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Metabolic Acidosis In Liver Failure

Metabolic Acidosis: Practice Essentials, Background, Etiology

Metabolic Acidosis: Practice Essentials, Background, Etiology

Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. An acid is a substance that can donate hydrogen ions (H+). A base is a substance that can accept H+ ions. The ion exchange occurs regardless of the substance's charge. Strong acids are those that are completely ionized in body fluids, and weak acids are those that are incompletely ionized in body fluids. Hydrochloric acid (HCl) is considered a strong acid because it is present only in a completely ionized form in the body, whereas carbonic acid (H2 CO3) is a weak acid because it is ionized incompletely, and, at equilibrium, all three reactants are present in body fluids. See the reactions below. The law of mass action states that the velocity of a reaction is proportional to the product of the reactant concentrations. On the basis of this law, the addition of H+ or bicarbonate (HCO3-) drives the reaction shown below to the left. In body fluids, the concentration of hydrogen ions ([H+]) is maintained within very narrow limits, with the normal physiologic concentration being 40 nEq/L. The concentration of HCO3- (24 mEq/L) is 600,000 times that of [H+]. The tight regulation of [H+] at this low concentration is crucial for normal cellular activities because H+ at higher concentrations can b Continue reading >>

Acid-base And Potassium Disorders In Liver Disease.

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 >>

Lactic Acidosis In Fulminant Hepatic Failure: Some Aspects Of Pathogenesis And Prognosis*

Lactic Acidosis In Fulminant Hepatic Failure: Some Aspects Of Pathogenesis And Prognosis*

Lactic acidosis in fulminant hepatic failure: Some aspects of pathogenesis and prognosis * Author links open overlay panel DavidBihari*** Get rights and content To obtain further evidence of tissue hypoxia in fulminant hepatic failure, we have measured the mixed venous lactate concentration and the acid-base status of 32 patients at the time of their admission, in grade III or IV encephalopathy. The mixed venous lactate was elevated in 26 of the 32 patients (median 5.0 mmol/l, range 0.821.1 mmol/l), and, in 17 patients, this was associated with evidence of a metabolic acidosis. Mixed venous lactate levels correlated inversely with the mean arterial pressure (r = 0.56, P < 0.005), systemic vascular resistance (r = 0.62, P < 0.001) and the oxygen extraction ratio (r = 0.44, P < 0.02). The 17 patients with a raised mixed venous lactate and metabolic acidosis had a significantly reduced systemic vascular resistance and oxygen extraction ratio compared with the other 15 (median systemic vascular resistances 944 and 1710 dynes/cm5/m2, respectively, P < 0.05, median oxygen extraction ratios 19 and 23%, respectively, P < 0.05). Survival was markedly reduced in the patients with hyperlactataemia and a metabolic acidosis, and only one out of the 17 survived compared with 12 of the remaining 15, P = 0.0002. These results suggest that lactic acid accumulation may be in part the consequence of tissue hypoxia that develops as a result of arteriovenous shunting, reflected in the reduction in systemic vascular resistance. This tissue hypoxia may occur despite apparently adequate systemic blood pressure, flow and oxygenation. Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

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

The Short Term Prognosis In Alcoholic Liver Disease With Metabolic Acidosis

The Short Term Prognosis In Alcoholic Liver Disease With Metabolic Acidosis

The Short Term Prognosis in Alcoholic Liver Disease with Metabolic Acidosis The Korean Journal of Hepatology 2004;10(2): 117-124. The Short Term Prognosis in Alcoholic Liver Disease with Metabolic Acidosis Ki Sun Bae , Kwon Yoo , You Kyung Cho , Ki Nam Shim , Sung Ae Jung , Il Hwan Moon Department of Internal Medicine, Ewha Womans University College of Medicine, Seoul, Korea Alcoholic liver disease with metabolic acidosis may have possible causes such as alcoholic ketoacidosis, diabetic ketoacidosis, lactic acidosis. Salicylate, methanol, and ethylene glycol intoxication should also be considered. The aim of this study was to investigate the short-term prognostic factors in patients with alcoholic liver disease with metabolic acidosis. Clinical data related to twenty-nine patients with alcoholic liver disease and metabolic acidosis was analysed retrospectively. Patients were divided into two groups according to the outcome (survival or death). Past medical history, and physical, laboratory and radiologic data at admission were compared. The amount of daily alcohol intake differed significantly between the two groups (P=0.034), but duration and total amount of alcohol intake did not differ significantly between the two groups (P=0.128; P=0.360). The presence of ascites differed significantly between two the groups (P=0.019). On laboratory testing, the following differed significantly: base excess (P=0.038), hemoglobin (P=0.019), platelet (P=0.040), total bilirubin (P=0.007), albumin (P=0.012), creatinine (P=0.014), phosphorus (P=0.021), chloride (P=0.010), ammonia (P=0.003), prothrombin time (P=0.033), fibrinogen (P=0.011) and D-dimer (P=0.024). Review of the medical history of the patients showed diabetes (10/29), cirrhosis (10/29), and hepatocellular carcinoma (1/29). Continue reading >>

Hypoketotic Hypoglycemia, Metabolic Acidosis, Toxic Liver Disease: Causes & Diagnoses | Symptoma.com

Hypoketotic Hypoglycemia, Metabolic Acidosis, Toxic Liver Disease: Causes & Diagnoses | Symptoma.com

Causes of metabolic acidosis There are many causes. [patient.info] Diseases and drugs that impair mitochondrial function can cause lactic acidosis. [merckmanuals.com] metabolic , Metabolic acidosis NOS , Metabolic Acidoses , Acidosis, Metabolic , Acidoses, Metabolic , Metabolic Acidosis , acidosis metabolic , metabolic acidosis disorder [fpnotebook.com] Also, severe electrolye abnormalities (hyponatremia, hypophosphatemia, hypokalemia, hypomagnesemia, also metabolic acidosis). [errolozdalga.com] Progress in liver diseases . 3 : 28298. [en.wikipedia.org] Instead of being harmlessly metabolized and bound to glucuronates and sulfates, excessive acetaminophen compounds enter CYP protein-mediated metabolic reactions in the liver [lecturio.com] Long Chain Hydroxyacyl-CoA Dehydrogenase Deficiency Treatment : It is important to avoid fasting to prevent hypoketotic hypoglycemia. [emilytam.com] Clinical considerations: Poor feeding, vomiting, lethargy Hypoglycemia Metabolic acidosis Hepatomegaly Cardiac insufficiency History of sudden unexpected death in a sibling [archildrens.org] Symptoms associated with LCHAD deficiency are due to low levels of energy and the toxic build-up of fatty acids in cells, especially in the liver and brain. [genetics.mytestingoptions.com] Toxic liver disease with hepatic necrosis K71.2 Toxic liver disease with acute hepatitis K71.3 Toxic liver disease with chronic persistent hepatitis K71.4 Toxic liver disease [icd10data.com] disease drug-induced toxic (predictable) liver disease Codes K71 Toxic liver disease K71.0 Toxic liver disease with cholestasis K71.1 Toxic liver disease with hepatic necrosis [icd10data.com] All medications should be evaluated for toxic effects on the liver. [aafp.org] Missing:Hypoketotic HypoglycemiaMetabolic Acidosis Urinary Continue reading >>

Acute Liver Failure - Wikipedia

Acute Liver Failure - Wikipedia

Acute liver failure (with hepatocellular necrosis and sinusoidal bleeding) from Marburg virus , a rare cause Acute liver failure is the appearance of severe complications rapidly after the first signs of liver disease (such as jaundice ), and indicates that the liver has sustained severe damage (loss of function of 8090% of liver cells). The complications are hepatic encephalopathy and impaired protein synthesis (as measured by the levels of serum albumin and the prothrombin time in the blood). The 1993 classification defines hyperacute as within 1 week, acute as 828 days, and subacute as 412 weeks. [1] It reflects the fact that the pace of disease evolution strongly influences prognosis. Underlying cause is the other significant determinant of outcome. [2] Acute liver failure is defined as "the rapid development of hepatocellular dysfunction, specifically coagulopathy and mental status changes (encephalopathy) in a patient without known prior liver disease". [3] page 1557 The diagnosis of acute liver failure is based on physical exam, laboratory findings, patient history, and past medical history to establish mental status changes, coagulopathy, rapidity of onset, and absence of known prior liver disease respectively. [3] page 1557 The exact definition of "rapid" is somewhat questionable, and different sub-divisions exist which are based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms. This is sub-divided into "fulminant hepatic failure", which requires onset of encephalopathy within 8 weeks, and "subfulminant", which describes onset of encephalopathy after 8 weeks but before 26 weeks. [4] Another scheme defi Continue reading >>

Fulminant Hepatic Failure In Small Animals

Fulminant Hepatic Failure In Small Animals

Fulminant Hepatic Failure in Small Animals Fulminant Hepatic Failure in Small Animals By Sharon A. Center, BS, DVM, DACVIM, Professor, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University Hepatobiliary Fluke Infection in Small Animals Fulminant hepatic failure is a syndrome defined by the abrupt loss of liver function, associated with hepatic encephalopathy (HE) and coagulopathy. Early, appropriate therapy is critical. In chronic or end-stage liver disease with an acute or chronic insult and in acute liver injury with no apparent underlying cause, treatment provides supportive care to allow time for hepatic regeneration and compensation. Specific treatment should be administered if an underlying cause is determined. Decontamination of oral, dermal, and enteric surfaces is mandatory if toxin exposure has occurred within 36 hr. If an adverse drug reaction is implicated, the drug in question must be discontinued and antidotes investigated. Life-threatening infection, cerebral edema, and coagulopathies are major complications. Attention to fluid, electrolyte, and acid-base balance, glycemic status, and nutritional support optimizes chance of survival. Restoration of intravascular volume and systemic perfusion may prevent or mitigate the severity of organ failure that often accompanies fulminant hepatic failure (eg, renal, cardiac, adrenal, pancreatic dysfunction). Lactated Ringers solution should be avoided in animals with compromised lactate metabolism, leading to lactic acidosis. Chronic vomiting and diarrhea often accompany fulminant hepatic failure and can lead to dehydration, hypokalemia, hypochloremia, and metabolic alkalosis. Alkalosis and hypokalemia can each escalate renal ammonia production, contributing to hyperammonemia and HE. Ne Continue reading >>

Liver Failure, Acute

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 >>

Respiratory Alkalosisdifferential Diagnoses

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 >>

Fulminant Hepatic Failure

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 >>

Acid-base And Potassium Disorders In Liver Disease

Acid-base And Potassium Disorders In Liver Disease

@article{89a276395fb14e7ba5b2dd13a5976c0d, title = "Acid-Base and Potassium Disorders in Liver Disease", abstract = "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.", keywords = "acid-base, hyperkalemia, kidney, liver disease, liver failure, metabolic acidosis, respiratory alkalosis", author = "Ahya, {Shubhada N.} and {Jos\{'e} Soler}, Maria and Josh Levitsky and Daniel Batlle", N2 - 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 c Continue reading >>

Acid-base Disorders In Liver Disease.

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 >>

Alterations In Arterial Blood Parameters In Patients With Liver Cirrhosis And Ascites

Alterations In Arterial Blood Parameters In Patients With Liver Cirrhosis And Ascites

Int J Med Sci 2007; 4(2):94-97. doi:10.7150/ijms.4.94 Alterations in Arterial Blood Parameters in Patients with Liver Cirrhosis and Ascites Konstantinos Charalabopoulos1,2, Dimitrios Peschos3, Leonidas Zoganas4, George Bablekos4, Christos Golias1, Alexander Charalabopoulos1, Dimitrios Stagikas1, Angi Karakosta1, Athanasios Papathanasopoulos5, George Karachalios2, Anna Batistatou3 1. Department of Physiology, Clinical Unit, Medical Faculty, University of Ioannina, Ioannina, Greece. 2. Department of Medicine, Red Cross Hospital, Athens, Greece. 3. Department of Pathology, Medical Faculty, University of Ioannina, Ioannina, Greece. 4. Department of Thoracic Surgery, Red Cross Hospital, Athens, Greece. 5. Department of Medicine, Gastroenterology Unit, Medical Faculty, University of Ioannina, Ioannina, Greece. This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License . See for full terms and conditions. Charalabopoulos K, Peschos D, Zoganas L, Bablekos G, Golias C, Charalabopoulos A, Stagikas D, Karakosta A, Papathanasopoulos A, Karachalios G, Batistatou A. Alterations in Arterial Blood Parameters in Patients with Liver Cirrhosis and Ascites. Int J Med Sci 2007; 4(2):94-97. doi:10.7150/ijms.4.94. Available from In cirrhotic patients, in addition to hepatocytes and Kuppfer cells dysfunction circulatory anatomic shunt and ventilation/perfusion (VA/ Q) ratio abnormalities can induce decrease in partial pressure of oxygen in arterial blood (PaO2), in oxygen saturation of hemoglobin (SaO2) as well as various acid-base disturbances. We studied 49 cases of liver cirrhosis (LC) with ascites compared to 50 normal controls. Causes were: posthepatic 37 (75.51%), alcoholic 7 (14.24%), cardiac 2 (4.08%), and cryptogenic 3 (6.12%). C Continue reading >>

Acid-base And Potassium Disorders In Liver Disease

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. [29] Lactic acidosis may be precipitated by biguanides as they inhibit mitochondrial respiration predominantly in the liver. ... Continue reading >>

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