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 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 >>
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 >>
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 >>
8.1 Lactic Acidosis
Lactic acidosis is a common cause of metabolic acidosis. 1,2,3 Each day the body has an excess production of about 1500 mmols of lactate (about 20 mmols/kg/day) which enters the blood stream and is subsequently metabolised mostly in the liver. This internal cycling with production by the tissues and transport to and metabolism by the liver and kidney is known as the Cori cycle. This normal process does not represent any net fixed acid production which requires excretion from the body. All tissues can produce lactate under anaerobic conditions but tissues with active glycolysis produce excess lactate from glucose under normal conditions and this lactate tends to spill over into the blood. Lactate is produced from pyruvate in a reaction catalysed by lactate dehydrogenase: This reaction is so rapid that pyruvate and lactate can be considered to be always in an equilibrium situation. Normally the ratio of lactate to pyruvate in the cell is 10 to 1. The ratio [NADH]/[NAD+] by the Law of Mass Action determines the balance between lactate and pyruvate. This ratio is also used to denote the redox state within the cytoplasm. Lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH. In the extracellular fluid, the H+ titrates bicarbonate on a one for one basis. Lactate is released from cells into the ISF and blood. At rest, the tissues which normally produce excess lactate are: During heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate.( 4,5 ) During pregnancy, the placenta is an important producer of lactate which passes into both the maternal and the foetal circulations. Lactate is metabolised predominantly in the liver (60%) and kidney (30%) 6 . Half is converted to glucose (gluconeogenesis) and Continue reading >>
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 >>
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 >>
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Lactic Acidosis Update For Critical Care Clinicians
Lactic Acidosis Update for Critical Care Clinicians Franz Volhard Clinic and Max Delbrck Center for Molecular Medicine, Medical Faculty of the Charit Humboldt University of Berlin, Berlin, Germany. Correspondence to Dr. Friedrich C. Luft, Wiltberg Strasse 50, 13125 Berlin, Germany. Phone: 49-30-9417-2202; Fax: 49-30-9417-2206; E-mail: luft/{at}fvk-berlin.de Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO3 increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO3 is of little value. Carbicarb is a mixture of Na2CO3 and NaHCO3 that buffers similarly to NaHCO3 but without net generation of CO2. The results from animal stud Continue reading >>
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 >>
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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 >>
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A Patient With Acute Liver Failure And Extreme Hypoglycaemia With Lactic Acidosis Who Was Not In Coma: Causes And Consequences Of Lactate-protected Hypoglycaemia
Background: Hepatotoxicity induced by malaria infection is commonly a significant cause of morbidity and mortality among humans. Hence, finding of medicinal plants that have hepatoprotective activity are urgently needed. Therefore, this study aimed to evaluate hepatoprotective effect of aqueous crude extract of Thunbergia laurifolia leaves against Plasmodium berghei infected mice. Methods: Aqueous crude extract of T. laurifolia leaves was prepared and tested for hepatoprotective effect in P. berghei infected mice. The standard 4-day suppressive test was undertaken in groups of ICR mice infected with 1x10 7 parasitized erythrocytes, and then orally treated with the extract at doses of 1000, 2000, and 4000 mg/kg for 4 consecutive days. Pyrimethamine (1 mg/kg) was used as positive control, and combination treatment with 4000 mg/kg of extract was also determined. All liver markers were subsequently measured including aspartate aminotransferase (AST), alanine aminotransferase (ALT), cholesterol, and albumin. Results: Hepatotoxicity was induced by malaria infection in mice as indicated by progressive increase of AST and ALT, and markedly decrease of cholesterol and albumin, particularly stared on day 4 after infection. Interestingly, hepatoprotective effect was found in infected mice treated with the extract in dose-dependent manner as indicated by the similar levels of all liver markers to normal mice, and the highest activity was found at dose of 4000 mg/kg. Moreover, combination treatment of pyrimethamine and the extract was recommended. Additionally, prolong survival time of infected mice treatment with the extract was also found. No side effect on normal mice of this extract was observed. Conclusion: Aqueous crude extract of T. laurifolia leaves presented hepatoprotecti Continue reading >>
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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 >>
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 >>
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 >>
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 >>
