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Nejm Lactic Acidosis

Welcome To Osmolality.com | Presented By Advanced Instruments, Inc.

Welcome To Osmolality.com | Presented By Advanced Instruments, Inc.

Bhagat, C.I., Garcia-Webb, P., Fletcher, E., Beilby, J.P. Calculated versus Measured Plasma Osmolalities Revisited. Clinical Chemistry, 30(10):1703 1984 Boyd, D.R., Mansberger, A.R., Serum Water and Osmolal Changes in Hemorrhagic Shock: An Experimental and Clinical Study, Am Surgeon, 34: 744 (1968) Dorwart, W.V., Chalmers, L., Comparison of Methods for Calculating Serum Osmolality from Chemical Concentrations, and the Prognostic Value of Such Computations, Clinical Chemistry, 21: 190 (1975) Eskew, L., Speicher, C.E., Using Anion and Osmolal Gaps to Diagnose the Cause of Intoxication, Diagnostic Medicine, p. 6 February 1985 Evans, J.R., Osmolal Gaps in Urine, Clinical Chemistry, 32(7): 1415 (1986) Evans, J.R., Yet More on Osmolal Gaps in Urine, Clinical Chemistry, 33(5): 736 (1987) Garg, A.K., Nanji, A.A., Osmolar Gap, Diagnostic Medicine, p. 38 Mar/Apr 1982 Neary, R.H., More on Osmolal Gaps in Urine, Clinical Chemistry, 32(12): 2225 (1986) Osterloh, J.D., Discrepancies in osmolal gaps and calculated alcohol concentrations -see comments-. Archives of Pathology Laboratory Medicine 1996; 120: 637-41. Soloway, H.B., What is an osmotic gap, and how is it used in diagnosis?, Diagnostic Medicine, p. 20 Nov/Dec 1983 Speicher, C.E., Anion and Osmolal Gaps, Consultation Casebook, Pathologist, 2: 117 (1984) Walker, J.A., Missing gap: pitfall in the diagnosis of alcohol intoxication by osmometry. Archives of Internal Medicine 1986; 146: 1843-4. Weisberg, H.F., Osmolality: Calculated, "Delta" and More Formulas. Clinical Chemistry, 21: 1182 (1975) 1. Bekeris, L., Baker, C., Fenton, J., Kimball, D., et al. Propylene Glycol as a Cause of Elevated Serum Osmolality. Am. Journal of Clinical Pathology, 72 (4): 633, October 1979. 2. Cate, J.C., Propylene Glycol Intoxication and Lactic Acid Continue reading >>

Asynchrony Em: I'm All About That (acid/) Base

Asynchrony Em: I'm All About That (acid/) Base

New to Asynchrony EM? It's an asynchronous learning course in its third year at Brown EM. Digital resources and #FOAMed are curated and packaged by topic, following Brown EM's curricular calendar. In the spirit of #FOAMed, we've started putting it out there for the EM community at large. Check out the theme song, the 'extras', and the discussion questions, and other modules -- and leave us your thoughts in the comments section. Follow us on Twitter at @AsynchronyEM. Note: Brown EM residents must complete the modules (including discussion/quiz) in Canvas to obtain credit hours. "Because you know I"m all about that bass..." Sing it, Meghan! Here we are, continuing in our endocrine/metabolic curricular block -- Holy moly, I CAN HEAR YOU GROANING FROM HERE!! Of course, you are notgroaning about my punny Meghan Trainor reference, but about the topics:ACID-BASE estimations and HYPONATREMIA, which are dry and difficult and one of several reasons why you are not training to be nephrologists. I get it. But I'm going to try to make this as painless and relevant as possible. There is LOTS of optionalcontent listed, because there's a LOT more you could be reading about this if you're so inclined. Also, some references are not open access #FOAMed, but worth finding if you have institutional access to the New England Journal of Medicine (Brown residents can link to the e-library through Canvas). However, you'll get enough from the #FOAM content that you'll know what you're talking about, and I've also summarized some of the points from the NEJM below. And you already know the theme song. "All About That Bass," Meghan Trainor: "Yeah, my mama, she told me, don't worry about chlor-i-ide..." (#alternativelyrics) ACID/BASE 'PARADIGM SHIFT': MEET STEWART AND SID Just when you thought you Continue reading >>

Lactic Acidosis (pdf Download Available)

Lactic Acidosis (pdf Download Available)

hypoxemia (e.g., summiting Mount Everest), lac- tate levels are either normal or only minimally elevated. Lactate is a major biofuel used for intra- cellular, intercellular, and interorgan shuttles, processes that appear to increase bioenergetic efficiency. It is doubtful that lactic acidosis is due to the release of protons from ATP hydrolysis, since no ATP depletion can be shown on mag- netic resonance spectroscopy, even in severe septic (although similarly unproven) lies with the Stewart, or strong ion, approach to acidbase physiology. Lactate is an anion that decreases the strong-ion difference and increases the dissociation of water Australian and New Zealand Intensive Care Research Centre No potential conflict of interest relevant to this letter was re- 1. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med 2. Garcia-Alvarez M, Marik P, Bellomo R. Sepsis-associated hy- 3. Garcia-Alvarez M, Marik P, Bellomo R. Stress hyperlactate- mia: present understanding and controversy. Lancet Diabetes 4. May CN, Ishikawa K, Wan L, et al. Renal bioenergetics dur- ing early gram-negative mammalian sepsis and angiotensin II infusion. Intensive Care Med 2012;38:886-93. 5. Kellum JA. Disorders of acid-base balance. Crit Care Med To the Editor: Kraut and Madias provide an ex- cellent overview of lactic acidosis. But the asser- tion that it remains unproven that the therapeu- tic administration of sodium bicarbonate may improve hemodynamics is inaccurate. Two pro- spective, randomized, blinded, crossover studies specifically examined the effects of sodium bi- carbonate or isovolemic aliquots of normal sa- line on hemodynamics in critically ill patients with lactic acidemia who required vasoactive sup- Mathieu et al. concluded that sodium bicarbon- ate did not improve hemodynamic vari Continue reading >>

Biolab Medical Unit London Uk - Tests

Biolab Medical Unit London Uk - Tests

Samples have to be separated and frozen immediately after collection D-lactate is produced from non-absorbed carbohydrates by colonic bacteria (which may also proliferate in the ileum). The absorption of large amounts of D-lactate can cause metabolic acidosis, altered mental status and a variety of other neurologic symptoms, in particular dysarthria and ataxia [2,3,4]. Its measurement is part of the differential diagnosis of chronic fatigue syndrome [5]. Although a temporal relationship has been described between elevations of plasma D-lactate and the accompanying encephalopathy, the exact neurological mechanisms remain undescribed [6]. Otherwise healthy children with gastroenteritis may also develop D-lactic acidosis. There are a number of other tests of gastro-intestinal function available from Biolab the gut fermentation test, the PEG profile (gut permeability), the measurement of plasma short-chain polypeptides and the lactulose breath hydrogen test. Each of these tests provides somewhat different information from the D-lactate test, which is specific for the presence of D-lactate-producing bacteria in the gut (probably Enterococcus and Streptococcus spp. [5]). Unaffected subjects have plasma concentrations of D-lactate of less than 60umol/L. Continue reading >>

Talk:lactic Acidosis

Talk:lactic Acidosis

This article is within the scope of WikiProject Physiology , a collaborative effort to improve the coverage of Physiology on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks. This article has been classified as relating to the kidneys and renal physiology . This article is within the scope of WikiProject Medicine , which recommends that medicine-related articles follow the Manual of Style for medicine-related articles and that biomedical information in any article use high-quality medical sources . Please visit the project page for details or ask questions at Wikipedia talk:WikiProject Medicine . This article has been rated as Mid-importance on the project's importance scale . Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles . Here are links to possibly useful sources of information about Lactic acidosis. Other potential sources include: Centre for Reviews and Dissemination and CDC Acidosis is not due to lactic acid[ edit ] As I have mentioned on the talk pages of Anaerobic Respiration and Lactic Acid , relatively recent research has clearly established that lactate production in anaerobic respiration does not cause acidosis. The reference I cited there is . Lim Wei Quan ( talk ) 06:44, 30 October 2008 (UTC) Personally until proven otherwise, I think it warrants staying placed on the wiki to keep a 'warning' as the prevailing ideology behind the article vs leaving it otherwise. Preceding unsigned comment added by 71.61.125.253 ( talk ) 07:34, 3 January 2009 (UTC) In humans, perhaps, but lactic acid buildup can cause such extreme acidosis in large reptiles (particularly croc Continue reading >>

Fluid Resuscitation

Fluid Resuscitation

Normal saline can cause a hyperchloremic metabolic acidosis, whereas lactated ringers can cause a metabolic alkalosis secondary to metabolism of lactate (which produces bicarbonate). Never use LR with blood products as the calcium will bind to the citrate. Dextrose-containing solutions should be avoided in patients with neurologic injuries as they may cause hyperglycemia, cerebral acidosis, and an osmotic diuresis [Stoelting et. al. Basics of Anesthesia, 5th ed. Elsevier China, p. 351, 2007]. It is well established that hypotonic fluids cause brain edema (thus do not use Lactated ringers for large volume resuscitation), although animal studies suggest that crystalloids increase cerebral edema and ICP only when they result in hypoosmolality [Crit Care Med 16: 862, 1988; Anesthesiology 67: 936, 1987] Half-life of albumin is 16 hours. Hydroxyethyl starch is made of either 6% MW hetastarch in saline [Hespan] or 6% MW hetastarch in balanced salt solution [Hextend]. 90% of hydroxylethyl starch particles last 17 days. Dextran comes in dextran 40 and dextran 70. Larger particles have a half-life in the order of days, thus dextran 70 is generally used for volume resuscitation, while dextram 40 is used to improve blood flow to the microcirculation. Hypersensitivity reactions to colloids are possible, but rare. Note that the dextrans can reduce platelet aggregation and adhesiveness, and that hydroxyethyl starch can reduce factor VIII and vWF, as mentioned in Barrons review of 113 studies (which stated Artificial colloid administration was consistently associated with coagulopathy and clinical bleeding, most frequently in cardiac surgery patients receiving hydroxyethyl starch) [Barron ME et. al. Arch Surg 139: 552, 2004]. All colloids share the following potential downsides volume Continue reading >>

Morning Report Pearls 9/6/17 Lactic Acidosis

Morning Report Pearls 9/6/17 Lactic Acidosis

UCSF Internal Medicine Chief Resident Hub Thank you Courtney and Nancy for presenting a diagnostic mystery! This elderly woman presented to the ED after an episode of witnessed syncope with headstrike complicated by SDH and SAH, transferred from neurosurgery to medicine for a profound metabolic acidosis lactate of 21!! Syncope its all about the history! There are 4 main categories: cardiac arrhythmias, structural cardiopulmonary disease, neurogenic, and orthostatic hypotension. Lactate make you nervous? Not all lactates come from sepsis use an algorithm to help flesh out the other causes of elevated lactate. Remember that medications can affect all of these categories! Check out this previous post all about syncope and the associated Evernote ! Global: shock of any type! Distributive, cardiogenic, neurogenic, obstructive Local: mesenteric ischemia, compartment syndrome, seizure, etc. Decreased delivery of O2: severe anemia, severe hypoxemia, methemoglobinemia, carbon monoxide, cyanide Lack of required cofactor: thiamine deficiency Mitochondrial toxicity: EtOH, ARVs, Propofol, Salicylates, mitochondrial d/o Warburg effect conversion to anaerobic metabolism within a high-grade malignancy Decreased clearance of lactate from any cause: WAY less commonly D-lactic acidosis the D-isomer of lactate associated with small bowel overgrowth, short gut syndrome, unusual causes of sepsis. Of note, our lab at UCSF does NOT detect the d-lactate isomer, so if you have an elevated lactate here, its the L-lactate isomer. To read more, here is a link to a 2014 review article from the NEJM on Lactic Acidosis by Kraut and Madias: For more specifically about Type B lactic acidosis as a complication of lymphoma and leukemia, check out this case series and review by Friedenberg, Brandoff, and Continue reading >>

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base disturbances in children, Acidosis, Alkalosis Acid-base disturbances in children, Acidosis, Alkalosis The pH of the blood is controlled via three systems: chemical buffering, respiratory function, and renal function. Acidosis means a clinical disturbance in which there is an increase in plasma acidity, whether due to increased production by the tissues, loss of buffering ability or decreased clearance by the kidneys. A multitude of problems, congenital and acquired, can result in metabolic acidosis. The hallmark of a metabolic acidosis is a low serum HCO3 level. Metabolic alkalosis means the patient has an elevated HCO3, most typically seen with administration of loop diuretics. A respiratory acidosis means an increase in the partial pressure of carbon dioxide in the blood (PaCO2) due to inadequate respiration. Respiratory alkalosis typically occurs in response to a metabolic stimulus, such as hyperammonemia (seen in urea cycle defects) or diabetic ketoacidosis (DKA). Metabolic and respiratory mechanisms affect the acid-base state. The relationship between the pH and PaCO2 is dependent upon the plasma bicarbonate-plasma carbonic acid pool. To estimate the effect of pH change, for every 10 mmHg PaCO2, the pH will change by approximately 0.08; for example, if the PaCO2 rises to 50 from a normal 40 mmHg, then the expected pH will be approximately 7.32, or decreased by 0.08. Comparison of the base excess with the reference range assists in determining whether an acid-base disturbance is caused by a respiratory, metabolic or mixed metabolic/respiratory problem. While CO2 defines the respiratory component of acid-base balance, base excess defines the metabolic component. To generalize, a metabolic acidosis will have a low serum HCO3 and a respiratory acidosis will Continue reading >>

Metformin Induced Lactic Acidosis Nejm

Metformin Induced Lactic Acidosis Nejm

by : incidence, management and prevention. Drug Saf 2010;33(9):727-40. 3. Kalantar-Zadeh K, Uppot RN, Lewandrowski KB. Case records of the Massachusetts General Hospital (Case 23-2013). A 54-year-old woman with abdominal pain, vomiting, and confusion. N Engl J Med 2013;Jan 22, 1998 Correspondence from The New England Journal of Medicine in Patients with Diabetes Treated with . Prepare to become a physician, build your knowledge, lead a health care organization, and advance your career with Group information and services. Dec 11, 2014 Using dialysis to provide bicarbonate can prevent a decrease in ionized calcium, prevent volume overload and hyperosmolality (potential complications of bicarbonate infusion), and remove substances associated with , such as . Through an alkalinizing effect, base administration,Aug 31, 1995 Such a mechanism of action might diminish the removal of lactate from plasma and present a risk of . .. On the other hand, if the - increase in the sensitivity of muscle to insulin included an anticatabolic effect of insulin on protein metabolism, one would expect no change inJan 2, 2003 is a toxic effect of linezolid whose mechanism is unknown. Other drugs, including and nucleoside reverse-transcriptase inhibitors, have been associated with . In the case of nucleoside reverse-transcriptase inhibitors, is thought to involve mitochondrialJul 26, 2013 Q: What are the characteristics of -? A: overdose or accumulation as the cause of is highly likely in any patient who has most or all of the following five criteria in the absence of a high level: a history of administration (e.g., in aMeSH terms. , /chemically *; Aged; Diabetes Mellitus/drug therapy; Female; Humans; Hypoglycemic Agents/adverse effects*; Male; /adverse effects*; Risk FactorsDec 14, 2017 cause Continue reading >>

Delta Gap And Delta Ratio - Deranged Physiology

Delta Gap And Delta Ratio - Deranged Physiology

The delta gap and delta ratio, advantages and disadvantages . Once one has calculated the anion gap and finds it raised, one is almost obliged to figure out whether those anions have been solely responsible for the acidosis, or whether another (non-anion-gap) cause is lurking in the background. A brief review of this can be found in the "Required Reading" section hidden among the CICM Fellowship Exam preparation material.For actual education, the exam candidates are directed to the LITFL delta ratio page , and to the excellent online works of Kerry Brandis. The delta gap is a straight-out difference between the change in anion gap and the change in bicarbonate. Delta gap = (change in anion gap) - (change in bicarbonate) (The normal anion gap is assumed to be 12, and the normal HCO3is assumed to be 24.) A simplified equation which does not require a bicarbonate value is also available: -6 = Mixed high and normal anion gap acidosis -6 to 6 = Only ahigh anion gap acidosis exists over 6 = Mixed high anion gap acidosis and metabolic alkalosis Delta gap is essentially a tool to determine whether or not there is also a normal anion gap metabolic acidosis present.The normal value for delta gap is zero, and it should remain zero as anion gap and bicarbonate changetogether (mole for mole, in opposite directions). If the bicarbonate is changing significantlyless than the anion gap, the delta gap will become more and more positive, reflecting the fact that an alkalosis is present. If the change in bicarbonateis significantly greater than the change in anion gap, there is clearly some acidosis present which is unrelated to the anion gap rise, and thedelta gap will be very negative. Why -6 and +6?Keith Wrenn established these parameters in 1990 , using the normal values supplied to Continue reading >>

Hypotension, Tachycardia, Tachypnea, Lactic Acidosis: Causes & Diagnoses | Symptoma.com

Hypotension, Tachycardia, Tachypnea, Lactic Acidosis: Causes & Diagnoses | Symptoma.com

The signs of MH include hypercarbia, muscle rigidity, fast-rising body temperature, tachycardia, myolysis, increased ETCO 2 , hyperkalemia, and acidosis. [ryanodex.com] Manifestations can include muscle rigidity, hyperthermia, tachycardia, tachypnea, rhabdomyolysis, and respiratory and metabolic acidosis. [msdmanuals.com] , cyanosis, hyperkalaemia, lactic acidosis, fever, and eventually (if untreated) death. [anaesthesia.mh.org.au] Later signs include complex arrhythmias, cyanosis, hypoxia, hypotension, electrolyte abnormalities, rhabdomyolysis and severe hyperthermia. [patient.info] Fever or hypothermia, leukocytosis or leukopenia, tachypnea, and tachycardia are the cardinal signs of the systemic response, that is often called the systemic inflammatory [accessmedicine.mhmedical.com] Components of SIRS include tachycardia, tachypnea, hyperthermia or hypothermia, and elevated white blood count. [medpagetoday.com] Sodium bicarbonate for the treatment of lactic acidosis. [enotes.tripod.com] Ketamine Drug of choice as it is relatively safe in hypotension and tachycardia. [emergencymedicinecases.com] Electrocardiography (ECG) often demonstrates sinus tachycardia. [symptoma.com] Diabetic ketoacidosis , hypoglycaemia , lactic acidosis , hypothyroidism . [patient.info] [] that you or the environment around you is spinning ataxia loss of physical co-ordination caused byunderlying damage to the brain and nervous system breathlessness and tachycardia [nhs.uk] Increased muscle activity and seizures should be treated with dantrolene or diazepam ; diazepam should only be given with appropriate respiratory support. [37] Hypotension [en.wikipedia.org] 12mcg 0.2 Mcg/kg.min Vasodilation,inotropy,tachycardia,hypotensio n MILRINONE 25-75mcg/kg bolus 0.1-0.75mcg/kg/min Vasodilation,inotrop Continue reading >>

Lactic Acidosis In An Infant Receiving Hiv Prophylaxis

Lactic Acidosis In An Infant Receiving Hiv Prophylaxis

Lactic Acidosis in an Infant Receiving HIV Prophylaxis The rate of vertical transmission of human immunodeficiency virus (HIV) has dramatically decreased with the administration of antiretroviral treatments (ART) to HIV-infected mothers and their infants. The Pediatric AIDS Clinical Trials Group 076 (PACTG 076) originally showed zidovudine, a nucleoside analogue reverse transcriptase inhibitor (NRTI), to be a safe and effective therapy in preventing vertical transmission when administered to both mother and child.1 Guidelines currently recommend zidovudine for HIV prophylaxis for 4-6 weeks for neonates exposed to HIV in utero.2 Despite the overall safety findings of zidovudine from PACTG 076, rare, but serious, side effects have been observed. Although data are conflicting, NRTIs have been linked to mitochondrial toxicity that leads to lactic acidosis, cardiac abnormalities, neurologic delays, and death.3-5 We present a case of presumed mitochondrial toxicity and lactic acidosis in an infant exposed to zidovudine for HIV prophylaxis. A 5-week-old female born to an HIV-positive mother presented to a referring hospital for excessive vomiting of 2 days duration. Emesis was reported to occur after each feed and was non-bloody, non-bilious, and non-projectile. She had been afebrile with no sick contacts. She did have a history of reflux and would have small spit-ups after each feed. Diet consisted of infant formula 2-4 oz every 2-4 hours, mixed appropriately. Prenatal history was notable for maternal HIV diagnosed 16 years prior to the pregnancy; the mother, however, did not start HAART until pregnancy was confirmed. Treatment was initiated with elvitegravir/cobicistat/emtricitabine/tenofovir 6 months prior to her giving birth. She received IV zidovudine intrapartum, and th Continue reading >>

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

Interpretation of Arterial Blood Gases (ABGs) Chief, Section of Pulmonary, Critical Care & Sleep Medicine Bridgeport Hospital-Yale New Haven Health Assistant Clinical Professor, Yale University School of Medicine (Section of Pulmonary & Critical Care Medicine) Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other health care personnel. ABG interpretation is especially important in critically ill patients. The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acid-base disorders. Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewarts strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the anion gap. Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation: If the pH and the [H+] are inconsistent, the ABG is probably not valid. Step 2: Is there alkalemia or acidemia present? Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 7.45) You will need to check the PaCO2, HCO3- and anion gap Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction. Decrease in [HCO3-] = 5( PaCO2/10) to 7( PaCO2/10) If the observed compensa Continue reading >>

[nejm]nutrition In The Acute Phase Of Critical Illness

[nejm]nutrition In The Acute Phase Of Critical Illness

[NEJM]Nutrition in the Acute Phase of Critical Illness N Engl J Med 2014; 370:1227-1236 March 27, 2014 DOI: 10.1056/NEJMra1304623 Critically ill patients requiring vital organ support in the intensive care unit (ICU) commonly have anorexia and may be unable to feed volitionally by mouth for periods ranging from days to months. Unless such patients are provided with macronutrients in the form of enteral or parenteral nutrition, they accumulate an energy deficit that rapidly reaches proportions that contribute to lean-tissue wasting and that are associated with adverse outcomes.1 The catabolic response to acute critical illness is much more pronounced than that evoked by fasting in healthy persons, since the energy deficit in acutely ill patients is often superimposed on immobilization and pronounced inflammatory and endocrine stress responses. Severe skeletal-muscle wasting and weakness occurring during critical illness are associated with a prolonged need for mechanical ventilation and rehabilitation.2 In many studies, the degree of energy deficit accumulating in critically ill patients is strongly associated with the duration of stay in the ICU, which, in turn, is associated with an increased incidence of infectious complications and risk of death.1 Until recently, however, the causality of these associations remained unclear, since the majority of studies that formed the basis of published recommendations for feeding ICU patients were either observational or small interventional studies.3,4 Recently, the field of critical care nutrition has been revived by the findings of several randomized, controlled trials, which have opened a new debate on nutritional practice in the ICU. For this review, we focus on evidence from randomized, controlled studies that met the follo Continue reading >>

Lactic Acidosis - Now@nejm Now@nejm

Lactic Acidosis - [email protected] [email protected]

Posted by Carla Rothaus December 11th, 2014 When lactic acidosis accompanies low-flow states or sepsis, mortality rates increase sharply. A new review summarizes our current understanding of the pathophysiological aspects of lactic acidosis, as well as the approaches to its diagnosis andmanagement. Lactic acidosis results from the accumulation of lactate and protons in the body fluids and is often associated with poor clinical outcomes. The effect of lactic acidosis is governed by its severity and the clinical context. Mortality is increased by a factor of nearly three when lactic acidosis accompanies low-flow states or sepsis, and the higher the lactate level, the worse theoutcome. Hyperlactatemia occurs when lactate production exceeds lactate consumption. In tissue hypoxia, whether global or localized, lactate is overproduced and underutilized as a result of impaired mitochondrial oxidation. Even if systemic oxygen delivery is not low enough to cause generalized hypoxia, microcirculatory dysfunction can cause regional tissue hypoxia and hyperlactatemia. Hyperlactatemia can also result from aerobic glycolysis, a term denoting stimulated glycolysis that depends on factors other than tissue hypoxia. Activated in response to stress, aerobic glycolysis is an effective, albeit inefficient, mechanism for rapid generation of ATP. In the hyperdynamic stage of sepsis, epinephrine-dependent stimulation of the (beta)2-adrenoceptor augments the glycolytic flux both directly and through enhancement of the sarcolemmal Na+,K+-ATPase (which consumes large quantities of ATP). Other disorders associated with elevated epinephrine levels, such as severe asthma (especially with overuse of beta2-adrenergic agonists), extensive trauma, cardiogenic or hemorrhagic shock, and pheochromocytoma, Continue reading >>

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