Epinephrine-induced Lactic Acidosis In The Setting Of Status Asthmaticus.
Epinephrine-induced lactic acidosis in the setting of status asthmaticus. Murphy FT(1), Manown TJ, Knutson SW, Eliasson AH. (1)Department of Medicine, Walter Reed Army Medical Center, Washington, DC 20307-5000, USA. A relationship between intravenous epinephrine infusion and the development oflactic acidosis has been well described. We report a temporal association betweenthe administration of subcutaneous epinephrine and the development of lacticacidosis in the setting of status asthmaticus. A 20-year-old woman with a historyof asthma came to the emergency service in acute respiratory distress and wastreated with subcutaneous epinephrine. Six hours later, serial arterial blood gasstudies revealed the onset of a primary metabolic acidosis. Additional diagnosticstudies revealed a serum lactate level of 9.5 mumol/L. The lactic acidosisresolved within 15 hours. The patient never exhibited signs of hypotension,hypoxemia, or sepsis, and other potential etiologies for lactic acidosis wereexcluded. We believe the events of this case constitute a new observation andtheorize a mechanism of peripheral vasoconstriction and transient tissuehypoperfusion mediated by the subcutaneous epinephrine. Continue reading >>
Lactic Acidosis
hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq Continue reading >>
Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass.
Epinephrine-induced lactic acidosis following cardiopulmonary bypass. Department of Intensive Care, Royal North Shore Hospital, St. Leonards, NSW, Australia. To determine if lactic acidosis occurring after cardiopulmonary bypass could be attributed to the metabolic or other effects of epinephrine administration. Postsurgical cardiothoracic intensive therapy unit. Thirty-six adult patients, without acidosis, requiring vasoconstrictors for the management of hypotension after cardiopulmonary bypass. Randomized administration of either epinephrine or norepinephrine by infusion. Hemodynamic and metabolic data were collected before commencement of vasoconstrictor therapy (time 0) and then 1 hr (time 1), 6 to 10 hrs (time 2), and 22 to 30 hrs (time 3) later. Six of the 19 patients who received epinephrine developed lactic acidosis. None of the 17 patients receiving norepinephrine developed lactic acidosis. In the epinephrine group, but not in the norepinephrine group, lactate concentration increased significantly at times 1 and 2 (p = .01), while pH and base excess decreased (p < or = .01). Blood glucose concentration was higher in the epinephrine group at time 2 (p = .02), while the cardiac index (p < .03) and the mixed venous Po2 (p = .04) were higher at time 1. compared with the norepinephrine group, the patients receiving epinephrine had higher femoral venous lactate concentrations (p = .03), increased lower limb blood flow (p = .05), and increased femoral venous oxygen saturations (p = .04). The use of epinephrine after cardiopulmonary bypass precipitates the development of lactic acidosis in some patients. This phenomenon is presumably a beta-mediated effect, and is associated with an increase in whole-body and lower limb blood flow and a decrease in whole-body and tran Continue reading >>
Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass
Objective To determine if lactic acidosis occurring after cardiopulmonary bypass could be attributed to the metabolic or other effects of epinephrine administration. Setting Postsurgical cardiothoracic intensive therapy unit. Patients Thirty-six adult patients, without acidosis, requiring vasoconstrictors for the management of hypotension after cardiopulmonary bypass. Interventions Randomized administration of either epinephrine or norepinephrine by infusion. Measurements and Main Results Hemodynamic and metabolic data were collected before commencement of vasoconstrictor therapy (time 0) and then 1 hr (time 1), 6 to 10 hrs (time 2), and 22 to 30 hrs (time 3) later. Six of the 19 patients who received epinephrine developed lactic acidosis. None of the 17 patients receiving norepinephrine developed lactic acidosis. In the epinephrine group, but not in the norepinephrine group, lactate concentration increased significantly at times 1 and 2 (p = .01), while pH and base excess decreased (p
(pdf) Epinephrine-induced Lactic Acidosis In The Setting Of Status Asthmaticus
Lactic acidosis is frequently encountered in the intensive care unit. It occurs when there is an imbalance between production and clearance of lactate. Although lactic acidosis is often associated with a high anion gap and is generally defined as a lactate level >5 mmol/L and a serum pH <7.35, the presence of hypoalbuminemia may mask the anion gap and concomitant alkalosis may raise the pH. The causes of lactic acidosis are traditionally divided into impaired tissue oxygenation (Type A) and disorders in which tissue oxygenation is maintained (Type B). Lactate level is often used as a prognostic indicator and may be predictive of a favorable outcome if it normalizes within 48 hours. The routine measurement of serum lactate, however, should not determine therapeutic interventions. Unfortunately, treatment options remain limited and should be aimed at discontinuation of any offending drugs, treatment of the underlying pathology, and maintenance of organ perfusion. The mainstay of therapy of lactic acidosis remains prevention. Hyperlactatemia and lactic acidosis are two syndromes that are associated with morbidity and mortality. Medicationinduced hyperlactatemia and lactic acidosis are diagnoses of exclusion and have the potential to be overlooked. The purpose of this systematic review is to identify published reports of medicationinduced lactate level elevations to aid clinicians in diagnosing and comprehending the underlying mechanism of this rare adverse drug effect, and to provide management strategies. The PubMed database was searched for case reports, case series, retrospective studies, and prospective studies describing cases of medicationinduced lactate level elevation, including lactic acidosis and hyperlactatemia, published between January 1950 and June 2017. A s Continue reading >>
Lactic Acidosis: Background, Etiology, Epidemiology
Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe Continue reading >>
Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass
The normal blood lactate level is 0-2 mmol/L, and a value above 3-5 mmol/L is variably used to define hyperlactatemia. In cardiac surgical patients, hyperlactatemia can arise from both hypoxic and non-hypoxic mechanisms. The major non-hypoxic mechanism is likely stress-induced accelerated aerobic metabolism, in which elevated lactate results from a mass effect on the lactate/pyruvate equilibrium. The lactate/pyruvate ratio is normal ( < 20) in this circumstance. Hyperlactatemia can also result from impaired global or regional oxygen delivery, in which case the lactate/pyruvate ratio is typically elevated ( > 20). Lactate is a strong anion that is virtually fully dissociated at physiological pH. As such, increased lactate concentration reduces the strong ion difference and exerts an acidifying effect on the blood. Hyperlactatemia in cardiac surgery patients has been categorized as either early or late onset. Early-onset hyperlactatemia is that which develops in the operating room or very early following intensive care unit (ICU) admission. Early-onset hyperlactatemia is strongly associated with adverse outcome and probably arises as a consequence of both hypoxic (e.g., microcirculatory shock) and nonhypoxic (accelerated aerobic metabolism) mechanisms. By contrast, late-onset hyperlactatemia is a benign, self-limiting condition that typically arises within 6-12 hours of ICU admission and spontaneously resolves within 24 hours. Late onset hyperlactatemia occurs in the absence of any evidence of global or regional tissue hypoxia. The mechanism of late onset hyperlactatemia is not understood. Hyperlactatemia is a common accompaniment to treatment with 2-agonists such as epinephrine. Epinephrine-induced hyperlactatemia is thought to be due to accelerated aerobic metabolism a Continue reading >>
Risk Factors Of Post-operative Severe Hyperlactatemia And Lactic Acidosis Following Laparoscopic Resection For Pheochromocytoma
Risk factors of post-operative severe hyperlactatemia and lactic acidosis following laparoscopic resection for pheochromocytoma Scientific Reportsvolume7, Articlenumber:403 (2017) Severe hyperlactatemia (SH)/lactic acidosis (LA) after laparoscopic resection of pheochromocytoma is an infrequently reported complication. The study aims to investigate the incidence of this complication and to determine the clinical risk factors. Patients who underwent laparoscopic resection for pheochromocytoma between 2011 and 2014 at Peking Union Medical College Hospital were enrolled. LA was defined as pH < 7.35, bicarbonate <20 mmol/L, and serum lactate 5 mmol/L; SH as lactate 5 mmol/L; and moderate hyperlactatemia (MH) as lactate 2.55.0 mmol/L without evidence of acidosis (pH > 7.35 and/or bicarbonate >20 mmol/L). Data concerning patient demographics, clinical history, and laboratory results were collected and statistical analyses were performed. Out of 145 patients, 59 (40.7%) developed post-operative hyperlactatemia. The incidences of MH and SH/LA were 25.5% and 15.2%, respectively. Multivariate analysis demonstrated that body mass index (BMI) (odds ratio [OR], 1.204; 95% confidence interval [CI], 1.0161.426), 24-hour urine epinephrine concentration (OR, 1.012; 95% CI, 1.0021.022), and tumor size (OR, 1.571; 95% CI, 1.1022.240) were independent predictors of post-operative SH/LA. The data show that post-operative SH/LA is not a rare complication after pheochromocytoma resection and may be closely associated with higher BMI, larger tumor size, and higher levels of urine epinephrine. Pheochromocytoma is a rare, catecholamine-producing neuroendocrine tumor originating from chromaffin cells of the adrenal medulla 1 . Cardinal manifestations of pheochromocytoma include episodic hypertens Continue reading >>
Journal Of The Korean Association Of Oral And Maxillofacial Surgeons
ORCID: Received April 4, 2016; Revised July 22, 2016; Accepted August 17, 2016.; Published online October 31, 2016. Korean Association of Oral and Maxillofacial Surgeons. All rights reserved. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract (J Korean Assoc Oral Maxillofac Surg 2016;42:295-300) Submucosal infiltration and the topical application of epinephrine as a vasoconstrictor produce excellent hemostasis during surgery. The hemodynamic effects of epinephrine have been documented in numerous studies. However, its metabolic effects (especially during surgery) have been seldom recognized clinically. We report two cases of significant metabolic effects (including lactic acidosis and hyperglycemia) as well as hemodynamic effects in healthy patients undergoing orthognathic surgery with general anesthesia. Epinephrine can induce glycolysis and pyruvate generation, which result in lactic acidosis, via 2-adrenergic receptors. Therefore, careful perioperative observation for changes in plasma lactate and glucose levels along with intensive monitoring of vital signs should be carried out when epinephrine is excessively used as a vasoconstrictor during surgery. Keywords: Epinephrine, Orthognathic surgery, Local anesthesia, Lactic acidosis, Topical administration Continue reading >>
Epinephrine-induced Lactic Acidosis In Orthognathic Surgery: A Report Of Two Cases
Epinephrine-induced lactic acidosis in orthognathic surgery: a report of two cases 1Department of Anesthesiology and Pain Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 1Department of Anesthesiology and Pain Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 1Department of Anesthesiology and Pain Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 1Department of Anesthesiology and Pain Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 2Department of Oral and Maxillofacial Surgery, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 1Department of Anesthesiology and Pain Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 2Department of Oral and Maxillofacial Surgery, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. Corresponding author: Jang-Ho Son. Department of Oral and Maxillofacial Surgery, Ulsan University Hospital, 877 Bangeojinsunhwan-doro, Dong-gu, Ulsan 44033, Korea. TEL: +82-52-250-7230, FAX: +82-52-250-7236, [email protected] Received 2016 Apr 4; Revised 2016 Jul 22; Accepted 2016 Aug 17. Copyright 2016 The Korean Association of Oral and Maxillofacial Surgeons. All rights reserved. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Submucosal infiltration and the topical application of epinephrine as a vasoconstrictor produce excellent hemostasis during surgery. The hemodynamic effec Continue reading >>
Causes Of Lactic Acidosis - Deranged Physiology
A discussion of the causes of a high anion gap metabolic acidosis are frequently required by the CICM SAQs, and lactate often comes up as a differential. Beyond that, there are a series of questions which ask specifically about the causes of lactic acidosis. These questions are numerous. There is practically one in every paper. Question 4.1 from the first paper of 2016 Question 3.3 from the second paper of 2015 Question 27 from the second paper of 2014 Question 23 from the second paper of 2013 Question 26.4 from the second paper of 2013 Question 28 from the second paper of 2012 Question 9.1 from the first paper of 2011 Question 15.3 from the second paper of 2009 Question 3.3 from the second paper of 2009 Many of these questions for some reason focus repetitively on the plight of a certain middle-aged diabetic with a history of alcohol abuse. A specific feature of these questions is the use of red cell transketolase as a test of thiamine deficiency, reminding the candidates that this is an important differential. Lactic acidosis is discussed at greater length in a series of chapters dedicated to acid-base disturbances in their various forms and permutations. In order to simplify revision, a tabulated list of aetiologies is offered below, organised according to an increasingly irrelevant classification system from the 1980s. The massively flawed Cohen-Woods classification Type A lactic acidosis: impaired tissue oxygenation Type B1 lactic acidosis, due to a disease state NRTIs (nucleoside reverse transcriptase inhibitors) Continue reading >>
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 >>
Trk Gs Kalp Damar Cerrahisi Dergisi
1Departments of Anesthesiology and Reanimation, Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, stanbul 2Departments of Cardiovascular Surgery, Siyami Ersek Thoracic and Cardiovascular Surgery Training and Research Hospital, stanbul Keywords (Turkish): Koroner arter bypass cerrahisi; hiperlaktatemi; mortalite Keywords (English): Coronary artery bypass graft; hyperlactatemia; mortality Background: This study aims to determine the risk factorsfor hyperlactatemia developing after coronary arterybypass grafting (CABG) surgery and to analyze its effecton mortality and the morbidity. Methods: Four-hundred and eighty-two consecutive patientswho had undergone elective CABG were prospectivelyincluded in the study and divided into two groups: group 1(n=260), patients who had high blood lactate levels in the firstmeasurement (>3.5 mmol/l) in the intensive care unit (ICU);group 2 (n=222), patients who had normal blood lactate levels(<3.5 mmol/l). The duration of cardiopulmonary bypass(CPB) and cross-clamping (CC), hyperglycemia (blood glucoselevel >140 mg/dL), the presence of hemodynamic instabilityand requirement for vasopressors during CPB, inotropicagent administration for more than three hours and thetemperature and lactate changes at five different time pointsduring ICU stay were measured. Postoperative neurologic,infectious and renal complications and the durations of ICUstay and mechanical ventilation were recorded. Results: The blood lactate levels were found significantlyhigher in patients with longer CPB and CC durations andperoperative hemodynamic instability. Postoperatively, thepatients who had high glucose levels and high inotropicagent needs also had higher lactate levels. The patients ingroup 1 had longer extubation times and ICU st Continue reading >>
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 >>
Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect
Volume 147, Issue 5 , May 2014, Pages 1698-1705 Acidosis is a very common pathologic process in perioperative management. However, how to correct severe acidosis to improve the efficacy of vasoconstrictors in hemodynamically unstable patients is still debated. The present study investigated whether severe extracellular acidosis influences the vasoactive properties of vasoconstrictors on human isolated arteries. Segments of intact distal internal mammary arteries were removed from 41 patients undergoing artery bypass grafting. The arterial rings were washed in Krebs-Henseleit solution and suspended in an organ bath. The rings were set at a pretension equivalent of 100 mm Hg, and the relaxation response to 10 M acetylcholine was verified. Concentrationresponse curves for epinephrine, norepinephrine, methoxamine (1A/D-adrenoceptor agonist), phenylephrine (equipotent agonist of 1A/B-adrenoceptors), and clonidine (2-adrenoceptor agonist) were achieved under control conditions (pH 7.40) and under acidic conditions by substitution of the Krebs-Henseleit solution with a modified solution. Decreasing the pH from 7.40 to 7.20, 7.0, or 6.80 did not significantly alter the potency and efficacy of epinephrine and norepinephrine, although the standardized effect size was sometimes large. Severe acidosis (pH6.80) did not significantly change the potency and efficacy of phenylephrine and clonidine, although it increased the efficacy and potency of methoxamine (P<.001 and P=.04 vs paired control conditions, respectively). Extracellular acidosis did not impair the vasoactive properties of epinephrine and norepinephrine in human medium-size arteries until pH 6.80. The results of the present study also suggest that acidosis might potentiate arterial responsiveness to vasoconstrictors, mos Continue reading >>
