Fulminating Hepatitis B secondary to a lifetime use of IV drug abuse - Research Paper Example

? Fulminating Hepatitis B secondary to a lifetime use of IV drug abuse Fulminating Hepatitis B secondary to a lifetime use of IV drug abuse Introduction Understanding how fulminant hepatitis occurs is an essential step in the management and treatment of acute hepatitis. This helps in identifying the initial treatment, as well as eliminating all contraindications to liver transplant. In addition, conducting proper prognosis helps in identifying patients who need a transplant and those who will survive without a liver transplant. Symptoms presented by fulminant hepatitis B require immediate medical interventions to prevent further damage on liver cells. However, in some patients, the condition is asymptomatic, which makes it difficult to detect. Patients of such nature may spread the condition to others unknowingly (Vandevante et al, 2011). Hepatitis B virus This paper looks into a case of a 51 year old patient suffering from fulminating Hepatitis B as a result of prolonged intravenous drug abuse. The fulminant condition under consideration is as a result of hepatitis B virus. Currently, hepatitis B virus (HBV) is the leading cause of fulminant hepatitis compared to other viral hepatitis. Hepatitis B virus attacks and replicates within hepatocytes. In terms of structure, hepatitis B virus has an outer shell and an inner core. The inner core bares the viral DNA, enzymes and proteins including hepatitis B virus core antigen (HBcAg) and HBVe antigen (HBeAg). The outer shell has the hepatitis B virus surface antigen (HbsAg), which is produced in excess by hepatocytes replicating the hepatitis B virus. In such situations, (HbsAg) appears in patients’ blood in the form of small spheres. Apart from (HbsAg), patients with acute hepatitis also have HBeAg in circulation (Carey, 2009). Pathophysiology In hepatitis B virus infections, destruction of hepatocytes is not as a result of the virus, but it is caused by the host’s immune response to the viral antigens. The cellular immune response is the primary cause of pathogenesis, but the humoral immune response is less significant. Antigen presenting cells initiate the cellular immune response by presenting the viral epitopes to antigen specific T-lymphocytes. After production, the T cells go through a stage of maturation and expansion and then later migrate into the liver. In cases of acute HBV, a bigger number of viral DNA is cleared from liver cells through a non-cytocidal process caused by inflammatory byproducts derived from CD8+ T lymphocytes. The release of inflammatory products occurs once CD+ T cells are stimulated by interferon-gamma and tumor necrosis factor-alfa, which are products of CD4+ T cells (Gish, 2009). The inflammatory byproducts lead to down regulation of viral replication as well as triggering direct lysis of infected liver cells. The destruction of infected hepatocytes through lysis occurs due to action of HBV specific CD8+ cytotoxic T cells. Major destruction of hepatocytes in fulminant viral hepatitis is also as a result of host immune factors. HumoralAb response in fulminant hepatitis B is usually enhanced (Gish, 2009). This leads to an increased rate of HBsAG clearance from the liver. High level of anti-HBsAb is evident in patients with fulminant hepatitis B on admission. Fulminating hepatitis B may either be hyperacute, acute, and subacute. In hyperacute, features present include encephalopathy within 7 days after the appearance of jaundice, and an increased rate of getting cerebral oedema (Aspinal at al., 2011). Acute condition presents itself with jaundice to encephalopathy within8-28 days and a high risk of cerebral oedema. In subacutecondition, development of jaundice to encephalopathy may occur within 5-26 wks, and there is a minimal risk of cerebral oedema. Main clinical features in fulminating hepatitis B include encephalopathy, jaundice, and hepatocellular carcinoma. The liver may appear enlarged during the initial stages, but later reduces in size. Other conditions include cerebral oedema, renal failure, and haemodynamic disturbances. The hallmark of fulminating hepatitis B is an acute elevation of transaminase activity in serum (Gomersall, 2012). Prevalence There are no well detailed statistics on the prevalence of fulminating hepatitis B, hence the use of statistics on HBV in general. Hepatitis B virus occurs worldwide, but the highest prevalence is found in developing countries due to poor medical facilities. In Asia and Africa, high prevalence of HBV occurs in infancy and childhood. In these two continents, the overall prevalence of HBV carriers is 10-15%. Low HBV prevalence is present in countries with high stands of health care (Carey, 2009). In North America, cases of HBV infections are high in young adults. Statistics indicate that about 5% of adults living in USA have anti HBc, and 0.5% of the same population has HBsAG. It is necessary to note that the prevalence of HBV may be high in certain high-risk groups of persons such as IV drug abusers (Cohen et al, 2008). Infections in adults usually cause acute hepatitis B that is easy to clear from the liver. However, 5-10% of infections in adults develop into chronic carrier state. Estimates of about 25% of all HBV carriers die as a result of cirrhosis or primary liver cancer. Prevalence of HBV is on a decline due to improved procedures in the screening of blood and blood products. Studies show that remarkably few countries do not conduct advanced blood screening (Aspinal et al, 2011). Screening of HBV There are several diagnostic techniques available for the screening of HBV. Available techniques include immunohistochemistry, immunofluorescence studies, thin section electron microscopy, and in situ hybridization. These techniques apply in the examination of antigens associated with HBV in pathological specimens. Information obtained in such screenings provides essential information on HBV DNA replication and expression of HBV gene. In HBV infected hepatocytes, HBsAG appears in the cytoplasm while HBcAG appears in the nucleus and cytoplasm. It is essential to note that it is impossible to detect all virions present in hepatocytes (Aspinal et al, 2011). The use of DNA hybridization techniques and RT-PCR assays revealed that almost all patients with HBsAg/HBeAg have detectable HBV DNA in serum. Patients who manage to recover from acute HBV test negative for HBV DNA. On the other hand, some chronically infected patients without HBsAG test positive for HBV DNA (Gish, 2009). Prognosis Poor prognosis occurs in adults with fulminant hepatitis. In patients who are lucky to survive, they recover fully, and there are no chronic infections or permanent liver damages. Prognosis in the absence of liver transplant indicates that 80% of patients die. About 30% of patients in specialized care units survive. Presence of spur cells in peripheral blood is a sign of poor prognosis. In addition, occurrence of jaundice for at least 1week before encephalopathy sets in indicates a poor prognosis. In cases of a liver transplant, up to 80% of patients survive (Gomersall, 2012). Medical and nursing interventions Transferring the patient as soon as possible to specialist units prevents the patient from getting a coma. In order for the transfer to be successful, the heath care provider should provide oxygen continuously. In situations where the nurse doubts about the supply of oxygen, it is advisable to incubate the patient. Other things to observe during the transfer include sitting posture, monitoring of blood glucose, pupils, and blood pressure. The transfer should be done by health care providers who can perform incubation in suboptimal conditions. In addition, concentrated solutions of glucose and mannitol should be availableto treat and prevent cerebral edema (Gomersall, 2012). Liver transplant is recommended in patients who have survival rates less than 80% and show no contraindication to liver transplant. The other medical intervention involves vaccination of persons at high risk of getting HBV, and IV drug users can get the vaccine. Important blood measurements to monitor close are systolic pressures > 200mmHg or sustained systolic pressure > 150 mmHg. Pupils should be monitored after every 10 minutes for signs of sluggishness, and cerebral “posturing”. Other investigations include monitoring of AST and ALT. Normal measurements for the two chemical substances are >40, but decline as the condition gets worse. Use of N-acetylcysteineas part of the treatment regimen helps in countering effects of paracetamol overdose. This intervention leads to hypotension and reduced cerebral oedema. Infusions cause increased cardiac output, enhanced oxygen delivery and consumption. Cases of insulin resistance are common in severe acute hepatitis. Therefore, patients should put under a resting energy expenditure of 1700Kcal/day and nitrogen loss of 7g/day (Gomersall, 2012. Conclusion Intravenous drug use is one way through which HBV is transmitted. Persons without any liver disorder are likely to suffer from fulminating hepatitis B once they inject themselves using needles contaminated with HBV. Fulminating hepatitis B is highly fatal, and chances of survival for infected persons are extremely minimal. However, quick nursing and medical interventions are essential in saving a patient’s life before the condition gets worse. Prognosis is poor where there are no any medical interventions, and over 80% of such patients die. The best way to prevent HBV is through vaccination in high risk population. References Aspinal, E. J., Hawkins, G., Fraser, A., Hutchinson, H, J. & Goldberg, D. (2011). Hepatitis B prevention, diagnosis, treatment and care: a review. Occupational Medicine 61 (8), 531-540. Cohen, C., Evans, A. A., London, W. T. Block, J., Conte, M., Block, T. (2008).Underestimation of chronic hepatitis B virus infection in the United States of America. Journal of Viral Hepatitis 15(1), 12–13. Carey, W. D. (2009). The Prevalence and Natural History of Hepatitis B in the 21st Century. Cleveland Clinic Journal of Medicine76 (3), S2-S5. Gomersall, C. (2012). Fulminant hepatic failure. Retrieved from: http://www.aic.cuhk.edu.hk/web8/fulminant_hepatic_failure.htm Gish, R. G. (2009). Hepatitis B treatment: Current best practices, avoiding resistance. Cleveland Clinic Journal of MedicineVol.76 Suppl. 3, S14-S1. Vandevanter, N., Kwon, S., Sim, S. C., Chun.K., Trinh-Shevrin, C. (2011). Evaluation of community-academic partnership functioning: center for the elimination of hepatitis B health disparities. Prog Community Health Partnership. 5 (3),223-33. Read More