Linfoma marginal del bazo asociado a acidosis láctica tipo B: Caso clínico / Type B lactic acidosis associated with marginal lymphoma of the spleen: Report of one case

Lactic acidosis in the absence of hypoxia or tissue hypoperfusion (type B) is very rare and is associated with the use of some drugs or malignancy. We report a 79-year-old woman, with a marginal non-Hodgkin's lymphoma of the spleen that was subjected to a splenectomy one year ago. She presented with unexplained tachypnea associated with pancytopenia and elevation of IgM to 10 times over the higher normal limit. Laboratory tests showed the presence of metabolic acidosis and high lactic acid levels in the absence of infection, tissue hypoxia or hypoperfusion. She was treated with sodium bicarbonate and steroids without obtaining a reduction in lactate levels. Twelve days after admission, a single dose of Rituximab quickly normalized lactate concentrations and platelet count. After the fourth dose of Rituximab, pancytopenia disappeared and IgM fell to 25% of its baseline concentration.

D-lactoacidosis como complicación del síndrome de intestino corto / D-lactoacidosis as short bowel syndrome complication

Short bowel syndrome is defined as the loss, congenital or acquired, anatomical or functional, of a large part of the small intestine that generates inadequate absorption of nutrients and the frequent need of prolonged parenteral nutrition. The etiology of short bowel is diverse and varies with age. The necrotizing enterocolitisis and the midgut volvulus are among the most frequent causes. The bacterial overgrowth is frequently observed in children with short bowel, due to the secondary dilation of the remaining small bowel and to the associated intestinal dysmotility. It is more frequent in absence of the ileocecal valve. We present a 6-year-old boy with short bowel syndrome secondary to extensive intestinal resection after a volvulous of the medium small intestine, 9 months before admission to the hospital, and who was on cyclical parenteral nutrition at home. The child developed ataxia, disarthria, dizziness and conscience compromise been admitted to de intensive care unit in deep sopor. An extensive work up including metabolic, infectious, toxicology and SNC imaging was negative except for metabolic acidosis. He was discharged on good conditions. Even though the child was on supportive therapy, the patient was readmitted few hours later with similar symptoms. D-lacto acidosis was suspected and confirmed with a value of 6.69 mmol/1 (normal range: 0,0-0,25). Literature about this uncommon complication and its mechanism is reviewed. D-lacto acidosis should be suspected in every patient with short bowel syndrome and unexplained metabolic acidosis associated with neurological symptoms.

El síndrome de intestino corto se define como la pérdida, congénita o adquirida, anatómica o funcional, de una extensa área del intestino delgado que genera inadecuada absorción de nutrientes y la frecuente necesidad de nutrición parenteral prolongada. Su etiología varía con la edad. Entre las causas más frecuentes están la enterocolitis necrotizante y el vólvulo de intestino medio. El sobrecrecimiento bacteriano es frecuente en estos pacientes, debido a la dilatación secundaria del remanente de intestino delgado y a la dismotilidad intestinal asociada. Objetivo: Comunicar un caso de acidosis D-láctica en un niño con Intestino corto. Caso clínico: Niño de 6 años con antecedente de intestino corto secundario a resección intestinal por vólvulo de intestino medio 9 meses previos al ingreso y que estaba recibiendo nutrición parenteral domiciliaria ciclada. El niño desarrolló ataxia, disartria, mareos y compromiso de conciencia, ingresando a la unidad de cuidados intensivos en sopor profundo. Un extenso estudio metabólico, infectológico, toxicológico y de neuroimágenes fue negativo, excepto por acidosis metabólica. Fue dado de alta en buenas condiciones. A pesar del tratamiento de soporte vuelve a ingresar horas después con similar cuadro clínico. Se sospecha y confirma elevación de D-lactato en sangre (6,69 mmol/1 con rango normal de 0,0-0,25). Se revisa la literatura acerca de esta infrecuente complicación y su mecanismo de producción. La D-lactoacidosis debiera ser sospechada en todos los pacientes portadores de intestino corto que presenten un cuadro de acidosis metabólica no explicada, especialmente si se acompaña de compromiso de conciencia y síntomas cerebelosos.

Uso de bicarbonato de sódio na acidose metabólica do paciente gravemente enfermo / Sodium bicarbonate in the critically ill patient with metabolic acidosis

A acidose lática é um distúrbio do equilíbrio ácido-base muito frequente em pacientes internados em unidades de terapia intensiva e está associado a um mau prognóstico. Embora exista um acúmulo substancial de evidências de que níveis cítricos de acidemia provocam inúmeros efeitos adversos sobre o funcionamento celular, a utilização de bicarbonato de sódio para o tratamento da acidose lática em pacientes gravemente enfermos permanece alvo de controvérsias. Neste artigo, pretendemos:1) analisar as principais diferenças entre as acidoses hiperclorêmicas e as acidoses orgânicas, com ânion gap (AG) elevado, visando embasar a discussão sobre os fundamentos da terapia com bicarbonato de sódio nas acidoses metabólicas; 2) avaliar os riscos associados à persistência de níveis críticos de acidemia, contrastando-os com os riscos do uso de bicarbonato de sódio; 3) analisar criticamente as evidências da literatura sobre o uso de bicarbonato de sódio no tratamento da acidose lática do paciente crítico, com ênfase em ensaios clínicos randomizados em seres humanos; 4) fornecer um fundamento para a utilização judiciosa de bicarbonato de sódio nesta situação.

Lactic acidosis is a disorder of acid-base balance very common in patients hospitalized in intensive care units and is associated with a poor prognosis. Although there is a substantial accumulation of evidence that levels of citric acidemia leading to numerous adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains a subject of controversies. In this article we will: 1) analyze the main differences between the hyperchloremic acidosis and organic acidosis with anion gap (AG) high, in order to base the discussion on the fundamentals of therapy with sodium bicarbonate in metabolic acidosis, 2) assess the risks associated with the persistence of critical levels of acidemia, contrasting them with the risks of using sodium bicarbonate, 3) critically examine the evidence in the literature about the use of sodium bicarbonate in treating lactic acidosis in critically ill patients, with emphasis on tests clinical trials in humans, 4) provide a foundation for the judicious use of sodium bicarbonate in this situation.

Cirugía de revascularización miocárdica: predictores de evolución / Myocardial revascularization surgery: evolution predictors

Introducción: El objetivo buscado en esta investigación científica es identificar los factores relacionados con la evolución posoperatoria en pacientes que se someten a cirugía de revascularización miocárdica (CRM) con circulación extracorpórea (CPB). Objetivo: Identificar los factores relacionados con la evolución posoperatoria en pacientes que se someten a cirugía de revascularización miocárdica (CRM) con circulación extracorpórea (CPB). Material y métodos: Diseño: estudio retrospectivo observacional analítico. Sujetos: Se incluyeron pacientes sometidos a CRM con CPB en el Hospital San Juan de Dios de La Plata, desde el 01/04/07 al 30/03/08. Se excluyeron los pacientes > 70 años y las urgencias. Se registraron como variables independientes: edad; sexo; ASA; experiencia del cirujano; diabetes; glucemias basal y de egreso; lactacidemias basal y de egreso; minutos de clampeo aórtico (XCL) y minutos al destete de CPB. Las variables de resultado fueron: horas de apoyo inotrópico (1); horas de ventilación mecánica (VM); días de estancia posoperatoria (EH) y mortalidad. Las comparaciones de porcentajes se realizaron con la prueba exacta de Fisher a una cola. Para comparar variables cuantitativas se utilizó prueba de Mann-Whitney. Resultados: Se analizaron los datos de 116 pacientes, de los cuales 15 fallecieron (12,93 por ciento). Conclusiones: Se observó peor evolución posoperatoria en mujeres en las que la CPB fue mayor que 90 minutos, en pacientes con valores de glucemia > 130 mg/dl y en aquellos con lactacidemia de egreso > 4 mmol/l. Los pacientes con ASA IV requirieron inotrópicos por más tiempo.

Introduction: To identify factors associated with postoperative evolution in patients undergoing myocardial revascularization surgery (CRM) with cardiopulmonary bypass (CPB). Materials and methods: Retrospective analytical observational study. Patients undergoing CRM with CPB between 01/04/07 and 30/03/08. Exclusions: patients > 70 years and emergencies. Registered independent variables: age, gender, ASA; surgeon's experience; diabetes; basal and end-of-surgery glycaemia and lactacidemia levels, aortic cross clamping time, CPB time and weaning time. Variable result: inotropic support (1) time, mechanical ventilation (VM) time; hospital postoperative stay (EPOP) and mortality. Percentage comparisons: Fisher exact test to a queue, quantitative variables: Mann-Whitney test. Results: Data Analysis of 116 patients, 12.93 per cent of whom died. Conclusions: complicated outcome in women, > 90 'CPB in patients with blood glucose > 130 mg/dl and lactacidemia > 4mmol/l at end of surgery. ASA IV patients required more inotropic time.

Introdução: O objetivo buscado nesta investigação científica é identificar os fatores relacionados com a evolução pós-operatória de pacientes submetidos a cirurgia de revascularização miocárdica (CRM) com circulação extracorpórea (CPB). Material e métodos: Desenho: estudo retrospectivo observacional analítico. Sujeitos: Foram incluídos pacientes submetidos a CRM com CPB no Hospital San Juan de Dios de La Plata no período de 1° de abril de 2007 a 30 de março de 2008, e excluídos os pacientes > 70 anos e as urgências. Registraram-se como variáveis independentes: idade; sexo; ASA; experiência do cirurgião; diabetes; glicemias basal e de egresso; lactacidemias basal e de egresso; minutos de clampeamento aórtico (XCL) e minutos até o desmame da CPB. As variáveis de resultado foram: horas de apoio inotrópico (1); horas de ventilação mecânica (VM); dias de estádio pós-operatório (EH) e mortalidade. Para as comparações das porcentagens foi utilizada a prova exata de Fisher, e para comparar variáveis quantitativas se uso u a prova de Mann-Whitney. Resultados: Foram analisados os dados de 116 pacientes, 15 dos quais faleceram (12,93 por cento). Conclusoes: Comprovou-se pior evolução pós-operatória em mulheres nas quais a CPB foi maior que 90 minutos, em pacientes com valores de glicemia > 130 mg/dl e em aqueles com lactacidemia de egresso > 4 mmol/l. Os pacientes com ASA IV requereram inotrópicos durante mais tempo.

A preliminary study of thiamine status in northeastern Thai children with acute diarrhea.

This study is a preliminary determination of thiamine status in children with diarrhea and metabolic acidosis admitted to hospital. Children with diarrhea (N = 14; age 2 m-6 yr) were divided into 2 groups according to anion gap type; group 1 (21.4%) with a normal anion gap (5.5 +/- 5.2 mmol/l) and group 2 (78.6%) with a wide anion gap (21.2 +/- 5.2 mmol/l). Blood was taken on the day of admission to determine thiamine and lactate levels. Sixty-six point seven percent of patients in group 1 had a normal lactate level (1.5 +/- 0.8 mmol/l) and 33.3% had a high lactate level (2.2 mmol/l); none had thiamine deficiency (TPPE < 20%). High lactate (3.5 +/- 1.4 mmol/l) was found in 54.5% of group 2 and thiamine deficiency was observed in 18.2% of this group. In conclusion, no thiamine deficiency was noted in patients with normal anion gap, but thiamine deficiency was not uncommon in patients with a wide anion gap, regardless of lactic acidosis.

Unmeasured anions account for most of the metabolic acidosis in patients with hyperlactatemia

PURPOSE: To characterize the different components of metabolic acidosis in patients with hyperlactatemia in order to determine the degree to which lactate is responsible for the acidosis and the relevance that this might have in the outcome of these patients. METHODS: Arterial blood gas, arterial lactate, Na+, K+, Ca2+, Mg2+, Cl-, phosphate, albumin, and creatinine were measured on admission to make a diagnosis of the acid-base disturbances present. Intensive Care Unit and in-hospital mortality were also recorded. RESULTS: A total of 58 patients with hyperlactatemia were included. They usually had a mild acidemia (pH 7.31 ± 0.12) and a significantly high Standard Base Deficit (7.6 ± 6.7 mEq/L). In addition to lactate (4.3 ± 2.3 mEq/L), chloride (106.9 ± 9.5 mEq/L) and unmeasured anions (8.6 ± 5.0 mEq/L) accounted for the metabolic acidosis. Unmeasured anions were primarily responsible for the acidosis in both Intensive Care Unit survivors and nonsurvivors (44.7 percent ± 26.0 percent and 46.0 percent ± 17.5 percent, respectively, P = 0.871). Lactate contributed in similar percentages to the acidosis in both groups (23.0 percent ± 11.8 percent and 24.2 percent ± 9.7 percent in Intensive Care Unit survivors and nonsurvivors, respectively; P = 0.753). Correlation between Standard Base Deficit and lactate was found only in Intensive Care Unit nonsurvivors (r = 0.662, P < 0.01). DISCUSSION: Hyperlactatemia is usually accompanied by metabolic acidemia, but lactate is responsible for a minor percentage of the acidosis; unmeasured anions account for most of the acidosis in patients with hyperlactatemia. The percentage of the acidosis due to hyperlactatemia was not relevant in terms of outcome.

OBJETIVO: Caracterizar os diferentes componentes da acidose metabólica de pacientes com hiperlactatemia de modo a verificar o quanto o lactato é responsável pela acidose e a relevância que isso possa ter no prognóstico desses pacientes. MÉTODOS: Gasometria arterial com dosagem de lactato, Na+, K+, Ca2+, Mg2+, Cl-, fosfato, albumina e creatinina séricas foram coletados no momento da admissão para fazer o diagnóstico dos possíveis distúrbios ácido-básicos presentes. Mortalidade na UTI e mortalidade hospitalar foram avaliadas. RESULTADOS: Um total de 58 pacientes com hiperlactatemia foram incluídos. Eles tinham na média uma acidemia leve (pH 7.31 ± 0.12) e o déficit de base significativamente elevado (7.6 ± 6.7 mEq/L). Além do lactato (4.3 ± 2.3 mEq/L), o cloro (106.9 ± 9.5 mEq/L) e os ânions não mensuráveis (8.6 ± 5.0 mEq/L) contribuíram para a acidose metabólica. Os ânions não mensuráveis foram responsáveis pela maior parcela da acidose tanto nos pacientes que tiveram alta da UTI como nos que faleceram (44.7 ± 26.0 por cento e 46.0 ± 17.5 por cento, respectivamente, p= 0.871). O lactato contribuiu em percentagens semelhantes para a acidose em ambos os grupos (23.0 ± 11.8 por cento nos sobreviventes e 24.2 ± 9.7 por cento nos óbitos, p= 0.753). Correlação entre o déficit de base e o lactato somente foi encontrada nos óbitos (r = 0.662, p < 0.01). DISCUSSÃO: Hiperlactatemia é comumente acompanhada de acidemia metabólica, porém o lactato corresponde a uma parcela minoritária da acidose; ânions não mensuráveis contribuem com a maior parte da carga ácida em pacientes hiperlactatêmicos. O percentual da acidose devido à hiperlactatemia não foi relevante em termos de prognóstico.

A typical presentation of acute myeloid leukemia.

A young man who presented with fever, altered sensorium and sudden onset tachypnea, is described. Arterial blood gas analysis, revealed the presence of severe high anion gap metabolic acidosis, with compensatory respiratory alkalosis and normal oxygen saturation. A detailed neurological, nephrological, biochemical and hematological evaluation, revealed the presence of Acute myeloid leukemia, with lactic acidosis and hyponatremia. There are very few reports of presentation of leukemia as lactic acidosis. This case report highlights the need for emergency room physicians, to consider the possibility of lactic acidosis, as one of the causes of high anion gap acidosis and to meticulously investigate the cause of lactic acidosis. We describe a rare clinical instance of lactic acidosis as the presenting manifestation of Acute myeloid leukemia.

Influence of disease and drug factors on metformin daily dose

Metformin may, in the presence of certain risk factors, cause serious lactic acidosis. The aim of this study was to investigate the presence of risk factors for lactic acidosis among diabetic patients and to determine whether metformin daily dose was influenced by the presence of these risk factors or not. One hundred and eighteen patients were included in the study. Information about disease status and medication profile of the patient was retrieved from patient's medical files who were having diabetes mellitus and prescribed metformin. Approximately, tow thirds [74/118, 62.7%] of the included patients had a least one disease risk factor for lactic acidosis. Of those patients, [48/74; 64.9%] had a dose adjustment, with congestive heart failure and renal impairment being the risk factors most likely to result in a dose adjustment. More than one third [38%] of metformin patients were co-prescribed ACE-I or NSAIDs. The dose of metformin was insignificantly influenced by the co-administration of drug risk factors. Metformin total dialy dose was significantly influenced by the presence of disease risk factors and was insignificantly influenced by the co-administration of drug risk factors. Short running title: Risk Factors and Metformin Dose

Acidosis láctica: algunas consideraciones / Some reflections on lactic acidosis

La hiperlactacidemia significa clínicamente problemas para los pacientes. La acidosis láctica es un trastorno ácido-básico consecutivo a la acumulación del ácido láctico, el cual se comporta en el nivel celular, como la contrapartida reducida del ácido pirúvico. Este último, resulta de la degradación de la glucosa en el citosol, proceso que se realiza de manera anaoeróbica y que puede culminar en CO2 H2O si sigue la vía del ácido cítrico de Krebs. El diagnóstico de esta entidad se confirma al medir la concentración sanguínea del lactato, aunque existen diversas características clínicas y de laboratorio que dan indicios de la existencia de este trastorno. Las causas de acidosis láctica se dividen en las producidas por hipoxia hística (tipo A) y las no producidas por este trastorno (tipo B); dentro de estas últimas se sitúan las debidas a alteraciones sistémicas, al uso de fármacos o toxinas y a las que acompañan a errores innatos del metabolismo

Biguanidas (metformin) y acidosis láctica. Reporte de un caso y revisión de la literatura / Biguanides (metformin) and lactic acidosis. case report

Introducción. El metformin puede desencadenar acidosis láctica en presencia de insuficiencia renal aguda. Objetivo. Reportar un caso de acidosis láctica secundaria a metformin en presencia de función renal normal. Reporte del caso. Un paciente de 45 años de edad con historia de diabetes mellitus no insulino-dependiente, tipo 2, ingresó a una ICU. Tenía vómito y debilidad después de 13 días de tratamiento con metformin (2,000 mg/d). Al ingreso tenía TA 80/40, FC 110/min. FR 32/min. Laboratorio: pH 6.77, PaCO2 10mmHg, PaO2 300 mmHg, glucosa 79 mg/dL, urea 191 mg/dL, creatinina 9.5 mg/dL, ácido láctico 34 mmol/L. Se realizaron maniobras enérgicas que incluyeron ventilación mecánica, administración de líquidos y diálisis peritoneal; se recuperó rápidamente y se dio de alta a su domicilio cinco días depués

Tratamiento de intoxicaciones / Treatment of the intoxications

Se trataron 8 pacientes intoxicados por diferentes métodos: hemoperfusión, hemodiálisis, diálisis peritoneal afectados de diferentes tóxicos (se desarrolla botulismo, bromato de potasio y metanol), se discuten las indicaciones de tratamiento

Acidosis láctica: diagnóstico y tratamiento; revisión bibliográfica / Lactic acidosis: diagnosis and treatment; bibliographic review

La acidosis láctica es una complicación poco frecuente de la diabetes, y no es exclusiva de la misma, sin embargo, es uno de los estados más grave al que puede evolucionar un diabético. La misma puede ocurrir cuando existe un aporte deficiente de oxígeno a los tejidos, o cuando hay un incremento en la producción de lactato o su eliminación está disminuida. Los trastornos sistémicos, drogas, toxinas y los defectos enzimáticos congénitos, también pueden ser causa de acidosis láctica. La aparición de hiperlactatemia y eventualmente, acidosis láctica en el diabético, está siempre relacionada con una diabetes complicada o en la que concurren alguna de las condiciones antes señaladas. El mejor conocimiento de las vías bioquímicas que modulan las concentraciones de lactato en el organismo ha dado lugar a nuevos enfoques terapéuticos, entre los que pueden señalarse: suspensión de las drogas implicadas, alcalinizantes, hemodiálisis, diálisis peritoneal, sustancias que facilitan el metabolismo del ácido láctico e insulinoterapia en algunos casos. El reconocimiento precoz y la institución de un tratamiento enérgico y adecuado, son de vital importancia en el tratamiento de estos enfermos