Acute liver disorders in left-sided heart failure

A case of apparent acute hepatitis developed during a mild attack of left-sided heart failure is reported. No shock or significant systemic hypotension was observed which are usually reported in such patients. The signs of the liver impairment were transient, subsiding with the successful treatment of the heart failure.     

急性肝衰竭最新认识

在美国生物化学、影像学和生物工程学研究所（NIBIB）及国立卫生研究院（NIH）罕见疾病部门的支持下,美国糖尿病、消化病和肾脏病研究所（NIDDK）于2007年12月4～5日在马里兰洲的贝斯达（Bethesda）举行了有关急性肝衰竭（ALF）认识和处置的研讨会。会议认为：ALF是一种少见而难治的临床综合征;其病因多样,在15％的成人患者和50％的儿童患者中不能明确具体病因。ALF病程不定,病死率高。     

Acute heart failure

Acute heart failure (AHF) is one of the most common causes for hospital admission and is associated with a high risk of mortality. Compared to chronic heart failure, there is less robust evidence to guide diagnosis, risk stratification and management of AHF. This state-of-the art review aims to summarize new developments in this field. We also highlight areas of ongoing work including novel vasoactive agents, alternative models to traditional hospital admission and strategies to improve patient engagement.     

Acute liver failure

Opinion statement Acute liver failure (ALF) is an uncommon medical emergency whose rapid progression and high mortality demand early diagnosis and expert management, including immediate transfer of any potential case to facilities for intensive care and orthotopic liver transplantation (OLT). All patients with ALF must be screened aggressively for acetaminophen toxicity (history, serum levels, “hyperacute” presentation with renal failure), for other drugs, and viral hepatitis; rare causes of ALF should also be considered. After an acetaminophen overdose, N-acetylcysteine must be given as early as possible, preferably in the emergency room, but any patient with ALF should promptly receive N-acetylcysteine if there is suspicion of acetaminophen toxicity irrespective of the time of ingestion. Supportive care for all patients with ALF includes adequate enteral nutrition, aggressive screening and treatment of infection, prophylactic broad-spectrum antibiotics, and antifungal agents. Sedation with propofol is given for severe agitation or mechanical ventilation. With advanced coma grades, intensive care is needed with hemodynamic monitoring, ventilatory support, continuous renal replacement for renal failure, and intracranial pressure monitoring. Intracranial hypertension is treated with mannitol and/or acute short-term hyperventilation, but if the patient is refractory to treatment, mild-moderate hypothermia is achieved by a cooling blanket that is continued throughout OLT. Barbiturate coma is only used in refractory cases as the last treatment modality. Seizures are aggressively treated with phenytoin, with additional diazepam as needed. Candidacy and activation for OLT should be completed as early as possible in the course of ALF, especially in “hyperacute” cases such as acetaminophen toxicity. The final decision to proceed with OLT is made when a donor organ becomes available. King’s College Hospital criteria for OLT are still the best prognostic assessment for fatal outcome in ALF, but the criteria fail to identify some patients who will die.     

Acute liver failure

Acute liver failure, also called fulminant hepatic failure, is characterized by sudden hepatic synthetic dysfunction associated with coagulopathy and hepatic encephalopathy. Acute liver failure has most recently been defined based on the timing from onset of jaundice to encephalopathy as follows: 1) hyperacute (1-7 days); 2) acute (8-28 days), and 3) subacute (29-60 days). Rapid onset of encephalopathy in hyperacute liver failure is paradoxically associated with highest rate of spontaneous recovery, and subacute liver failure is associated with worst prognosis. The etiology of liver failure is established by history, serologic assays, and exclusion of alternative causes. Acute liver failure is most frequently caused by drug hepatotoxicity, including acetaminophen toxicity and idiosyncratic drug reactions, with viral hepatitis playing a lesser role in recent surveys. A substantial number of cases have an indeterminate etiology. Major complications of acute liver failure that require active intervention include metabolic disorders, coagulopathy, cerebral edema, renal failure, and infection. The focus of management of acute liver failure is comprehensive supportive care in an intensive care unit and assessment of the need for liver transplantation.     

Acute liver failure

Acute liver failure is characterized by a dynamic clinical course associated with high mortality. The main prognostic determinant is the development of extrahepatic complications. Close monitoring is mandatory, and prophylactic measures to avoid complications should be initiated. In case of complications, early and aggressive treatment is indicated. To date, artificial liver support devices are still in the experimental phase. Liver transplantation should be considered in patients with predictors of a poor spontaneous prognosis. Therefore, a transplant center should be contacted in every case of acute liver failure.     

Acute liver failure

Acute liver failure (ALF) is defined as hepatic encephalopathy complicating acute liver injury. The most common etiologies are acute viral hepatitis A and B, medication overdose (e.g., acetaminophen), idiosyncratic drug reactions, ingestion of other toxins (e.g., amanita mushroom poisoning), and metabolic disorders (e.g., Reye's syndrome). Despite advances in intensive care management, mortality continues to be high (40-80%) and is partly related to ALF's complications, such as cerebral edema, sepsis, hypoglycemia, gastrointestinal bleeding, and acute renal failure. Several prognostic models have been developed to determine which patients will spontaneously recover. Treatment is directed at early recognition of the complications and general supportive measures. The only proven therapy for those who are unlikely to recover is liver transplantation. Therefore, recognition of ALF is paramount, and urgent referral to a transplant center is critical to assess transplantation status.     

Acute liver failure

Untreated acute liver failure (ALF) has a poor outcome and so rapid diagnosis and management is vital if the patient is to survive. ALF has such profound and widespread physiological consequences that whenever possible, patients with ALF should be managed in an intensive care unit. Management is to support the physiology and treat the underlying cause. Advice should be sought from a centre capable of performing liver transplantation. Should recovery seem unlikely, liver transplantation is a viable treatment option in some cases.     

Acute liver failure

Acute liver failure (ALF) (sometimes referred to as fulminant hepatic failure) is a clinical syndrome from a variety of causes resulting from rapid loss in hepatocyte function, typically associated with coagulopathy and encephalopathy in a patient without preexisting liver disease or cirrhosis. Cerebral edema is a cardinal feature and may produce uncal herniation, yielding brain stem compression and death. The typical interval from onset of symptoms to onset of encephalopathy is 1 to 2 weeks, but cases evolving more slowly, up to 6 months, may still be included in the definition. ALF is rare, affecting 2000 patients annually in the United States, and comprises ～7% of liver transplants annually. Currently, in the United States, acetaminophen accounts for ～50% of all cases of ALF, but other etiologies include hepatitis, drug-induced liver injury, autoimmune hepatitis. Prior to the availability of liver transplantation (LT), mortality of ALF was extremely high, often exceeding 90%; most common causes of death were multiorgan failure, hemorrhage, infection, and cerebral edema. Fortunately, survival has improved considerably in the last 3 decades (overall survival now exceeds 60%). In large part, this improved survival reflects the option of LT but also reflects the high frequency of acetaminophen toxicity as a cause of ALF. In fact, most patients with ALF are not candidates for LT. Critical care of patients with ALF is key to their survival, and decisions must sometimes be made with inadequate information. We review standard practices (medical, pharmacological, and LT) and new research initiatives and findings for this interesting but vexing orphan disease. Particular attention will be paid to practical matters for clinicians to consider in approaching the ALF patient.     

Tissue damage and calcification may be independent mechanisms of bioprosthetic heart valve failure

BACKGROUND AND AIM OF THE STUDY: Porcine bioprosthetic valves have excellent hemodynamics and do not require anticoagulation, but have limited durability. Cusp tearing is a major cause of bioprosthetic valve failure. It has been suggested that the mechanism of bioprosthetic valve failure is stiffening by calcification, which leads to elevated stresses and secondary collagen fiber damage and leaflet tearing. This thesis was tested in explanted porcine bioprostheses. METHODS: A total of 60 explanted porcine bioprosthetic valves was tested mechanically, and 15 explanted valves were examined grossly and histologically. Circumferentially and radially oriented samples of cusp tissue were tested uniaxially in a materials testing machine and compared with five controls. RESULTS: Mean (+/-SD) duration of implantation was 10.9+/-5.6 years. Circumferential specimens from explants were less extensible than controls (11.0+/-5.5% versus 24.5+/-2.8% strain, p <0.001), and failed at lower tensions (973+/-733 versus 3075+/-911 N/m, p = 0.001) and at lower strains (21.2+/-8.1% versus 47.3+/-7.1% strain, p <0.001). Radial specimens from explants were less extensible (28.7+/-6.8% versus 39.2+/-5.9% strain, p = 0.002) and failed at lower strains (60.3+/-17.3% versus 112.2+/-24.9% strain, p <0.001) than the controls. The stiffness of the explants was unchanged from controls in both circumferential and radial samples. There were no differences between explants and controls in radial and circumferential stiffness, and in radial failure strength. Calcification was mild and diffuse in most of the tested samples. Tears were found in areas without calcific deposits, along with breaks in collagen fiber bundles. CONCLUSION: These results do not support the thesis that calcification stiffens glutaraldehyde-fixed porcine bioprostheses, except when the entire cusp is transformed into a solid mass of mineral. Rather, leaflet tears may develop as a result of accumulated mechanical damage that is independent of calcification.     

Acute liver failure: clinical-epidemiological characteristics

In order to ascertain the clinical and epidemiological features of acute liver failure (ALF), we analyzed the clinical histories of 22 patients from La Plata city, with the diagnosis of ALF (prothrombin level or factor V below 50%) seen between November 1996 and November 2000. Age, sex, hepatic encephalopathy, reason for consultation, etiology, hepatic biochemical tests, serum creatinine, glycemia, digestive hemorrhage, course and treatment variables were analyzed. What is remarkable is the high frequency of the toxic etiology and of infection by HDV, as well as the high prevalence of ascites and the low incidence of hepatic encephalopathy. We think that the high survival rate we found is due to the early diagnosis and early referral of the patients to the intensive care unit and to centers with programs for liver transplantation.     

Acute cardiogenic liver injury caused by heart failure in an adolescent

To the Editor: Heart failure is a systemic clinical syndrome characterized by multiple organ systems involvements [1] . With the progression of heart failure, p...     

"Flush-free niacin": dietary supplement may be "benefit-free"

This report describes a patient with coronary artery disease who was instructed to take extended-release niacin to treat low high-density lipoprotein cholesterol and instead purchased "flush-free niacin" available at the pharmacy. There was no significant change in his lipids. Once the patient switched to extended-release niacin, the anticipated beneficial effects were seen. The article reviews the composition of flush-free niacin, its purported and real lipid effects, and warns against the effects of misleading marketing.