RESUMO
BACKGROUND: Our objective was to identify possible associations between clinical and laboratory variables and the risk of developing acute kidney injury (AKI) in severely injured patients admitted to the intensive care unit (ICU) for whom creatine kinase (CK) levels were available. METHODS: For this retrospective observational study, we analyzed adult trauma patients admitted to the ICU from 2011 to 2015 at Fundación Valle del Lili (FVL) University Hospital. Our primary outcome was the incidence of AKI. Multivariate regression analysis was used to assess risk factors for this outcome. RESULTS: A total of 315 patients were included. The trauma mechanisms were blunt (n = 130), penetrating (n = 66) and blast (n = 44) trauma. The median (interquartile range, IQR) of injury severity score (ISS) was 21 (16-29). AKI developed in 75 patients (23.8%). Multivariate regression analysis revealed that the thoracic abbreviated injury scale (AIS) value (median (IQR) in the AKI group: 3 (0-4)), Acute Physiology and Chronic Health Evaluation (APACHE II) score (median (IQR) in the AKI group: 18 (10-27)), CK greater than 5000 U/L, lactic acid concentration at admission, and dobutamine administration were independently associated with AKI. CONCLUSION: We found that age, APACHE II score, thoracic trauma, lactic acidosis, and dobutamine administration were independently associated with AKI. Trauma surgeons need to be aware of the increased odds of AKI if one of these factors is identified during the evaluation and treatment of injured patients.
Assuntos
Injúria Renal Aguda/sangue , Ferimentos e Lesões/complicações , APACHE , Acidose Láctica/complicações , Acidose Láctica/fisiopatologia , Injúria Renal Aguda/epidemiologia , Injúria Renal Aguda/fisiopatologia , Adulto , Colômbia/epidemiologia , Creatina Quinase/análise , Creatina Quinase/sangue , Feminino , Hospitalização/estatística & dados numéricos , Humanos , Incidência , Escala de Gravidade do Ferimento , Unidades de Terapia Intensiva/organização & administração , Unidades de Terapia Intensiva/estatística & dados numéricos , Modelos Logísticos , Masculino , Estudos Retrospectivos , Fatores de Risco , Ferimentos e Lesões/sangue , Ferimentos e Lesões/epidemiologiaRESUMO
Lactic acidosis is the most common metabolic acidosis in hospitalized patients-the result from an underlying pathogenic process. To successfully manage lactic acid production, its cause needs to be eliminated. Patients with cancer have many risk factors for developing lactic acidosis, including the cancer diagnosis itself. Patients with lactic acidosis are critically ill, requiring an intense level of nursing care with accompanying frequent cardiopulmonary and renal assessments. The mortality rate from lactic acidosis is high. Therefore, appropriate nursing interventions may include end-of-life and palliative care.
Assuntos
Acidose Láctica/complicações , Neoplasias/complicações , Acidose Láctica/enfermagem , Humanos , Fatores de RiscoRESUMO
OBJECTIVE: To determine the frequency of mitochondrial DNA depletion syndrome (MDS) in infants with cholestasis and liver failure and to further clarify the clinical, biochemical, radiologic, histopathologic, and molecular features associated with MDS due to deoxyguanosine kinase (DGUOK) and MPV17 gene mutations. STUDY DESIGN: We studied 20 infants with suspected hepatocerebral MDS referred to our tertiary care center between 2007 and 2013. Genomic DNA was isolated from blood leukocytes, liver, and/or skeletal muscle samples by standard methods. Mitochondrial DNA copy number relative to nuclear DNA levels was determined in muscle and/or liver DNA using real-time quantitative polymerase chain reaction and compared with age-matched controls. Nuclear candidate genes, including polymerase γ, MPV17, and DGUOK were sequenced using standard analyses. RESULTS: We identified pathogenic MPV17 and DGUOK mutations in 11 infants (6 females) representing 2.5% of the 450 cases of infantile cholestasis and 22% of the 50 cases of infantile liver failure referred to our center during the study period. All of the 11 patients manifested cholestasis that was followed by a rapidly progressive liver failure and death before 2 years of life. Mitochondrial DNA depletion was demonstrated in liver or muscle for 8 out of the 11 cases where tissue was available. Seven patients had mutations in the MPV17 gene (3 novel mutations), 4 patients had DGUOK mutations (of which 2 were novel mutations). CONCLUSION: Mutations in the MPV17 and DGUOK genes are present in a significant percentage of infants with liver failure and are associated with poor prognosis.
Assuntos
Colestase/complicações , Falência Hepática/complicações , Proteínas de Membrana/genética , Proteínas Mitocondriais/genética , Mutação , Fosfotransferases (Aceptor do Grupo Álcool)/genética , Acidose Láctica/complicações , Alanina Transaminase/sangue , Aspartato Aminotransferases/sangue , Bile , Colestase/mortalidade , DNA Mitocondrial/análise , Feminino , Humanos , Lactente , Recém-Nascido , Leucócitos/química , Fígado/química , Falência Hepática/mortalidade , Masculino , Doenças Mitocondriais/genética , Doenças Mitocondriais/mortalidade , Músculo Esquelético/química , alfa-Fetoproteínas/análise , gama-Glutamiltransferase/sangueRESUMO
PURPOSE OF REVIEW: To summarize the properties of thiamine and evaluate current evidence on thiamine status and supplementation, for different populations of critically ill patients. RECENT FINDINGS: Thiamine, in the form of thiamine pyrophosphate, is a critical co-factor in the glyocolysis and oxidative decarboxylation of carbohydrates for energy production. Different studies have shown that critical illness in adults and children is characterized by absolute or relative thiamine depletion, which is associated with an almost 50% increase in mortality. Thiamine deficiency should be suspected in different clinical scenarios such as severe sepsis, burns, unexplained heart failure or lactic acidosis, neurological disorder in patients with previous history of alcoholism, starvation, chronic malnutrition, long-term parenteral feeding, hyperemesis gravidarum, or bariatric surgery. Nonetheless, thiamine supplements are not routinely given to critically ill patients. Clinicians should be able to suspect and recognize risk factors for the occurrence of severe neurological disorders secondary to thiamine deficiency, as early treatment can prevent the appearance of permanent neurological damage. SUMMARY: Symptoms and signs associated with thiamine deficiency lack sensitivity and specificity in critically ill patients. Consequently, depletion is frequently unrecognized and underdiagnosed by clinicians. Potentially deleterious consequences of thiamine depletion should be avoided by early and appropriate supplementation.
Assuntos
Estado Terminal/terapia , Suplementos Nutricionais , Deficiência de Tiamina/tratamento farmacológico , Tiamina Pirofosfato/administração & dosagem , Complexo Vitamínico B/administração & dosagem , Acidose Láctica/complicações , Acidose Láctica/tratamento farmacológico , Descarboxilação/efeitos dos fármacos , Relação Dose-Resposta a Droga , Humanos , Necessidades Nutricionais , Síndrome da Realimentação/complicações , Síndrome da Realimentação/tratamento farmacológico , Fatores de Risco , Sepse/complicações , Sepse/tratamento farmacológico , Deficiência de Tiamina/complicações , Encefalopatia de Wernicke/complicações , Encefalopatia de Wernicke/tratamento farmacológicoRESUMO
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.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso de 80 Anos ou mais , Acidose Láctica/complicações , Acidose Láctica/etiologia , Acidose Láctica/metabolismo , Bicarbonato de Sódio/uso terapêutico , Cetoacidose Diabética/diagnóstico , Cetoacidose Diabética/etiologia , Cetoacidose Diabética/terapia , Choque Séptico/metabolismo , Choque Séptico/terapia , Pacientes InternadosRESUMO
OBJECTIVE: To compare systemic hemodynamics with microcirculatory changes at different vascular beds during progressive hemorrhage. SETTING: University-based research laboratory. SUBJECTS: Twelve anesthetized, mechanically ventilated sheep. INTERVENTIONS: Sheep were randomly assigned to HEMORRHAGE or CONTROL group. In the HEMORRHAGE group (n = 8), three stepwise bleedings of 5 ml/kg at 30-min intervals were performed to add up 15 ml/kg. In the CONTROL group (n = 4), sheep had the same surgical preparation but were not bled. MEASUREMENTS AND MAIN RESULTS: Progressive bleeding decreased cardiac output, and superior mesenteric artery blood flow, and systemic and intestinal oxygen transports from the first step of bleeding whereas systemic and intestinal oxygen consumption remained unchanged. Mean arterial blood pressure, arterial pH and base excess, and intramucosal-arterial PCO(2) were only significantly modified in the last step of bleeding. Arterial lactate increased and sublingual, and intestinal serosal and mucosal capillary microvascular flow indexes and red blood cell velocities progressively decreased after the first step of bleeding (3.0 +/- 0.1 vs. 2.3 +/- 0.4, 3.2 +/- 0.2 vs. 2.4 +/- 0.6, 3.0 +/- 0.0 vs. 2.0 +/- 0.2, and 1,082 +/- 29 vs. 977 +/- 79, 1,042 +/- 24 vs. 953 +/- 60, 287 +/- 65 vs. 262 +/- 16 mum/s; P < 0.05 for all). CONCLUSIONS: Alterations in sublingual, intestinal microcirculation, and arterial lactate simultaneously arose from the first step of bleeding. The microcirculatory changes were identified either by semi-quantitative flow index or by quantitative red blood cell velocity measurements.
Assuntos
Hemorragia/fisiopatologia , Intestinos/irrigação sanguínea , Microcirculação/fisiologia , Fluxo Sanguíneo Regional/fisiologia , Língua/irrigação sanguínea , Acidose Láctica/complicações , Acidose Láctica/fisiopatologia , Animais , Velocidade do Fluxo Sanguíneo , Capilares/fisiologia , Débito Cardíaco/fisiologia , Progressão da Doença , Hemorragia/complicações , Mucosa Intestinal/metabolismo , Artéria Mesentérica Superior/fisiopatologia , Oxigênio/metabolismo , Distribuição Aleatória , Respiração Artificial , OvinosRESUMO
Se presenta el caso clínico de un recién nacido que debutó con hipoglicemia y severa acidosis láctica que se controló con paralización muscular, ventilación asistida y aporte de bicarbonato. Posteriormente desarrolló una insuficiencia hepática progresiva, falleciendo a los 25 días de edad. Los elementos clínicos y de laboratorio sugieren dos posibles diagnósticos: una alteración de la función mitocondrial o un déficit de piruvato carboxilasa. Se discuten las alternativas de estudio de ambos diagnósticos
Assuntos
Humanos , Recém-Nascido , Masculino , Acidose Láctica/complicações , Insuficiência Hepática/complicações , Acidose Láctica/terapia , Diagnóstico Diferencial , Hipoglicemia/complicações , Respiração Artificial , Bicarbonato de Sódio/uso terapêuticoRESUMO
An infant with feeding difficulties, hypotonia, lactic acidemia, and severe hypoketotic hypoglycemia died at the age of 7 months of liver disease. Electron microscopy revealed abnormal mitochondria. Biochemical studies of mitochondrial enzymes in liver showed a decreased activity of complexes I, III, and IV. Mitochondrial DNA (mtDNA) content was reduced in liver 7% of the mean value in control subjects) and in muscle (50%). In kidney, brain, and heart, the mtDNA content was normal. The liver-specific mtDNA depletion syndrome in this patient manifested itself with features of both a respiratory chain defect and a mitochondrial fatty acid oxidation defect. Syndromes involving depletion of mtDNA can be diagnosed only when the activity of the respiratory chain enzymes and the content of mtDNA are investigated in the most affected tissues.
Assuntos
Acidose Láctica/complicações , DNA Mitocondrial/isolamento & purificação , Hipoglicemia/complicações , Falência Hepática/metabolismo , Transporte de Elétrons , Evolução Fatal , Humanos , Lactente , Falência Hepática/enzimologia , Falência Hepática/etiologia , Falência Hepática/patologia , Masculino , Mitocôndrias Hepáticas/enzimologia , Mitocôndrias Hepáticas/genética , Oxirredutases/metabolismoRESUMO
An 18-month-old girl with an oxidative phosphorylation defect had neonatal onset of chronic lactic acidosis, lipid storage myopathy, bilateral cataracts, and primary adrenal insufficiency. Chronic lactic acidosis responded to treatment with dichloroacetate. Sequential muscle biopsies demonstrated resolution of the lipid storage myopathy associated with the return to normal muscle free carnitine levels. This case demonstrates a new clinical phenotype associated with a defect in oxidative phosphorylation and the need to consider mitochondrial disorders in the differential diagnosis of primary adrenal insufficiency in childhood.
Assuntos
Acidose Láctica/metabolismo , Hormônio Adrenocorticotrópico/deficiência , Erros Inatos do Metabolismo Lipídico/metabolismo , Mitocôndrias Musculares/metabolismo , Fosforilação Oxidativa , Acidose Láctica/complicações , Acidose Láctica/tratamento farmacológico , Catarata/complicações , Ácido Dicloroacético/uso terapêutico , Feminino , Humanos , Recém-Nascido , Erros Inatos do Metabolismo Lipídico/complicações , FenótipoRESUMO
A 5-year-old boy had recurrent vomiting and lethargy with lacticacidemia and ketoacidemia since birth. Lipoamide dehydrogenase deficiency was found in muscle and fibroblasts. Therapy with sodium dichloroacetate, thiamine, and carnitine was associated with reduction of the severity and frequency of the decompensation episodes and near normal plasma lactate levels. At 5 years of age, the patient has normal cognitive function and moderate motor impairment.
Assuntos
Acidose Láctica/metabolismo , Di-Hidrolipoamida Desidrogenase/deficiência , Cetose/metabolismo , Acidose Láctica/complicações , Acidose Láctica/tratamento farmacológico , Carnitina/uso terapêutico , Ácido Dicloroacético/uso terapêutico , Di-Hidrolipoamida Desidrogenase/metabolismo , Fibroblastos/metabolismo , Humanos , Lactente , Cetose/complicações , Cetose/tratamento farmacológico , Lactatos/sangue , Masculino , Transtornos dos Movimentos/etiologia , Músculos/metabolismo , Tiamina/uso terapêuticoAssuntos
Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Intestinos/irrigação sanguínea , Suco Gástrico/química , Lactatos , Insuficiência de Múltiplos Órgãos/diagnóstico , Acidose Láctica/complicações , Lactatos/sangue , Manometria/instrumentação , Insuficiência de Múltiplos Órgãos/fisiopatologiaAssuntos
Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Lactatos/diagnóstico , Insuficiência de Múltiplos Órgãos/diagnóstico , Suco Gástrico/química , Intestinos/irrigação sanguínea , Insuficiência de Múltiplos Órgãos/fisiopatologia , Manometria/instrumentação , Lactatos/sangue , Acidose Láctica/complicaçõesRESUMO
Accidental hypothermia, a condition seldomly seen in Chile, is defined as a spontaneous core temperature reduction to less than 35§ C and is associated with great morbidity and mortality. We report a 16 years old female intoxicated with liquefied petroleum gas that was admitted in coma, hypothermic, with severe hemodynamic derangement, lactic acidosis, rhabdomyolysis and iliofemoral phlebothrombosis. Peritoneal dialysis with solutions at 27§ C was used as a quick and safe means to revert hypothermia and avoid its complications
Assuntos
Humanos , Feminino , Adolescente , Intoxicação por Gás/complicações , Hipotermia/terapia , Diálise Peritoneal , Tromboflebite/complicações , Trombose , Transtornos da Consciência/complicações , Hipotermia/complicações , Hipotermia/fisiopatologia , Hipotermia/terapia , Acidose Láctica/complicações , Hipotensão/complicações , Rabdomiólise/complicaçõesRESUMO
The authors describe a family (mother, son and two daughters) with mitochondrial myopathy. The mother was asymptomatic. Two daughters had lactic acidosis and myoclonic epilepsy, mild dementia, ataxia, weakness and sensory neuropathy. The son suffered one acute hemiplegic episode due to an ischemic infarct in the right temporal region. All the patients studied had hypertension. EEG disclosed photomyoclonic response in the proband patient. Muscle biopsy disclosed ragged-red fibers and abnormal mitochondria by electron microscopy. Biochemical analysis showed a defect of cytochrome C oxidase in mitochondria isolated from skeletal muscle. Several clinical and genetic aspects of the mitochondrial encephalomyopathies are discussed.
Assuntos
Epilepsias Mioclônicas/genética , Mitocôndrias Musculares/ultraestrutura , Doenças Musculares/genética , Acidose Láctica/complicações , Adulto , Eletromiografia , Complexo IV da Cadeia de Transporte de Elétrons/metabolismo , Epilepsias Mioclônicas/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Mitocôndrias Musculares/metabolismo , Músculos/patologia , Doenças Musculares/sangue , Doenças Musculares/complicações , Doenças Musculares/diagnóstico , LinhagemRESUMO
Metabolic acidosis results from a disequilibrium between production and excretion of acid. Loss of base from the body through the gastrointestinal tract or in the urine or an increase in metabolic acid production are the three major mechanisms from which metabolic acidosis is generated. Uncomplicated metabolic acidosis is manifested by an increase in blood acidity, hypobicarbonatemia, and hypocapnea. The magnitude of these changes defines the severity wf the acidosis. It is convenient to divide metabolic acidosis into two general categories (hyperchloremic and normochloremic), based on the observed anion gap, as this serves to narrow the differential diagnosis. The normal anion gap is that amount of plasma anion not measure by routine laboratory screening that accounts for the difference between the measured sodium cation (Na+) and anions (Cl +/- HCO3-). Metabolic acidosis; causes; diagnosis; clinical manifestations.
Assuntos
Desequilíbrio Ácido-Base/metabolismo , Acidose/metabolismo , Espaço Extracelular/metabolismo , Acidose/classificação , Acidose/diagnóstico , Acidose/etiologia , Acidose Láctica/complicações , Acidose Láctica/etiologia , Acidose Láctica/metabolismo , Acidose Láctica/terapia , Bicarbonatos/metabolismo , Bicarbonatos/urina , Cloretos/metabolismo , Humanos , Concentração de Íons de Hidrogênio , Rim/metabolismo , Falência Renal Crônica/metabolismo , Desequilíbrio HidroeletrolíticoRESUMO
Os autores descrevem uma família de raça negra (mäe e três filhos) com miopatia mitocondrial. Duas irmäs tinham acidose láctica concomitante e epilepsia mioclônica. Outros achados observados nos membros mais afetados foram demência, ataxia, fraqueza muscular e neuropatia sensitiva. A mäe era assintomática. Um filho sofreu acidente vascular cerebral isquêmico envolvendo a regiäo temporal direita. Todos os membros da família estudados eram hipertensos. EEG mostrou resposta fotomioclônica na paciente probanda. Biópsia muscular mostrou
Assuntos
Adulto , Pessoa de Meia-Idade , Humanos , Masculino , Feminino , Doenças Musculares/genética , Mitocôndrias Musculares/ultraestrutura , Acidose Láctica/complicações , Doenças Musculares/complicações , Doenças Musculares/diagnóstico , Eletroencefalografia , Complexo IV da Cadeia de Transporte de Elétrons/metabolismo , Epilepsias Mioclônicas/complicações , Mitocôndrias Musculares/metabolismo , Músculos/patologia , LinhagemRESUMO
Clinical findings are presented for 30 patients with lactic acidemia in whom activity of the pyruvate dehydrogenase complex in fibroblasts was significantly (P = less than 0.01) below that of control cell lines. Residual activity of the activated complex ranged from 1.6% to 68.5% of control activity. Seven patients died before 6 months of age, and another five before reaching 2 years of age. Sixteen of the surviving patients and the five who died between 6 months and 2 years all had psychomotor retardation. Seventeen children had structural central nervous system damage, as determined either by computed tomography or at autopsy. The extent and location of damage varied from cerebral atrophy to the development of cystic lesions in the cerebral cortex, basal ganglia, and brain stem. Two patients had ataxic episodes only and were not developmentally delayed. This cohort of patients strongly resembles a comparable group assembled from various other reports.
Assuntos
Doença da Deficiência do Complexo de Piruvato Desidrogenase , Acidose Láctica/complicações , Adolescente , Encefalopatias/complicações , Células Cultivadas , Criança , Pré-Escolar , Ácido Dicloroacético/farmacologia , Fibroblastos/enzimologia , Humanos , Lactente , Recém-Nascido , Deficiência Intelectual/complicações , Hipotonia Muscular/complicações , Pele/enzimologiaRESUMO
Se estudiaron retrospectivamente 5 pacientes con diagnóstico de acidosis láctica en la Unidad de Cuidados Intensivos del Hospital General Docente "Enrique Cabrera" en el período comprendido entre 1983 y septiembre de 1986, al considerar que 5 de ellas reunían los criterios de la misma. Todas las pacientes correspondían al sexo femenino, 3 de ellas eran insulinodependientes y 2 no insulinodependientes. La duración promedio de la enfermedad fue menor de 5 años. La causa fundamental del desarrollo de la acidosis láctica fue la sepsis asociada o no al abandono del tratamiento. Ninguna paciente utilizaba diabefén como tratamiento de su diabetes. Dos pacientes fallecieron durante el curso de la enfermedad. Se valora la utilidad o no del tratamiento con bicarbonato, de acuerdo con la información obtenida en la literatura consultada