Acute Liver Failure

2016 ◽  
Vol 27 (4) ◽  
pp. 420-429 ◽  
Author(s):  
Ami Grek ◽  
Lisa Arasi

Acute liver failure, also known as fulminant hepatic failure, is a rare life-threatening disease that has a high mortality rate and affects many organ systems. Causes of acute liver failure vary—it can be attributed to drugs, viruses, and other uncommon sources. Complications of liver failure can include encephalopathy, cerebral edema, sepsis, renal failure, gastrointestinal bleeding, and respiratory failure. Fortunately, with advances in critical care medicine and emergent liver transplant, mortality rates have decreased in the past decade. This article reviews acute liver failure, its manifestations in different organ systems, and its treatment.

1970 ◽  
Vol 31 (2) ◽  
pp. 89-92
Author(s):  
Gauri Shankar Shah ◽  
Manoj Kumar Singh ◽  
Dheeraj Shah

Introduction: Hepatic encephalopathy is a potentially reversible neurophyschiatric abnormality in the setting of liver failure. Acute liver failure (ALF) is a potentially life-threatening disorder in children. Objectives: The present study evaluated the clinical profile, outcome and factors influencing the outcome of children presenting with acute liver failure and hepatic encephalopathy presenting to a referral hospital of Eastern Nepal. Methodology: Thirty children (17 males and 13 females) were admitted with this diagnosis during two year period.Prospective study. Results: The most common cause of acute liver failure was mushroom poisoning seen in 30% of cases. Only 37% (11 out of 30) children survived, most of them in early stages (Stage I and II) of encephalopathy. Bleeding manifestations were significantly more common (P=0.002) in deaths as compared to survivors. Conclusion: As liver failure is associated with high mortality rates especially in absence of facilities for liver transplantation, efforts should be directed in favor of implementing preventive measures such as vaccination and community education to prevent toxin ingestion. Key Words: Acute liver failure; Hepatic encephalopathy; Mushroom poisoning DOI: 10.3126/jnps.v31i2.4639 J Nep Paedtr Soc 2010;31(2):89-92


2019 ◽  
Vol 11 (1) ◽  
pp. 70-74 ◽  
Author(s):  
Oliver D Tavabie ◽  
William Bernal

Acute liver failure (ALF) is a rare but life-threatening clinical syndrome with a broad range of causes. Significant improvements in outcome have occurred over the last 50 years, resulting not only from incremental improvements in specialist critical care and a step-change following the introduction of transplantation for this indication, but also better and more effective treatment started early at the site of first presentation.1 2 Emergency liver transplantation (LTx) remains an important intervention and the decision regarding the need for LTx remains key to management, though non-transplant therapies now appear effective for many causes of the condition. In this short review, we will outline issues in the recognition and management of ALF and ongoing challenges in its treatment.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1329-1329
Author(s):  
Honar Cherif ◽  
Jan Hansen ◽  
Mats Kalin ◽  
Magnus Bjorkholm Prof

Abstract Background: Appropriately aggressive treatment of haematological malignancies can be complicated by a variety of life threatening events. Despite high hospital mortality rates for such patients admitted to intensive care units (ICU) it is now generally considered to be appropriate to offer intensive care to selected cases, provided there is a reasonable prospect of cure or at least worthwhile palliation. Aims and Methods: We conducted a retrospective observational study to assess outcome and prognostic indicators in consecutive patients with hematological diseases admitted to the ICU during a 6-year-period. Results: From 1996 through 2001, a total of 95 patients with hematological diseases and a median age of 57 years (range 16–86) were admitted to the ICU. The median duration of ICU stay was 1 day (mean 4.2 days: range 1–67 days). The Mean Acute Physiology and Chronic Health Evaluation II (APACHE II) score was 20 (± 9). The large majority of patients underwent active treatment of a hematological malignancy (90%) with acute leukaemia (27%), non-Hodgkin lymphoma (24%) and multiple myeloma (10%) dominating. Respiratory failure (46%), sepsis (24%), cardiovascular complications (9%) and bleeding disorders (7%) were the major reasons for ICU admission. A total of 49 patients (51%) had a microbiologically verified infection and 21 (22%) had bacteremia. Crude ICU, 4-week and 6-month mortality rates were 28%, 45%, and 57%, respectively. An APACHE II score > 30 predicted a high short-term mortality rate (p= 0.0001). However, age > 65 years, respiratory failure, bacteremia, and a diagnosis of acute leukemia were not significantly associated with a poor short-term survival (p> 0.05). A total of 30 patients (31%) were alive after a minimum follow up of 3.5 years. Conclusion: The lower mortality rate as compared with most other series is probably explained by a more liberal attitude towards ICU admission. Not withstanding this, for a substantial proportion of critically ill hematological patients a short time care at an ICU is life saving. Patients with life threatening complications of haematological disease should be offered intensive care unless or until it is clear that there is no prospect of recovery from the acute illness or that the underlying malignancy cannot be controlled.


2013 ◽  
Vol 33 (1) ◽  
pp. 48-56 ◽  
Author(s):  
Holly Castello ◽  
Lisa Schoch ◽  
Tracy A. Grogan

Acute fatty liver of pregnancy is a rare and life-threatening disease associated with a defect in fatty acid metabolism in the fetus that causes liver disease in the mother. Prompt diagnosis and management are critical to the outcome of both the mother and the fetus and require involvement of several medical specialties, including hepatology, obstetrics, and, possibly, critical care. The included case study describes a woman with acute fatty liver of pregnancy decompensating to acute liver failure complicated by encephalopathy, cerebral edema, and intracranial hypertension. Subsequent management of these conditions, including the woman’s progression to liver transplant, is provided.


2019 ◽  
Vol 19 (12) ◽  
pp. 980-987 ◽  
Author(s):  
Mohammad Ridwane Mungroo ◽  
Ayaz Anwar ◽  
Naveed Ahmed Khan ◽  
Ruqaiyyah Siddiqui

Pathogenic free-living amoeba are known to cause a devastating infection of the central nervous system and are often referred to as “brain-eating amoebae”. The mortality rate of more than 90% and free-living nature of these amoebae is a cause for concern. It is distressing that the mortality rate has remained the same over the past few decades, highlighting the lack of interest by the pharmaceutical industry. With the threat of global warming and increased outdoor activities of public, there is a need for renewed interest in identifying potential anti-amoebic compounds for successful prognosis. Here, we discuss the available chemotherapeutic options and opportunities for potential strategies in the treatment and diagnosis of these life-threatening infections.


2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Bertram K. Woitok ◽  
Shawki Bahmad ◽  
Gregor Lindner

Background.Exertional heat stroke is a life-threatening condition often complicated by multiorgan failure. We hereby present a case of a 25-year-old male presenting with syncope after a 10  km run in 28°C outside temperature who developed acute liver failure. Case Presentation. Initial temperature was found to be 41.1°C, and cooling measures were rapidly applied. He suffered from acute renal failure and rhabdomyolysis and proceeded to acute liver failure (ASAT 6100 U/l and ALAT 6561 U/l) due to hypoxic hepatitis on day 3. He did not meet criteria for emergency liver transplantation and recovered on supportive care. Conclusions. Acute liver failure due to heat stroke is a life-threatening condition with often delayed onset, which nevertheless resolves on supportive care in the majority of cases; thus, a delayed referral to transplant seems to be reasonable.


1995 ◽  
Vol 6 (5) ◽  
pp. 1379-1385
Author(s):  
J Coresh ◽  
M Walser ◽  
S Hill

Concerns have been raised about the possibility of protein restriction resulting in malnutrition and poor subsequent survival on dialysis. However, no studies have examined patients treated with protein restriction to determine their subsequent survival on dialysis. This study prospectively monitored 67 patients with established chronic renal failure (mean initial serum creatinine of 4.3 mg/dL) who were treated with a very low-protein diet (0.3 g/kg per day) supplemented with either essential amino acids or a ketoacid-amino acid mixture and observed closely for clinical complications. Forty-four patients required dialysis. Once dialysis was started, dietary treatment was no longer prescribed. The cumulative mortality rate during the first 2 yr after starting dialysis was 7% (95% confidence interval, 0 to 16%). During this period, only two deaths occurred compared with 11.5 deaths expected on the basis of national mortality rates adjusted for age, sex, race, and cause of renal disease (P = 0.002). However, the protective effect was limited to the first 2 yr on dialysis. Thereafter, mortality rates increased, resulting in a total of 10 deaths during 96.4 person-years of follow-up, which was not significantly lower than the 14.9 deaths expected (P = 0.25). Extrapolation of sequential serum creatinine measurements made before dietary treatment suggests that the improved survival cannot be due to the early initiation of dialysis. Although the lack of an internal control group and data on dialysis lends uncertainty, the large difference in mortality rate between these patients and the nationwide experience indicates that protein restriction and close clinical monitoring predialysis does not worsen and may substantially improve survival during the first 2 yr on dialysis. These findings point out the importance of studying predialysis treatments as a means for lowering mortality on dialysis.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3344-3344
Author(s):  
Selim Corbacioglu ◽  
Simone Cesaro ◽  
Maura Faraci ◽  
Bernd Gruhn ◽  
Jaap Jan Boelens ◽  
...  

Abstract Abstract 3344 Poster Board III-232 Background: Hepatic VOD is a life-threatening complication following SCT with a high incidence in children. Development of VOD is one of the most common causes of early death after SCT. Busulfan (BU), an alkylating agent with a very narrow therapeutic index is a commonly used conditioning agent in pediatric stem cell transplantation (SCT) with a strong correlation between AUC and both efficacy and toxicity. Oral BU (poBU) has significant age-related and interpatient pharmacokinetic differences and was linked with an increased risk for VOD. IV busulfan (ivBU) yielded promising results in some studies to be associated with low toxicity profile, especially with a reduced incidence of VOD. Methods: Patients <18 years with myeloablative SCT were included in a prospective multicenter phase II/III trial to evaluate the efficacy of Defibrotide (DF). Eligibility criteria included conditioning with BU (iv and po) and melphalan (MEL). Pts were prospectively randomized to the control arm or to receive DF. Primary endpoint was the incidence of hepatic VOD by D+30 using modified Seattle criteria (2 or more of the following: bilirubin > 2 mg/dL, hepatomegaly, ascites and/or unexplained weight gain > 5%). VOD was assessed by physical exam; hepatomegaly and ascites were confirmed by ultrasound. A blinded IRC of 3 expert hematologists confirmed the diagnosis of VOD. Although the study was not powered to assess mortality, a composite score was assessed as a secondary endpoint that incorporated VOD-associated toxicity (respiratory failure, renal failure, encephalopathy) and mortality. The additional analysis of the influence of BU on VOD was not planned and is therefore explorative. Results: 360 pts were enrolled between January 2006 and January 2009 by 28 centers in the EU and Israel. An Intent-to-Treat (ITT) analysis was performed on all pts who signed informed consent (n=356). 251 (71%) pts from the ITT population were conditioned with BU (64% ivBU; 36% poBU). 202 (55%) were treated with BU and Melphalan (MEL) (60% ivBU; 40% poBU). In 49 (14%) BU was used without MEL (80% ivBU; 20% poBU). In children <2yrs 44 (12%) were conditioned with BU/MEL (59% ivBU; 41% poBU) and 26 (7%) were conditioned without MEL (85% ivBU; 15% poBU). The median age of patients with iv BU was 3.65 yrs and 5,13 yrs with poBU; 28% infants, 50% children (ages 2-11 yrs) and 22% adolescents (evenly distributed). 45% female, 55% male (evenly distributed). Allo-SCT was performed in 69% with ivBU and 46% with poBU (remaining with auto-SCT). The diagnoses were evenly distributed between poBU and ivBU. Except in AML 18% were conditioned with ivBU and 32% with poBU. Preexisting liver disease was present in 23% ivBU and 9% poBU pts, of which 46% (17/37) ivBU and 37% (3/8) poBU had elevated transaminases. Overall VOD was experienced by 23% of the infants, 14% of the children and 13% of the adolescents. The overall incidence of VOD in pts treated with BU was 18%. VOD was diagnosed in 24% ivBU vs 8% poBU pts. In pts treated with BU/MEL VOD was diagnosed in 16%. VOD in ivBU/MEL was 21% (26) vs 8% (6) in poBU/MEL. In BU without MEL VOD was diagnosed in 27% (13/49). 31% (12/39) in ivBU pts and 10% (1/10) in poBU pts. In infants treated with BU/MEL the incidence of VOD in the ivBU group was 23% (6/26) and 11% (2/18) in poBU. In BU without MEL in infants the incidences were 41% (9/22) ivBU versus none (0/4) in poBU. The diagnosis of VOD independent of severity was associated with a higher mortality and equaled 24.6% (14/57) compared to 7% in pts without VOD (21/299). Respiratory failure was observed in 10% (16/161) of ivBU vs 2% (2/90) of poBU pts (9% (11/122) vs 1% (1/80) iv vs po BU/MEL); renal failure in 5% (8/161) ivBu vs 1% (1/90) poBU (5% (6/122) vs none in iv vs po BU/MEL). The incidence of multi-organ-failure (MOF) by day +100 was 12% (19/161) in ivBU vs 3% (3/90) in poBU (p=0.022). Compared to all other pts the risk to develop VOD in infants treated with allo-SCT and ivBU is 2.4 times higher (p=0.003). Conclusions: Although the scope of this trial was not to assess the influence of BU on the incidence of VOD and there was an imbalanced distribution of liver diseases and a potential bias for other risk factors the incidence of VOD in ivBU was unexpectedly high especially in infants. Inasmuch this is due to a high interpatient variability of the AUC should be explored prospectively. Disclosures: Corbacioglu: Gentium S.p.A.: Consultancy, Research Funding.


2017 ◽  
Vol 54 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Fabiano Moraes MIGUEL ◽  
Elizângela Gonçalves SCHEMITT ◽  
Josieli Raskopf COLARES ◽  
Renata Minuzzo HARTMANN ◽  
Maria Isabel MORGAN-MARTINS ◽  
...  

ABSTRACT BACKGROUND Severe Acute Liver Failure (ALF) is a life-threatening clinical syndrome characterized by hepatocyte necrosis, loss of hepatic architecture, and impairment of liver functions. One of the main causes of ALF is hepatotoxicity from chemical agents, which damage hepatocytes and result in increase of reactive oxygen species. The vitamin E isoform is the one with the strongest biological antioxidant activity. OBJECTIVE To evaluate the antioxidant effect of vitamin E in this ALF model. METHODS We used 56 rats (mean weight of 300 g) divided into eight groups, four groups assessed at 24 hours and 4 assessed at 48 hours after induction: control group (CO); Vitamin E (Vit. E); Thioacetamide (TAA) and Thioacetamide + Vitamina E (TAA+Vit.E). Rats were submitted to injections of thioacetamide (400 mg/kg i.p.) at baseline and 8 hours later. Vitamin E (100 mg/kg ip) was administered 30 minutes after the second dose of thioacetamide. The 48-hour group rats received two additional doses of vitamin E (24h and 36h). At 24h or 48 hours after the administration of the first dose of TAA, rats were weighed and anesthetized and their blood sampled for evaluation of liver integrity through enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Liver tissue was sampled for assessment of lipid peroxidation (LPO) by the technique TBARS, antioxidant enzymes SOD, CAT, GPx and GST activity, levels of the NO 2 /NO 3 and histology by H&E in two times. The results were expressed as mean ± standard deviation and statistically analyzed by ANOVA followed by Student-Newman-Keuls, with P <0.05 considered as significant. RESULTS After treatment with vitamin E, we observed a reduction in liver enzymes AST (U/L) (101.32±19.45 in 24 hours and 97.85±29.65 in 48 hours) related to the TAA group (469.56± 0.69 in 24 hours and 598.23±55.45 in 48 hours) and ALT (U/L) (76.59±8.56 in 24 hours and 68.47±6.49 in 48 hours) compared to the TAA group (312.21±10.23 in 24 hours and 359.15±17.58 in 48 hours). There was a reduction of LPO (nmol/mg Prot) in the TAA+Vit.E group (0.77±0.07 in 24 hours and 0.95±0.08 in 48 hours) compared to the TAA group (1.50±0.07 in 24 hours e 1.65±0.16 in 48 hours). SOD decreased in the TAA+Vit.E group (49.48±9.47 in 24 hours and 62.45±18, 47 in 48 hours), related to the TAA group (98.46±15.48 in 24 hours and 154.13±21.46 in 48 hours), as well as GST (nmol/min/mg Prot) in the TAA+Vit.E group (350.57±36.93 in 24 hours and 453.29±13.84 in 48 hours) compared to the TAA group (561.57±64.56 in 24 hours and 673.43±38.13 in 48 hours). There was an increase in CAT (pmol/min/mg Prot) in the TAA+Vit.E group (3.40±0.44 in 24 hours and 3.0±0.35 in 48 hours) compared to the TAA group (1.65±0.21 in 24 hours and 1.86±0.42 in 48 hours). The GPx (nmol/min/mg Prot) increased in 24 hours in the TAA+Vit.E group (1.01±0.16) compared to the TAA group (0.41±0.04) and decreased in 48 hours (1.19±0.17) compared to the TAA group (1.76±0.21). There was a reduction in NO2/NO3 (mmol/L) levels in the TAA+Vit.E group (31.47±4.26 in 24 hours and 38.93±5.20 in 48 hours) compared to the TAA group (49.37±5.12 in 24 hours and 53.53±5.97 in 48 hours). The histopathological evaluation showed a decrease in liver injury (necrosis and inflammation) in both studied times. CONCLUSION These results suggest that vitamin E was able to protect the liver from lesions caused by thioacetamide.


Sign in / Sign up

Export Citation Format

Share Document