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Can Sepsis Cause Metabolic Acidosis?

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 >>

Sepsis - Wikipedia

Sepsis - Wikipedia

For the genus of flies of this name, see Sepsis (genus) . Blood culture bottles: orange label for anaerobes , green label for aerobes , and yellow label for blood samples from children Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs. [8] Common signs and symptoms include fever , increased heart rate , increased breathing rate , and confusion . [1] There also may be symptoms related to a specific infection, such as a cough with pneumonia , or painful urination with a kidney infection . [2] In the very young, old, and people with a weakened immune system , there may be no symptoms of a specific infection and the body temperature may be low or normal, rather than high . [2] Severe sepsis is sepsis causing poor organ function or insufficient blood flow. [9] Insufficient blood flow may be evident by low blood pressure , high blood lactate , or low urine output . [9] Septic shock is low blood pressure due to sepsis that does not improve after reasonable amounts of intravenous fluids are given. [9] Sepsis is caused by an immune response triggered by an infection. [2] [3] Most commonly, the infection is bacterial , but it may also be from fungi , viruses , or parasites . [2] Common locations for the primary infection include lungs, brain, urinary tract , skin, and abdominal organs . [2] Risk factors include young or old age, a weakened immune system from conditions such as cancer or diabetes , major trauma , or burns . [1] An older method of diagnosis was based on meeting at least two systemic inflammatory response syndrome (SIRS) criteria due to a presumed infection. [2] In 2016, SIRS was replaced with qSOFA which is two of the following three: increased breathing rate, change in level of con Continue reading >>

Lactic Acidosis

Lactic Acidosis

Background 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 Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac 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 >>

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 >>

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 >>

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 >>

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 >>

Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine

Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine

Montagnani and Nardi: Lactic Acidosis, Hyperlactatemia and Sepsis Lactic Acidosis, Hyperlactatemia and Sepsis [1] Division of Internal Medicine, Misericordia Hospital, Grosseto [2] Division of Internal Medicine, Maggiore Hospital, Bologna, Italy Correspondence to: Ospedale Misericordia di Grosseto, via Senese, 58100 Grosseto, Italy. +39.0564.485330. [email protected] Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic a Continue reading >>

Metabolic Acidosis In Sepsis.

Metabolic Acidosis In Sepsis.

Intensive Care Unit, Emergency Department, Hospital das Clinicas, University of Sao Paulo Medical School, Sao Paulo, Brazil. Endocr Metab Immune Disord Drug Targets. 2010 Sep;10(3):252-7. Metabolic acidosis is very common in critically ill septic patients. Acidosis may be a result of the underlying pathophysiology, but it also may be the result of the way in which those patients are managed. Chloride-associated acidosis is frequent and is potentially aggravated during fluid resuscitation. The severity of metabolic acidosis is associated with poor clinical outcomes; however, it remains uncertain whether or not there is a causal relationship between acidosis and the pathophysiology of septic syndromes. Several experimental findings have demonstrated the impact of acidosis modulation on the release of inflammatory mediators and cardiovascular function. Treatment of metabolic acidosis is based on control of the underlying process and support of organ dysfunction, although the use of intravenous chloride-poor balanced solutions seems an attractive option to prevent the worsening of metabolic acidosis during fluid resuscitation. Continue reading >>

Physicochemical Characterization Of Metabolic Acidosis Induced By Normal Saline Resuscitation Of Patients With Severe Sepsis And Septic Shock

Physicochemical Characterization Of Metabolic Acidosis Induced By Normal Saline Resuscitation Of Patients With Severe Sepsis And Septic Shock

OBJECTIVE: The aim of this study was to characterize and quantify metabolic acidosis that was caused by initial volume expansion during the reanimation of patients with severe sepsis and septic shock. METHODS: A blood sample was drawn for physicochemical characterization of the patient's acid-base equilibrium both before and after volume expansion using 30 mL/kg 0.9% saline solution. The diagnosis and quantification of metabolic acidosis were based on the standard base excess (SBE). RESULTS: Eight patients with a mean age of 58 13 years and mean APACHE II scores of 20 4 were expanded using 2,000 370 mL of 0.9% saline solution. Blood pH dropped from 7.404 0.080 to 7.367 0.086 (p=0.018), and PCO2 increased from 30 5 to 32 2 mmHg (p=0.215); SBE dropped from -4.4 5.6 to -6.0 5.7 mEq/L (p=0.039). The drop in SBE was associated with the acidifying power of two factors, namely, a significant increase in the strong ion gap (SIG) from 6.1 3.4 to 7.7 4.0 mEq/L (p = 0.134) and a non-significant drop in the apparent inorganic strong ion differences (SIDai) from 40 5 to 38 4 mEq/L (p = 0.318). Conversely, the serum albumin levels decreased from 3.1 1.0 to 2.6 0.8 mEq/L (p = 0.003) with an alkalinizing effect on SBE. Increased serum chloride levels from 103 10 to 106 7 mEq/L (p < 0.001) led to a drop in SIDai. CONCLUSION: Initial resuscitation using 30 mL/kg of 0.9% saline solution for patients with severe sepsis and septic shock is associated with worsened metabolic acidosis, as measured by SBE. This worsened SBE can be ascribed to a serum increase in the levels of unmeasurable anions and chloride. Keywords: Ketosis; Intensive care units; Sepsis; Shock, septic/therapy; Acid-base equilibrium; Saline solution, hypertonic/therapeutic use In Brazil, approximately 26% of patients who ar Continue reading >>

Hypercapnia And Acidosis In Sepsis:a Double-edged Sword? | Anesthesiology | Asa Publications

Hypercapnia And Acidosis In Sepsis:a Double-edged Sword? | Anesthesiology | Asa Publications

The effects of hypercapnia in sepsis may be a function of the hypercapnia or the acidosis per se . As discussed, the effects of HCA on the immune response seem to be predominantly a function of the acidosis, rather than the hypercapnia per se , but the fact that the acidosis is hypercapnic rather than metabolic is of importance. The potential exists for hypercapnia to exert direct effects, independent of pH changes. A specific example is the binding of carbon dioxide to free amine groups on proteins to form carbamates, which can alter certain protein behavior or activity. The classic example is hemoglobin in which carbamino formation alters HbO2affinity. In addition, the potential for buffering of a HCA to modulate its effects in sepsis is also of importance. Buffered hypercapnia, that is, hypercapnia in the presence of normal pH, seems to worsen lung injury induced by intrapulmonary bacterial instillation. 36 To avoid the confounding effects of the administration of exogenous acid and/or alkali, animals were first exposed to environmental hypercapnia until renal buffering had restored pH to the normal range. These animals were then subjected to intrapulmonary inoculation of E. coli , and the severity of lung injury produced during a 6-h period was compared with that seen in similarly inoculated animals exposed to normocapnia. Buffered hypercapnia significantly increased E. coli -induced lung injury when compared with normocapnic controls, as assessed by arterial oxygenation, lung compliance, proinflammatory pulmonary cytokine concentrations, and measurements of structural lung damage. Of interest, buffered hypercapnia did not reduce the phagocytic capacity of neutrophils and did not increase lung bacterial load. These findings contrast markedly with the protective eff 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 >>

Causes Of Lactic Acidosis In Sepsis - Deranged Physiology

Causes Of Lactic Acidosis In Sepsis - Deranged Physiology

This topic is for some reason the subject of one frequently repeated question. Notable duplicates include the following: Question 6.4 from the first paper of 2013 (a detailed discussion is carried out here) Question 22.2 from the second paper of 2011 Question 6.4 from the first paper of 2011 Mechanisms responsible for lactic acidosis in sepsis Endogenous catecholamine release and use of catecholamine inotropes Circulatory failure due to hypoxia and hypotension Inhibition of pyruvate dehydrogenase (PDH) by endotoxin Slowed hepatic blood flow, impairing clearance So the lactate in sepsis is raised. What of it? The college seems to favour this concept as an exam topic. It has come up repeatedly in the past papers. It seems important for the trainees to understand that in septic shock the lactate elevation is not purely a feature of tissue hypoperfusion, but rather the outcome of complex metabolic changes. The mechanism of lactate elevation in sepsis is discussed in greater detail in a chapter dedicated to these metabolic changes . Instead of revisiting that elaborate explanation, I will instead produce some references, and this confusing flowchart diagram: Jones, Alan E., and Michael A. Puskarich. "Sepsis-induced tissue hypoperfusion." Critical care clinics25.4 (2009): 769. Continue reading >>

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting

A Profile Of Metabolic Acidosis In Patients With Sepsis In An Intensive Care Unit Setting

A profile of metabolic acidosis in patients with sepsis in an Intensive Care Unit setting Department of Internal Medicine, Amrita Institute of Medical Sciences, Kochi, Kerala, India 1Department of Emergency Medicine, Amrita Institute of Medical Sciences, Kochi, Kerala, India Address for correspondence: Dr. Kartik Ganesh, Department of Nephrology, Amrita Institute of Medical Sciences, Kochi - 682 041, Kerala, India. E-mail: [email protected] Author information Copyright and License information Disclaimer Copyright : International Journal of Critical Illness and Injury Science This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. This article has been cited by other articles in PMC. Metabolic acidosis is frequently found in patients with severe sepsis. An understanding of types of acidosis in sepsis and their evolution over the course of treatment may give us insight into the behavior of acidbase 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 nonsurvivors. A prospective study conducted at Amrita Institute of Medical Sciences, Kochi, Kerala, in the Department of Internal Medicine. Seventy-five consecutive patients admitted in the medical ICU with sepsis and metabolic acidosis were assessed. Arterial blood gas and serum electrolytes were measured during the first five days of admission or until death, renal replacement or discharge supervened. Continue reading >>

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