tubular dysfunction. It is usually well tolerated, especially with appropriate respiratory compensation. The prognosis is largely that of the underlying condition. If associated with hyperkalemia, think of hypo-aldosteronism (Type 4 RTA), especially if diabetic. With persistent hypokalemia, think of RTA Types 1 and 2. Hyperchloremic acidosis is usually well tolerated in the Continue reading >>

Hyperchloremic Acidosis | Definition Of Hyperchloremic Acidosis By Medical Dictionary

Hyperchloremic Acidosis | Definition Of Hyperchloremic Acidosis By Medical Dictionary

Hyperchloremic acidosis | definition of hyperchloremic acidosis by Medical dictionary Related to hyperchloremic acidosis: Lactic acidosis , hypochloremic alkalosis 1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH. 2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidotic. Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma. In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to a Continue reading >>

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>

Hyperchloremic Acidosisclinical Presentation

Hyperchloremic Acidosisclinical Presentation

Hyperchloremic AcidosisClinical Presentation Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Metabolic acidosis, per se, has no specific symptoms and signs, unless it is extremely severe or of acute onset; however, it can produce symptoms and signs from changes in pulmonary, cardiovascular, neurologic, and musculoskeletal function. If the acidosis is marked and/or of acute onset, the patient may report headache, lack of energy, nausea, and vomiting. Neurologic abnormalities such as mental confusion progressing to stupor, when observed, are not usually secondary to the acidosis but are the cause of the acidosis itself. In general, neurologic abnormalities are less common in persons with metabolic acidosis than in persons with respiratory acidosis. An increase in minute ventilation of up to 4- to- 8-fold may occur in persons with respiratory compensation. Persistent tachypnea or hyperpnea (affecting the depth more than the rate of ventilation) may be the only clinical clue to an underlying acidotic state. This type of tachypnea/hyperpnea characteristically persists in sleep or interferes with sleep. Effects on the cardiovascular system include direct impairment of myocardial contraction (especially at a pH < 7.2), tachycardia, and increased risk of ventricular fibrillation or heart failure with pulmonary edema. Patients may report dyspnea upon exertion or, in severe cases, at rest. In advanced stages, overt cardiovascular collapse may occur from impaired catecholamine release. Chronic acidemia, as is observed in RTA, can lead to a variety of skeletal problems. This is probably due in part to the release of calcium and phosphate during bone buffering of the excess protons. Decreased tubular absorption of calcium secondary t 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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