Acute liver failure with a massive upper GI bleed meeting the criteria of MIS-C.

Multisystem inflammatory syndrome in children (MIS-C) is a known complication of COVID-19. There is still limited knowledge about this condition. Here, we report the case of a previously healthy toddler boy, who presented with acute liver failure and duodenal lesions resulting in severe haematemesis and haemorrhagic shock, requiring intensive care unit care. The patient had persistent transaminitis, a deranged coagulation profile, inflammatory markers were elevated, and laboratory tests were negative for common infectious hepatitis aetiologies as well as COVID-19 Reverse transcription polymerase chain reaction. His COVID-19 antibody was reactive. Upper gastrointestinal endoscopy revealed a Forrest grade III duodenal ulcer. Looking into the constellation of symptoms and laboratory findings a confirmed diagnosis of acute viral hepatitis caused by MIS-C was made. Hence, he was given intravenous methylprednisolone along with intravenous immunoglobulins, after which he improved clinically and transaminitis resolved. The patient was discharged on clinical improvement and was doing fine on follow-up up to 6 months.

Prevalence, Associated Factors, and Outcomes of Severe Acute Kidney Injury in Pediatric Acute Liver Failure: Single-Center Retrospective Study, 2003-2017.

OBJECTIVES: Our aim was to determine the prevalence and explanatory factors associated with outcomes in children with acute liver failure (ALF) admitted to the PICU, who also develop severe acute kidney injury (AKI). DESIGN: Retrospective cohort, 2003 to 2017. SETTING: Sixteen-bed PICU in a university-affiliated tertiary care hospital. PATIENTS: Admissions to the PICU with ALF underwent data review of the first week and at least 90-day follow-up. Patients with stages 2-3 AKI using the British Association of pediatric Nephrology definitions, or receiving continuous renal replacement therapy (CRRT) for renal indications, were defined as severe AKI. We excluded ALF cases on CRRT for hepatic-only indications. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Baseline characteristics, proportion with severe AKI, illness severity and interventions, and outcomes (i.e., transplant, survival with native liver, overall survival, duration of PICU stay, and mechanical ventilation). Ninety-four children with ALF admitted to the PICU were included. Over the first week, 29 had severe AKI, and another eight received CRRT for renal/mixed reno-hepatic indications; hence, the total severe AKI cohort was 37 of 94 (39.4%). In a multivariable logistic regression model, peak aspartate aminotransferase (AST) and requirement for inotropes on arrival were associated with severe AKI. Severe AKI was associated with longer PICU stay and duration of ventilation, and lower spontaneous survival with native liver. In another model, severe AKI was associated with greater odds of mortality (odds ratio 7.34 [95% CI, 1.90-28.28], p = 0.004). After 90 days, 3 of 17 survivors of severe AKI had serum creatinine greater than the upper limit of normal for age. CONCLUSIONS: Many children with ALF in the PICU develop severe AKI. Severe AKI is associated with the timecourse of PICU admission and outcome, including survival with native liver. Future work should look at ALF goal directed renoprotective strategies at the time of presentation.

Clinical presentation and outcomes of patients with rhabdomyolysis: A tertiary care center experience.

OBJECTIVES: To evaluate the clinical and laboratory features, complications, and outcomes of patients with rhabdomyolysis in the Saudi population. METHODS: Retrospectives descriptive study of adult patients who presented to King Abdulaziz Medical City (KAMC) withrhabdomyolysis between January 2016 and December 2022. RESULTS: Most of the participants (84.5%) were male, with a median age of 41 years and a body mass index of 26.5 kg/m2. Medications, mainly statins (22.4%) and illicit drugs (15.5%), constituted the root causes of rhabdomyolysis in the cohort (44.8%). The most common presenting complaints were myalgia (63.8%) and fatigue (37.9%). More than one-third of the participants (32.8%) developed AKI, with 3 patients requiring temporary hemodialysis, and only 8.6% developed acute liver failure (ALF). Intensive care unit (ICU) admission was required for 10 patients (17.2%), and the overall mortality rate was 8.6%. Patients who developed complications (composite outcomes of AKI, ALF, multiorgan failure, or death) had significantly reduced kidney function and higher levels of blood urea nitrogen, anion gap, and uric acid upon admission than those who did not. CONCLUSION: This study offers a thorough understanding of clinical and laboratory features, causes, complications, and outcomes of rhabdomyolysis among Saudi patients. The insights gained enhance our understanding of rhabdomyolysis within this population, providing a foundation for future research and improvements in clinical management.

Acute kidney injury in acute liver failure: A narrative review.

Acute kidney injury (AKI) is a frequent complication of acute liver failure (ALF) and it worsens the already worse prognoses of ALF. ALF is an uncommon disease, with varying etiologies and varying definitions in different parts of the world. There is limited literature on the impact of AKI on the outcome of ALF with or without transplantation. The multifaceted etiology of AKI in ALF encompasses factors such as hemodynamic instability, systemic inflammation, sepsis and direct nephrotoxicity. Indications of renal replacement therapy (RRT) for AKI in ALF patients extend beyond the conventional criteria for dialysis and continuous renal replacement therapy (CRRT) may have a role in transplant-free survival or bridge to liver transplantation (LT). LT is a life-saving option for ALF, so despite somewhat lower survival rates of LT in ALF patients with AKI, LT is not usually deferred. In this review, we will discuss the guidelines' recommended definition and classification of AKI in ALF, the impact of AKI in ALF, the pathophysiology of AKI and the role of CRRT and LT in ALF patients with AKI.

Menace of hepatitis E in pregnancy: unleashing the threat of fulminant liver failure.

This case report presents a primigravida in her 20s with a history of seizure disorder and chronic cholecystitis, who presented at 30 weeks and 6 days of gestation with upper abdominal pain, fever and vomiting. Initially diagnosed with acute calculous cholecystitis, the patient's condition rapidly deteriorated, resulting in fetal demise and the development of severe complications. Subsequent investigations revealed an enlarged fatty liver and signs of acute liver failure. The diagnosis of acute fatty liver of pregnancy was initially considered but later ruled out, and the patient was diagnosed with hepatitis E based on positive anti-hepatitis E virus IgM antibodies. Prompt termination of pregnancy was performed, followed by intensive care management. After a prolonged hospital stay, the patient recovered and was discharged in stable condition. This case emphasises the importance of considering hepatitis E as a potential cause of acute liver failure in pregnant women and the need for early recognition and multidisciplinary management to achieve favourable outcomes.

Acute liver failure after out-of-hospital cardiac arrest: An observational study.

RATIONALE: Apart from hypoxic hepatitis (HH), the hepatic consequences of out-of-hospital cardiac arrest (OHCA) have been little studied. This cohort study aimed to investigate the characteristics of liver dysfunction resulting from OHCA and its association with outcomes. METHODS: Among the conventional static liver function tests used to define acute liver failure (ALF), we determined which one correlated more closely with the reference indocyanine green (ICG) clearance test in a series of OHCA patients from the CYRUS trial (NCT01595958). Subsequently, we assessed whether ALF, in addition to HH (i.e., acute liver injury), was an independent risk factor for death in a large cohort of OHCA patients admitted to two intensive care units between 2007 and 2017. RESULTS: ICG clearance, available for 22 patients, was impaired in 17 (77.3%) cases. Prothrombin time (PT) ratio was the only static liver function test that correlated significantly (r = -0.66, p < 0.01) with ICG clearance and was therefore used to define ALF, with the usual cutoff of < 50%. Of the 418 patients included in the analysis (sex ratio: 1.4; median age: 64 [53-75] years; non-shockable rhythm: 73%), 67 (16.0%) presented with ALF, and 61 (14.6%) had HH at admission. On day 28, 337 (80.6%) patients died. Following multivariate analysis, ALF at admission, OHCA occurring at home, absence of bystander, non-cardiac cause of OHCA, low-flow duration ≥ 20 min, and SOFA score excluding liver subscore at admission were independently associated with day 28 mortality. CONCLUSIONS: ALF occurred frequently after OHCA and, unlike HH, was independently associated with day 28 mortality.

ACG Clinical Guideline: disorders of the hepatic and mesenteric circulation

Disorders of the mesenteric, portal, and hepatic veins and mesenteric and hepatic arteries have important clinical consequences and may lead to acute liver failure, chronic liver disease, noncirrhotic portal hypertension, cirrhosis, and hepatocellular carcinoma. Although literature in the field of vascular liver disorders is scant, these disorders are common in clinical practice, and general practitioners, gastroenterologists, and hepatologists may benefit from expert guidance and recommendations for management of these conditions. These guidelines represent the official practice recommendations of the American College of Gastroenterology. Key concept statements based on author expert opinion and review of literature and specific recommendations based on PICO/GRADE analysis have been developed to aid in the management of vascular liver disorders. These recommendations and guidelines should be tailored to individual patients and circumstances in routine clinical practice.

Fulminant hepatic failure caused by herbal supplies

The consumption of botanicals for therapeutic purposes has increased significantly in recent years. Drug-induced liver disease (DILI) is a frequent cause of acute liver injury, around 50% in the United States, and about 1% is secondary to the use of phytotherapeuticals and herbal supplies. Ruellia bahiensis, a plant species of the Acanthaceae family, is a tropical plant distributed in Northeastern Brazil. In folk medicine in the state of Bahia, the species is known as "mãe-boa" and is commonly used. L.S.S, a 23-year old, female, patient was admitted at University Hospital of Bahia-Brazil with signs and symptoms of acute hepatitis. She had made daily use of an herbal supply popularly known as "mãe-boa" for at least two years prescribed by a physician. Diagnostic investigation was negative for viral and autoimmune hepatitis, leptospirosis, dengue, and CMV (cytomegalovirus). The patient had to undergo liver transplantation. Explant revealed massive hepatic necrosis. According to histological findings, and after exclusion of other etiologies, liver damage was assigned to herbal supply. The prolonged use of Ruellia bahiensis infusions may have caused the liver dysfunction.

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure / Modificações da hemodinâmica e metabolismo cerebral na insuficiência hepatica fulminante

ABSTRACT Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.

RESUMO O edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.

Hipotermia terapêutica como ponte até transplante em pacientes com falência hepática fulminante / Therapeutic hypothermia as a bridge to transplantation in patients with fulminant hepatic failure

Os tópicos mais importantes na falência hepática fulminante são o edema cerebral e a hipertensão intracraniana. Dentre todas as opções terapêuticas, tem sido relatado que a hipotermia sistêmica induzida em níveis entre 33 - 34ºC reduz a elevação da pressão e aumenta o tempo durante o qual os pacientes podem tolerar um enxerto. Esta revisão discutiu as indicações e os efeitos adversos da hipotermia.

The most important topics in fulminant hepatic failure are cerebral edema and intracranial hypertension. Among all therapeutic options, systemic induced hypothermia to 33 - 34ºC has been reported to reduce the high pressure and increase the time during which patients can tolerate a graft. This review discusses the indications and adverse effects of hypothermia.

Terapia com células da medula óssea em modelo experimental de insuficiência hepática aguda induzida por acetominofen / Therapy with bone marrow cells in an experimental model of heart failure liver induced by acute acetaminophen

Introdução e objetivos: a insuficiência hepática aguda (IHA), apesar de rara, permanece como uma condição rapidamente progressiva e frequentemente fatal. A intoxicação por acetaminofen (APAP) induz necrose hepática maciça e frequentemente leva à morte por edema cerebral. Terapias celulares são de grande interesse como potenciais tratamentos para IHA. Neste projeto foi avaliado o potencial terapêutico das células mononucleares da medula óssea (CMMO) em um modelo experimental de IHA induzida por APAP em camundongos. Métodos: A IHA foi induzida em camundongos C57Bl/6, previamente submetidos à dieta alcoólica por três semanas, através da administração de APAP na dose de 300 mg/kg por via intraperitoneal. Após a indução da IHA, os camundongos foram transplantados, por via endovenosa, com 107 CMMO...

Introduction and objectives: a cute liver failure (IHA), although rare, remains a rapidly progressive and often fatal condition. Poisoning by acetaminophen (APAP) induces a massive hepatic necrosis and often leads to death by cerebral edema. Cell therapies are of great interest as potential treatments for IHA. In this project we evaluated the therapeutic potential of bone marrow mononuclear cells (BMC) in an experimental model of IHA induced by APAP in mice. Methods: The IHA was induced in C57BL/6 mice previously submitted to the alcohol diet for three weeks by the administration of APAP at a dose of 300 mg / kg, intraperitoneally. After induction of IHA, the mice were transplanted intravenously with 107 BMC...

A new experimental model for acute hepatic failure in rats / Novo modelo experimental em ratos para insuficiência hepática aguda

PURPOSE: To develop a reliable surgical model of acute hepatic failure and hyperammonemia in rats that avoids porto-systemic shunt and bile duct ligation, applicable to hepatic encephalopathy research. METHODS: The pedicles of right lateral and caudate lobes were exposed and clamped. One hour later, the animal was reopened, clamps were released and anterior subtotal hepatectomy (resection of median and left lateral lobes) was performed, comprising 75 percent of liver removal. Four hours after hepatectomy, blood samples and liver tissues were collected from ALF and control groups. RESULTS: Differences between ALF and control groups were significant for ALT, AST, total and direct bilirubin, sodium, potassium, alkaline phosphatasis, gamma-glutamyltransferase and most important, ammonia. Histologically, significant differences were noticed between groups. CONCLUSION: The model is useful for the study of specific aspects of ALF and the development of new therapeutic approaches.

OBJETIVO: Desenvolver um modelo cirúrgico de IHA e hiperamonemia em ratos, que evita o shunt porto-sistêmico e a ligadura do ducto biliar, que seja aplicável à pesquisa de encefalopatia hepática. MÉTODOS: Após anestesia geral e laparotomia mediana, os pedículos dos lobos laterais direito e caudado foram isolados e clampeados. Após 1 hora, o animal foi reaberto, os clampes retirados e foi realizada hepatectomia anterior subtotal (ressecção dos lobos médio e lateral esquerdo), compreendendo a remoção de 75 por cento do parênquima. Quatro horas após a hepatectomia, amostras de sangue e tecido hepático foram coletadas nos grupos IHA e controle. RESULTADOS: Diferenças entre os grupos IHA e controle foram significativas para ALT, AST, bilirrubina total e direta, sódio, potássio, fosfatase alcalina, gama glutamiltransferase e principalmente amônia. Histologicamente, diferenças significativas foram observadas entre os grupos. CONCLUSÃO: O modelo é útil para o estudo de aspectos específicos da IHA e o desenvolvimento de novas abordagens terapêuticas.

Curso de atualização em emergências médicas: aula 18: insuficiência hepatica aguda / Course of updating in medical emergencies: class 18: acute hepatic failure

A insuficiência hepática aguda (IHA) é uma síndrome clínica extremamente grave, de diagnóstico precoce difícil, evolução rápida e alta mortalidade. Nesta revisão buscamos reunir as informações mais atuais sobre classificação, etiologia, diagnóstico e tratamento, discutindo as diversas controvérsias sobre o tema. O diagnóstico da IHA é difícil e engloba o quadro clínico e laboratorial de hepatite aguda (grave), tempo de protrombina alargado, com qualquer alteração do sensório, além de pesquisa cuidadosa na história do paciente, incluindo o uso de medicações ou ervas e presença de diagnóstico prévio de hepatopatia. O diagnóstico etiólogico inclui infecções virais, medicamentos e toxinas, causas cardíacas e vasculares, metabólicas, além da hepatite autoimune, doenças de Wilson e neoplasias. O tratamento da IHA é dado em duas etapas, sendo a primeira constituída pelas medidas de suporte, prevenção e tratamento das complicações, que devem ser oferecidas a todos os pacientes, e a segunda pelas medidas específicas, que serão direcionadas dependendo da etiologia. O transplante hepático é a única terapia definitiva para os pacientes que não conseguem o restabelimento da função hepática.

Acute hepatic failure (AHF) is one extremely serious clinical syndrome of difficult pre-emptive diagnosis, rapid evolution and high mortality. In this review we summarized the current information regarding its classification, etiology, diagnosis and treatment, and discussed the controversies about the issue. The diagnosis of the AHF is difficult and includes laboratorial and clinical findings of severe acute hepatitis, increased prothrombin time and presence of hepatic encephalopathy. It is necessary that a careful history of the patient be obtained especially with respect to utilization of medications, herbs as well as the presence of previous diagnosis of liver disease. The possible etiologies include viral infections, cardiac and vascular affections, medications and toxins, metabolic causes, auto-immune hepatitis, Wilson's disease and neoplasm. The treatment of AHF requires support measures, prevention and treatment of complications that must be offered all patients and specific measures which should be offered according to the etiology of AHF. Liver transplant is the only definitive therapy for patients who do not recover the hepatic function.

Hipotermia intravascular inducida en el manejo de la hipertensión intracraneana en insuficiencia hepática aguda: caso clínico / Intravascular hypothermia for the management of Intracranial hypertension in acute liver failure: case report

Acute liver failure has a mortality rate in excess of 80 percent. Most deaths are attributed to brain edema with intracranial hypertension and herniation of structures, where ammonium plays a major role in its generation. We report an 18 year-old female with a fulminant hepatic failure caused by virus A infection. The patient developed a profound sopor and required mechanical ventilation. A CT scan showed the presence of brain edema and intracranial hypertension. A Raudemic® catheter was inserted to measure intracranial pressure and brain temperature. Intracranial hypertension became refractory and intravascular hypothermia was started, reducing brain temperature to 33°C. Seventy two hours later, a liver transplantation was performed. After testing graft perfusion, rewarming was started, completing 122 hours of hypothermia at 33°C. The patient was discharged in good conditions after 69 days of hospitalization.

Intraparenchymal intracranial pressure monitoring in patients with acute liver failure / Monitoreo intraparenquimatoso de presión intracraneana en pacientes con falla hepática aguda

BACKGROUND: Elevated intracranial pressure (ICP) is a common cause of death in acute liver failure (ALF) and is determinant for decision-making regarding the timing of liver transplantation. The recommended type ICP monitoring device is controversial in ALF patients. Epidural devices had less risk of hemorrhagic complications, but they are less reliable than intraparenchymal ones. METHOD: Twenty-three patients with ALF were treated, and 19 of them received a liver transplant. Seventeen patients had ICP monitoring because of grade III-IV encephalopathy. All patients received fresh plasma (2-3 units) before and during placing the intraparenchymal device. RESULTS: Eleven cases (64.7 percent) had elevated ICP, and 6 patients (35.2 percent) had normal values. One patient (5.9 percent) had an asymptomatic small intraparenchymal haemorrhage <1cm³ in CTscan, which did not prevent the liver transplantation. CONCLUSION: In our experience, intraparenchymal ICP monitoring in patients with ALF seems to be an accurate method with a low risk of complications.

ANTECEDENTES: La presión intracraneana elevada (PIC) es una causa frecuente de muerte en la falla hepática aguda (FHA) y es determinante para la toma de decisiones respecto del momento del transplante hepático. El tipo de dispositivo para el monitoreo de OIC es controversial em los pacientes em FHA. Los dispositivos epidurales tienen menos riesgo de complicaciones hemorrágicas, pero son menos confiables que los intraparenquimatosos. MÉTODO: Veintitrés pacientes con FHA fueron tratados, y 19 de ellos recibieron un transplante hepático. diecisiete pacientes tuvieron monitoreo de PIC debido a encefalopatía grado III-IV. Todos los pacientes recibieron plasma fresco (2-3 unidades) antes y durante la colocación de la fibra intraparenquimatosa. RESULTADOS: Once casos (64.7 por ciento) tuvieron PIC elevada, y 6 pacientes (35.2 por ciento) tuvieron valores normales. Un paciente (5.9 por ciento) tuvo una pequeña hemorragia intraparenquimatosa asintomática <1cm³ en TAC, la cual no impidió el transplante hepático. CONCLUSIÓN: En nuestra experiencia, el monitoreo intraparenquimatoso de presión intracraneana en pacientes con FHA parece ser un método preciso y con bajo riesgo de complicaciones.

Factores pronósticos en insuficiencia hepática aguda / Prognoses factors in acute hepatic insufficiency

Introducción. La insuficiencia hepática aguda (IHA) es un síndrome poco frecuente aunque con elevada mortalidad. El objetivo de este estudio fue determinar las características clínico-epidemiológicas de la IHA. Materiales y métodos: Estudio abierto, prospectivo, descriptivo de pacientes con diagnóstico de IHA hospitalizados en la Unidad de Hígado del HNERM desde Febrero 1999 hasta Enero 2003. Resultados. Se estudiaron 15 casos. La edad promedio fue 63 años (30-81), la relación M/F fue 2/1. La etiología fue hepatitis viral B (53.3 por ciento), reacciones tóxicas por idiosincracia (20 por ciento), indeterminada (20 por ciento) y hepatitis A (6.7 por ciento). En el momento del diagnóstico el 80 por ciento presentó encefalopatía Grado I y el 20 por ciento encefalopatía III. El 13.3 por ciento no tuvo ascitis y el 86.7 por ciento ascitis leve-moderada. El 53.3 por ciento tenía como antecedente una enfermedad crónica (diabetes, insuficiencia renal crónica, cardiopatía y otros). Los valores de laboratorio fueron: albúmina media 2.5 gr./dl, bilirrubina media 25.9 mg/dl, tiempo de protrombina media 29'' y Factor V media 40.7 por ciento. Las complicaciones más frecuentes fueron la sepsis y el edema cerebral. La mortalidad global fue 80 por ciento. El tiempo de sobrevida media fue 16.6 días. Conclusiones. La mayoría de casos tuvieron más de 60 años. La principal causa de IHA fue la hepatitis viral B, esta enfermedad puede prevenirse con la inmunización activa. La infección y el edema cerebral fueron causas importantes de muerte. La IHA aunque rara, es una entidad rápidamente progresiva y fatal.

Introduction. Acute Hepatic Insufficiency (AHI) is a rare syndrome but has a highmortality rate. The purpose of this study was to determine the clinico-epidemiological characteristics of AHI. Materials and Methods. Open study, prospective, descriptive of patients diagnosed with AHI in the Liver Unit of the Edgardo Rebagliati Martins State Hospital (HNERM) from February 1999 until January 2003. Results. Fifteen (15) cases were studied. The average age was 63 (30-81), the M-Fratio was 2/1. The diagnosis was viral Hepatitis B (53.3 per cent), toxic idiosyncratic reactions(20 per cent), undetermined (20 per cent) and Hepatitis A (6.7 per cent). At the time of diagnosis 80 per cent had Grade I encephalopathyand 20 per cent Grade III encephalopathy; 13.3 per cent did not have ascites and 86.7 per cent had mild-moderate ascites; 53.3 per cent had a history of chronic illness (diabetes, chronic renal insufficiency, cardiopathy and others). Average laboratory values were: albumin 2.5 gr./dl, bilirubin 25.9 mg/dl, prothrombin time 29” and Factor V 40.7 per cent. The most frequent complications were sepsis and cerebral oedema. Global mortality was 80 per cent. The average survival time was 16.6 days.Conclusions. In most cases the patients were over 60 years of age. The main cause of AHI was viral Hepatitis B, a disease which can be prevented with active immunisation. Infection and cerebral oedema were common causes of death. AHI, although rare, is a rapidly degenerative and fatal condition.

Hepatite fulminante: do diagnóstico ao transplante de fígado / Fulminant hepatitis: from diagnosis to liver transplantation

A insuficiência aguda grave do fígado é rara, e potencialmente letal. A identificação precoce dessa síndrome, o manejo adequado dentro do ambiente de terapia intensiva e a transferência para centros transplantadores são mandatórios. A realização do transplante hepático nos pacientes com mau prognóstico salva esses indivíduos de uma morte quase certa. O autor revisa as estratégias atuais do suporte à vida nesses pacientes críticos de maneira multidisciplinar, enfatizando a monitorização invasiva para definir o momento oportuno do transplante hepático.

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

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% (p<0,001). O Grupo SSH apresentou maior estabilidade hemodinâmica, nos primeiros 5 min da reperfusão hepática, a pressão arterial média no Grupo SSH aumentou 21,1% e no Grupo Controle diminuiu 11,1% (p<0,001). Nos primeiros 5 min da reperfusão a pressão de perfusão cerebral no Grupo SSH aumentou 28,3% e no Grupo Controle diminuiu 28,5% (p< 0,001). A natremia no final da fase anepáica e após 3 horas da reperfusão foi significativamente maior no Grupo SSH (153.00 ± 2.66 and 149.00 ± 1.73 mEq/L) que no Grupo Controle (143.71 ± 3.30 and 142.43 ± 1.72 mEq/L), p=0.003 e p< 0.001 respectivamente.CONCLUSÃO: Estes resultados sugerem que a solução salina hipertônica pode ser utilizada com sucesso como medida neuroprotetora no transplante de fígado para hepatite fulminante, promovendo diminuição efetiva da pressão intracraniana e estabilidade cardiocirculatória, proporcionando aumento sustentado da PPC durante a cirurgia.

Hepatotoxidad por acetaminofeno en un escolar con ingesta habitual de alcohol: caso clínico / Acetaminophen hepatotoxicity in a teenager with excessive alcohol intake

Acetaminophen hepatotoxicity in a teenager with excessive alcohol intake We report a 12 years old male with a history of excessive alcohol intake, that developed a severe liver failure after the use of acetaminophen in therapeutic doses. He presented with encephalopathy, jaundice, fever and an upper gastrointestinal bleeding. Serum aspartate aminotransferase values were 5 250 IU/L. The patient received supportive care and oral corticosteroids, remained severely compromised for 72 hours and had a good evolution thereafter. The association of acetaminophen use and excessive alcohol intake in a patient who developed an acute hepatic failure and the absence of serological evidence of hepatitis A or B viral infection, support the diagnosis of drug induced liver failure