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Lactic Acidosis Treatment Guidelines

High Incidence Of Lactic Acidosis And Symptomatic Hyperlactatemia In Women Receiving Highly Active Antiretroviral Therapy In Soweto, South Africa | Clinical Infectious Diseases | Oxford Academic

High Incidence Of Lactic Acidosis And Symptomatic Hyperlactatemia In Women Receiving Highly Active Antiretroviral Therapy In Soweto, South Africa | Clinical Infectious Diseases | Oxford Academic

Background. Lactic acidosis and symptomatic hyperlactatemia may complicate nucleoside reverse-transcriptase inhibitor use. Females may be at increased risk for such complications. Our study evaluated the incidence of lactic acidosis and symptomatic hyperlactatemia by sex, analyzed clinical features, and described the safety of reintroducing highly active antiretroviral therapy (HAART) with zidovudine replacing stavudine. Methods. A retrospective cohort analysis was performed for 1735 adults (63% of whom were female) who initiated HAART from April 2004 through August 2005 in Soweto, South Africa, with follow-up until February 2006. Patients with lactate levels 4.5 mmol/L and no potential cause of elevated lactic acidosis other than receipt of HAART were included in the study. Results. A total of 23 patients (22 of whom were female) experienced lactic acidosis. The overall incidence was 10.6 cases per 1000 patient-years; the incidence was 16.1 cases per 1000 patient-years in female patients and 1.2 cases per 1000 patient-years in male patients. Seven (30.4%) of the patients died. Eight (34.8%) of the patients were obese (body mass index [calculated as weight in kilograms divided by the square of height in meters], <30) at HAART initiation. Forty-four patients (37 of whom were female) had symptomatic hyperlactatemia. The overall incidence was 20.2 cases per 1000 patient-years, with an incidence of 27.0 cases per 1000 patient-years in female patients and 8.7 cases per 1000 patient-years in male patients. None of the patients died. Nine (20.4%) of the patients were obese at HAART initiation. Sixty-six of 67 patients were receiving stavudine, and 5 patients were receiving didanosine. Among 56 patients who restarted HAART with zidovudine for a cumulative nucleoside reverse-tr Continue reading >>

Metformin Associated Lactic Acidosis

Metformin Associated Lactic Acidosis

Emma Fitzgerald, specialist trainee year 2 in anaesthetics 1, Stephen Mathieu, specialist registrar in anaesthetics and intensive care medicine1, Andrew Ball, consultant in anaesthesia and intensive care medicine1 1Dorset County Hospital, Dorchester, Dorset DT1 2JY Correspondence to: E Fitzgerald zcharm6{at}hotmail.com Dehydration in patients taking metformin can lead to metformin associated lactic acidosis, a potentially fatal condition Metformin, a dimethylbiguanide, is a widely used oral antihyperglycaemic drug used in the long term treatment of type 2 diabetes mellitus. More recently it has also been used to improve fertility and weight reduction in patients with polycystic ovary syndrome. Many large studies have shown that intensive glucose control with metformin in overweight patients with type 2 diabetes is associated with risk reductions of 32% (P=0.002) for any diabetes related end point, 42% (P=0.017) for diabetes related death, and 36% (P=0.011) for all cause mortality compared with diet alone.1 Furthermore, metformin reduces microvascular end points, and its degree of glycaemic control is similar to that sulphonylureas and insulin. Metformin is considered to be first line treatment in overweight patients with type 2 diabetes whose blood glucose is inadequately controlled by lifestyle interventions alone and should be considered as a first line glucose lowering treatment in non-overweight patients with type 2 diabetes because of its other beneficial effects.2 It may also be useful in overweight patients with type 1 diabetes. A potential complication of metformin is the development of type B (non-hypoxic) lactic acidosis. Although metformin associated lactic acidosis is a rare condition, with an estimated prevalence of one to five cases per 100 000 population 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 >>

Metformin-induced Lactic Acidosis: No One Left Behind

Metformin-induced Lactic Acidosis: No One Left Behind

Abstract Metformin is a safe drug when correctly used in properly selected patients. In real life, however, associated lactic acidosis has been repeatedly, although rarely, reported. The term metformin-induced lactic acidosis refers to cases that cannot be explained by any major risk factor other than drug accumulation, usually due to renal failure. Treatment consists of vital function support and drug removal, mainly achieved by renal replacement therapy. Despite dramatic clinical presentation, the prognosis of metformin-induced lactic acidosis is usually surprisingly good. In the previous issue of Critical Care, Friesecke and colleagues demonstrate that the survival rate of patients with severe lactic acidosis due to metformin accumulation can be strikingly higher than expected based on the initial clinical evaluation [1]. Metformin is nowadays the first-line drug of choice for the treatment of adults with type 2 diabetes [2]. This drug is the sixth most frequently prescribed in the USA (> 50 million prescriptions in 2009) and is taken by almost 1.5% of the Italian population [3, 4]. Metformin is a safe drug when correctly used in properly selected patients. In particular, no cases of lactic acidosis (a relatively common side effect of other biguanide compounds) were reported in 347 trials with 70,490 patient-years of metformin use [5]. Real life can differ from research settings, however, and lactic acidosis has been repeatedly, although rarely, observed in patients treated with metformin. The number of inquiries to the Swedish Poison Information Centre for metformin intoxication has increased 10 times during the past decade, with 25 cases of severe lactic acidosis reported in 2007 and 2008 [6]. According to the American Association of Poison Control Centers, metform Continue reading >>

Treatment Of Lactic Acidosis.

Treatment Of Lactic Acidosis.

Severe lactic acidosis is often associated with poor prognosis. Recognition and correction of the underlying process is the major step in the treatment of this serious condition. Intravenous administration of sodium bicarbonate has been the mainstay in the treatment of lactic acidosis. Aggressive use of this therapeutic modality, however, can lead to serious complications and should therefore be considered with caution. Peritoneal dialysis and hemodialysis provide large amounts of alkali without causing the hypernatremia or hypervolemia commonly associated with bicarbonate infusion. Peritoneal dialysis with bicarbonate-based dialysate, in particular, appears to be an ideal means of delivering physiologic buffer. Administration of methylene blue was initially thought to increase lactate metabolism by altering the cellular oxidative state. Its subsequent clinical use, however, showed little efficacy. Sodium nitroprusside has been advocated for the treatment of some forms of lactic acidosis as a method of alleviating regional hypoperfusion. Insulin therapy has been found to be quite useful in the treatment of phenformin-associated lactic acidosis and is recommended in this setting. Since dichloroacetate activates pyruvate dehydrogenase and enhances lactate metabolism, it may be a useful adjunct in the treatment of lactic acidosis. Continue reading >>

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Open Access funded by Sociedad Colombiana de Anestesiologa y Reanimacin Lactic acidosis is defined as the presence of pH <7.35, blood lactate >2.0mmol/L and PaCO2 <42mmHg. However, the definition of severe lactic acidosis is controversial. The primary cause of severe lactic acidosis is shock. Although rare, metformin-related lactic acidosis is associated with a mortality as high as 50%. The treatment for metabolic acidosis, including lactic acidosis, may be specific or general, using sodium bicarbonate, trihydroxyaminomethane, carbicarb or continuous haemodiafiltration. The successful treatment of lactic acidosis depends on the control of the aetiological source. Intermittent or continuous renal replacement therapy is perfectly justified, shock being the argument for deciding which modality to use. We report a case of a male patient presenting with metformin poisoning as a result of attempted suicide, who developed lactic acidosis and multiple organ failure. The critical success factor was treatment with continuous haemodiafiltration. Definimos acidosis lctica en presencia de pH <7.35, lactato en sangre >2.0mmol/L y PaCO2 <42mmHg. Por otro lado, la definicin de acidosis lctica grave es controvertida. La causa principal de acidosis lctica grave es el estado de choque. La acidosis lctica por metformina es rara pero alcanza mortalidad del 50%. La acidosis metablica incluyendo a la acidosis lctica puede recibir tratamiento especfico o tratamiento general con bicarbonato de sodio, trihidroxiaminometano, carbicarb o hemodiafiltracin continua. El xito del tratamiento de la acidosis lctica yace en el control de la fuente etiolgica; la terapia de reemplazo renal intermitente o continua est perfectamente justificada, donde el argumento para decidir cul utilizar ser el estado de 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 >>

Can You Treat Lactic Acidosis By Dialysis?

Can You Treat Lactic Acidosis By Dialysis?

Can you treat lactic acidosis by dialysis? 10 Comments on Can you treat lactic acidosis by dialysis? Managing patients with lactic acidosis, especially the type A variety, is really hard! Usually they have multiple problems, are septic, hypotensive, often on multiple machines and the lactate keeps going up. The choices are between giving soda bicarb, carbicarb or dichloroacetate. The main purpose is to avoid some of complications of severe acidosis such arrhythmias, decreased response to cathechloamines, or reduced contractility. Bicarbonate therapy is a double-edged sword, however, because of the several side-effects such as decreased cardiac output, reduced ionized cardiac output, increased CO2 generation, volume overload and increased lactate generation. Paradoxically, it can also worsen intracellular acidosis. Staff managing these patients think that it would be great to simply clear it out using an extracorporeal therapy, such as hemodialysis or CRRT. Unfortunately it usually does not work. Lactate clearance by dialysis is only 3% of the overall clearance, most of which is in the tissue. In one study, they evaluated the utility of continuous venovenous hemofiltration with dialysis, to calculate lactate clearance by the hemofilter in 10 critically ill patients with acute renal failure and stable blood lactate concentrations. They found that the median blood lactate concentration increased despite renal replacement therapy. The median total plasma lactate clearance was 1379 ml/min (range, 754 to 1881 ml/min), and the median filter lactate clearance was 24 ml/min (range, 7 to 36 ml/min). The authors concluded that continuous venovenous hemofiltration with dialysis cannot meet lactate overproduction. Moreover, the generation of lactic acid is at least order of magnitu Continue reading >>

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update for Critical Care Clinicians Franz Volhard Clinic and Max Delbrck Center for Molecular Medicine, Medical Faculty of the Charit Humboldt University of Berlin, Berlin, Germany. Correspondence to Dr. Friedrich C. Luft, Wiltberg Strasse 50, 13125 Berlin, Germany. Phone: 49-30-9417-2202; Fax: 49-30-9417-2206; E-mail: luft/{at}fvk-berlin.de Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO3 increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO3 is of little value. Carbicarb is a mixture of Na2CO3 and NaHCO3 that buffers similarly to NaHCO3 but without net generation of CO2. The results from animal stud Continue reading >>

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... 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 a Continue reading >>

Treatment Of Metformin-associated Lactic Acidosis With Closed Recirculation Bicarbonate-buffered Hemodialysis

Treatment Of Metformin-associated Lactic Acidosis With Closed Recirculation Bicarbonate-buffered Hemodialysis

Treatment of Metformin-Associated Lactic Acidosis With Closed Recirculation Bicarbonate-Buffered Hemodialysis To the Editor. The use of massive amounts of intravenous (IV) sodium bicarbonate in the management of lactic acidosis seems necessary as soon as the acidosis becomes severe.1 However, some patients have an apparent resistance to this alkali therapy.2 In addition, intensive administration of sodium bicarbonate carries the combined risks of volume and sodium overload. Several authors tried hemodialysis (HD) or peritoneal dialysis (PD) but, most of the time, the precarious hemodynamic state of these patients limits the use of conventional HD.3,4 The new possibilities allowing the use of dialysate containing bicarbonate in HD have led us to try this method in the case of a metformin-treated diabetic with severe lactic acidosis.5 Report of a Case. A 64-year-old woman was admitted to the hospital in severe shock. Despite chronic renal failure (serum creatinine level of 300 moles/L, she was given 1,700 mg/day of metformin for six Continue reading >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Hiv & Aids Information :: Factsheet Lactic Acidosis

Hiv & Aids Information :: Factsheet Lactic Acidosis

Please enter the email address. Separate multiple addresses with a comma. Lactic acidosis refers to a build-up of lactic acid in the blood. It is a rare but dangerous side-effect of some anti-HIV drugs most of these are no longer in regular use. Your HIV clinic will use blood tests to check your levels of lactic acid. Lacticacidosis is very rare. Nevertheless, it is an important subject to understandbecause people who develop the condition can become dangerously ill. Lacticacidosis is a serious side-effect of the nucleosidereverse transcriptaseinhibitor (NRTI)class of anti-HIV drugs. This class includes abacavir (Ziagen),didanosine (ddI, Videx), lamivudine (3TC, Epivir), stavudine (d4T,Zerit), tenofovir (Viread) andzidovudine (AZT, Retrovir). The drugsmost linked with lactic acidosis are stavudine and didanosine. However, neitherof these drugs is now used if any other treatment options are available, mainlybecause of the side-effects they can cause. Lactic acidosis is also apotential, but rare, side-effect of other drugs, including the commonlyprescribed diabetes drug, metformin. The term lactic acidosis is used to describehigh levels of a substance called lactate in the blood. Lactate is a by-productof the processing of sugar within the body. Lacticacidosis is one of several conditions which are believed to be caused by damage to mitochondria . Mitochondriaare found in all human cells and are involved in the production of energy.Other possible side-effects ofNRTIs which may also be associated withdamage to mitochondria include peripheral neuropathy (numbness or pain in the feetand hands); bone marrow suppression; pancreatitis (inflammation of thepancreas); hepatic steatosis (accumulation of fat in the liver); and myopathy(muscle damage). "Lactic acidosis may occurat a Continue reading >>

Lactic Acidosis - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i Continue reading >>

Sustained Low-efficiency Dialysis As A Treatment Modality In A Patient With Lymphoma-associated Lactic Acidosis

Sustained Low-efficiency Dialysis As A Treatment Modality In A Patient With Lymphoma-associated Lactic Acidosis

Sustained low-efficiency dialysis as a treatment modality in a patient with lymphoma-associated lactic acidosis Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Correspondence and offprint requests to: M. Prikis, Division of Nephrology, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA. Email: [email protected] Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works by this author on: Division of Nephrology, Fletcher Allen Health Care and the University of Vermont College of Medicine and 2Division of Pulmonary and Critical Care, Department of Medicine, Fletcher Allen Health Care and the University of Vermont College of Medicine, 1 South Prospect Street, Rehab 201, 05401-1473 Burlington VT, USA Search for other works Continue reading >>

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