History of Presenting Illness (HPI)
BA is a 40-year-old male who presents to the emergency department accompanied by his relatives with vomiting blood and yellowing of the eyes. The blood vomiting is sudden in onset, and it is fresh red blood. It is not mixed with any food contents, and the patient has no history of peptic ulcer disease. The yellowness of the started a week ago and had become more yellow as days elapse. The patient does not have any known hematological disease. Of significance is that BA is a known alcoholic for the past twenty years and has been rehabilitated for the same
Past Medical History
Patient has no known chronic medical conditions. He has no known drug or food allergies. BA is a chronic alcoholic for the past twenty years. He takes beer, wines, and spirits that cannot be quantified. However, he does not use any hard drugs. He has been admitted 4 times before. His first admission lasted 5 days, and they were discharged on antibiotics after a diagnosis of amoeba. His second admission lasted 10 days they were discharged with a diagnosis of impaired hepatic function whereas his 3rd admission was 6 months ago and the doctor said that his liver was not functioning properly due to excess alcohol consumption.
General examination: BA is an elderly man who has been brought in a stretcher. He looks sick. His clothes are bloody On exam: he has both palmar and plantar pallor, he is dehydrated, jaundiced, and not cyanosed but has grade 3 finger clubbing. There is no lymphadenopathy, the patient is edematous but not wasted.
Gastrointestinal Examination (GIT): On inspection, the abdomen is distended, there are no obvious therapeutic scars or marks.
On palpation, light palpation elicited no tenderness or obvious masses in any of the abdominal quadrants. However, on deep palpation, a mass was present on the right hypochondriac region extending into the right lumbar quadrant. The mass extended about 8 cm below the coastal margin. The mass moved downwards with inspiration, was consistent, and the edges were regular.
On percussion, the rest of the abdomen was tympanic except the right upper quadrant, which was dull on percussion. Neither shifting dullness nor fluid thrills were elucidated.
On auscultation, abdominal sounds were present and bruits were also heard.
Investigations: Blood tests revealed low levels of blood albumin, Liver tests revealed moderate elevation of AST and CRP. The levels of ALT were mildly elevated hence the AST/ALT ratio was greater than one. Liver function tests revealed increased prothrombin time. On ultrasonography, the liver was apparently enlarged as well as diffusely hyperechoic.
Diagnosis: the diagnosis was alcoholic liver disease. However, there're were also some differential diagnoses including Hepatitis B, Hepatitis C, and chronic pancreatitis.
Management: The management of the patient included referral to chemical dependency team for rehabilitation. The patient also underwent nutritional support providing vitamins and minerals to improve liver functions. The patient also received parenteral Vitamin K.
Treatment: Glucocorticosteroids were administered to the patient to reduce hepatic injury and enhance regeneration of the hepatic tissue.
Most commonly, alcoholic liver disease presents as a mild condition, with short-term prognosis requiring no specific treatment (Tilg, Moschen, & Szabo, 2016, p. 959). However, cessation or abstinence from of alcohol use is normally a necessity (Younossi et al., 2016, p. 75). Likewise, care has to be taken to ensure that the patient provided with good nutrition and supplementation of vitamins as well as minerals such as folate and thiamine. For coagulopathic patients, parenteral vitamin K is a necessity (Tilg, Moschen, & Szabo, 2016, p. 959). Moreover, symptoms of alcohol withdrawal such as delirium tremens should not only be anticipated but also managed adequately, the main reason as to why the patient was referred to chemical dependency team (Crossan et al., 2015, p. 34).
However, patients with severe acute alcoholic liver disease face a high risk of mortality at a rate of about 50% within a month. The strongest factors, which are predictive of such a short-term mortality include hepatic encephalopathy, hyperbilirubinemia, as well as coagulopathy (Szabo, 2015, p. 890). As a result, patients exhibiting such findings as azotemia and GI bleeding should be hospitalized. In severe alcoholic liver disease, it is necessary to reduce injury to the hepatocytes, enhance regeneration, and suppress inflammation. Glucocorticosteroids are indicated for this purpose (Tilg, Moschen, & Szabo, 2016, p. 959).
Appraisal of the Patient's Wellbeing
Reports from previous studies indicate an impairment not only in the physical but also in the physical but also in the mental dimension of quality of life as well as wellbeing of patients with alcoholic liver disease (Anstee, Daly, & Day, 2015, p. 677). However, few documentations have been made on the impact of alcoholic liver disease on the social support of the patient, even though, it could have adverse effects on the same. In most instances, the patient would be depressed, as Mathurin and Bataller (2015, p. 40) state that 50% of patients treated for alcoholic liver disease experiences depression in relation to clinical symptoms. Patients with alcoholic liver disease exhibit signs of psychological distresses as well as depression in accordance to the provisions of Beck depression inventory as well psychological wellbeing index, in relation to how severe the disease is (Tilg, Moschen, & Szabo, 2016, p. 959). In turn, such psychological expressions have adverse effects on their social support, as they get worried about the condition of the patient.
Appraisal of Cost Effectiveness of Ultrasonography
Ultrasonography is one of the imaging modalities, which is effective in early investigation of alcoholic liver disease (Zeybel et al, 2015, p. 20). However, researchers have had doubts about cost effectiveness of ultrasonography in the investigation of alcoholic liver disease. Owing to the fact that ultrasonography is a non-invasive procedure, which does not expose the patient to dangerous radiological waves, it is of great significance in the diagnosis of alcoholic liver disease. However, its cost effectiveness has been in doubt. According to a study by Tsochatzis and Gluud (2016, p. 581) ultrasonography is cost effective in the investigation of alcoholic liver disease if compared to other imaging modalities such as magnetic resonance imaging and abdominal x-ray. However, if compared to other laboratory tests such liver tests, liver function tests, and blood tests, ultrasonography is not cost effective since is not highly specific for alcoholic liver disease and must be used alongside other tests (Louvet & Mathurin, 2015, p. 231). If used alone in the diagnosis of alcoholic liver disease, the results form ultrasonography would not be soecific for the underlying condition hence confirmatory tests will be necessary, as a result, ultrasonography is not cost effective in the diagnosis of alcoholic liver disease as in the case of BA (Tilg, Moschen, & Szabo, 2016, p. 959).
Anstee, Q.M., Daly, A.K. and Day, C.P., 2015, November. Genetics of alcoholic liver disease. In Seminars in liver disease (Vol. 35, No. 04, pp. 361-374). Thieme Medical Publishers.
Chen, P., Starkel, P., Turner, J.R., Ho, S.B. and Schnabl, B., 2015. Dysbiosisinduced intestinal inflammation activates tumor necrosis factor receptor I and mediates alcoholic liver disease in mice. Hepatology, 61(3), pp.883-894.
Crossan, C., Tsochatzis, E.A., Longworth, L., Gurusamy, K., Davidson, B., Rodriguez-Peralvarez, M., Mantzoukis, K., O'Brien, J., Thalassinos, E., Papastergiou, V. and Burroughs, A., 2015. Cost-effectiveness of non-invasive methods for assessment and monitoring of liver fibrosis and cirrhosis in patients with chronic liver disease: systematic review and economic evaluation.
Louvet, A. and Mathurin, P., 2015. Alcoholic liver disease: mechanisms of injury and targeted treatment. Nature Reviews Gastroenterology and Hepatology, 12(4), p.231.
Mathurin, P. and Bataller, R., 2015. Trends in the management and burden of alcoholic liver disease. Journal of hepatology, 62(1), pp.S38-S46.
Szabo, G., 2015. Gut-liver axis in alcoholic liver disease. Gastroenterology, 148(1), pp.30-36.
Tilg, H., Moschen, A.R. and Szabo, G., 2016. Interleukin1 and inflammasomes in alcoholic liver disease/acute alcoholic hepatitis and nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Hepatology, 64(3), pp.955-965.
Younossi, Z.M., Koenig, A.B., Abdelatif, D., Fazel, Y., Henry, L. and Wymer, M., 2016. Global epidemiology of nonalcoholic fatty liver disease-Metaanalytic assessment of prevalence, incidence, and outcomes. Hepatology, 64(1), pp.73-84.
Zeybel, M., Hardy, T., Robinson, S.M., Fox, C., Anstee, Q.M., Ness, T., Masson, S., Mathers, J.C., French, J., White, S. and Mann, J., 2015. Differential DNA methylation of genes involved in fibrosis progression in non-alcoholic fatty liver disease and alcoholic liver disease. Clinical epigenetics, 7(1), p.25.
Pavlov, C.S., Casazza, G., Nikolova, D., Tsochatzis, E. and Gluud, C., 2016. Systematic review with metaanalysis: diagnostic accuracy of transient elastography for staging of fibrosis in people with alcoholic liver disease. Alimentary pharmacology & therapeutics, 43(5), pp.575-585.
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Alcoholic Liver Disease: Case Study. (2022, May 21). Retrieved from https://proessays.net/essays/alcoholic-liver-disease-case-study
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