American Thoracic Society - Liver Dysfunction And Severe Lactic Acidosis In A Previously Healthy Man
Liver dysfunction and severe lactic acidosis in a previously healthy man A man in his eighth decade presented to his primary doctor three weeks prior to admission with easy bruising. A complete blood count revealed low counts in all three major cell lines and a subsequent bone marrow biopsy demonstrated B-cell follicular lymphoma. Other biochemical parameters, including tests of liver transaminases and bilirubin, were normal. Two weeks later he developed a cough and shortness of breath and he received a diagnosis of acute bronchitis, for which he was prescribed azithromycin along with an inhaler of salmeterol and fluticasone. His cough and dyspnea did not improve and he was admitted to another hospital for further evaluation. A diagnosis of liver failure was made based on elevated liver function tests (aspartate aminotransferase=995 U/L, alanine aminotransferase=552 U/L, total bilirubin=7.2 mg/dL, direct bilirubin=5.5 mg/dL); worsening pancytopenia was noted. Evaluation of the acute liver failure did not reveal an etiology, and he was transferred to a tertiary care hospital for further evaluation and care. Thyroid cancer, s/p partial thyroidectomy Denies excessive alcohol and illicit drug use 40 pack-year cigarette smoking history, stopped in 2004 Laboratory investigation did not reveal occult infectious hepatitis or autoimmune disease. Diagnostic imaging of the liver revealed a large intra-hepatic mass and trans-jugular liver biopsy showed extensive hepatic infiltration by lymphoma. His respiratory status became increasingly tenuous and his trachea was intubated and positive-pressure mechanical ventilation was initiated. He was transferred to the ICU but suffered the rapid onset of shock despite infusions of sodium bicarbonate and norepinephrine. After a conversation Continue reading >>
Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification The Cohen-Woods classification categorizes causes of lactic acidosis as: Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids. Symptoms in humans include all those of typical m Continue reading >>
Review. Perioperative Management Of Lactic Acidosis In End-stage Liver Disease Patient
1. Kreisberg RA. Lactate Homeostasis and Lactic Acidosis, Ann. of Int. Med. 1980;92: 227-237. 2. Gunnerson KJ1, Saul M, He S, Kellum JA. Lactate versus nonlactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients Crit Care 2006; 10:R22. 3. Cohen RD, Woods HF. Clinical and biochemical aspects of lactic acidosis. Blackwell Scientific Publication, Oxford, 1976 pp.46-64. 4. Kraut J., Madias N. Lactic Acidosis N Engl J Med. 2014 Dec 11;371:2309-19. 5. Jeppesen JB, Mortensen C, Bendtsen F, Mller S. Lactate metabolism in chronic liver disease. Scand J Clin Lab Invest Scand J Clin Lab Invest. 2013;73:293-9. 6. Bakker J, Nijsten MW, Jansen TC. Clinical use of lactate monitoring in critically ill patients. Ann Intensive Care. 2013 May 10;3:12. 7. Murphy ND, Kodakat SK, Wendon JA, et al. Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation. Crit Care Med 2001; 29: 2111-8. 8. Oster JR, Perez GO. Acid-base disturbances in liver disease. J Hepatol 1986; 2: 299-306. 9. Walsh TS, Mclellan S, Mackenzie SJ, et al. Hyperlactatemia and pulmonary lactate production in patients with fulminant hepatic failure. Chest 1999; 116: 471-6. 10. Bernardi M, Predieri S. Disturbances of acid-base balance in cirrhosis: a neglected issue warranting further insights. Liver Int 2005;25:463-6. 11. Funk G., Doberer D., Kneidinger N., et al. Acid-base disturbances in critically ill patients with cirrhosis. Liver International 2007 ISSN 1478-3223 p.901-909. 12. Fencl V, Leith D. Stewarts quantitative acid-base chemistry: Applications in biology and medicine Resp. Physiol. 1993;91: 1-16. 13. Fencl V, Jabor A, Kazda A, Figge J. Diagnosis of metabolic acidbase disturbances in critically ill patients. Am J Respir Crit Care Continue reading >>
Fulminant Hepatic Failure
markedly increased susceptibility to bacterial infections (bacteraemia in 30%, fungaemia in 10%) significantly more common in patients with renal failure. respiratory (47%) or urinary tract origin most common Gram +ve most common in first week, gram -ve in second week and fungal infection in third week ECG: multiple VEs, heart block, bradycardia common EEG: hepatic encephalopathy has characteristic pattern HAV IgM, HBcAb (IgM) - high sensitivity and specificity for acute infection with these 2 viruses. Assay for antibody to hepatitis C not very useful as it is rarely positive in the acute stages of the disease. Usually becomes positive for the first time only 3-6 months after the onset. The presence of HB IgM Ab to core Ag usually required for diagnosis as surface antigen is rapidly cleared lamivudine for patients with hepatitis B treated with steroids (to prevent acute liver failure on withdrawal of steroids) NB Early liason with and transfer to specialist unit before patient develops grade IV coma. 90% ofpatients in grade III coma progress to grade IV. N-acetylcysteine of benefit in patients following paracetamol overdose evenwhen there is evidence of encephalopathy and coagulopathy. Results in lesshypotension and less cerebral oedema. Infusion results in increased cardiacoutput, oxygen delivery and consumption in patients with FHF. Mechanism ofaction is not clear. Attention to metabolic homeostasis important lactulose - aim to produce 2 soft motions/day - diarrhoea aggravates anyabnormality of fluid and electrolyte balance. Reduces colonic production ofammonia in addition to having a laxative effect. NB insulin resistance occurs in severe acute hepatitis. Resting energy expenditure 1700 kcal/day with nitrogen loss of 7g/day (butheavily dependent on whether or not di Continue reading >>
2.5 Acid Base Role Of The Liver
The liver is important in acid-base physiology and this is often overlooked. It is important because it is a metabolically active organ which may be either a significant net producer or consumer of hydrogen ions. The amounts of acid involved may be very large. The acid-base roles of the liver may be considered under the following headings: Carbon dioxide production from complete oxidation of substrates Metabolism of organic acid anions (such as lactate, ketones and amino acids) Production of plasma proteins (esp albumin) Complete oxidation of carbohydrates and fat which occurs in the liver produces carbon dioxide but no fixed acids. As the liver uses 20% of the bodys oxygen consumption, this hepatic metabolism represents 20% of the bodys carbon dioxide production also. The CO2 diffuses out of the liver and reactions in red cells result in production of H+ and HCO3-. The metabolism of various organic anions in the liver results in consumption of H+ and regeneration of the extracellular bicarbonate buffer. These anions may be: Exogenous (eg citrate in blood transfusion, acetate and gluconate from Plasmalyte 148 solution, lactate from Hartmanns solution), or Endogenous (eg lactate from active glycolysis or anaerobic metabolism, keto-acids produced in the liver) The term acid anion is used because they are anions produced by dissociation of an acid. That is: HA -> H+ + A- (where HA is the acid and A- is the acid anion). The anions are the conjugate base of the acid (Bronsted-Lowry system) and are not themselves acids. This is an important distinction to make because they are often referred to as though they were acids and this leads to confusion. If the endogenous production of these anions is followed by later consumption in the liver then there is no net production of ac Continue reading >>
For Patients And Visitors
Definition Metabolic acidosis is a condition in which there is too much acid in the body fluids. Alternative Names Acidosis - metabolic 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: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Prolonged lack of oxygen from shock, heart failure, or severe anemia Seizures Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Severe dehydration 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 function Continue reading >>
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Liver Failure, Acute
These correspond to diseases that can cause LFTs in the 1000s, which actually carries a fairly limited differential diagnosis: Acetaminophen - accounts for the majority of cases in the US. Other drugs/toxins including isoniazid, antibiotics, anticonvulsants, PTU, and poison mushrooms. Importantly, alcohol does not really cause LFTs in the 1000s nor does it cause acute liver failure!!! Hep B > Hep A, not really Hep C. Also Hep D (with Hep B coinfection) and Hep E (esp pregnant women). Rarely, other viruses such as HSV, CMV, adenovirus, and others can cause ALF especially in immunocompromised patients. 3. Vascular: "Shock liver" from extreme hypotension, Budd-Chiari, Veno-occlusive disease Wilson's Disease - accounts for 2-3% of ALF - presents usually in young adults with hemolytic anemia and acute liver failure, often with characteristically low Alk Phos. Other metabolic causes include complications related to pregnancy - Acute Fatty Liver of Pregnancy and HELLP syndrome. Reye's syndrome - associated with children taking ASA while suffering from viral illness (influenza, varicella). 5. Autoimmune Hepatitis - often is the first presentation, can be fulminant. Overview of ALF Manifestions and Basic Management 1. Neuro - Hepatic Encephalopathy, Cerebral Edema, Seizures. Cerebral edema is common in severe encephalopathy and is a major cause of death in acute liver failure (the other common cause of death is sepsis). Unclear pathophysiology but likely related to osmotic derangements in astrocytes, alterations in cerebral blood flow, and other hand-waving theories. Management involves raising the head of the bed, hyperventilation (low PCO2 cerebral vasoconstriction), mannitol (hyperosmolar solution and osmotic diuresis leading to plasma hyperosmolarity and hypernatremia), hyp Continue reading >>
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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: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>
Metabolic Acidosis: Causes, Symptoms, And Treatment
The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>
Acid-base And Potassium Disorders In Liver Disease
Northwestern University, Feinberg school of Medicine, Chicago Acid-base and potassium disorders occur frequently in the setting of liver disease. As the liver's metabolic function worsens, particularly in the setting of renal dysfunction, hemodynamic compromise, and hepatic encephalopathy, acid-base disorders ensue. The most common acid-base disorder is respiratory alkalosis. Metabolic acidosis alone or in combination with respiratory alkalosis also is common. Acid-base disorders in patients with liver disease are complex. The urine anion gap may help to distinguish between chronic respiratory alkalosis and hyperchloremic metabolic acidosis when a blood gas is not available. A negative urine anion gap helps to rule out chronic respiratory alkalosis. In this disorder a positive urine anion gap is expected owing to suppressed urinary acidification. Distal renal tubular acidosis occurs in autoimmune liver disease such as primary biliary cirrhosis, but often is a functional defect from impaired distal sodium delivery. Potassium disorders are often the result of the therapies used to treat advanced liver disease. Do you want to read the rest of this article? ... Patients with decompensated liver disease, in the setting of sepsis or hemorrhage, may have increased serum lactate levels due to poor utilization and metabolism.  Lactic acidosis may be precipitated by biguanides as they inhibit mitochondrial respiration predominantly in the liver. ... Continue reading >>
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. 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 >>
Does this test have other names? Carbon dioxide test, CO2 test What is this test? This test measures the amount of bicarbonate, a form of carbon dioxide, in your blood. Bicarbonate, also known as HCO3, is a byproduct of your body's metabolism. Your blood brings bicarbonate to your lungs, and then it is exhaled as carbon dioxide. Your kidneys also help regulate bicarbonate. Bicarbonate is excreted and reabsorbed by your kidneys. This regulates your body's pH, or acid balance. Bicarbonate also works with sodium, potassium, and chloride, also called electrolytes. These are usually measured at the same time as bicarbonate. This test is usually part of a comprehensive series of blood tests to check for certain health conditions. Why do I need this test? You may need this test to monitor issues that affect pH levels in your blood. You may also have this test if you have kidney disease, liver failure, or other conditions related to metabolism. What other tests might I have along with this test? Your healthcare provider may also order several other tests. These may include: Arterial blood gas analysis Electrolyte (sodium, potassium, and chloride) testing as part of a basic or comprehensive metabolic panel Urine pH testing Anion gap blood testing What do my test results mean? Test results may vary depending on your age, gender, health history, the method used for the test, and other things. Your test results may not mean you have a problem. Ask your healthcare provider what your test results mean for you. Results are given in milliequivalents per liter (mEq/L) or millimoles per L (mmol/L). Normal bicarbonate levels are: 23 to 30 mEq/L in adults A high level of bicarbonate in your blood can be from metabolic alkalosis, a condition that causes a pH increase in tissue. Metabolic al Continue reading >>
Acid-base Disorders In Liver Disease.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Department of Respiratory and Critical Care Medicine, Otto Wagner Spital, Vienna, Austria. Department of General Internal Medicine & Emergency Medicine, Hirslanden Klinik Im Park, Zurich, Switzerland. Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria. Division of Oncology and Hematology, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria. Department of Respiratory and Critical Care Medicine, Otto Wagner Spital, Vienna, Austria. Electronic address: [email protected] J Hepatol. 2017 Nov;67(5):1062-1073. doi: 10.1016/j.jhep.2017.06.023. Epub 2017 Jul 3. Alongside the kidneys and lungs, the liver has been recognised as an important regulator of acid-base homeostasis. While respiratory alkalosis is the most common acid-base disorder in chronic liver disease, various complex metabolic acid-base disorders may occur with liver dysfunction. While the standard variables of acid-base equilibrium, such as pH and overall base excess, often fail to unmask the underlying cause of acid-base disorders, the physical-chemical acid-base model provides a more in-depth pathophysiological assessment for clinical judgement of acid-base disorders, in patients with liver diseases. Patients with stable chronic liver disease have several offsetting acidifying and alkalinising metabolic acid-base disorders. Hypoalbuminaemic alkalosis is counteracted by hyperchloraemic and dilutional acidosis, resulting in a normal overall base excess. When patients with liver cirrhosis become critically ill (e.g., because of sepsis or bleeding), this fragile eq Continue reading >>
Respiratory Alkalosisdifferential Diagnoses
Respiratory AlkalosisDifferential Diagnoses Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more... Hyperthyroidism: Hyperthyroidism increases the ventilation chemoreflexes, thereby causing hyperventilation. These chemoreflexes return to normal with treatment of the hyperthyroidism. Pregnancy: Progesterone levels are increased during pregnancy. Progesterone causes stimulation of the respiratory center, which can lead to respiratory alkalosis. Chronic respiratory alkalosis is a common finding in pregnant women. [ 3 ] Congestive heart failure: Patients with congestive heart failure (and other low cardiac-output states) hyperventilate at rest, during exercise, and during sleep. Owing to pulmonary congestion, pulmonary vascular and interstitial receptors are stimulated. Additionally, the low cardiac-output state and hypotension stimulate breathing via the arterial baroreceptors. Chronic/severe liver disease: Several mechanisms have been hypothesized to explain the hyperventilation associated with liver disease. Increased levels of progesterone, ammonia, vasoactive intestinal peptide, and glutamine can stimulate respiration. Patients with severe disease or portal hypertension may have small pulmonary arteriovenous anastomoses in the lungs or portal-pulmonary shunts, which result in hypoxemia. This stimulates the peripheral chemoreceptors and leads to hyperventilation. The degree of respiratory alkalosis correlates with the severity of hepatic insufficiency. [ 3 ] Salicylate overdose: Initially, a respiratory alkalosis occurs, which is followed by a metabolic acidosis that induces secondary hyperventilation. Fever and sepsis: Fever and sepsis may manifest as hyperventilation, even before hypotension develops. The exact mechanism is not known but is Continue reading >>
Acid-base And Potassium Disorders In Liver Disease.
Acid-base and potassium disorders in liver disease. Division of Nephrology and Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. [email protected] Acid-base and potassium disorders occur frequently in the setting of liver disease. As the liver's metabolic function worsens, particularly in the setting of renal dysfunction, hemodynamic compromise, and hepatic encephalopathy, acid-base disorders ensue. The most common acid-base disorder is respiratory alkalosis. Metabolic acidosis alone or in combination with respiratory alkalosis also is common. Acid-base disorders in patients with liver disease are complex. The urine anion gap may help to distinguish between chronic respiratory alkalosis and hyperchloremic metabolic acidosis when a blood gas is not available. A negative urine anion gap helps to rule out chronic respiratory alkalosis. In this disorder a positive urine anion gap is expected owing to suppressed urinary acidification. Distal renal tubular acidosis occurs in autoimmune liver disease such as primary biliary cirrhosis, but often is a functional defect from impaired distal sodium delivery. Potassium disorders are often the result of the therapies used to treat advanced liver disease. Continue reading >>