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ABSTRACT Introduction: hemorrhagic shock is a significant cause of trauma-related deaths in Brazil and worldwide. This study aims to compare BE and lactate values at ICU admission and twenty-four hours after in identifying tissue hypoperfusion and mortality. Methods: examines a historical cohort of trauma patients over eitheen years old submittet to damage control resuscitation approch upon hospital admission and were then admitted to the ICU. We collected and analyzed ISS, mechanism and type of trauma, need for renal replacement therapy, massive transfusion. BE, lactate, pH, bicarbonate at ICU admission and twenty-four hours later, and mortality data. The patients were grouped based on their BE values (≥-6 and <-6mmol/L), which were previously identified in the literature as predictors of severity. They were subsequently redivided using the most accurate values found in this sample. In addition to performing multivariate binary logistic regression. The data were compared using several statistical tests due to diversity and according to the indication for each variable. Results: there were significant changes in perfusion upon admission to the Intensive Care Unit. BE is a statistically significant value for predicting mortality, as determined by using values from previous literature and from this study. Conclusion: the results demonstrate the importance of monitoring BE levels in the prediction of ICU mortality. BE proves to be a valuable bedside marker with quick results and wide availability.

RESUMO Introdução: o choque hemorrágico é a principal causa reversível de morte no trauma no Brasil e no mundo. Objetivo: comparar o valor de BE ao do lactato na admissão da UTI e vinte e quatro horas após o internamento na identificação de hipoperfusão tecidual e predição de mortalidade Método: coorte histórica de pacientes traumatizados, maiores de dezoito anos, submetidos à estratégia de controle de danos na admissão hospitalar, seguido de internamento em UTI. Foram coletados e analisados ISS, mecanismo e tipo de trauma, necessidade de terapia de substituição renal e transfusão maciça; BE, lactato, pH e bicarbonato coletados na admissão da UTI e vinte e quatro horas após, e a mortalidade. Os pacientes foram divididos em grupos conforme valores de BE (≥-6 e <-6mmol/L) já descritos na literatura como preditores de gravidade, e após redivididos de acordo com os valores de melhor acurácia encontrados nesta amostra, além de realização de regressão logística binária multivariada. Os dados foram comparados através de diversos testes estatísticos devido a diversidade e conforme a indicação para cada variável. Resultados: houve alterações perfusionais impactantes já na admissão da UTI. BE manteve-se com valor estatisticamente significativo para predição de mortalidade tanto quando utilizado os valores já conhecidos da literatura como quando aplicados os valores neste estudo identificados. Conclusão: valores de BE e de lactato foram capazes de predizer hipoperfusão tecidual e mortalidade nos dois momentos estudados, quando comparados, o BE tem boa performance como preditor de mortalidade, com rápido resultado e ampla disponibilidade.

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La metformina es el fármaco preferido en el manejo inicial de la diabetes mellitus tipo 2 (DMT2). Aunque se recomienda su uso ampliamente, se debe tener precaución al prescribirla a poblaciones susceptibles a condiciones de riesgo de hipoperfusión sistémica, ya que puede provocar acumulación en el organismo y alteraciones metabólicas que desemboquen en acidosis láctica asociada a metformina, una complicación grave que a menudo es subdiagnosticada. Con el propósito de promover un mejor conocimiento sobre este tema, la presente revisión se centra en el análisis de la clínica, fisiopatología, diagnóstico y manejo de la acidosis láctica asociada a metformina, prestando especial atención al manejo mediante terapias de reemplazo renal. El análisis se basará en la experiencia de una serie de casos de acidosis láctica asociada a metformina atendidos en un centro clínico hospitalario en Chile.

Metformin is the preferred medication for the initial management of type 2 diabetes mellitus (T2DM). Although its use is widely recommended, caution should be exercised when prescribing it to populations susceptible to systemic hypoperfusion conditions, as it can lead to accumulation in the body and metabolic disturbances that may result in metformin-associated lactic acidosis. This severe complication is often underdiagnosed. To promote a better understanding of this topic, the present review focuses on the analysis of the clinical, pathophysiological, diagnostic, and management aspects of metformin-associated lactic acidosis, with particular attention to management through renal replacement therapies. The analysis will be based on the experience of a series of cases of metformin-associated lactic acidosis treated at a hospital clinical center in Chile.

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Resumen Introducción. El síndrome de encefalopatía mitocondrial, acidosis láctica y episodios similares a un accidente cerebrovascular (MELAS, por su sigla en inglés) es una de las enfermedades mitocondriales más frecuentes. Estas patologías se caracterizan por ser hereditarias, multisistémicas y progresivas, y por causar un compromiso predominantemente neurológico que provoca discapacidad y mortalidad, por lo que el diagnóstico temprano y la consejería genética son de gran importancia para mejorar el pronóstico de estos pacientes. Presentación del caso. Paciente femenina de cinco años quien fue llevada a consulta al servicio de pediatría por convulsión y ataxia, y en quien se evidenció retraso psicomotor. Aunque los estudios de neuroimagen fueron normales, se observó hiperlactatemia. Se encontró una relación lactato/piruvato >20, por lo que se sospechó enfermedad mitocondrial. Seis meses después, la paciente presentó deterioro neurológico progresivo caracterizado por alteración de la consciencia, mioclonías y hemiparesia. Se realizó tomografía axial computarizada de cráneo y resonancia magnética por espectroscopia que permitieron identificar una lesión isquémica occipital y aumento del lactato cerebral, respectivamente. Para confirmar el diagnóstico de síndrome MELAS, se solicitó estudio de ADN mitocondrial, en el que se observó la mutación m.3243A>G en el gen MT-TL1. La paciente tuvo un rápido deterioro, presentando una involución de las capacidades adquiridas, falleciendo a los cuatro años del inicio de los signos clínicos. Conclusión. Las enfermedades mitocondriales deben ser consideradas en pacientes con antecedentes de epilepsia y otras alteraciones neurológicas como ataxia e involución del neurodesarrollo.

Abstract Introduction: MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke) syndrome is the most common mitochondrial disease. These diseases are hereditary, multi-systemic and progressive, and lead to a predominant neurological involvement that causes disability and death, so early diagnosis and genetic counseling are of great importance for improving the prognosis of these patients. Case presentation: Five-year-old female patient who was taken to the pediatrics service of the hospital due to epileptic seizure, psychomotor retardation and ataxia. Although in the first medical consultation her neuroimaging studies were normal, hyperlactatemia was identified. In addition, a lactate to pyruvate ratio >20 was observed, so a mitochondrial disease was suspected. Six months later, the patient showed progressive deterioration of her health condition. A cranial CT scan and a magnetic resonance spectroscopy allowed the identification of an ischemic lesion in the occipital lobe and increased cerebral lactate levels, respectively. In order to confirm the MELAS syndrome diagnosis, a mitochondrial DNA study was requested, in which the m.3243A>G mutation was found. Unfortunately, the patient had a rapid deterioration of her health condition, showing a regression of her acquired functions, and died four years after the onset of the clinical signs. Conclusion: Mitochondrial diseases diagnosis should always be considered in patients with a history of epilepsy and other neurological disorders such as ataxia and neurodevelopmental regression.

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O objetivo deste artigo foi abordar as controvérsias científicas acerca dos distúrbios ácido-base nas doenças hepáticas. Nos estágios avançados da doença hepática, os distúrbios ácido-base atuam de forma complexa, comprometendo a qualidade de vida do paciente e desafiando o manejo clínico. A literatura apresenta a alcalose respiratória como uma das principais alterações, porém há uma longa discussão sobre o mecanismo fisiopatológico; em especial, citam-se a hipóxia, a hipocapnia e o nível de progesterona. Nas desordens metabólicas, com destaque para a acidose, os estudos apontam principalmente o lactato, os unmeasured ions ou íons não medidos e as alterações hidroeletrolíticas, mas cada componente desse sobressai-se dependendo da fase da doença estudada, compensada ou descompensada. As controvérsias dos distúrbios ácido-base nas doenças hepáticas devem-se ora à complexidade da fisiopatologia da própria doença, ora à necessidade de mais estudos esclarecedores.

The aim of this study is to address the scientific controversy about acid-base disorders in liver diseases. In the end stage of liver diseases, the acid-base disorder has a complex performance, impairing the patient's quality of life and challenging the clinic management. Although the literature shows respiratory alkalosis as one of the main alterations, there is a long discussion about the pathophysiological mechanism, specially regarding hypoxia, hypocapnia, and progesterone level. In metabolic disorders, especially acidosis, the studies mainly indicate the lactate, unmeasured ions, and hydroelectrolytic alterations, but, depending on the disease phase, either compensated or decompensated, each element has a particular action. The controversy about acid-base disorders in liver diseases is associated with the complexity of this condition, as well as with the necessity of more specialized research.

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RESUMEN La metformina es uno de los medicamentos más utilizados como primera línea para control de la diabetes mellitus tipo 2; tiene un papel benéfico en la mortalidad cardiovascular y bajo riesgo de producir hipoglucemia; sin embargo, no está exenta de efectos adversos, de los cuales, el más temido es la acidosis láctica, cuya incidencia es de 7,4 casos por 100.000 usuarios del medicamento por año. Los principales factores de riesgo para desarrollar dicha complicación son la insuficiencia renal aguda o crónica, la falla cardíaca, la enfermedad hepática y el uso concomitante de medicamentos que bloquean la cadena respiratoria de la mitocondria. El tratamiento incluye la reanimación hídrica, el soporte y, en algunos casos, el bicarbonato. La terapia de reemplazo renal ha sido exitosa en estos pacientes, pero las indicaciones para hacerla aún no son claras porque la metformina es una molécula parcialmente dializable y se requiere hemodiálisis prolongada para reducir suficientemente sus niveles. A pesar del tratamiento intensivo, la mortalidad asociada a esta complicación continúa siendo muy alta. El diagnóstico temprano y el tratamiento oportuno son fundamentales para mejorar el pronóstico.

SUMMARY Metformin lactic acidosis. Report of two cases Metformin is recommended as a first-line treatment for patients with diabetes mellitus type 2; it has a cardiovascular protective effect, and low risk of hypoglycemia. However, a severe but infrequent complication of its use is lactic acidosis, which has high morbidity and mortality rates. The estimated incidence of metformin lactic acidosis is 7,4 cases per 100.000 patients per year. Main risk factors are acute or chronic renal disease, congestive heart failure, hepatic failure, and concomitant use of drugs that affect metformin clearance or energy metabolism. Treatment includes hydration with crystalloids, support measures, and intravenous bicarbonate. Renal replacement therapy has been successful for treating metformin-associated lactic acidosis, but there are still no clear indications for it, because metformin is a partially dialyzable molecule and prolonged hemodialysis is required to reduce its levels sufficiently. Despite current treatment, mortality remains high. Early diagnosis and prompt multidisciplinary support are essential to improve outcome in these patients.

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Metformin-associated lactic acidosis is a severe and infrequent adverse event. Early diagnosis is essential to start an early treatment, which often has favorable results. We report a 56 years old non-insulin-requiring type 2 diabetic female who developed a severe metabolic acidosis associated with metformin in relation to an acute renal failure secondary to infectious diarrhea. Early treatment with bicarbonate and continuous hemofiltration allowed a quick improvement of the patient. Metformin-associated lactic acidosis has an elevated mortality (50-80%) and has a specific and effective treatment. Therefore, the condition must be born in mind.

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We report a 74-year-old man with diabetes mellitus type 2 and hypertension, who recently underwent coronary bypass surgery due to severe triple vessel disease receiving cardiological and combined antidiabetic therapy, including metformin 4 g/day. He was admitted with abdominal pain, nausea, vomiting, diarrhea and loss of consciousness. At admission, he was disoriented and agitated with signs of poor perfusion. His blood pressure was 80/70 mmHg, pulse rate 40 beats/min, respiratory rate 20-breaths/min, and axillary temperature 35°C. Biochemical profile revealed an extreme hyperkalemia of 15.4 mEq/L (double checked), elevated creatinine, uremia and brain natriuretic peptide; hypoglycemia (blood glucose 68 mg/dl) and normal C Reactive Protein. Arterial blood gases revealed severe lactic acidemia. The electrocardiogram showed sinus bradycardia, simple AV block, widened QRS with prominent T wave and prolonged QT. He was admitted to the Intensive Care Unit (ICU) with the suspicion of lactic acidosis associated with metformin, receiving fluid management, intravenous hypertonic glucose plus insulin and sodium bicarbonate, mechanical ventilation, vasopressor therapy, a temporary pacemaker lead, in addition to continuous venovenous hemodiafiltration. Two days later, the patient experienced a significant clinical improvement with normalization of the acid-base status, plasma lactate and potassium levels. On day 9, diuresis was recovered, creatinine and uremia returned to normal levels and the patient was discharged from the ICU.

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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.

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Propofol infusion syndrome (PRIS) is a rare but potentially lethal complications. This disorder is triggered under unknown circumstances by a propofol infusion of more than 5 mg/kg/h for more than 48 h. PRIS is characterized by a multiorgan failure and rhabdomyolysis and is induced by a disturbance in mitochondrial long chain fatty acid oxidation. We report a 43 year-old woman who underwent brain surgery due to a vascular malformation. In the immediate postoperative period, she had an unexplained and severe lactic acidosis. During anaesthesia, she received a propofol infusion of 7 mg/kg/h that continued in the UCI at a rate of 3.5 mg/kg/h, for 8 hours more. The suspicion of PRIS motivated immediate discontinuation of propofol with rapid correction of lactic acidosis and full recovery of the patient.

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