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Metabolic Acidosis In Sepsis Pathophysiology

Week 4 - Pathophysiology Of Sepsis, Shock

Week 4 - Pathophysiology Of Sepsis, Shock

What defines sepsis (something + something)? infection + systemic inflammatory response (SIRS) temperature > 38 C or <36 C, HR > 90 bpm, respirations > 20/min, WBC count >12,000/mm3 or <4000/mm or >10% immature neutrophils sepsis with >1 sign of organ failure - respiratory, hepatic, hematologic, CNS, metabolic acidosis What are the signs of neurologic organ failure? altered consciousness, confusion, psychosis What are the signs of respiratory organ failure? tachypnea, PaO2 <70 mmHg, SaO2 <90%, PaO2/FiO2 < 300 What are the signs of hepatic organ failure? jaundice, increased enzymes, decreased albumin, increased PT What are the signs of cardiovascular organ failure? tachycardia, hypotension, altered CVP, altered PAOP What are the signs of renal organ failure? What are the signs of coagulation (organ) failure? decreased platelets, increased PT/APTT, decreased protein C, increased D dimer sepsis with signs of end organ profusion deficiency: MAP < 65 mmHg or lactate > 4 mmol/L Is severe sepsis increasing or decreasing in incidence? Why is the incidence of sepsis increasing? aging population, increased use of immunomodulating therapy, longer survival in cancer patients, increased transplantation What are the main groups of organisms causing sepsis (3)? gram negative bacteria, gram positive bacteria, fungi What is the most common site of infection in severe sepsis? Continue reading >>

Sepsis And Septic Shock

Sepsis And Septic Shock

(Video) How to do Cardiopulmonary Resuscitation (CPR) in Adults By Paul M. Maggio, MD, MBA, Associate Professor of Surgery, Associate Chief Medical Officer, and Co-Director, Critical Care Medicine, Stanford University Medical Center Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection. In septic shock, there is critical reduction in tissue perfusion; acute failure of multiple organs, including the lungs, kidneys, and liver, can occur. Common causes in immunocompetent patients include many different species of gram-positive and gram-negative bacteria. Immunocompromised patients may have uncommon bacterial or fungal species as a cause. Signs include fever, hypotension, oliguria, and confusion. Diagnosis is primarily clinical combined with culture results showing infection; early recognition and treatment is critical. Treatment is aggressive fluid resuscitation, antibiotics, surgical excision of infected or necrotic tissue and drainage of pus, and supportive care. Sepsis represents a spectrum of disease with mortality risk ranging from moderate (eg, 10%) to substantial (eg, > 40%) depending on various pathogen and host factors along with the timeliness of recognition and provision of appropriate treatment. Septic shock is a subset of sepsis with significantly increased mortality due to severe abnormalities of circulation and/or cellular metabolism. Septic shock involves persistent hypotension (defined as the need for vasopressors to maintain mean arterial pressure 65 mm Hg, and a serum lactate level > 18 mg/dL [2 mmol/L] despite adequate volume resuscitation [1] ). The concept of the systemic inflammatory response syndrome (SIRS), defined by certain abnormalities of vital signs and laboratory results, has long 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 >>

Sepsis Pathophysiology

Sepsis Pathophysiology

-> Gram +ve cocci (staphylococci, streptococci) -> Gram ve bacilli (E.coli, Klebsiella, Pseudomonas aeruginosa) NF-KB = nuclear factor-KB -> induction of immune response genes pathogen binds to toll-like receptors (TLRs) on surface of immune cells (monocytes) -> increased NO synthase activity on endothelial cells -> endothelial injury and activation of coagulation cascade Inflammation > neutrophil chemotaxis, increased capillary permeability, macrophage activation, lytic enzyme induction Fibrinolytic pathway suppression > decreased APC and tPa activity -> decreased plasmin production = microvascular thrombosis -> ischaemia -> organ dysfunction -> death DO2 increased in septic shock from increased Q VO2 increased c/o raised tissue metabolic activity -> mitochondrial dysfunction impaired regional microvascular blood flow & autoregulation mitochondrial dysfunction with impaired pyruvate oxidation excess catecholamines may impair hepatic lactate extraction (by reducing regional hepatic blood flow) lactate clearance is decreased because pyruvate dehydrogenase activity is reduced in both skeletal muscle and liver. tissue hypoxia may not be a major mechanism & NMR spectroscopy suggests that hyperlactaemia may occur without tissue hypoxia net lactate production from the hepatosplanchnic bed is uncommon in sepsis Andrades M, Morina A, Spasi S, Spasojevi I. Bench-to-bedside review: sepsis from the redox point of view. Critical care. 15(5):230. 2011. [ pubmed ] [ free full text ] Angus DC, van der Poll T. Severe sepsis and septic shock. The New England journal of medicine. 369(9):840-51. 2013. [ pubmed ] Annane D, Bellissant E, Cavaillon JM. Septic shock. Lancet (London, England). 365(9453):63-78. 2005. [ pubmed ] Bosmann M, Ward PA. The inflammatory response in sepsis. Trends in Continue reading >>

Septic Shock: Practice Essentials, Background, Pathophysiology

Septic Shock: Practice Essentials, Background, Pathophysiology

Sepsis is defined as life-threatening organ dysfunction due to dysregulated host response to infection, and organ dysfunction is defined as an acute change in total Sequential Organ Failure Assessment (SOFA) score greater than 2 points secondary to the infection cause. [ 1 ] Septic shock occurs in a subset of patients with sepsis and comprises of an underlying circulatory and cellular/metabolic abnormality thatis associated with increased mortality. Septic shock is defined by persisting hypotension requiring vasopressors to maintain a mean arterial pressure of65 mm Hg or higher and a serum lactate level greater than 2 mmol/L (18 mg/dL) despite adequate volume resuscitation. [ 1 ] This new 2016 definition, also called Sepsis-3, eliminates the requirement for the presence of systemic inflammatory response syndrome (SIRS) to define sepsis, and it removed the severe sepsis definition. What was previously called severe sepsis is now the new definition of sepsis. Detrimental host responses to infection occupy a continuum that ranges from sepsis to severe sepsis to septic shock and multiple organ dysfunction syndrome (MODS). The specific clinical features depend on where the patient falls on that continuum. Signs and symptoms of sepsis are often nonspecific and include the following: Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23. 315 (8):801-10. [Medline] . Solomkin JS, Mazuski JE, Bradley JS, Rodvold KA, Goldstein EJ, Baron EJ, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis. 2010 Jan Continue reading >>

Metabolic Acidosis In Patients With Sepsis: Epiphenomenon Or Part Of The Pathophysiology?

Metabolic Acidosis In Patients With Sepsis: Epiphenomenon Or Part Of The Pathophysiology?

Metabolic acidosis in patients with sepsis: epiphenomenon or part of the pathophysiology? Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 1526, USA. To review the mechanisms of metabolic acidosis in sepsis. Articles and published reviews on metabolic acidosis in sepsis. Sepsis affects millions of patients each year and efforts to limit mortality have been limited. It is associated with many features one of which is acidosis which may be a result of the underlying pathophysiology (e.g. respiratory failure, shock, renal failure) or may also result from the way in which we manage critically ill patients. Lactic acidosis identifies septic patients at risk and aggressive fluid resuscitation (along with inotropes and blood in some patients) to reverse acidosis and improve venous oxygen saturation will improve mortality. However, most patients with severe sepsis or septic shock receive 0.9% saline and therefore may develop hyperchloraemic acidosis as a consequence of their resuscitation. Therefore alterations in acid-base balance are almost always in the background in the management of patients with sepsis. What is unknown is whether acidosis is in the causal pathway for organ dysfunction or whether it is simply an epiphenomenon. Changes in acid-base balance, of the type and magnitude commonly encountered in patients with sepsis, significantly alter the release of inflammatory mediators. Less significant changes in the immune response have already been implicated in influencing outcome for patients with sepsis and a reduction in acidosis in septic patients may have the same effect. Understanding the effects of acid-base on the inflammatory response is relevant as all forms of metabolic acidosis appear to be associated with pro Continue reading >>

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting Ganesh K, Sharma R N, Varghese J, Pillai M - Int J Crit Illn Inj Sci

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting Ganesh K, Sharma R N, Varghese J, Pillai M - Int J Crit Illn Inj Sci

Metabolic acidosis is frequently found in patients with severe sepsis. Several studies have shown that the amount of metabolic acidosis and its evolution over hospital stay has an effect on the prognosis. However, the precise composition of metabolic acidosis in these patients is not well known. Metabolic acidosis in severe sepsis may be secondary to lactic acidosis, but studies have shown that there is an unidentified anion contributing to high anion gap metabolic acidosis in addition to lactate. [1] Alterations in acid-base balance occur both as part of the pathophysiology of the underlying disease and as part of therapeutic interventions. [2] Thus, an understanding of types of acidosis in sepsis and their evolution over the course of treatment may give us insight into the behavior of acid-base balance in these patients. To describe at Intensive Care Unit (ICU) admission and over the first 5 days the composition of metabolic acidosis in patients with sepsis and to evaluate and compare acidosis patterns in survivors and non survivors. It was a prospective study conducted at Amrita Institute of Medical Sciences, Kochi, Kerala, in the Department of Internal Medicine and done on patients with sepsis as defined by the standard criteria. ICU consecutive patients admitted in the medical ICU with sepsis and metabolic acidosis were assessed. This sample size had an allowable error of 28% on the estimate of mortality. Arterial blood gas and serum electrolytes were measured during the first 5 days of admission or until death, renal replacement, or discharge supervened. The arbitrary period of 5 days was decided based on previous studies conducted. [3] Hereafter, for the purpose of discussion, day 1 indicates the day of admission and last day indicates either day 5 after admissi Continue reading >>

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris 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. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and 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 >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Relationship Between Oxygen Demand And Oxygen Supply In Severe Sepsis

Relationship Between Oxygen Demand And Oxygen Supply In Severe Sepsis

Relationship Between Oxygen Demand and Oxygen Supply in Severe Sepsis Severe sepsis is characterized by an increase in oxygen demand, which is related to the inflammatory response to severe infection or other types of serious injury. This inflammatory process is simultaneously responsible for the peripheral alterations associated with sepsis. The pathophysiology of the alterations in systemic oxygen extraction is complex and can include: (a) microvascular obstruction by the activated cellular elements, (b) the release of various circulating mediators, and (c) alterations in endothelial cells resulting in a reduction in arteriolar tone, an abnormal distribution of blood flow, and the formation of peripheral edema that may compress the microvasculature and increase the diffusion gradient for oxygen from the capillaries to the mitochondria. Septic ShockSevere SepsisLactic AcidosisTissue HypoxiaAdult Respiratory Distress Syndrome 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. Abel FL (1989) Myocardial function in sepsis and endotoxin shock. Am J Physiol 257:R1265R1281. PubMed Google Scholar Weisel R, Vito L, Dennis R, Valeri R, Hechtman H (1977) Myocardial depression during sepsis. Am J Surg 144:510521. Google Scholar Vincent JL, Weil MH, Puri V, Carlson RW (1981) Circulatory shock associated with purulent peritonitis. Am J Surg 142:262270. PubMed CrossRef Google Scholar Parker MM, Shelhamer JH, Bacharach SL et al (1984) Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 100:483490. PubMed Google Scholar Vincen Continue reading >>

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Kimmoun et al.; licensee BioMed Central.2015 The Erratum to this article has been published in Critical Care 2017 21:40 Lactic acidosis is a very common biological issue for shock patients. Experimental data clearly demonstrate that metabolic acidosis, including lactic acidosis, participates in the reduction of cardiac contractility and in the vascular hyporesponsiveness to vasopressors through various mechanisms. However, the contributions of each mechanism responsible for these deleterious effects have not been fully determined and their respective consequences on organ failure are still poorly defined, particularly in humans. Despite some convincing experimental data, no clinical trial has established the level at which pH becomes deleterious for hemodynamics. Consequently, the essential treatment for lactic acidosis in shock patients is to correct the cause. It is unknown, however, whether symptomatic pH correction is beneficial in shock patients. The latest Surviving Sepsis Campaign guidelines recommend against the use of buffer therapy with pH 7.15 and issue no recommendation for pH levels <7.15. Furthermore, based on strong experimental and clinical evidence, sodium bicarbonate infusion alone is not recommended for restoring pH. Indeed, bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. This review addresses the principal hemodynamic consequences of shock-associated lactic acidosis. Despite the lack of formal evidence, this review also highlights the various adapted supportive therapy options that could be putatively added to causal treatment in attempting to reverse the hemodynamic consequences of shock-associated lactic Continue reading >>

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 >>

Acidbase Disturbances In Intensive Care Patients: Etiology, Pathophysiology And Treatment

Acidbase Disturbances In Intensive Care Patients: Etiology, Pathophysiology And Treatment

Acidbase disturbances in intensive care patients: etiology, pathophysiology and treatment Center for Critical Care Nephrology, CRISMA Center, Department of Critical Care Medicine Correspondence and offprint requests to: John A. Kellum; E-mail: [email protected] Search for other works by this author on: Center for Critical Care Nephrology, CRISMA Center, Department of Critical Care Medicine Nephrology Dialysis Transplantation, Volume 30, Issue 7, 1 July 2015, Pages 11041111, Mohammed Al-Jaghbeer, John A. Kellum; Acidbase disturbances in intensive care patients: etiology, pathophysiology and treatment, Nephrology Dialysis Transplantation, Volume 30, Issue 7, 1 July 2015, Pages 11041111, Acidbase disturbances are very common in critically ill and injured patients as well as contribute significantly to morbidity and mortality. An understanding of the pathophysiology of these disorders is vital to their proper management. This review will discuss the etiology, pathophysiology and treatment of acidbase disturbances in intensive care patientswith particular attention to evidence from recent studies examining the effects of fluid resuscitation on acidbase and its consequences. acidbase physiology , acidosis , alkalosis , anion gap , strong ion difference The modern intensive care unit is a place where complex acidbase and electrolyte disorders are common, with one study, showing that 64% of critically ill patients have acute metabolic acidosis [ 1 ]. Although it is generally believed that most cases of acidbase derangement are mild and self-limiting, extremes of blood pH in either direction, especially when happening quickly, can have significant multiorgan consequences. Advances in evaluating acidbase balance have helped in understanding the impact of fluids in the critic Continue reading >>

Understanding Lactate In Sepsis & Using It To Our Advantage

Understanding Lactate In Sepsis & Using It To Our Advantage

You are here: Home / PULMCrit / Understanding lactate in sepsis & Using it to our advantage Understanding lactate in sepsis & Using it to our advantage Once upon a time a 60-year-old man was transferred from the oncology ward to the ICU for treatment of neutropenic septic shock. Over the course of the morning he started rigoring and dropped his blood pressure from 140/70 to 70/40 within a few hours, refractory to four liters of crystalloid. In the ICU his blood pressure didn't improve with vasopressin and norepinephrine titrated to 40 mcg/min. His MAP remained in the high 40s, he was mottled up to the knees, and he wasn't making any urine. Echocardiography suggested a moderately reduced left ventricle ejection fraction, not terrible but perhaps inadequate for his current condition. Dobutamine has usually been our choice of inotrope in septic shock. However, this patient was so unstable that we chose epinephrine instead. On an epinephrine infusion titrated to 10 mcg/min his blood pressure improved immediately, his mottling disappeared, and he started having excellent urine output. However, his lactate level began to rise. He was improving clinically, so we suspected that the lactate was due to the epinephrine infusion. We continued the epinephrine, he continued to improve, and his lactate continued to rise. His lactate level increased as high as 15 mM, at which point the epinephrine infusion was being titrated off anyway. Once the epinephrine was stopped his lactate rapidly normalized. He continued to improve briskly. By the next morning he was off vasopressors and ready for transfer back to the ward. This was eye-opening. It seemed that the epinephrine infusion was the pivotal intervention which helped him stabilize. However, while clinically improving him, the epineph Continue reading >>

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