diabetestalk.net

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Curr Opin Crit Care. 2008 Aug;14(4):379-83. doi: 10.1097/MCC.0b013e3283069d5c. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? University of British Columbia, Critical Care Research Laboratories, Vancouver, British Columbia, Canada. Bicarbonate therapy for severe lactic acidosis remains a controversial therapy. The most recent 2008 Surviving Sepsis guidelines strongly recommend against the use of bicarbonate in patients with pH at least 7.15, while deferring judgment in more severe acidemia. We review the mechanisms causing lactic acidosis in the critically ill and the scientific rationale behind treatment with bicarbonate. There is little rationale or evidence for the use of bicarbonate therapy for lactic acidosis due to shock. We agree with the Surviving Sepsis guidelines recommendation against the use of bicarbonate for lactic acidosis for pH at least 7.15 and we further recommend a lower target pH of 7.00 or less. If bicarbonate is used, consideration must be given to slow infusion and a plan for clearing the CO2 that is produced and measuring and correcting ionized calcium as the resultant 10% drop may decrease cardiac and vascular contractility and responsiveness to catecholamines. When continuous renal replacement therapy is used during severe acidosis, we recommend bicarbonate-based replacement fluid over citrate as citrate may increase the strong ion gap. Effective therapy of lactic acidosis due to shock is to reverse the cause. Continue reading >>

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- and Intracellular Alkalinization Improves Cardiovascular Functions in Severe Lactic Acidosis Induced by Hemorrhagic Shock From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Bra Continue reading >>

Sodium Bicarbonate - Journal Of Emergency Medical Services

Sodium Bicarbonate - Journal Of Emergency Medical Services

Your paramedic crew responds to a cardiac arrest in a large shopping complex. Fortunately, the patient has all the links in the chain of survival in place. Bystander CPR has been initiated, and an automated external defibrillator (AED) was in place in the shopping complex and deployed, the 9-1-1 system was accessed, and your unit arrived rapidlywithin six minutes from the time of call. As you approach, you assess the situation, interview bystanders and begin the final linkearly advanced care. For patients in cardiac arrest, the American Heart Association (AHA) has determined this provides the best opportunity for someone to survive cardiac arrest in the prehospital environment. The patient remains in ventricular fibrillation (v fib) despite several AED shocks. You gain IV access and begin pharmacological therapy. After administering epinephrine and amiodarone, you consider sodium bicarbonate as directed by protocol. You recognize that over the past several years AHA has deemphasized the use of sodium bicarbonate. But what is the controversy? When is it appropriate to give sodium bicarbonate, and are paramedics using it to its fullest advantage? Seasoned paramedics will recall giving multiple ampules of sodium bicarbonate during a cardiac arrest, but today it appears to be an afterthought. Sodium bicarbonate (NaHCO3) is used primarily to combat acidosis, although its the treatment of choice in certain cases of overdose. It works by mixing with lactic acid that forms in low perfusion states and in periods of inadequate oxygenation, such as shock and cardiac arrest. It is then converted to a form of carbonic acid that turns into carbon dioxide, and in turn, is expelled through the lungs during ventilation. Primarily, NaHCO3 works as a buffer by mixing with acids within th Continue reading >>

Metabolic Acidosis; Gap Positive

Metabolic Acidosis; Gap Positive

Metabolic acidosis is defined by low serum pH (less than 7.35-7.45) and low serum bicarbonate. It occurs by one of three major mechanisms: 1. Increased endogenous acid (i.e., lactic acidosis, diabetic ketoacidosis). 2. Decreased renal acid excretion (i.e., renal failure). In determining the underlying etiology for a metabolic acidosis, the serum anion gap must be calculated by subtracting the major measured anions (chloride and bicarbonate) from the major measured cation (sodium). If the result is greater than 12 meq/L (which is the normal value for most laboratories), the acidosis is said to be an anion gap acidosis. The expected anion gap should is lower in hypoalbuminemia and should be corrected - for each decrease of 1gm/dl in albumin, the normal anion gap should be decreased by approximately 2.5 meq/L. A. What is the differential diagnosis for this problem? Anion gap acidosis can be the result from: 1. A fall in unmeasured cations (as seen in hypomagnesemia or hypocalcemia). The most common reasons for a rise in anions are ingestions, lactic acidosis, ketoacidosis and renal failure. Ingestions of multiple different toxins can result in unmeasured anions causing a metabolic gap acidosis. Most commonly salicylate and the alcohols (methanol and ethylene glycol) can lead to severe acidosis. The inhalant toluene may also be a culprit. Lactic acidosis is the most common cause of an elevated anion gap acidosis in hospitalized patients, occurring with decreased perfusion causing relative tissue ischemia. This leads to increased lactic acid production and impaired renal excretion with resultant acid accumulation (Type A lactic acidosis). Type B lactic acidosis occurs in patients without overt tissue and can be seen in diabetics on metformin, patients with hematologic and s Continue reading >>

Sodium Bicarbonate (baking Soda): Side Effects, Dosages, Treatment, Interactions, Warnings

Sodium Bicarbonate (baking Soda): Side Effects, Dosages, Treatment, Interactions, Warnings

What Is Sodium Bicarbonate and How Does It Work? Sodium bicarbonate is indicated in the treatment of metabolic acidosis which may occur in severe renal disease , uncontrolled diabetes , circulatory insufficiency due to shock or severe dehydration , extracorporeal circulation of blood , cardiac arrest and severe primary lactic acidosis . Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate- protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products. Sodium bicarbonate also is indicated in severe diarrhea , which is often accompanied by a significant loss of bicarbonate. Treatment of metabolic acidosis should, if possible, be superimposed on measures designed to control the basic cause of the acidosis e.g., insulin in uncomplicated diabetes, blood volume restoration in shock. But since an appreciable time interval may elapse before all of the ancillary effects are brought about, bicarbonate therapy is indicated to minimize risks inherent to the acidosis itself. Vigorous bicarbonate therapy is required in any form of metabolic acidosis where a rapid increase in plasma total CO2 content is crucial e.g., cardiac arrest, circulatory insufficiency due to shock or severe dehydration, and in severe primary lactic acidosis or severe diabetic acidosis. Adult and Pediatric Dosage Forms and Strengths Dosage Considerations Should be Given as Follows: Adult, Initial: 1 mEq/kg/dose intravenous (IV) x1; base subsequent doses on results of arterial blood pH and PaCO2 as well as calculation of base deficit Repeat doses may be considered in the se Continue reading >>

Sodium Bicarbonate - Intravenous (iv) Dilution

Sodium Bicarbonate - Intravenous (iv) Dilution

The authors make no claims of the accuracy of the information contained herein; and these suggested doses and/or guidelines are not a substitute for clinical judgment. Neither GlobalRPh Inc. nor any other party involved in the preparation of this document shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user's use of or reliance upon this material. PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER. Standard Dilutions [Amount of drug] [Infusion volume] [Infusion rate] May add ordered dose to empty viaflex bag or dilute in 50-1000ml. Monitor ABG's q2-3 hours to assess response. Administer IV either undiluted or diluted in other IV fluid (50-1000ml) depending on fluid status. Osmolarity: 2Na + gluc/18 + BUN/2.8 (nml: 280-295). **Note: treat hypokalemia or hypocalcemia first if present. In all cases, the primary goal in treating metabolic acidosis is to focus on reversal of the underlying process causing the acidosis. Examples: (1) Renal failure: dialysis if needed. (2) Alcoholic ketoacidosis: fluids, electrolytes, thiamine, folic acid. (3) Sepsis/shock: volume resuscitation, vasopressors, etc. (4) Salicylate intoxication: IV fluids, alkalinization of the urine, .... If there is a severe deficit (HCO3- < 10-12 mEq/L and pH<7.2) correct with sodium bicarbonate. Sodium bicarb is also useful if the acidosis is due to inorganic acids (especially if renal disease is present). However, when the acidosis results from organic acids (lactic acid, acetoacetic acid, etc) the role of bicarbonate is controversial. In most cases of DKA or sever lactic acidosis the administration of sodium bicarbonat Continue reading >>

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Is there a role for sodium bicarbonate in treating lactic acidosis from shock? 30 Jul 2008 | Controversial, Review / Commentary The review again brings to light the important issue of treatment of acute severe metabolic acidosis with base. The authors also summarize the mechanism of lactic acidosis and the evidence for and against base therapy and come to the conclusion that there is no support for this treatment presently when blood pH is higher than 7.15. The use of sodium bicarbonate in the treatment of severe lactic acidosis, defined as blood pH lower... To read the rest of this recommendation and access over 145,000 article recommendations from 3,700+ journals across biomedicine, register Send a recommendation to your institution's librarian or information manager to request an extended free trial for articles in biology and medicine, contributed inclusion in F1000Prime to help you filter recommendations, plus relevant articles as engine clusters of related articles and be alerted as soon as similar articles appear in If you think you should be able to access this content, please contact us . If you've forgotten your password, please enter your email address below and we'll send you instructions on how to reset your password. The email address should be the one you originally registered with F1000. Email address not recognised, please try again We are unable to reset your password, please contact [email protected] to reactivate your account, quoting error code UACC/DEL You registered with F1000 via Google, so we cannot reset your password. If you still need help with your Google account password, please click here . You registered with F1000 via Facebook, so we cannot reset your password. If you still need help with your Facebook account password, please click here . 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 >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany 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. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment of acute non-anion gap metabolic acidosis Medical and Research Services VHAGLA Healthcare System, Division of Nephrology, VHAGLA Healthcare System Correspondence to: Jeffrey A. Kraut; E-mail: [email protected] Search for other works by this author on: Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Jeffrey A. Kraut, Ira Kurtz; Treatment of acute non-anion gap metabolic acidosis, Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acidbase disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide migh Continue reading >>

Lactic Acidosis Treatment & Management

Lactic Acidosis Treatment & Management

Approach Considerations Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery. The former is addressed by various therapies, including administration of appropriate antibiotics, surgical drainage and debridement of a septic focus, chemotherapy of malignant disorders, discontinuation of causative drugs, and dietary modification in certain types of congenital lactate acidosis. Cardiovascular collapse secondary to hypovolemia or sepsis should be treated with fluid replacement. Both crystalloids and colloids can restore intravascular volume, but hydroxyethyl starch solutions should be avoided owing to increased mortality. [21] Excessive normal saline administration can cause a nongap metabolic acidosis due to hyperchloremia, which has been associated with increased acute kidney injury. [32] Balanced salt solutions such as Ringer lactate and Plasma-Lyte will not cause a nongap metabolic acidosis and may reduce the need for renal replacement therapy; however, these can cause a metabolic alkalosis. [33] No randomized, controlled trial has yet established the safest and most effective crystalloid. If a colloid is indicated, albumin should be used. Despite appropriate fluid management, vasopressors or inotropes may still be required to augment oxygen delivery. Acidemia decreases the response to catecholamines, and higher doses may be needed. Conversely, high doses may exacerbate ischemia in critical tissue beds. Careful dose titration is needed to maximize benefit and reduce harm. Lactic acidosis causes a compensatory increase in minute ventilation. Patients may be tachypneic initially, but respiratory muscle fatigue can ensue rapidly and mechanical ventilation may be necessary. Alkali therapy remains controversial Continue reading >>

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium bicarbonate in the critically Ill patient with metabolic acidosis Uso de bicarbonato de sdio na acidose metablica do paciente gravemente enfermo Lactic acidosis is an acid-base imbalance frequently found in critically ill patients. It is associated with a poor prognosis. Despite the substantial body of evidence that critical levels of acidemia have several adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains highly controversial. This article aimed at: 1) analyzing the main differences between hyperchloremic and organic acidoses, with high anion gap; 2) comparing the risks associated with critical levels of acidemia with those associated with the use of sodium bicarbonate; 3) critically analyzing the literature evidence about the use of sodium bicarbonate for the treatment of lactic acidosis in critically ill patients, with an emphasis on randomized control trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation. Descriptors: lactic acidosis, diabetic ketoacidosis, sodium bicarbonate, septic shock. A acidose ltica um distrbio do equilbrio cido-base muito frequente em pacientes internados em unidades de terapia intensiva e est associado a um mau prognstico. Embora exista um acmulo substancial de evidncias de que nveis crticos de acidemia provocam inmeros efeitos adversos sobre o funcionamento celular, a utilizao de bicarbonato de sdio para o tratamento da acidose ltica em pacientes gravemente enfermos permanece alvo de controvrsias. Neste artigo, pretendemos: 1) analisar as principais diferenas entre as acidoses hiperclormicas e as acidoses orgnicas, com nion gap (AG) elevado, visando embasar a discusso sobre os fundamentos da terapia Continue reading >>

Sodium Bicarbonate To Treat Severe Acidosis In The Critically Ill ((bicar-icu))

Sodium Bicarbonate To Treat Severe Acidosis In The Critically Ill ((bicar-icu))

Design: randomized multiple center clinical trial, open label Arms: intravenous 4.2% Sodium Bicarbonate vs no additional treatment Inclusion: age of 18 yo or above, critically ill patient with a SOFA score of 4 or above, lactatemia of 2mmol/l or above, with pH of 7.20 or below and PaCO2 of 45mmHg or below and bicarbonatemia of 20mmol/l or below Exclusion: single respiratory disorder (PaCO2 > 50 mmHg, Bicarbonatemia equal or higher than (PaCO2-40)/10 + 24 ; acute diarrhea, ileostomy or biliary drainage ; stage IV kidney failure or chronic dialysis ; tubular acidosis, ketoacidosis, high anion gap acids poisoning (PEG, aspirin, methanol) ; PaCO2 equal to 45mmHg or above and spontaneous breathing, pregnancy, protected patients, moribund patient (life expectancy of 48h or below) Randomization: website randomization with stratification on age, presence of sepsis at inclusion, renal failure Intervention: experimental arm: intravenous 4.2% Sodium Bicarbonate 125 to 250ml in 30min up to 1000ml/24h. The target is a plasma pH of 7.30 or above. An interim statistical analysis is planned when 200 patients will be included Evolution of the organ failure scores [TimeFrame:Day 0 to Day 28] use of SOFA score to assess the outcome 2 Duration of renal replacement therapy (days) [TimeFrame:Day 0 to Day 28] Duration of mechanical ventilation and ventilatory free days (days) [TimeFrame:Day 0 to Day 28] duration of mechanical ventilation and ventilatory free days Duration of vasopressors administration (h) [TimeFrame:Day 0 to Day 28] need for vasopressors and fluids using duration of vasopressor infusion (D0 to D28) Hospital acquired infections (incidence) [TimeFrame:Day 0 to Day 28] hospital acquired infections using United States Centers for Disease Control definitions and a dedicated docu Continue reading >>

Shock (circulatory) - Wikipedia

Shock (circulatory) - Wikipedia

"Acute shock" redirects here. For the psychological condition, see Acute stress reaction . Shock is a life-threatening medical condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function. [1] [2] The typical signs of shock are low blood pressure , rapid heart rate , signs of poor end-organ perfusion (i.e., low urine output, confusion, or loss of consciousness), and weak pulses. The shock index (SI), defined as heart rate divided by systolic blood pressure, is an accurate diagnostic measure that is more useful than hypotension and tachycardia in isolation. [3] Under normal conditions, a number between 0.5 and 0.8 is typically seen. Should that number increase, so does suspicion of an underlying state of shock. Blood pressure alone may not be a reliable sign for shock, as there are times when a person is in circulatory shock but has a stable blood pressure. [4] Circulatory shock is not related to the emotional state of shock . Circulatory shock is a life-threatening medical emergency and one of the most common causes of death for critically ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac and/or respiratory arrest . [5] One of the key dangers of shock is that it progresses by a positive feedback mechanism. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. This is normally very useful to match up blood supply level with tissue demand for nutrients. However, if enough tissue causes this, it will deprive vital nutrients from other parts of the body. Additionally, the ability 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 >>

More in ketosis