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At least 19 recordsLinked to original sources
PubMedDate not supplied

Antiarrhythmic drug therapy in patients with renal failure, liver failure, and congestive heart failure.

Commonly prescribed antiarrhythmic agents--and several recently developed agents--are reviewed with respect to their use in patients with renal failure, hepatic failure, and congestive heart failure. Because removal of electrophysiologically active agents from the systemic circulation in most cases depends on either renal elimination, hepatic metabolism, or both, patients with preexisting kidney or liver disease may be at increased risk of treatment-related drug toxicity, including proarrhythmia. These susceptibilities should be anticipated, with drug selection and/or dosage modified accordingly. Patients with left ventricular dysfunction and heart failure also are at increased risk of treatment-related complications, including proarrhythmia and hemodynamic intolerance. In addition, the metabolism of antiarrhythmic drugs may be impaired in these patients. Preference should be given to drugs with a proven safety profile, such as amiodarone, in patients with heart failure.

Anti-Arrhythmia Agents↗
PubMed1996

The lived experience of end-stage liver failure and liver transplantation.

This phenomenological study examined the lived experience of an individual who underwent end-stage liver failure and liver transplantation. The participant was asked to respond to the question, what was it like for you having experienced end-stage liver failure and liver transplantation? Permission was granted to tape-record the interview. Themes derived from the data analysis were identified, analyzed, and sorted. As a result, four categories were delineated: (1) uncertainty, (2) control, (3) social support, and (4) spirituality. Categories and themes contributing to a description of one individual's experience with end-stage liver failure and liver transplantation may provide direction for interventional studies designed to effect change in the lived experiences of those undergoing similar phenomena.

Fear↗
PubMed2006

The brain glutamate system in liver failure.

Liver failure results in significant alterations of the brain glutamate system. Ammonia and the astrocyte play major roles in such alterations, which affect several components of the brain glutamate system, namely its synthesis, intercellular transport (uptake and release), and function. In addition to the neurological symptoms of hepatic encephalopathy, modified glutamatergic regulation may contribute to other cerebral complications of liver failure, such as brain edema, intracranial hypertension and changes in cerebral blood flow. A better understanding of the cause and precise nature of the alterations of the brain glutamate system in liver failure could lead to new therapeutic avenues for the cerebral complications of liver disease.

Animals↗
PubMed1993

Managing the patient with liver failure.

Liver failure affects virtually all aspects of body functioning, which challenges medical-surgical nurses to deliver effective comprehensive care. Managing patients with liver failure requires a thorough understanding of hepatic physiology and the pathophysiology of liver disease failure.

Acid-Base Imbalance↗
PubMed1980

Evidence for liver cell proliferation during fatal acute liver failure.

Liver cell regeneration was assessed by determining the mitotic index and the frequency of liver cells with interploid DNA values in livers from patients dying from fulminant hepatitis. For comparison, the same parameters were determined in patients with uncomplicated hepatitis. We found comparable levels of regeneration in the two groups, indicating that the rate of liver cell destruction is a major determinant in the prognosis of acute liver failure. Accordingly, measures to prevent liver cell necrosis seem at least as important as stimulation of regeneration. Judged from available experimental evidence, substances with documented hepatotrophic effect in animals, such as insulin and glucagon, may therefore not be effective in acute liver failure unless the patient has impaired secretion of these substances.

Adult↗
PubMed2002

Managing liver failure.

Liver disease is rare in childhood, but important new developments have altered the natural history and outcome. It is important that clinicians are aware of these diseases and their management. Acute liver failure is most often due to viral hepatitis, paracetamol overdose, or inherited metabolic liver disease. The clinical presentation includes jaundice, coagulopathy, and encephalopathy. Early diagnosis is necessary to prevent complications such as cerebral oedema, gastrointestinal bleeding, and renal failure. Early supportive management, in particular intravenous N-acetylcysteine, may be effective but liver transplantation is usually the definitive treatment and thus early referral to a specialist unit for liver transplantation is mandatory. Chronic liver failure may be due to unresolved neonatal liver disease, either inherited biliary hypoplasia or extrahepatic biliary atresia, while in older children, autoimmune liver disease or cystic fibrosis are the commonest causes. Treatment includes specific medication, nutritional support, and liver transplantation, which now has a 90% survival with good quality life.

Child↗
PubMedDate not supplied

Serum acute-phase protein level as indicator for liver failure after liver resection.

BACKGROUND/AIMS: We investigated the relationship between postoperative liver failure and serum acute-phase protein level before and after liver resection. METHODOLOGY: Thirty-four patients who underwent liver resection were prospectively included. Serum concentrations of negative (albumin, prealbumin and retinol-binding protein) and positive (orosomucoid, haptoglobin and C-reactive protein) acute-phase proteins were assayed prior to surgery (baseline) and on postoperative day 3, 12 and 45. Postoperative liver failure was defined as serum bilirubin more than 50 micromol/L or prothrombin time less than 50% on postoperative day 7. Univariate analysis was performed to compare patients who did and did not present postoperative liver failure. RESULTS: Postoperative liver failure occurred in 8 cases and was correlated with: 1) higher negative and lower positive acute-phase protein levels (p<0.04) at baseline, 2) lower negative and lower positive acute-phase protein levels on postoperative day 3, 12 or 45 (p< or =0.05). CONCLUSIONS: Early onset of inflammatory serum protein profile was correlated with absence of postoperative liver failure. Serum acute-phase protein could be used as predictor as well as early postoperative diagnosis marker of postoperative liver failure. Relationship between preoperative inflammation and postoperative liver failure warrants further investigations because of potential therapeutic consequences.

Acute-Phase Proteins↗
PubMed2002

[Intensive care treatment of post-traumatic liver failure].

Liver failure following trauma or surgery is associated with a mortality of between 15-->50%, depending on the extent of the operation, pre-operative functional impairment of the liver as well as the occurrence of concomitant infectious disease. The liver can be the source as well as the target of posttraumatic liver failure (PLF). PLF can be caused by a reduction of liver perfusion due to hypotension, catecholamines or increased intraabdominal pressure. Further contributing factors include prolonged parenteral nutrition, endotoxemia, and potentially hepatotoxic drugs (sedatives, anticonvulsive drugs, antibiotics etc.). PLF is mostly associated with MOF. The Child classification and the APACHE score may predict prognosis before surgery and serum bilirubin levels thereafter. Prevention and therapy is based on treatment of shock and tissue hypoxia. It should be accompanied by appropriate diagnostic measures and followed by an aggressive medical and surgical approach.

APACHE↗
PubMed2003

Neonatal liver failure.

Liver failure in the neonatal period is challenging to diagnose and manage, and still carries a high mortality. With ongoing developments in the field of metabolic disorders and antiviral therapy, and the ability to offer liver transplantation to small babies, an overall survival of 40% has been achieved. Early recognition of liver failure, good supportive care and prompt referral to a paediatric liver transplant centre are essential elements in improving the outcome for these babies. Decisions about contra-indications to and timing of transplantation are complex as many of the disease processes are still evolving in the neonatal period, and extrahepatic disease, which cannot be corrected by a transplant, may appear later.

Humans↗
PubMed2006

Review article: non-biological liver support in liver failure.

Liver failure, whether acute or acute-on-chronic, remains an important cause of morbidity and mortality. The lack of liver detoxification, metabolic and regulatory functions of the liver leads to life-threatening complications, such as renal failure, altered immune response, hepatic coma and systemic haemodynamic dysfunction, eventually culminating in multiorgan failure. Current medical therapy involves the management of the precipitating event and treatment of complications until the liver eventually recovers, leaving us with no other treatment options than transplantation if these attempts fail. However, the shortage in cadaveric organs and other transplant-related problems, have prompted the need for alternative methods to provide liver support. As liver failure is often potentially reversible, considerable effort has been invested in the development of liver support systems. Currently, most of the experience is available for non-biological support systems. They represent the focus of this review, which aims to define the goals of liver support, to describe the design of the different existing devices and to analyse the available data to determine their current status in the management of patients with liver failure.

Albumins↗
PubMed2001

Extracorporeal detoxification using the molecular adsorbent recirculating system for critically ill patients with liver failure.

Liver failure resulting from different causes and its concomitant complications represent difficult-to-treat conditions with high mortality rates, despite improved therapeutic modalities in intensive care medicine. The accumulation of albumin-bound metabolites that are normally cleared by the liver, such as bilirubin and bile acids, contributes substantially to the development of multiorgan dysfunction in these clinical situations. The molecular adsorbent recirculating system (MARS) represents a cell-free, extracorporeal, liver assistance method for the selective removal of albumin-bound substances. Moreover, it enables the removal of excess water and water-soluble substances via an inbuilt dialysis step. Since 1993, >400 patients have been treated in 53 centers in Europe, the United States, and Asia. Diseases treated with MARS included acute exacerbation of chronic hepatic failure, hepatorenal syndrome, acute hepatic failure, and primary nonfunction/poor function after liver transplantation and major liver resection. Treatments were well tolerated. No severe adverse events were observed. Six- to 8-h MARS treatments resulted in significant (P < 0.05) removal of bilirubin, bile acids, tryptophan, short- and middle-chain fatty acids, aromatic amino acids, and ammonia. Clearance rates for strongly albumin-bound substances were between 10 and 60 ml/min. The removal of albumin-bound toxins resulted in decreases in hepatic encephalopathy, increases in mean arterial pressure, and improvements in kidney and liver function. In the first randomized clinical trial of the MARS method for treatment of the hepatorenal syndrome, significant prolongation of survival was observed for the MARS-treated group. It is concluded that the MARS method can contribute to the treatment of critically ill patients with liver failure and different underlying diseases.

Critical Illness↗
PubMed2001

Living donor liver transplantation for children with liver failure and concurrent multiple organ system failure.

Liver transplantation for pediatric patients in liver failure and multiple organ system failure (MOSF) often results in poor patient survival. Progression of organ failure occurs while awaiting a cadaveric allograft. Therefore, we considered living donor liver transplantation (LDLT) in this critically ill group of children and report our initial results with comparison to a similar group who received cadaveric donation (CAD). A retrospective chart review was performed on all pediatric liver transplant recipients who met criteria for MOSF at the time of transplantation. Data collection involved pretransplantation patient profiles, as well as postoperative complications and patient survival. Eight patients in MOSF received living donor transplants and 11 patients received a cadaveric allograft. Mean wait time was 3.5 days in the LDLT group and 6.5 days in the CAD group. Pretransplantation patient profiles and postoperative complications were similar between groups. Mean cold ischemia times were 3.8 hours in the LDLT group and 7.9 hours in the CAD group (P = .0002). Thirty-day and 6-month survival rates of the LDLT group were 88% and 63% compared with 45% and 27% in the CAD group, respectively. Living donor transplant recipients in MOSF had decreased wait times to transplantation, as well as decreased cold ischemia times, compared with cadaveric transplant recipients. Patients in the LDLT group had markedly improved survival compared with the CAD group. Timely transplantation before worsening organ failure may account for these findings.

Cadaver↗
PubMed1996

The American experience with transplantation for acute liver failure.

Liver transplantation has become the major therapy for acute liver failure (ALF) in the United States. Survival rates range from 46% to 89%. Appropriate patient selection, timely referral, and management of common complications have improved survival. Donor organ shortage may prompt further use of extracorporeal support systems and auxillary transplantation in the future. This article reviews the American experience of liver transplantation in patients with ALF.

Contraindications↗
PubMed1995

Progression from idiopathic portal hypertension to incomplete septal cirrhosis with liver failure requiring liver transplantation.

We report the case of a 30-year-old male patient suffering from what was initially thought to be end-stage cryptogenic cirrhosis with portal hypertension and liver failure, who underwent liver transplantation. Histological examination of the surgical specimen showed incomplete septal cirrhosis. At the age of 17 this patient had presented pancytopenia and splenomegaly, which were treated by splenectomy. The surgeon discovered portal hypertension. Re-examination of the wedge liver biopsy taken at this time revealed features of idiopathic portal hypertension. This case clearly shows that incomplete septal cirrhosis may be a late manifestation of idiopathic portal hypertension. The presence of sinusoidal dilatation and peliosis as well as early evidence of fibrosis which are already visible on the initial biopsy and are still present on the late specimen, are indirect evidence of a continuous process which ultimately led to incomplete cirrhosis with liver failure.

Adult↗
PubMed2002

Intestinal endotoxemia as a pathogenetic mechanism in liver failure.

Liver injury induced by various pathogenic factors (such as hepatitis virus, ethanol, drugs and hepatotoxicants, etc.) through their respective special pathogenesis is referred to as primary liver injury (PLI). Liver injury resulted from endotoxin (lipopolysaccharide, LPS) and the activation of Kupffer cells by LPS while intestinal endotoxemia (IETM) occurred during the occurrence and development of hepatitis is named the secondary liver injury (SLI). The latter which has lost their own specificities of primary pathogenic factors is ascribed to IETM. The secondary liver injury is of important action and impact on development and prognosis of hepatitis. More severe IETM commonly results in excessive inflammatory responses, with serious hepatic necrosis, further severe hepatitis and even induces acute liver failure. The milder IETM successively precipitates a cascade, including repeated and persistent hepatocytic impairment accompanied by infiltration of inflammatory cells, hepatic fibrosis, cirrhosis and hepatocarcinoma. Generally, the milder IETM ends with chronic hepatic failure. If PLI caused by various pathogenic factors through their independent specific mechanismis regarded as the first hit on liver, then SLI mediated by different chemical mediators from KCs activated by IETM in the course of hepatitis is the second hit on liver. Thus, fusing and overlapping of the primary and scondary liver injuries determine and influeuce the complexity of the illness and outcome of the patient with hepatitis. For this reason, the viewpoint of SLI induced by the second hit on liver inflicted by IETM suggests that medical professionals should attach great importance to both PLI and SLI caused by IETM. That is, try to adjust the function of KS(s) and eliminate endotoxemia of the patient.

Animals↗
PubMed2002

Inappropriate pemoline therapy leading to acute liver failure and liver transplantation.

A 36-year-old female, presenting with jaundice, developed acute liver failure requiring orthotopic liver transplantation. On admission, none of the known causative factors for acute hepatitis, including use of drugs, were found to be present. Several days after hospitalization, the patient admitted taking therapy prescribed by a "non-traditional" physician, that she had been using for several years due to overweight and which had recently been modified with the introduction of pemoline. A considerable body of evidence exists in the medical literature showing that pemoline, which is a central nervous system stimulant, has variable hepatotoxic effects, ranging from a mild transient increase of serum transaminases to liver failure, including some lethal cases.

Adult↗
PubMed1978

Liver failure.

Liver failure is a complication of viral hepatitis, as well as a consequence of acute mushroom or drug poisoning. The different therapies to be employed in a "pre emergency" state, or in case of "emergency" (resistant to medical treatment or starting as "fulminant" hepatic failure) are summarized. The percentage of survival, even by means of sophisticated treatment, does not overcome 30%.

Adrenal Cortex Hormones↗