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Lactic Acidosis Liver Failure

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe 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 >>

Lactic Acidosis

Lactic Acidosis

hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq 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 >>

Lactic Acid In Shock And Liver Failure

Lactic Acid In Shock And Liver Failure

Metabolic acidosis during prolonged shock is a well-recognised and documented fact. As shown by Cournand et al. (1) in 1943, acidosis is linked with lactate accumulation in extracellular fluid, which is due to an imbalance between tissue oxygen supply and metabolic needs. Septic ShockBlood LactateLactate LevelLactate ConcentrationBase Deficit These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access. Unable to display preview. Download preview PDF. COURNAND, A., RILEY, R.L., BRADLEY, S.E., BREED, E.S., NOBEL, R.O., LAUSON, H.D., GREGERSEN, M.I., RICHARDS, D.W.: Studies of circulation in clinical shock. Surgery 13, 964 (1943) Google Scholar PERETZ, D.I., McGREGOR, M., DOSSETOR, J.B.: Lactic acidosis: a clinically significant aspect of shock. Can. Med. Assoc. J. 90, 673 (1964) PubMed Google Scholar BRODER, G., WEIL, M.H.: Excess lactate: an index of reversibility of shock in human patients. Science 143, 1457 (1964) PubMed CrossRef Google Scholar HUCKABEE, W.E.: Relationship of pyruvate and lactate during anaerobic metabolism. II. Exercise and formation of O2 debt. J. Clin. Invest. 37, 255 (1958) PubMed CrossRef Google Scholar ROSENBERG, J.C., RUSH, B.J.: Blood lactic acid levels in irreversible hemorrhagic and lethal endotoxin shock. Surg. Gynecol. Obstet. 126, 1247 (1968) PubMed Google Scholar ROWELL, L.B., KRANING, K.K., EVANS, T.O., KENNEDY, J.W., BLACKMAN, J.R., KUSUMI, F.: Splanchnic removal of lactate and pyruvate during prolonged exercise in man. J. Appl. Physiol. 21, 1773 (1966) PubMed Google Scholar SCHIMASSEK, H.: Der Einflu der Leber auf den extrazellulren Redox-Quotienten Lactat/Pyruvat. Versuche Continue reading >>

The Effect Of Liver Disease On Lactate Normalization In Severe Sepsis And Septic Shock: A Cohort Study

The Effect Of Liver Disease On Lactate Normalization In Severe Sepsis And Septic Shock: A Cohort Study

The effect of liver disease on lactate normalization in severe sepsis and septic shock: a cohort study Sterling, Puskarich, and Jones: The effect of liver disease on lactate normalization in severe sepsis and septic shock: a cohort study DOI: The effect of liver disease on lactate normalization in severe sepsis and septic shock: a cohort study Sarah A. Sterling , Michael A. Puskarich , Alan E. Jones Department of Emergency Medicine, University of Mississippi Medical Center, Jackson, MS, USA Correspondence to: Alan E. Jones Department of Emergency Medicine, University of Mississippi Medical Center, 2500 N State Street, Jackson, MS 39216, USA E-mail: [email protected] Received: July 16, 2015 Revised: September 28, 2015 Accepted: September 30, 2015 Copyright 2015 The Korean Society of Emergency Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ). To describe the effect of liver disease (LD) on lactate clearance during early sepsis resuscitation. This is a multicenter randomized clinical trial. An initial lactate >2 mmol/L and subsequent serum lactate measurement within 6 hours were required for inclusion. LD was categorized by two methods: 1) past medical history (PMH) categorized as no LD, mild LD (no Childs score criteria, but PMH of hepatitis B/C), cirrhosis; and 2) measurable liver dysfunction determined by the liver component of the sequential organ failure assessment (L-SOFA) score as no dysfunction (L-SOFA score 0), mild dysfunction (score 1), moderate-severe dysfunction (score 2 to 4). Primary outcome was the rate of lactate normalization. One hundred eighty-seven patients were included. When categorized by PMH, 169 patients had no LD, 6 mild LD, and 12 cirrhosis. 63/169 (37%) of patients Continue reading >>

What Is A Lactic Acid Blood Test?

What Is A Lactic Acid Blood Test?

It’s a test that measures the amount of lactic acid (also called “lactate”) in your blood. This acid is made in muscle cells and red blood cells. It forms when your body turns food into energy. Your body relies on this energy when its oxygen levels are low. Oxygen levels might drop during an intense workout or when you have an infection or disease. Once you finish your workout or recover from the illness, your lactic acid level tends to go back to normal. But sometimes, it doesn't. Higher-than-normal lactic acid levels can lead to a condition called lactic acidosis. If it’s severe enough, it can upset your body’s pH balance, which indicates the level of acid in your blood. Lactic acidosis can lead to these symptoms: It’s a simple blood test. Your doctor will draw blood from a vein or artery using a needle. In rare cases, he may take a sample of cerebrospinal fluid from your spinal column during a procedure called a spinal tap. Normally, you don’t have to adjust your routine to prepare for the test. If your lactic acid level is normal, you don’t have lactic acidosis. Your cells are making enough oxygen. It also tells your doctor that something other than lactic acidosis is causing your symptoms. He’ll likely order other tests to find out what it is. If your lactic acid level is high, it could be caused by a number of things. Most often, it’s because you have a condition that makes it hard for you to breathe in enough oxygen. Some of these conditions could include: Severe lung disease or respiratory failure Fluid build-up in your lungs Very low red blood cell count (severe anemia) A higher-than-normal lactic acid level in your blood can also be a sign of problems with your metabolism. And, your body might need more oxygen than normal because you have o Continue reading >>

Significant Lactic Acidosis With Acute Liver Failure At Presentation In Haemophagocytic-lymphohistiocytosis

Significant Lactic Acidosis With Acute Liver Failure At Presentation In Haemophagocytic-lymphohistiocytosis

The causes of acute liver failure in early infancy require prompt recognition and treatment to improve the prognosis. High serum lactate levels typically lead the clinician to consider mitochondrial or other metabolic disorders. We describe a series of young infants with Haemophagocytic Lymphohistiocytosis (HLH) who initially presented with unusually high lactate levels. Retrospective case note analysis of children with a final diagnosis of HLH who had high lactate levels at presentation. We identified 5 infants (M: F 3:2) with a median age of 34 (3-270) days, all presenting with pyrexia, poor feeding, deranged liver function tests and worsening coagulopathy. All had hepatosplenomegaly and ascites detected clinically or by ultrasound examination. Significant lactic acidosis was present early in the illness (median 14.2 (10.5-29.8) mmol/l) despite adequate perfusion and renal function in 4 out of the 5 infants. Extensive investigations for possible metabolic causes did not yield an alternative diagnosis. All were thrombocytopenic (median19,000 (7,000-23,000)/mm3) and had low fibrinogen levels (0.5 (0.5-0.7) g/l). Hyperferritinaemia (32,055 (20,000-180,370) nanogram/ml) and elevated triglyceride levels were documented in four in whom this was measured. The diagnosis of HLH was confirmed by bone marrow evidence of haemophagocytosis in 4 but one infant was only diagnosed by post-mortem examination. Only one child survived long term, following a bone marrow transplant. Clinically significant lactic acidosis in association with acute-onset liver dysfunction was seen in our series of infants with HLH. Continue reading >>

Unusual Case Of Severe Lactic Acidosis In A Liver Transplant Patient

Unusual Case Of Severe Lactic Acidosis In A Liver Transplant Patient

Unusual Case of Severe Lactic Acidosis in a Liver Transplant Patient 1Department of Anesthesiology, Drexel University College of Medicine/Hahnemann University Hospital, Philadelphia, PA, USA 2Department of Surgery, Drexel University College of Medicine/Hahnemann University Hospital, Philadelphia, PA, USA Correspondence should be addressed to Michael S. Green Received 1 September 2017; Revised 30 October 2017; Accepted 3 December 2017; Published 17 December 2017 Copyright 2017 Shweta Yemul Golhar et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Lactic acidosis is a standard indicator for oxygen debt and some other very significant causes. We describe a case of liver transplant patient presenting with vague abdominal pain and lactic acidosis without any liver dysfunction/failure/ischemia/rejection or sepsis. The imaging studies showed vague bowel edema and normal hepatic perfusion. The patient continued to deteriorate with rising lactic acidosis when a repeat CT abdomen eventually showed signs of lymphomatosis peritonei. Biopsy revealed the unusual diagnosis of posttransplant lymphoproliferative disorder. Immediate discontinuation of immunosuppression and initiation of chemotherapy led to clinical improvement. Our intention of presenting this case is to increase awareness of posttransplant lymphoma and propose lactic acidosis as not only an indicator of liver dysfunction or rejection but also an aid for diagnosis of this unusual but fatal and potentially curable condition. Lactic acidosis is a universally accepted marker for adequacy of perfusion. It is the end product of anaerobic metabolism and thu Continue reading >>

Lactic Acidosis

Lactic Acidosis

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[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] 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[edit] 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.[2] Symptoms in humans include all those of typical m Continue reading >>

Renal Fellow Network: Differential Diagnosis: Lactic Acidosis

Renal Fellow Network: Differential Diagnosis: Lactic Acidosis

As discussed in a recent post describing the success of early goal-directed therapy for sepsis, the test for serum lactate has enjoyed a rise in prominence in recent years. However, all that is lactic acid is not necessarily sepsis! Here's a differential diagnosis for lactic acidosis: 1. Shock--especially cardiogenic and septic shock, which is indicative of an inability of the circulatory system to match the metabolic demands of tissue. 2. Bowel Ischemia--mesenteric ischemia, necrotic bowel, etc.--the necrosis of cells in the intestine will release free lactate into the bloodstream. 3. Cirrhosis/Liver Failure--since lactate is metabolized to bicarbonate by the liver, patients with end-stage liver disease often have elevated lactate levels, which is NOT necessarily indicative of shock/hypoperfusion (although this group of patients often represents a conundrum in that they are precisely the type of patient who can get septic & die rapidly.) 4. Grand-mal Seizures: can lead to a transient increase in serum lactate which typically reverses on its own pretty quickly. 5. Thiamine Deficiency: thiamine is a cofactor for enzymes in the glycolytic pathway; its absence prevents adequate cellular metabolism and lactate can build up. 6. Citrate Toxicity in patients on CVVH given citrate-based replacement solution--this is heralded by an increased total calcium concentration along with a decreased ionized calcium concentration. 7. D-lactic acidosis: this atypical form of lactic acidosis occurs when bacterial overgrowth (as might occur in patients with GI bypass surgery) results in the metabolic synthesis of the D-isoform of lactic acidosis, which is not metabolizable to bicarbonate endogenously as is the naturally-occurring L-isoform of lactate. 8. Severe alkalosis: an increase in la Continue reading >>

Metformin‐associated Lactic Acidosis In A Patient With Liver Disease

Metformin‐associated Lactic Acidosis In A Patient With Liver Disease

Sir, Metformin is an orally active biguanide, and was found to reduce mortality and complications in obese diabetic patients in the UK Prospective Diabetes Study.1 As a result, the drug is widely used as first‐line therapy for patients with obesity and type 2 diabetes. We would like to remind prescribers of a rare, but commonly fatal complication of metformin therapy in patients with liver or renal disease. A 40‐year‐old Gujerati man was admitted through accident and emergency. On admission, little history was available from the patient, and no corroborative history was available, apart from the fact that he was diabetic and on metformin. He was short of breath at rest, with oxygen saturation of 84% on air, and had a Glasgow Coma Score of 13/15. Capillary blood glucose was 1.7 mmol/l. Arterial blood gas analysis on 60% oxygen revealed severe metabolic acidosis: pH 6.62, pCO2 8.3 kPa, pO2 47.8 kPa, base excess −31.2, bicarbonate 6.4 mmol/l, anion gap 37 mmol/l. Serum lactate was extremely high at >20 mmol/l. He had a low urea of 2.4 mmol/l, normal creatinine of 63 µmol/l, a raised aspartate transaminase (110 IU/l, NR 10–50), bilirubin (64 µmol/l, NR 2–17) and alkaline phosphatase (323 IU/l, NR 40–135). He had a macrocytic anaemia (haemoglobin 9.7 g/dl, NR 13.0–17.0; MCV 99.0 fl, NR 76.0–96.0), and deranged clotting (PT 30 s, control 12 s; KPTT 65 s, control 35 s), but normal platelet count (152×109/l, NR 135–450). Hypoglycaemia was confirmed by a venous plasma glucose of 1.9 mmol/l. On review of his medical notes, he had been diagnosed with type 2 diabetes 3 years prior to admission. He had not been seen at diabetic clinic for over 2 years, when his diabetes was well controlled with metformin 850 mg twice daily. Eighteen months previously, he was a Continue reading >>

Lactic Acidosis With Acute Fatty Liver And Hepatic Dysfunction

Lactic Acidosis With Acute Fatty Liver And Hepatic Dysfunction

Acute Fatty Liver with Lactic Acidosis and Hepatic Dysfunction Description. Acute fatty liver with lactic acidosis and hepatic dysfunction is a dramatic and distinctive clinical syndrome associated with medications that affect mitochondrial function. The hallmark of the syndrome is hepatic microvesicular steatosis (small droplet fat) accompanied by lactic acidosis and clinical and laboratory features of hepatic failure, such as stupor, coma, encephalopathy, hyperammonemia, hypoglycemia and coagulopathy. Latency to Onset. The onset of hepatic steatosis and lactic acidosis varies with the causative agent and pathophysiology of mitochondrial failure. Drugs that directly inhibit mitochondrial function or protein synthesis directly cause this syndrome within 7 to 28 days, as is typical with aspirin in Reye syndrome and intravenous tetracycline particularly when given to pregnant women. For agents that inhibit mitochondrial DNA synthesis and cause mitochondrial failure as a result of lack of replacement of mitochondria, such as the nucleoside analogues, this syndrome arises after 2 to 3 months of continuous therapy. Symptoms. Initial symptoms are nonspecific and vague and include nausea, poor appetite, weight loss and abdominal discomfort. These prodromal symptoms precede evidence of hepatic injury by 1 to 4 weeks. With onset of lactic acidosis, shortness of breath and weakness arise followed by stupor and coma. Jaundice occurs late and is usually mild. Once lactic acidosis is present, this syndrome is life threatening. Serum Enzyme Elevations. Serum aminotransferase levels are usually minimally elevated even with the onset of hepatic failure. Decrease in serum albumin, prolongation of prothrombin time, appearance of hyperammonemia, hypoglycemia and lactic acidosis often pre Continue reading >>

American Thoracic Society - Liver Dysfunction And Severe Lactic Acidosis In A Previously Healthy Man

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 >>

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