Doctor’s Login   Patient's Login       Visitors    |    Bulletin Board    |    Videos    |    Register               Profile Liver Biology Liver Diseases Liver Transplant Liver FAQ Consult the Doctor Contact Founder’s Profile Dr. M.R. Rajasekar MS(Madras), FRCS, MD(UK), Currently Senior Consultant Surgeon in Liver Surgery (HPB) Dr.Rajasekar graduated from university of Madras with MBBS and Master of Surgery Degree. He was the best out ...     What’s New? Entecavir is a guanosine analogue with marked activity against HBV DNA ... The European Medicines Evaluation Agency has granted marketing ...      Testimonials Liver transplant in India- no regrets! Rakesh, at 33 years of age was told that a liver transplant alone could save his life. His family was shattered by the news...   Events Chat live: with Dr. M.R. Rajasekar on Every Monday from 8.00 am onwards       Frequently Asked Questions on Liver     Questions.   Q1.What is the prognosis without liver transplant? Q2.Is there any way to avoid a liver transplant? Q3.When should I get prepared for a liver transplant? Q4.What is the success rate of liver transplant? Q5.Whole liver or partial liver: which is better? Q6.Will liver transplant restore all my functions and quality of life? Q7.What is the long term effect of transplant and post transplant medications? Q8.What is the cost of liver transplant and after care? Q9.Is there any difference in liver transplant in India and abroad? Q10. What is Liver Function Tests (LFT's) ? Q11. What is Albumin (ALB) (4-6)? Q12. What is Alkaline Phosphatase (ALK PHOS) (30-120)? Q13. What is Alanine Aminotransferase (ALT or SGPT) (<35)? Q14. Whats is Total Bilirubin (TOT BILI) (<1.0)? Q15. How To Differentiate Alcoholic Hepatitis From Alcoholic Cirrhosis And Is The Differentiation Important?     Answers   Q1.What is the prognosis without liver transplant? Patients with advanced chronic liver failure can survive for a median time range of 18 months from the time of diagnosis without liver transplant. However as the disease advances they will require frequent medical admissions, some of which may be fatal. Q2.Is there any way to avoid a liver transplant? Patients with alcohol related liver failure may stabilize if they stop alcohol consumption and show some clinical improvement. Some of the patients with early cirrhosis due to viral hepatitis may improve if the virus is eradicated from their system by treatment. By and large liver cirrhosis is a progressive disorder and does not reverse by medical treatment; hence liver replacement remains the only cure. Q3.When should I get prepared for a liver transplant? It is advisable to undergo an evaluation as soon as you meet at least 2 of the criteria listed under absolute indications. This allows the author to list you for a suitable cadaver liver straight away. The cadaver livers are offered on first come first serve basis when the offer comes from some part of the country. While on waitlist one can explore the option of living donor transplant if any suitable relative is available. Q4.What is the success rate of liver transplant? The success of liver transplant depends on the medical condition of the patient. Or good risk patients who go for the surgery early enough, the 5 year survival is 85%. Patients who have additional risk factors like kidney dysfunction, malnutrition, cancer, portal vein occlusion, previous abdominal surgery and hepatitis-C type I are bound to have lower survival rates. Q5.Whole liver or partial liver: which is better? Whole cadaver liver is any day preferable to a partial liver from living donors. Whole liver transplant is technically less complex and hence will have lower chance of technical complication. However in India, the availability of cadaver liver is very limited and the partial liver donation is a more practical option. The long term outcome is more or less comparable between the two types of transplant.   Q6.Will liver transplant restore all my functions and quality of life? All the metabolic abnormalities are corrected by a liver transplant. Hence patients can have normal diet without restrictions soon after the transplant. Restoration of physical strength will be gradual and will take around three months to be restored fully. One can plan to return to work involving moderate physical strain by 4 months. Active sports can be resumed by six months. Education in school and college is usually commenced within 6 months after the transplant. Children will grow normally and may suffer attention deficit in academic pursuit which will improve with training. Normal sexual functions are restored in 60% by 3-4 months and some may require medical help. Q7.What is the long term effect of transplant and post transplant medications? Liver transplant per say does not have any sequel. Scar and rarely herniation from the wound can occur. However the life long medications do have certain effects. Q8.What is the cost of liver transplant and after care? It is now possible to have a successful liver transplant for 15 Lakh Rs (30000 USD), for patients who come early. With the author's effort it may be possible to lower the cost further for economically under privileged. There is an average monthly expense of Rs 10,000 per month (250 USD/pm), for medications and blood tests and this will be life long. In the long run the cost may come down by half (these figures are applicable to Indian citizens). Q9.Is there any difference in liver transplant in India and abroad? No hospital in India is as good as the best run hospitals in the West. To achieve such high standards will increase the cost of transplant. However the technical expertise of the doctors and nurses is comparable to that in the West. The infrastructure is also comparable. The results of liver transplant (in the author's series), is also comparable to the results of established centers. It is a very good deal for the price that is ten times cheaper than either the Western centers or those in Far East and Singapore. In any case 99% of Indian citizens cannot afford to spend > Rs 15 million that is required for liver transplant abroad. Q10. What is Liver Function Tests (LFT's) ? Liver function studies is a battery of tests that give your doctor an idea of how well your liver is working. From these studies, your doctor can identify possible liver disease or infections like hepatitis. Several different tests comprise LFT's. Q11. What is Albumin (ALB) (4-6)? Albumin is a protein produced by the liver that helps maintain osmotic pressure in the vascular space. By maintaining this pressure, fluid stays in the vascular system instead of leaking out into the tissues resulting in swelling (edema). Albumin also carries certain minerals in the blood stream. Elevated: Usually indicates dehydration. Below normal: Can indicate liver dysfunction or insufficient protein intake. Q12. What is Alkaline Phosphatase (ALK PHOS) (30-120)? Alkaline phosphatase is an enzyme found in many organs in the body, including the liver. Elevated: A warning sign that there is some type of liver dysfunction resulting in liver tissue damage. Below normal: Usually not significant. Q13. What is Alanine Aminotransferase (ALT or SGPT) (<35)? This protein is found primarily in the liver. It is released into the blood when there has been some sort of liver tissue damage. Elevated: Indicates tissue damage as a result of such things as obstruction, hepatitis, or cirrhosis. Below normal: Usually not significant. Q14. Whats is Total Bilirubin (TOT BILI) (<1.0)? Bilirubin is a normal component of red blood cells. When these cells break down free bilirubin is released in the blood. Bilirubin is then carried to the liver where it is broken down and excreted. When the liver is not functioning properly, bilirubin builds up in the body, causing jaundice (yellowing of the skin and eyes and darkening of the urine). Elevated:Usually caused by a dysfunction of the system that breaks down bilirubin which includes the liver. Such an elevation can be caused by an obstruction or liver failure. Q15. How To Differentiate Alcoholic Hepatitis From Alcoholic Cirrhosis And Is The Differentiation Important? The association of alcohol abuse and liver damage is known since the times of ancient Greeks and is also recognised in Ayurveda. The clinical spectrum of alcoholic liver injury varies from asymptomatic hepatomegaly to profound hepatocellular failure with portal hypertension. The clinical picture tends to be more florid in individuals with more advanced liver injury. Alcoholic liver injury appears to progress from fatty changes through alcoholic hepatitis to cirrhosis. Majority of the individuals who abuse alcohol will develop fatty changes in their liver at some stage of their drinking career. However only 20% of such individuals will develop cirrhosis. The apparent predisposition of certain people to develop alcoholic cirrhosis is unknown. Fatty liver, though indicating a profound metabolic disturbance within the liver, is not necessarily harmful. Certainly, cirrhosis may develop in an alcoholic who has never had fatty change and isolated fatty change has not been shown to proceed directly to cirrhosis. Alcoholic hepatitis develops in only a proportion of drinkers even after decades of abuse and is assumed to be a precirrhotic lesion, although its natural history is not well understood. Thus in approximately 50% of individuals alcoholic hepatitis may persist for several years and in 10% of individuals the lesion may heal despite continued alcohol abuse. It has therefore been suggested that although alcoholic hepatitis may contribute, when present, to the evolution towards cirrhosis, it is not a sine qua non of such progression. Though most of the alcoholics may have a combination of alcoholic hepatitis and cirrhosis on biopsy and more or less similar clinical and biochemical features, there are certain features which may help in differentiating the two conditions as given in the Table 1 below. Since alcoholic hepatitis is reversible and hepatic function improves over a period of time with abstinence, management consists predominantly of abstinence from alcohol and supportive care; whereas alcoholic cirrhosis once established is irreversible and hepatic function may not improve over time, management consists of abstinence from alcohol, treatment of complications and liver transplantation may be a viable option in carefully selected patients. Liver transplantation should not be done in patients with pure alcoholic hepatitis. Hence it is very essential to differentiate a patient having alcoholic from the one having alcoholic cirrhosis as the management and prognosis is different.   Table 1 Differentiation betweenalcoholic hepatitis and alcoholic cirrhosis   Alcoholic hepatitis   Alcoholic cirrhosis   Symptomatology   Symptomatology   ::Patients with alcoholic hepatitis have been abusing alcohol till the time of presentation; they look more ill and being symptomatic present to a physician.   ::Patients with alcoholic cirrhosis may not have abused alcohol for many years prior to presentation; most of them are well compensated, with only one-third being symptomatic.   ::Jaundice is usually one of the most common symptom. Some common mode of presentations are: jaundice - 50% of the patients, ascites in 30 - 60% and splenomegaly - 15% of the patients.   ::Ascites is usually the common symptom. Some common mode of presentations are: 40%, dilated abdominal wall veins - 60% and splenomegaly - 25% of the patients.   ::Fever (even high grade) is seen in upto 50% of the subjects.   ::High grade fever is not seen (unless there is superadded infection).   ::Symptoms of variceal bleeding and hepatic encephalopathy are uncommon.   ::Variceal bleeding and hepatic encephalopathy are quite common.   Clinical Signs   Clinical Signs   ::Spider naevi and palmar erythema may be florid.8   ::Spider naevi and palmar erythema though seen, may not be florid.   ::Features of portal hypertension - Ascites, dilated abdominal wall veins, splenomegaly and oesophageal varices are not a prominent features of pure alcoholic hepatitis.   ::Features of portal hypertension are a prominent feature of alcoholic cirrhosis   ::Liver is very large and tender on palpation; its surface is smooth and consistency is soft to firm.   ::Liver is mild to moderately enlarged or may not be palpable in advance cirrhosis and when palpable it is nontender, irregular with palpable nodules and firm in consistency.   ::Arterial bruit may be heard over the liver area.   ::Unless there is superadded hepatocellular Unless there is superadded hepatocellular   Investigations   Investigations   ::Polymorphonuclear leucocytosis (upto) 20,000/mm3) is quite common.   ::Polymorphonuclear leucocytosis though seen may not be as high as in alcoholic hepatitis.   ::Platelet function is depressed, but there may not be thrombocytopenia. There is no evidence of hypersplenism.   ::Both platelet function and number are reduced and there is evidence of hypersplenism.   ::SGOT and SGPT are elevated upto 300 to 400 IU with SGOT/SGPT ratio > 2.   ::SGOT and SGPT are usually normal.   ::Highest levels of rise of gamma glutamyl transpeptidase, glutamate dehydrogenase and tumour necrosis factor are seen in alcoholic hepatitis.   ::There is mild to moderate rise of gamma glutamyl transpeptidase and glutamate dehydrogenase in alcoholic cirrhosis.   ::Most of the elevated enzymes fall back to normal level within 1 week of abstinence.   ::No significant fall in enzyme levels are seen over a period of time, even if abstinent.   ::Isotope liver scan may show total absence of radiotracer uptake by the hepatic parenchyma ("Medical hepatectomy") with avid uptake by the spleen and the bone marrow of vertebrae and the ribs. After a period of recovery, the liver scan may show normal tracer uptake.   ::Isotope liver scan show inhomogeneous tracer distribution in the liver, with left lobe uptake greater than the right lobe, colloid shift to the spleen ("Hot spleen") and visualisation of the bone marrow of the vertebrae. Liver scan picture does not show improvement over time.   Liver biopsy histology   Liver biopsy histology   Three obligatory features for the histologic diagnosis are -   On liver biopsy the following features are seen-   - ballooning degeneration of hepatocytes, with areas of necrosis.   - parenchymal necrosis   - inflammatory cell infiltrates, predominantly   - regeneration      - scarring   polymorphonuclear leucocytes      :- fibrosis, both pericellular (producing a lattice-like or chicken wire appearance) and perivenular (centrolobular).      ::20% of alcoholics show features of hepatitis on 18.3% of alcoholics show features of cirrhosis (6.7%) or in combination with cirrhosis (13.4%).8 Alcoholic hepatitis rarely is seen as an isolated pathology on liver biopsy. On most occasions it is seen in combination with either fatty liver or cirrhosis.   ::18.3% of alcoholics show features of cirrhosis on biopsy; 5% as only cirrhosis and 13.4% in combination with alcoholic hepatitis. Thus alcoholic cirrhosis may be the only pathology alcoholic cirrhosis may be the only pathology   Management   Management   ::Alcoholic hepatitis is usually reversible on Alcoholic cirrhosis is generally considered to   ::Alcoholic cirrhosis is generally considered to be an irreversible lesion once it is established   ::Treatment consists of abstinence and proper nutritional support. Liver transplantation is not recommended at this stage.   ::Apart from abstinence and treatment of complications, liver transplantation may be a viable option.   Prognosis   Prognosis   ::Though high initial in hospital mortality of about 50%, long term prognosis of those who abstain from alcohol is very good.   ::Though initial in hospital mortality may not be high (but depends on the mode of decompensation), long term prognosis is presentation and degree of hepatic dismal with nearly 50% 5 year mortality   ::The Maddrey discrimination function is a simple equation in which the serum bilirubin and prothrombin time are used to indicate the presence of severe alcoholic hepatitis (4.6 x (PT in secs - control time) + serum bilirubin in mg/dl). A score greater than 32 indicates severe alcoholic hepatitis with poor prognosis.   ::Child-Pugh score is used to determine the prognosis using the following parameters - ascites, encephalopathy, bilirubin, albumin and prothrombin time. Child class A has the best prognosis and child class C has the worst   Summary Alcoholic Hepatitis Alcoholic Cirrhosis Acute debauch, continued alcohol consumption Ill patient (may be febrile) Presents usually with jaundice which may be deep (Cholestatic!) Tender, large and smooth hepatomegaly Florid spider angioma and palmar erythema No major signs of portal hypertension Arterial bruit over the liver Polymorphonuclear leucocytosis GGT, SGOT and SGPT elevated - usually upto 300 IU/L Gold standard for diagnosis is liver biopsy Poor prognosis for Maddrey’s score > 32. Probably a past drinker Relatively well preserved (unless severely decompensated) Presents usually with ascites or GI bleeding Non tender, firm, irregular and nodular liver Spider angioma and palmar erythema present Signs of portal hypertension present Arterial bruit over liver only with hepatoma Minimal polymorphonuclear leucocytosis Liver enzymes usually in normal range Gold standard for diagnosis is liver biopsy Poor prognosis for Child class C.       Home   l   Founder's Profile   l   Liver Biology   l   Newsletter   l   Enquiry   l  FAQ   l  Member's Login   l   Sitemap  l   Contact Us © 2010, Global Healthcare Solutions All Rights Reserved. Dr M. R. Rajasekar. design: mayuri infomedia