31 research outputs found

    Resucitación Hemostática en el Choque Hemorrágico Traumático: Relato de Caso

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    ResumenJustificativa y objetivos: El objetivo de este artículo es relatar un caso en que la estrategia damage control (control de daños [RDC]) con resucitación hemostática, fue usada con éxito en paciente politraumatizada con choque hemorrágico grave.Relato de caso: Paciente de 32 años, con choque hemorrágico grave por politraumatismo con fractura de cadera, que evolucionó con acidosis, coagulopatía e hipotermia. Durante la resucitación volémica, la paciente recibió transfusión de hemocomponentes a una razón de PFC/CP/CH de 1:1:1. Evolucionó en el período intraoperatorio, con una mejoría de los parámetros perfusionales y no necesitó fármacos vasoactivos. Al término de la operación, la paciente fue derivada a la unidad de cuidados intensivos y tuvo su alta al séptimo día del postoperatorio.Conclusiones: La terapéutica ideal del choque hemorrágico traumático todavía no ha quedado establecida, pero la rapidez en el control de la hemorragia y del rescate perfusional, junto con protocolos terapéuticos bien definidos, sientan las bases para evitar la progresión de la coagulopatía y la refractariedad del choque

    O pré-condicionamento com solução salina hipertônica reduz o stress oxidativo na isquemia reperfusão hepática com hipotermia

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    A lesão isquemia/reperfusão (IR) hepática desencadeia uma reação inflamatória que influencia diretamente na sobrevivência do enxerto após o transplante de fígado. A hipotermia reduz drasticamente a lesão IR, sendo a base da preservação dos órgãos. No entanto, outras estratégias são necessárias para aumentar a viabilidade do enxerto. Em trabalho anterior realizado no nosso LIM, foi demonstrado que a solução salina hipertônica(SSH) reduz a lesão hepática após a IR hepática normotérmica. O objetivo deste estudo foi avaliar os efeitos do condicionamento do fígado com SSH na IR hepática com hipotermia tópica do fígado. [...

    Experimental Model of Non-Controlled Hemorrhagic Shock in Pigs

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    SummaryBackground and objectivesA better understanding of pathophysiologic changes associated to trauma and hemorrhagic shock can help the development of therapies capable of reducing trauma-related mortality. The objective of this study was to describe a model of non-controlled hemorrhagic shock in pigs.MethodsAnimals received ketamine and midazolam as pre-anesthetic medications. Anesthesia was induced with propofol, and tracheal intubation was performed with the animals on spontaneous ventilation. After intubation neuromuscular blockade was performed. Animals were maintained in controlled mechanical ventilation and normocapnia. Anesthesia was maintained with propofol and fentanyl as needed. Saline was infused during the entire preparation period.MonitoringCardioscope, pulse oximeter, invasive blood pressure, volumetric catheter in the pulmonary artery, and urine output by cystostomy were used. Experimental model: after the initial recording of hemodynamic, metabolic, and coagulation variables, right subcostal incision and left lobe liver biopsy were performed. Anesthetic infusion was reduced while the infusion of saline was interrupted. An incision 12cm long 2cm deep was performed in the right liver lobe followed by digital divulsion of the wound. During the hemorrhagic phase, an aspiration probe was placed close to the wound and the volume of aspirated blood was recorded. When mean arterial pressure reached 40mmHg and bleeding was above 700mL the intervention phase was initiated according to the type of study.ConclusionThe development of experimental models to reduce high mortality and costs related to trauma is important

    Solução salina hipertônica aumenta a pressão de perfusão cerebral no transplante do fígado para hepatite fulminante: resultados preliminares

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    During orthotopic liver transplantation for fulminant hepatic failure, some patients may develop sudden deterioration of cerebral perfusion and oxygenation, mainly due to increased intracranial pressure and hypotension, which are likely responsible for postoperative neurological morbidity and mortality. In the present study, we hypothesized that the favorable effects of hypertonic saline solution (NaCl 7.5%, 4 mL/kg) infusion on both systemic and cerebral hemodynamics, demonstrated in laboratory and clinical settings of intracranial hypertension and hemorrhagic shock resuscitation, may attenuate the decrease in cerebral perfusion pressure that often occurs during orthotopic liver transplantation for fulminant hepatic failure. METHODS: 10 patients with fulminant hepatic failure in grade IV encephalopathy undergoing orthotopic liver transplantation with intracranial pressure monitoring were included in this study. The effect on cerebral and systemic hemodynamics in 3 patients who received hypertonic saline solution during anhepatic phase (HSS group) was examined, comparing their data with historical controls obtained from surgical procedure recordings in 7 patients (Control group). The maximal intracranial pressure and the corresponding mean arterial pressure values were collected in 4 time periods: (T1) the last 10 min of the dissection phase, (T2) the first 10 minutes at the beginning of anhepatic phase, (T3) at the end of the anhepatic phase, and (T4) the first 5 minutes after graft reperfusion. RESULTS: Immediately after hypertonic saline solution infusion, intracranial pressure decreased 50.4%. During the first 5 min of reperfusion, the intracranial pressure remained stable in the HSS group, and all these patients presented an intracranial pressure lower than 20 mm Hg, while in the Control group, the intracranial pressure increased 46.5% (P < 0.001). The HSS group was the most hemodynamically stable; the mean arterial pressure during the first 5 min of reperfusion increased 21.1% in the HSS group and decreased 11.1% in the Control group (P < 0.001). During the first 5 min of reperfusion, cerebral perfusion pressure increased 28.3% in the HSS group while in the Control group the cerebral perfusion pressure decreased 28.5% (P < 0.001). Serum sodium at the end of the anhepatic phase and 3 hours after reperfusion was significantly higher in the HSS group (153.00 &plusmn; 2.66 and 149.00 &plusmn; 1.73 mEq/L) than in the Control group (143.71 &plusmn; 3.30 and 142.43 &plusmn; 1.72 mEq/L), P = 0.003 and P < 0.001 respectively. CONCLUSION: Hypertonic saline solution can be successfully used as an adjunct in the neuroprotective strategy during orthotopic liver transplantation for fulminant hepatic failure, reducing intracranial pressure while restoring arterial blood pressure, promoting sustained increase in the cerebral perfusion pressure.Neste estudo testamos a hipótese de que os efeitos benéficos decorrentes da administração da solução salina hipertônica (NaCl 7,5%, 4 mL/kg) sobre a hemodinâmica sistêmica e cerebral na hipertensão intracraniana e no choque hemorrágico, possam atenuar a diminuição da pressão de perfusão cerebral que freqüentemente acompanha o transplante do fígado para hepatite fulminante. MÉTODO: Foram estudados 10 pacientes com hepatite fulminante em encefalopatia grau IV e monitorização de pressão intracraniana submetidos ao transplante do fígado. A hemodinâmica sistêmica e cerebral de 3 pacientes que receberam solução salina hipertônica durante a fase anepática (Grupo SSH) foi analisada comparando com os dados obtidos de 7 pacientes transplantados anteriormente nas mesmas condições (Grupo Controle). Os valores de pressão intracraniana máxima e a correspondente pressão arterial média foram coletados em quatro tempos: (T1) nos últimos 10 min da fase de disseccão, (T2) nos primeiros 10 minutos da fase anepática, (T3) no final da fase anepática e (T4) nos primeiros 5 min da reperfusão RESULTADO: Imediatamente após a infusão da solução salina hipertônica a pressão intracraniana diminuiu 50,4%. Nos primeiros 5 min da reperfusão a pressão intracraniana no Grupo SSH se manteve estável e todos os pacientes apresentavam pressão intracraniana menor que 20 mmHg enquanto no Grupo Controle a pressão intracraniana aumentou 46,5% (

    Independent early predictors of mortality in polytrauma patients: a prospective, observational, longitudinal study

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    OBJECTIVES: Trauma is an important public health issue and associated with substantial socioeconomic impacts and major adverse clinical outcomes. No single study has previously investigated the predictors of mortality across all stages of care (pre-hospital, emergency room, surgical center and intensive care unit) in a general trauma population. This study was designed to identify early predictors of mortality in severely injured polytrauma patients across all stages of care to provide a better understanding of the physiologic changes and mechanisms by which to improve care in this population. METHODS: A longitudinal, prospective, observational study was conducted between 2010 and 2013 in São Paulo, Brazil. Patients submitted to high-energy trauma were included. Exclusion criteria were as follows: injury severity scor

    Hyperkalemia Accompanies Hemorrhagic Shock and Correlates with Mortality

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    OBJECTIVE: This study was designed to evaluate the effects of terlipressin versus fluid resuscitation with normal saline, hypertonic saline or hypertonic-hyperoncotic hydroxyethyl starch, on hemodynamics, metabolics, blood loss and short-term survival in hemorrhagic shock. METHOD: Twenty-nine pigs were subjected to severe liver injury and treated 30 min later with either: (1) 2 mg terlipressin in a bolus, (2) placebo-treated controls, (3) 4 mL/kg 7.5% hypertonic NaCl, (4) 4 mL/kg 7.2% hypertonic-hyperoncotic hydroxyethyl starch 200/0.5, or (5) normal saline at three times lost blood volume. RESULTS: The overall mortality rate was 69%. Blood loss was significantly higher in the hypertonic-hyperoncotic hydroxyethyl starch and normal saline groups than in the terlipressin, hypertonic NaCl and placebo-treated controls groups (p<0.005). Hyperkalemia (K>5 mmol/L) before any treatment occurred in 66% of the patients (80% among non-survivors vs. 22% among survivors, p=0.019). Post-resuscitation hyperkalemia occurred in 86.66% of non-survivors vs. 0% of survivors (p<0.001). Hyperkalemia was the first sign of an unsuccessful outcome for the usual resuscitative procedure and was not related to arterial acidemia. Successfully resuscitated animals showed a significant decrease in serum potassium levels relative to the baseline value. CONCLUSION: Hyperkalemia accompanies hemorrhagic shock and, in addition to providing an early sign of the acute ischemic insult severity, may be responsible for cardiac arrest related to hemorrhagic shock

    Hepatite fulminante: estudo dos fatores associados à mortalidade hospitalar de 100 pacientes priorizados para transplante de fígado

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    Introdução. A despeito dos avanços nos cuidados de terapia intensiva e no transplante de fígado (TF), a hepatite fulminante (HF) ainda hoje apresenta alta taxa de mortalidade. A identificação de fatores prognósticos de maior acurácia deve ajudar a otimizar a priorização dos pacientes em lista de espera para o TF. Objetivo. Avaliar fatores prognósticos de mortalidade hospitalar dos pacientes com HF priorizados para TF. Métodos. Foram estudados retrospectivamente 100 pacientes adultos (78 mulheres, idade média 35,5 ± 14,7 anos) com HF priorizados para TF, em um único centro, de fevereiro de 2002 a junho de 2011. O diagnóstico etiológico foi hepatite viral em 17% dos casos, medicamentosa em 29%, autoimune em 13%, criptogênica em 34% e outras causas em 7%. A indicação do TF foi determinada de acordo com os critérios de O’Grady. Foram avaliados: idade, sexo, etiologia, intervalo icterícia/encefalopatia, intervalo entre a priorização e o TF, grau de encefalopatia, tempo de internação, RNI, fator V, bilirrubina, creatinina, AST, ALT, lactato e Model for End-Stage Liver Disease (MELD). Todos os dados foram coletados do dia da priorização. Resultados. O intervalo entre a priorização e o TF foi de 1,5 dias (0 a 9) e o tempo de internação foi de 18 ± 27 dias. A mortalidade hospitalar foi de 69%. Os pacientes não sobreviventes apresentaram na priorização maior grau de encefalopatia [3 (1 a 4) vs. 2 (1 a 4)], MELD (41 ± 9 vs. 38 ± 7) e lactato (62,2 ± 45,2 vs. 33,9 ± 16,0 mg/dL) quando comparados com os sobreviventes (p&lt;0,05). Dos 100 pacientes, 69% foram submetidos ao TF, os outros 31% morreram antes do TF. Os pacientes não transplantados apresentaram maior grau de encefalopatia [4 (1 a 4) vs. 3 (1 a 4)], MELD (44 ± 8 vs. 38 ± 8), lactato (78,4 ± 48,3 vs. 41,8 ± 30,6 mg/dL) e creatinina (2,60 ± 2,34 vs. 1,55 ± 1,54 mg/dL) quando comparados aos pacientes submetidos ao TF (p&lt;0.05). Conclusão. No momento da priorização para o TF, os pacientes com HF que apresentam condição clínica mais grave, com encefalopatia graus 3 ou 4, insuficiência renal, escores mais elevados de MELD e lactato elevado, têm maior taxa de mortalidade hospitalar mesmo quando submetidos ao TF, indicando pior prognóstico
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