Posted: March 18th, 2023
Alcoholic Liver Disease
CAUSES AND IMPACT
Causes, Incidence, Risk Factors, Impact
Alcohol use has been linked with liver disease mortality and increased social and economic costs (NCBI, 2014; Bruha et al., 2009). Most recent statistics say that disorders in alcohol consumption afflict millions of people worldwide. The incidence has been increasing along with increasing alcohol consumption. Alcohol liver disease takes the form of acute alcoholic hepatitis and chronic liver disease, such as steatosis, steatohepatitis, fibrosis and cirrhosis. Seriousness and prognosis depend on the amount consumed, the pattern of drinking and the length of time of consumption, the presence of liver inflammation, diet and nutritional and genetic disposition. While steatosis is virtually benign, morbidity and mortality are both high in liver cirrhosis. Survival rate for advanced cirrhosis is 1 to 2 years and 50% mortality risk for those with severe acute alcoholic hepatitis have as much as 50% mortality (NCBI, 2014). Long-term intake of more than 30 grams of absolute alcohol a day raises the risk of alcoholic liver disease or ALD. Liver disease is almost sure to develop from long-term consumption of more than 80 grams of absolute alcohol a day (Bruha et al.).
Alcohol liver disease or ALD or Alcohol-related disease or ARLD is damage to the liver by alcohol mis-use (NCBI, 2014). The symptoms do not manifest until the liver has been seriously damaged. I is the most complex organ in the body second only to the brain. It filters toxins from the blood, helps digest food, regulates blood sugar and cholesterol levels, and helps fight infection and disease. It is very resilient and can regenerate itself. But every alcohol consumption destroys some liver cells. While it can produce new cells to replace those that die, prolonged alcohol use for a number of years reduces its capabilities and soon damages it (NCBI).
The three stages of ARLD or ALD are alcoholic fatty liver disease, alcoholic hepatitis, and cirrhosis (NCBI, Bruha et al. 2009). Fatty liver disease can result from heavy drinking for even a few days. It is reversible and liver health can be restored if drinking is stopped for two weeks. Alcoholic infectious hepatitis results from continued alcohol over-consumption, which inflames the liver. Liver health can be restored if drinking is stopped permanently. Otherwise, it is a life-threatening illness. And cirrhosis is the last stage in which the liver is substantially scarred. It is generally irreversible but immediate cessation can reduce further damage and largely increase life expectancy. Otherwise, life expectancy is limited to at least 5 years at 50%. Complications are likely and life-threatening, including internal bleeding, increased toxins in the brain or encephalopathy, fluid accumulation in the abdomen or ascites linked to kidney failure, and liver cancer (NBCI, Bruha et al.).
Signs and Symptoms
ALD or ARLD produces conditions and associated symptoms (NHS, 2013). The symptoms do not appear until the liver has been seriously damaged. Early symptoms are malaise, weight loss, loss of appetite, jaundice or yellowing of the eyes and skin, swelling of the ankles and the abdomen, drowsiness or confusion, vomiting of blood or blood in the stools, and diarrhea. Advanced symptoms develop when the liver becomes more severely damaged. These include jaundice, edema or swelling of the extremities because of fluid build-up, ascites or build up of abdominal fluid, strong skin itch, hair loss, clubbed fingers, blotchy red palms, considerable weight loss, muscle wasting, weakness, confusion and memory disruption, insomnia, personality changes because of toxin build-up in the brain, vomiting of blood, black stools because of internal bleeding, frequent bruises and bleeding and increases sensitivity to alcohol and drugs. The last is the result of the failure of the liver to process alcohol and drugs (NHS).
Physical examination often reveals an enlarged and smooth but seldom tender liver (NHS, 2013). The signs of chronic liver disease, such as spider angiomas, ascites or asterixix, are likely absent. Symptoms may be non-specific and mild. These include loss of appetite and weight loss, painful or distended stomach, nausea or vomiting. Physical manifestations can include enlarged liver or hepatomegaly, jaundice, ascites, spider angiomas, fever and encephalopathy. Alcoholic cirrhosis may present itself in the form of decompensation even when fatty liver or alcoholic hepatitis did not precede it. It may also be diagnosed along with acute alcoholic hepatitis. The symptoms and signs of alcoholic cirrhosis are not distinguishable from its causes. The person may have jaundice, pruritus, abnormal laboratory findings, or complications of portal hypertension, such as variceal bleeding, ascites, or hepatic encephalopathy. Symptoms are often absent until the advanced stage (NHS).
Treatment and Effects
Abstinence is the ultimate goal of treatment as it improves ALD in all its stages (EASL, 2012). Disulfiram used to be the only effective medication for alcoholism until the discovery of its ill effects of possible hepatotoxicity. More recent medications have been developed without this risk and to complement psychosocial treatments. These are naltrexone and acamprosate. Both drugs were approved for the treatment of alcoholism although they have not been tested on cirrhosis (EASL).
A large trial found that the intramuscular application of naltrexone in alcoholism has been effective (EASL, 2012). However, it has not been tested on ALD and has therefore not been recommended for those with this illness. Acamprosate, the other approved drug, is a modulator. A meta-analysis of 24 randomized controlled trials provided evidence of its effectiveness as an alcoholism treatment. The use of gamma-hydroxybutyric acid has been approved for use as medicine in European countries, like Italy and Austria, for alcoholism. But the risk of gamma-hydroxybutyric acid abuse requires additional research. However, these two drugs are still recommended for alcohol dependency without advance ALD in combination with counseling for alcohol reduction consumption and the prevention of relapse (EASL).
With abstinence as goal, alcohol withdrawal syndrome is almost certain to occur (EASL, 2012). Benzodiazepines are recognized as the “gold standard” therapy for withdrawal. They are effective in reducing both withdrawal symptoms and risks of seizures and/or delirium tremens. Short and intermediate-acting benzodiazepines are safer for older patients and those with some hepatic problems (EASL).
Nursing Care Strategies for the First 24 Hours Upon Admission
A positive assessment of patients with unhealthy alcohol use satisfies the standard criteria for admission (Makdissi & Stewart, 2013). The patient is first assessed as to whether he has an alcohol use disorder or not. Those without are subjected to a brief intervention strategy, consisting of a minimum feedback on his alcohol use and condition, advice on how to reduce use, an explanation on why consumption should be limited, a non-confrontation inquiry on his interest in reducing consumption and a determined plan to reduce drinking. Outpatient referral shall be integrated into the brief intervention strategy (Makdissi & Stewart).
If the patient must be hospitalized and had priori severe withdrawal or unstable medical disease, the management should be prevention for acute alcohol withdrawal (Makdissi & Stewart, 2013). He will be given fixed dose benzodiazepines at 50mg every 6 hours for the first 24 hours upon admission. This will be followed by 25 mg every 6 hours for the next 48 hours. He will
The patient will be monitored for over-sedation or insufficient dosage. Benzodiazepine will be administered in case of active withdrawal but in decreased use and shorter duration of treatment. Shorter-acting benzodiazepines will be given to prevent recurrence of symptoms. First treatment of severe withdrawal will consist of intravenous benzodiazepines of 2-4 mg or 5-10 mg of diazepam. In case, additional dose is needed, which is seldom, the patient will be subjected to intensive monitoring and treatment with barbiturates or propofol. Phenobarbital is, however, most frequently used in this situation at 30mg, which is equivalent to 2 mg lorazepam, 25 mg chlodiazepoxide or 10 mg diazepam (Makdissi & Stewart).
An alternative to benzodiazepines is pentoxifylline, as some suggest, as first-line treatment in a patient with severe alcoholic liver disease (Frazier, 2011). This is in combination with enteral nutrition as a suitable preference to corticosteroids in a patient with alcoholic severe hepatitis. Pentoxifylline or PTX was demonstrated to improve the condition of a patient with alcoholic hepatitis through the down regulation of pro-inflammatory cytokines. At the same time, it possesses antibiotic effects that respond to disease severity. Furthermore, it asserts antifibriotic effects by enhancing both profibrogenic cytokine and procollagen effects. And lastly, it reduces mortality by reducing the incidence of hepatorenal syndrome by improving renal microcirculation and hemodynamic mechanism (Frazier).
If the patient is a chronic heavy drinker, he is likely to suffer from other disorders related to drinking (Makdissi & Stewart, 2013). A chronic heavy drinker consumes at least 50-60 grams of alcohol daily. These disorders include pneumonia, wound infections, bleeding, myocardial dysfunction and increased stress responses. These disorders will be addressed with detoxification and abstinence before applying further procedures. These succeeding procedures will likely be parenteral thiamine, electrolyte replacement, and rigid monitoring and treatmemtnf for post-operative withdrawal. Benzodizepines will be used to prevent acute withdrawal. Morphine will be used to reduce post-operative pneumonia by correcting endocrine and immune imbalances produced by chronic heavy drinking and peri-operative abstinence (Makdissi & Stewart).
Bruha, R., et al. (2009). Alcoholic liver disease. Vol. 110 # 3m Prague Medical Report:
PubMed Central. Retrieved on April 6, 2014 from http://www.ncbi.nlm.nih.gov/pubmed/19655694
EASL (2012). EASL clinical practical guidelines: management of alcoholic liver disease. Vol. 51 # 1, Journal of Hepatology: European Association for the Study of the liver. Retrieved on April 6, 2014 from http://www.easl.eu/assets/application/files/5e1b5512fb2cabb_file.pdf
Frazier, T.H. (2011). Treatment of alcoholic liver disease. Vol. 4 # 1, Therapeutic
Advances in Gastroenterology: PubMed Central. Retrieved on April 6, 2014 from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3036962/
Makdissi, R. And Steward, S.H. (2013). Care for hospitalized patients with unhealthy alcohol use: a narrative review. Makdissi and steward Addiction Science and Clinical
Practice. Retrieved on April 6, 2014 from http://www.ascpjournal.org/content/pdf/1940-0640-8-11.pdf
NCBI (2014). Alcoholic-related liver disease. National Center for Biotechnology:
US National Library of Medicine. Retrieved on April 6, 2014 from http://www.ncbi.nlm.nih.go/pubmedhealth/PMH0047841
NHS (2013). Alcohol-related liver disease: symptoms. National Health Services: NHS
England. Retrieved on April 6, 2014 from http://www.nhs.uk/Conditions/liver_disease_(alcoholic)/Pages/symptoms.aspx
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