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Lactic Acidosis An Update

Lactic Acidosis | Nejm

Lactic Acidosis | Nejm

This article is available to subscribers. Subscribe now . Already have an account? Sign in Review Article Disorders of Fluids and ElectrolytesFree Preview When lactic acidosis accompanies low-flow states or sepsis, mortality rates increase sharply. This review summarizes our current understanding of the pathophysiological aspects of lactic acidosis, as well as the approaches to its diagnosis and management. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. Dr. Kraut reports holding pending patents related to the use of selective NHE1 inhibitors in the treatment of metabolic acidosis (lapsed without the filing of a nonprovisional application) and systems, methods, and compositions for improved treatment of acidosis. No other potential conflict of interest relevant to this article was reported. From Medical and Research Services, Membrane Biology Laboratory, and the Division of Nephrology, David Geffen School of Medicine, University of California, Los Angeles, and the Veterans Affairs Greater Los Angeles Healthcare System both in Los Angeles (J.A.K.); and the Department of Medicine, Division of Nephrology, St. Elizabeths Medical Center, and the Department of Medicine, Tufts University School of Medicine both in Boston (N.E.M.). Address reprint requests to Dr. Kraut at the Division of Nephrology, VHAGLA Healthcare System, 11301 Wilshire Blvd., Los Angeles, CA 90073; or at [emailprotected] ; or to Dr. Madias at the Department of Medicine, St. Elizabeths Medical Center, 736 Cambridge St., Boston, MA 02135, or at [emailprotected] . Continue reading >>

Differential Diagnosis Of Elevated Serum Lactate 1,2

Differential Diagnosis Of Elevated Serum Lactate 1,2

Sinus tachycardia, LVH, secondary repolarization abnormalities No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax. No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis. Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening. There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities. Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance. The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified. Despite the patients reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patients significant lower extremity edema was more suggestive of chronic venous stasis. One notable laboratory abnormality that Continue reading >>

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some people's bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus , especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acidosis is higher in people with diabetes who Continue reading >>

Lactic Acidosis: An Update

Lactic Acidosis: An Update

Clinical Chemistry and Laboratory Medicine (CCLM) Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R. Source Normalized Impact per Paper (SNIP) 2016: 1.112 [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * *Prices in US$ apply to orders placed in the Americas only. Prices in GBP apply to orders placed in Great Britain only. Prices in represent the retail prices valid in Germany (unless otherwise indicated). Prices are subject to change without notice. Prices do not include postage and handling if applicable. RRP: Recommended Retail Price. Department of Anaesthesia and Critical Care, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Department of Clinical Chemistry, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Published Online: 2016-08-15 | DOI: Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences Continue reading >>

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further clarifying the relationship between metformin, acute kidney injury and lactic acidosis Subscribe to Nature Reviews Nephrology for full access: Diabetes mellitus: complex interplay between metformin, AKI and lactic acidosis Bell, S., Soto-Pedre, E., Connelly, P., Livingstone, S. & Pearson, E. Clarifying the relationship between metformin, acute kidney injury and lactic acidosis . Nat. Rev. Nephrol. , (2017). Rhee, C. M., Kovesdy, C. P. & Kalantar-Zadeh, K. Risks of metformin in type 2 diabetes and chronic kidney disease: lessons learned from Taiwanese data Risk of acute kidney injury and survival in patients treated with metformin: an observational cohort study Acute kidney injury, plasma lactate concentrations and lactic acidosis in metformin users: a GoDarts study . Diabetes Obes. Metab. 19, 1579–1586 (2017). Inzucchi, S. E., Lipska, K. J., Mayo, H., Bailey, C. J. & McGuire, D. K. Metformin in patients with type 2 diabetes and kidney disease: a systematic review Restricting metformin in CKD: continued caution warranted . Am. J. Kidney Dis. 66, 1101–1102 (2015). Should restrictions be relaxed for metformin use in chronic kidney disease? Yes, they should be relaxed! What's the fuss? Should restrictions be relaxed for metformin use in chronic kidney disease? No, we should never again compromise safety! Metformin in chronic kidney disease: more harm than help? Lancet Diabetes Endocrinol. 3, 579–581 (2015). Metformin use in type 2 diabetes mellitus With CKD: is it time to liberalize dosing recommendations? Kalantar-Zadeh, K., Uppot, R. N. & Lewandrowski, K. B. Case records of the Massachusetts General Hospital. Case 23–2013. A 54-year-old woman with abdominal pain, vomiting, and confusion United States Renal Data System. USRDS 2017 Annual Data Report: Atlas Continue reading >>

Lactic Acidosis

Lactic Acidosis

WHAT YOU NEED TO KNOW: What is lactic acidosis and what causes it? Lactic acidosis is the buildup of lactic acid in your blood. Lactic acid is a substance that can build up in your body if you are not getting enough oxygen. It can also occur if you have a condition that causes an increased need for oxygen. The following may cause lactic acidosis: Shock from trauma or severe blood loss Sepsis (a serious condition that occurs when the body overreacts to an infection) Seizures Heart attack or heart failure Severe lung disease Liver or kidney disease Cancer or AIDS Diabetic ketoacidosis Certain medicines such as metformin (diabetes medicine) or some HIV medicines Intense exercise What are the signs and symptoms of lactic acidosis? Muscular weakness Breathing faster than normal Nausea and vomiting Coma How is lactic acidosis diagnosed and treated? Lactic acidosis is diagnosed with a blood test. The blood test measures the amount of lactate in your blood. Treatment depends on the cause of your lactic acidosis. The condition that caused lactic acidosis will need to be treated. When should I contact my healthcare provider? Your symptoms return. You have questions or concerns about your condition or care. Care Agreement You have the right to help plan your care. Learn about your health condition and how it may be treated. Discuss treatment options with your caregivers to decide what care you want to receive. You always have the right to refuse treatment. The above information is an educational aid only. It is not intended as medical advice for individual conditions or treatments. Talk to your doctor, nurse or pharmacist before following any medical regimen to see if it is safe and effective for you. © 2017 Truven Health Analytics Inc. Information is for End User's use only and Continue reading >>

Acute Lactic Acidosis

Acute Lactic Acidosis

Author: Bret A Nicks, MD, MHA; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Metabolic acidosis is defined as a state of decreased systemic pH resulting from either a primary increase in hydrogen ion (H+) or a reduction in bicarbonate (HCO3-) concentrations. In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in PaCO2. Chronically, renal compensation occurs by means of reabsorption of HCO3. [ 1 , 2 ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may result from numerous conditions. [ 2 , 3 , 4 ] It remains the most common cause of metabolic acidosis in hospitalized patients. The normal blood lactate concentration in unstressed patients is0.5-1 mmol/L. Patients with critical illness can be considered to have normal lactate concentrations of less than 2 mmol/L. Hyperlactatemia is defined as a mild to moderate persistent increase in blood lactate concentration (2-4 mmol/L) without metabolic acidosis, whereas lactic acidosis is characterized by persistently increased blood lactate levels (usually >4-5 mmol/L) in association with metabolic acidosis. [ 1 , 5 ] Elevated lactate levels, while typically thought of as a marker of inadequate tissue perfusion with concurrent shift toward increased anaerobic metabolism, can be present in patients in whom systemic hypoperfusion is not present and therefore should be considered wit Continue reading >>

D-lactic Acidosis In Humans: Review Of Update

D-lactic Acidosis In Humans: Review Of Update

Your browser does not support the NLM PubReader view. Go to this page to see a list of supporting browsers. D-Lactic Acidosis in Humans: Review of Update Electrolyte Blood Press. 2006 Mar;4(1):53-56. Electrolyte Blood Press. 2006 Mar;4(1):53-56. English. Published online March 31, 2006. Copyright 2006 The Korean Society of Electrolyte and Blood Pressure Research D-Lactic Acidosis in Humans: Review of Update Kyung Pyo Kang, M.D.,Sik Lee, M.D. and Sung Kyew Kang, M.D. Department of Internal Medicine, and Research Institute of Clinical Medicine, Chonbuk National University Medical School, Chonbuk, Korea. Correspondence author: Sung Kyew Kang, M.D., Department of Internal Medicine, Chonbuk National University Medical School, Chonbuk, Korea. Tel: 063)250-1677, Fax: 063)254-1609, Email: [email protected] This article has been cited by 2 articles inPubMed Central. D-Lactic acidosis has been well documented in ruminants. In humans, D-lactic acidosis is very rare, but D-lactic acidosis may be more common than generally believed and should be looked for in a case of metabolic acidosis in which the cause of acidosis is not apparent. The clinical presentation of D-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The entity should be considered as a diagnosis in a patient who presents with metabolic acidosis accompanied by high anion gap, normal lactate level, negative Acetest, history of short bowel syndrome or malabsorption, and characteristic neurologic manifestations. Low carbohydrate diet, bicarbonate treatment, rehydration, and oral antibiotics would be helpful in controlling symptoms. Keywords: D-lactic acidosis; Metabolic acidosis; Humans D-Lactic acidosis has been well documented in ruminants. In humans, however, D-lactic acidosis is Continue reading >>

Metformin And Fatal Lactic Acidosis

Metformin And Fatal Lactic Acidosis

Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major Continue reading >>

Metformin-associated Lactic Acidosis Undergoing Renal Replacement Therapy In Intensive Care Units: A Five-million Population-based Study In The North-west Of Italy

Metformin-associated Lactic Acidosis Undergoing Renal Replacement Therapy In Intensive Care Units: A Five-million Population-based Study In The North-west Of Italy

Abstract Background: Metformin-associated lactic acidosis (MALA) is a severe complication of drug administration with significant morbidity and mortality. So far no study in large population areas have examined the incidence, clinical profile and outcome of acute kidney injury (AKI)-MALA patients admitted in intensive care units (ICUs) and treated by renal replacement therapy (MALA-RRT). Methods: Retrospective analysis over a 6-year period (2010-2015) in Piedmont and Aosta Valley regions (5,305,940 inhabitants, 141,174 diabetics treated with metformin) of all MALA-RRT cases. Results: One hundred and seventeen cases of AKI-MALA-RRT were observed (12.04/100,000 metformin treated diabetics, 1.45% of all RRT-ICU patients). Survival rate was 78.3%. The average duration of RRT was 4.0 days at mean dialysis effluent of 977 mL/kg/day. At admission most patients were dehydrated, and experienced shock and oliguria. Conclusion: Our data showed that MALA-RRT is a common complication, needing more prevention. Adopted policy of early, extended, continuous and high efficiency dialysis could contribute to an observed high survival rate. Video Journal Club “Cappuccino with Claudio Ronco” at © 2017 S. Karger AG, Basel Introduction Metformin, an old drug known for more than 45 years, is the first-line treatment for type 2 diabetes mellitus in the world [1]. Metformin reduces the risk of mortality and morbidity in diabetic population [2] and decreases insulin resistance [3]. Generally speaking, metformin is considered a safe drug, with some limitations. Due to increased risk of lactic acidosis, metformin is contraindicated in patients with organ dysfunction such as congestive heart failure, renal, or hepatic insufficiency, and in very elderly patients [4]. Since metformin prescription Continue reading >>

Role Of Lactate In Critically Ill Children Agrawal S, Sachdev A, Gupta D, Chugh K

Role Of Lactate In Critically Ill Children Agrawal S, Sachdev A, Gupta D, Chugh K

Lactic acidosis is a common finding in critically ill patients. It has been used as a prognostic marker of the outcome in Pediatric Intensive Care Unit patients. Lactic acid is produced as a product of anaerobic glycolysis and is reversibly converted to pyruvate in the presence of favorable metabolic environment. All the body tissues can produce and consume lactate with few having predominant function of production and others of consumption. Liver is a major organ for lactate consumption and it is the liver, which metabolizes the increased lactic acid produced in regional tissue beds.The lactate levels can be done on arterial, venous, or mixed venous blood and can be measured by various methods. Serial lactate concentrations and the difference in arterial and mixed venous lactate levels or between the arterial and regional blood lactate levels like jugular venous lactate levels have been shown to have better correlation with the outcome. High initial blood lactate levels and persistently high lactate levels have been correlated with poor outcome.There are various causes of lactic acid overproduction, which may produce either hyperlactatemia or lactic acidosis. High blood lactate levels are found in critically ill patients with shock of any etiology and sepsis due to various reasons, which include increased catecholamine induced glucose flux apart from the tissue hypoperfusion and hypoxia. Various other illnesses can cause an increase in blood lactate levels like acute lung/liver injury, severe asthma, poisoning, post cardiac surgery etc.Treating the underlying disease leading to lactic acidosis is the best measure to control lactic acidosis. Some therapeutic choices are available to neutralize the effect of lactic acid on cell function, but none has stood the test of t Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis is defined as a state of decreased systemic pH resulting from either a primary increase in hydrogen ion (H+) or a reduction in bicarbonate (HCO3-) concentrations. In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in PaCO2. Chronically, renal compensation occurs by means of reabsorption of HCO3. [ 1 , 2 ] Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may result from numerous conditions. [ 2 , 3 , 4 ] It remains the most common cause of metabolic acidosis in hospitalized patients. Cohen R, Woods H. Clinical and Biochemical Aspects of Lactic Acidosis. London, United Kingdom: Blackwell Scientific Publications; 1976. Suetrong B, Walley KR. Lactic acidosis in sepsis: It's not all anaerobic. Implications for diagnosis and management. Chest. 2015 Sep 17. [Medline] . Forrest DM, Russell JA. Metabolic acidosis. Webb A, Shapiro M, Singer M, Suter P, eds. Oxford Textbook of Critical Care. Oxford, United Kingdom: Oxford University Press; 1999. 573-7. Seheult J, Fitzpatrick G, Boran G. Lactic acidosis: an update. Clin Chem Lab Med. 2017 Mar 1. 55 (3):322-33. [Medline] . [Full Text] . Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med. 1992 Jan. 20(1):80-93. [Medline] . Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA. Lactate clearance vs central venous oxygen saturation as goal Continue reading >>

Review: Lactate & Sepsis

Review: Lactate & Sepsis

On this snowy, Stockholm Sunday, I look out from my quarters on the Mlardrottningen across the still, icy waters and I think about a cirrhotic patient for whom I recently cared. She presented with significant dyspnea as she had stopped taking her diuretics. Instead, she was using excessivedoses of her friends albuterol inhaler to treat her shortness of breath. Additionally, she had been drinking alcohol heavily for seven days prior to admission. Her venous pH was 7.38, and her lactate concentration was over 7.0 mmol/L a sepsis alert was called. In a very recent and fantastic review by Suetrong and Walley , the mechanisms of lactate formation are revisited. Notably, a distinction is made between hyperlactatemia an elevated concentration of lactate in the blood and lactic acidosis, which is comprised of both hyperlactatemia and systemic acidosis. The authors discuss the mechanisms by which lactate is formed and aptly detail that many of these processes do not result in acid formation. Notably, while the generation of pyruvate from glucose does generate [H+], the conversion of pyruvate to lactate consumes an equimolar amount of [H+] such that the production of lactate does not result in a net gain of protons [i.e. acidosis]. So where does the acidosis with which we are so familiar come from? The excess protons are the result of an impaired Krebs Cycle. In states of true tissue oxygen debt, intracellular protons can no longer be consumed during the Krebs Cycle; consequently, intracellular acidosis and acidemia ensue. It is this latter means of hyperlactatemia to which we attach the label type A or lactic acidosis with clinical evidence of tissue hypoxia. However, as described 40 years ago , excessive lactate may come from clinical states where there is no evidence of tissu Continue reading >>

Lactic Acidosis Update For Critical Care Clinicians

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 >>

Propofol Infusion Syndrome In Adults: A Clinical Update

Propofol Infusion Syndrome In Adults: A Clinical Update

Propofol Infusion Syndrome in Adults: A Clinical Update Department of Internal Medicine, Saint Joseph Hospital, 2900 N. Lake Shore, Chicago, IL 60657, USA Received 24 November 2014; Revised 21 March 2015; Accepted 28 March 2015 Copyright 2015 Aibek E. Mirrakhimov 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. Propofol infusion syndrome is a rare but extremely dangerous complication of propofol administration. Certain risk factors for the development of propofol infusion syndrome are described, such as appropriate propofol doses and durations of administration, carbohydrate depletion, severe illness, and concomitant administration of catecholamines and glucocorticosteroids. The pathophysiology of this condition includes impairment of mitochondrial beta-oxidation of fatty acids, disruption of the electron transport chain, and blockage of beta-adrenoreceptors and cardiac calcium channels. The disease commonly presents as an otherwise unexplained high anion gap metabolic acidosis, rhabdomyolysis, hyperkalemia, acute kidney injury, elevated liver enzymes, and cardiac dysfunction. Management of overt propofol infusion syndrome requires immediate discontinuation of propofol infusion and supportive management, including hemodialysis, hemodynamic support, and extracorporeal membrane oxygenation in refractory cases. However, we must emphasize that given the high mortality of propofol infusion syndrome, the best management is prevention. Clinicians should consider alternative sedative regimes to prolonged propofol infusions and remain within recommended maximal dose limits. Propofol is a sedative-hypnotic m Continue reading >>

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