Ricardo Souza Nani

Hyperkalemia accompanies hemorrhagic shock and correlates with mortality

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.

Potassium in hemorrhagic shock: a potential marker of tissue hypoxia.

BACKGROUND This study was designed to evaluate serum potassium level variation in a porcine model of hemorrhagic shock (HS). METHODS Eight pigs were studied in a controlled hemorrhage model of HS. Blood withdrawal began at a 50 mL/min to 70 mL/min rate, adjusted to reach a mean arterial pressure (MAP) level of 60 mm Hg in 10 minutes. When MAP reached 60 mm Hg, the blood withdrawal rate was adjusted to maintain a MAP decrease rate of 10 mm Hg every 2 minutes to 4 minutes. Arterial and mixed venous blood samples were collected at MAP levels of 60 mm Hg, 50 mm Hg, 40 mm Hg, 30 mm Hg, 20 mm Hg, and 10 mm Hg and analyzed for oxygen saturation, Po2, Pco2, potassium, lactate, bicarbonate, hemoglobin, pH, and standard base excess. RESULTS Significant increase in serum potassium occurred early in all animals. The rate of rise in serum potassium and its levels accompanied the hemodynamic deterioration. Hyperkalemia (K >5 mmol/L) incidence was 12.5% at 60 mm Hg and 50 mm Hg, 62.5% at 40 mm Hg, 87.5% at 30 mm Hg, and 100% at 20 mm Hg. Strong correlations were found between potassium levels and lactate (R = 0.82), SvO2 (R = 0.87), DeltapH (R = 0.83), and DeltaPco2 (R = 0.82). CONCLUSIONS Serum potassium increase accompanies the onset of HS. The rise in serum potassium was directly related to the hemodynamic deterioration of HS and strongly correlated with markers of tissue hypoxia.

Hypertonic saline solution increases cerebral perfusion pressure during clinical orthotopic liver transplantation for fulminant hepatic failure: preliminary results

UNLABELLED 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 +/- 2.66 and 149.00 +/- 1.73 mEq/L) than in the Control group (143.71 +/- 3.30 and 142.43 +/- 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.

Ressuscitação hemostática no choque hemorrágico traumático: relato de caso

JUSTIFICATIVA E OBJETIVOS: O objetivo deste artigo e relatar um caso em que a estrategia damage control (RDC) com ressuscitacao hemostatica foi usada com sucesso em paciente politraumatizada com choque hemorragico grave. RELATO DE CASO: Paciente de 32 anos com choque hemorragico grave por politraumatismo com fratura de bacia, que evoluiu com acidose, coagulopatia e hipotermia. Durante a ressuscitacao volemica, a paciente recebeu transfusao de hemocomponentes - plasma fresco congelado/concentrado de plaquetas/concentrado de hemacias, na razao de 1:1:1. Evoluiu no periodo intraoperatorio, com melhora dos parâmetros perfusionais, e prescindiu de drogas vasoativas. No fim da operacao a paciente foi levada para unidade de terapia intensiva e teve alta no setimo dia de pos-operatorio. CONCLUSAO: A terapeutica ideal do choque hemorragico traumatico ainda nao esta estabelecida, porem a rapidez no controle da hemorragia e do resgate perfusional e protocolos terapeuticos bem definidos sao as bases para se evitar a progressao da coagulopatia e a refratariedade do choque.

Hemostatic resuscitation in traumatic hemorrhagic shock: case report

Abstract Background and objectives The aim of this paper is to report a case in which the damage control resuscitation (DCR) approach was successfully used to promote hemostatic resuscitation in a polytraumatized patient with severe hemorrhagic shock. Case report Female patient, 32 years of age, with severe hemorrhagic shock due to polytrauma with hip fracture, who developed acidosis, coagulopathy, and hypothermia. During fluid resuscitation, the patient received blood products transfusion of fresh frozen plasma/packed red blood cells/platelet concentrate at a ratio of 1:1:1 and evolved intraoperatively with improvement in perfusion parameters without requiring vasoactive drugs. At the end of the operation, the patient was taken to the intensive care unit and discharged on the seventh postoperative day. Conclusion The ideal management of traumatic hemorrhagic shock is not yet established, but the rapid control of bleeding and perfusion recovery and well-defined therapeutic protocols are fundamental to prevent progression of coagulopathy and refractory shock.

Experimental model of non-controlled hemorrhagic shock in pigs

BACKGROUND AND OBJECTIVES A 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. METHODS Animals 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. MONITORING Cardioscope, 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. CONCLUSION The development of experimental models to reduce high mortality and costs related to trauma is important.

Modelo experimental de choque hemorrágico não controlado em porcos

JUSTIFICATIVA Y OBJETIVOS: Una comprension mejor de las alteraciones fisiopatologicas asociadas al trauma y al choque hemorragico, puede ayudar en el desarrollo de las terapeuticas capaces de reducir la mortalidad relacionada con el trauma. El objetivo de este estudio es describir un modelo de choque hemorragico no controlado en cerdos. METODOS: Como medicacion preanestesica, los animales recibieron cetamina y midazolan. La anestesia fue inducida con propofol, y la intubacion traqueal fue realizada con la respiracion espontanea. Despues de la intubacion, se realizo el bloqueo neuromuscular. Los animales se mantuvieron bajo respiracion mecanica controlada y normocapnia. La anestesia se mantuvo con propofol y fentanil, a tono con la necesidad. Una solucion de suero fisiologico al 0,9% fue infundida durante todo el periodo de la preparacion. MONITOREO: Se usaron el cardioscopio, oximetro de pulso, medida de presion arterial invasiva, cateter volumetrico de arteria pulmonar y medida de debito urinario por cistostomia. Modelo experimental: despues del registro inicial de las variables hemodinamicas, metabolicas y de coagulacion, se realizaron la incision subcostal derecha y la biopsia hepatica del lobulo izquierdo. La infusion de anestesicos fue reducida, mientras que la solucion de salina isotonica se interrumpio. Una incision de 12 cm de extension por 2 cm de profundidad se hizo en el lobulo hepatico derecho, seguida de una divulsion digital de la herida. Durante la fase de hemorragia, una sonda de aspiracion fue posicionada junto a la herida, y el volumen de sangre aspirado fue registrado. Cuando la presion arterial promedio llego a 40 mmHg y el sangramiento fue superior a 700 mL, pudo iniciarse la fase de intervencion de acuerdo con el tipo de estudio. CONCLUSION: Es importante continuar desarrollando modelos experimentales con el objetivo final de reducir la alta mortalidad y los costes asociados al trauma.

Anestesia para trasplante hepático en hepatitis fulminante

SUMMARY Fulminant hepatic failure (FHF) is defined by sudden onset of encephalopathy, coagulopathy and jaundice in an otherwise normal individual. Fulminant hepatic failure results in progressive multi-organ failure with a dramatic impact in the brain. Severe cerebral edema is a frequent finding that ultimately lead to intracranial hypertension and death The management of patients with FHF is aimed mainly in prevent or reversing increased intracranial pressure associated with support treatment for other failing organs. The definitive treatment for patients with FHF is liver transplantation. This article aims to present a practical approach to anesthesia care and intraoperative management of patients with FHF.

O remifentanil pode diminuir o diâmetro das alças intestinais

4,5 . Considerando a observacao da equipe cirurgica, desenvolvemos projeto de pesquisa clinico para avaliacao da hipotese de efeito indesejavel do remifentanil sobre o diâmetro das alcas intestinais. Apos a aprovacao pela Comissao de Etica institucional e assinatura do termo de consentimento livre e esclarecido, realizamos medidas do diâmetro das alcas jejunais antes e apos infusao continua de remifentanil em dois pacientes adultos submetidos a hepatectomia. Foram excluidos pacientes que apresentassem fatores de interferencia na contratilidade intestinal, como diabetes melito, neuropatias perifericas, insuficiencia renal cronica, doenca de Chagas, doenca inflamatoria intestinal, colagenoses, desnutricao grave, sindromes de ma-absorcao, jejum por tempo superior a 48 horas ou ocorrencia de nauseas, vomitos ou diarreia no pre-operatorio. O diâmetro das alcas intestinais foi aferido utilizando-se um paquimetro mecânico de aco inoxidavel (Starrett4,5 . Considerando a observacao da equipe cirurgica, desenvolvemos projeto de pesquisa clinico para avaliacao da hipotese de efeito indesejavel do remifentanil sobre o diâmetro das alcas intestinais. Apos a aprovacao pela Comissao de Etica institucional e assinatura do termo de consentimento livre e esclarecido, realizamos medidas do diâmetro das alcas jejunais antes e apos infusao continua de remifentanil em dois pacientes adultos submetidos a hepatectomia. Foram excluidos pacientes que apresentassem fatores de interferencia na contratilidade intestinal, como diabetes melito, neuropatias perifericas, insuficiencia renal cronica, doenca de Chagas, doenca inflamatoria intestinal, colagenoses, desnutricao grave, sindromes de ma-absorcao, jejum por tempo superior a 48 horas ou ocorrencia de nauseas, vomitos ou diarreia no pre-operatorio. O diâmetro das alcas intestinais foi aferido utilizando-se um paquimetro mecânico de aco inoxidavel (Starrett