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LIVER DISEASES IN GENERAL PRACTICE

O P Kapoor
Hon. Visiting Physician, Jaslok Hospital and Bombay Hospital, Mumbai,
Ex. Hon. Prof. of Medicine, Grant Medical College and JJ Hospital, Mumbai 400 008.




Gone are the days when every gastrointestinal symptom was diagnosed to be due to "weak" liver. If the blood test of "liver profile" (liver function tests) is normally, sure enough the liver is functioning normally. Not only that, the vague diagnosis of "hepatitis" or hepatopathy should never be used as a label. At present, with the help of modern imaging and various serological tests and "markers" an accurate diagnosis of the "type" of hepatitis can be made.

A general practitioner should not worry about the involvement of the liver in systemic disorders like connective tissue disorders (e.g. systemic lupus erythematosus) and many others. Diagnosis of "primary" liver disease should be mastered. Also following points should be remembered:-
  1. Jaundice is not hyperbilirubinaemia and more important hyperbilirubinaemia is not same as jaundice. Hyperbilirubinaemia is a theoretical finding and often does not indicate "Primary" liver disease. Therefore ignore it and continue your differential diagnosis and sorting out the complaints of your patient. Examples are patients suffering from typhoid, malaria and viral fevers. More important examples are surgical, orthopaedic, gynaec, obstetric and severely ill patients in intensive care units - who will very often show raised levels of bilirubin and alkaline phosphatase with minimal elevation of SGPT - which is part of the systemic illness. In all such patients, serum bilirubin is usually less than 3 mg and no clinical jaundice is observed. But if the patient has clinical jaundice (Icterus) and the bilirubin level is 3 to 4 mg or more, "Primary" liver disease should be thought off.

  2. 5% population has raised levels of bilirubin which is not due to disease but abnormal "metabolism" and calls for no treatment or panic reaction because it would last life time. In such patients the bilirubin is usually 2 or 3 mg (but could increase to double during any infection in the body), but SGPT remains normal. If this bilirubin is "indirect" type and is not present in urine, Gilberts disease is the label given. But if it is of direct type and present in urine, Dubin Johnson disease or BRIC is the label given to these patients. No treatment is required. These patients are wrongly diagnosed by doctors and G. Ps as having "repeated" attacks of hepatitis!!

  3. Sonographers have introduced a very common terminology (equivalent to increased BV markings on X-ray chest) that the liver is enlarged and fatty. Again it is common to get this type of liver in fatty or anaemic or diabetic patients and SGPT will always be normal. No treatment is required. But if SGPT is increased, a rare liver disease NASH may be diagnosed which is again an inherited disease with abnormal metabolism causing fatty liver where fatty foods would have to be permanently avoided. More often in alcoholic patients if SGOT (not SGPT) is elevated, then, the fatty liver is a pathologically important finding. It is at this stage that omission of alcohol can reverse the process to a normal liver.

  4. It is worth remembering that alcohol anddrugs (mainly anti-TB drugs - INH, rifampicin and possibly pyrazinamide) can mimic any liver disease and must be excluded before diagnosing a "Primary" liver disease.

  5. Imaging of liver (sonography and scanning) is only reliable to exclude a space occupying lesion like an abscess or a malignancy. Again only blood tests and clinical history can differentiate these two illnesses. An increased level of alpha feto protein with a positive HBsAg test will favour diagnosis of hepatoma. A high titre of IHA (Indirect haemagglutination test of amoebiasis) will favour the diagnosis of amoebic abscess (otherwise it is pyogenic liver abscess).

  6. Do not waste your patientís money on costly "liver profile" blood tests. Blood tests for SGPT and bilirubin are enough to indicate liver damage. Serum alkaline phosphatase or GGT elevation would confirm that the jaundice is due to cholestasis. If jaundice is more than 21/2 to 3 monthsí duration, and SGPT is raised 4-5 times more than normal, then serum albumin and globulin ratio will help to diagnose chronic liver disease (chronic active hepatitis). Albumin levels go down to less than 3G and globulins increase to more than 2G. Prothombin time is the most sensitive test to indicate poor prognosis. For example, if it is 60 seconds (without any anti-coagulant), the jaundiced patient will hardly survive. Raised bilirubin levels by themselves (even upto 30, 40 or 50 mg) or very high SGPT levels (even upto 5 to 10 thousand or more) do not indicate bad prognosis.
Coming to the primary liver diseases basically one can divide them into acute and chronic illness, though both can present with acute onset. I must stress the fact, that a chronic liver illness can remain in the body silently and may be picked up only on routine check up. Examples are - a firm nodular enlarged cirrhotic liver in an alcoholic patient or a huge enlarged liver with or without a mass in the liver with underlying hepatoma. This does not occur in acute illness like acute viral hepatitis and amoebic liver abscess.

Acute illnesses of the liver : Fortunately, there are only 3 primary illnesses of the liver. These are in order of frequency -
    1. acute viral hepatitis
    2. acute drug hepatitis
    3. amoebic liver abscess (ALA)
The incidence of ALA is falling day by day and has now become as rare an entity as cancer of the liver. Also if the patient is not taking anti-TB drugs, majority of the cases of clinical jaundice as explained earlier (bilirubin more than 3-4 mg) are all suffering from acute viral hepatitis. However, I would like to discuss these illnesses in detail. I would like to repeat that I am not discussing mild abnormality of the liver function tests and hyperbilirubinaemia which can occur in all common and uncommon fevers like malaria, typhoid, abdominal tuberculosis, dengue fever and other illnesses due to viruses like inf. mononucleosis (EB virus), cytomegalic virus, herpes simplex virus, etc. Most of these illnesses do not cause clinical jaundice and are not worth remembering by the family physicians, though they can upset the patient, the family members and the family physicians because of the fear of the liver involvement.

Acute Viral Hepatitis : It can be due to virus A,B,C,D,E. The virus A infection occurs commonly in children and not in adults. Virus E is the commonest infection in adults. Both these viruses are benign and the patients invariably recover. Therefore, the blood tests for these viruses need not be done in private practice as these are very costly. Rarely these tests are done to exclude or diagnose drug hepatitis (by their absence).

Virus D is not to be remembered by family physicians because it is connected to Virus B and is a dependent of that virus. That leaves only virus B and C. Virus C comes mainly through blood transfusion. Thus if any patient who has had a bloodtransfusion develops an attack of viral hepatitis, anti HCV antibodies should be looked for in the blood (again costly test). Otherwise, in a straight forward patient of viral hepatitis, virus C should not become a differential diagnosis (while in cirrhosis patient it is an important investigation). The only other indication for asking anti HCV is anybody who is found to have "persistent" (done on more than one occasion at an interval of a month or two) abnormal liver function tests detected on a routine examination. This leaves only virus B.
    1. In 5% patients this virus can persist and can cause chronic liver damage.
    2. The blood test for this virus that is HBsAg, is quite cheap (about Rs.100/-)
    3. This virus could be transmitted very easily through physical contact in normal population (through the blood)
    4. And since the test for viral E, (anti HEV) in adult is very costly (about Rs. 500/-) . . . . .in every case of viral hepatitis it will be worthwhile to ask for the test of HBsAg to rule out viral B infection. If found positive, next blood test for anti HBc IgM should be asked for to confirm the diagnosis of virus B infection (only positive HBsAg may be present in asymptomatic carrier); and if found to be positive HBsAg should be repeated after 6 months to see if it is still persisting when the patient should be sent to a specialist.
Thus, virus E is the commonest cause of jaundice in hepatitis in adults provided the patient is not on anti-TB drugs. The clinical picture is in 3 stages:
  1. The patient gets the usual attack of fever like any other viral fever with bodyache, malaise, etc. but loss of appetite, nausea (and may be vomiting) are out of proportion to the fever. This stage usually lasts about a few days and at the end of it, the patient might notice that the urine is becoming dark coloured (like light black tea).
  2. At this stage the urine colour becomes darker and the patient develops clinical jaundice which the relations might notice. As the jaundice increases, loss of appetite, nausea and vomiting gradually decrease. This stage may also last for few days to a week.
  3. In the 3rd stage, the patient appears like a healthy man with no fever, nausea or vomiting and has good appetite, but he and the relations are only worried about the jaundice which may be associated with itching due to cholestasis. This stage can last for a few days upto a week or two.

TREATMENT OF VIRAL HEPATITIS

    1. Isolation of the family members is useless by the time jaundice appears in the patient.
    2. The usual prescription given by the doctors for this disease includes -

      i. Tonics for appetite
      ii. inj. Glucose25 per cent IV
      iii.
      Inj. Calcium Gluconate IV
      iv. Inj. B. Complex
      v. Inj. Vit. C
      vi. Inj. Vit. K
      vii. Antibiotics
      vii. Prednisolone 1 tab. BD or TDS
      ix. Inj. Liver Extract
      x. Methionine and Choline containing liver tonics
      xi. Sedatives

All the above drugs are more or less useless and in fact, the last two drugs are even harmful because they can precipitate hepatic coma.

It is very important to understand that the viral hepatitis is a "viral" disease and there is no specific treatment for this disease. (At presentantiviral drugs are used only for "chronic" Virus B and C hepatitis). The liver which is necrosed, recovers most of the times with the help of nature. All we have to do is to help nature by giving complete rest to the patient as long as jaundice lasts. Therefore, the most important part of the treatment is rest at home (not necessarily in bed) till jaundice disappears. IV Glucose should be given only if there is persistent vomiting.


Regarding diet in Viral Hepatitis, some doctors prescribe fat-free diet, others prescribe a high protein diet containing casilan powder or protinex and still others prescribe a high carbohydrate diet with plenty of glucose. Ideally, till the patient has loss of appetite and nausea, which is approximately the first week of illness, the patient is asked to take whatever he likes but the stress should be on liquids specially sugar cane juice or fruit juices.


A normal diet (except fried or spicy food), which the rest of the family members are eating, should be prescribed to all the patients as soon as their appetite returns. The fats are omitted from the diet only if the stools become white coloured which rarely occurs for 2-3 days during the course of this illness. Most of the doctors starve their patients and specially tell them to avoid fats (which normally make the food palatable). The result is, that these patients lose too much weight at the end of the illness, not because of the disease itself, but because of the wrong advise given by the GP.


DRUGS IN VIRAL HEPATITIS

Perinorm could be used if there is a lot of nausea. Nowadays Domstal (Domperidol) is the best drug to be used.


Regarding rest of the drugs, antibiotics do not work in Viral Hepatitis, and in fact may increase nausea and vomiting. The tonics get the wrong credit. Normally, in all these patients, appetite returns as soon as jaundice starts deepening, a paradox which the doctors are not aware of, thus giving the wrong credit to the tonics. Methionine, Choline and sedatives should not be used in Viral Hepatitis since they may precipitate Hepatic Coma. The numerous injections used in this disease may be used for psychological treatment of the patient for whom "Liver Disease" is a dangerous disease. The only useful injection is Glucose 25 per cent IV, which should be used "only" for patients having severe vomiting. All the rest can have Glucose by mouth. Cane sugar juice or other fruit juices can replace glucose. Vit B and C tablets may be given orally.


Following are the danger signals : the presence of any one of them indicates oncoming Hepatic Coma and death. 1. Drowsiness, 2. Reversal of sleep rhythm e.g. sleeping at day time and waking up at night time. 3. Abnormal behaviour. 4. Irritability. 5. Tremors or tremulousness.


With the appearance of any one of them, the patient should be sent to the hospital or a specialistís opinion should be sought. Deep jaundice as such is not a sign of danger.

DIFFERENTIAL DIAGNOSIS OF PATIENTS WITH DEEP JAUNDICE

'Sonography' should be asked for to see dilatation of the biliary tree. Isotope Liver Scan is not required to be done if your sonographer doctor is reliable and experienced enough. CT Scan, wherever available is a very costly Ďalternativeí to sonography and should be left to the specialist to order. CT Scan is the best and most accurate investigation out of all other non-invasive methods of diagnosing a case of undiagnosed "deep jaundice". (If the bile duct is dilated, patient should be sent to a Gastroenterologist for ERCP or MRCP examination to study the type of biliary obstruction).


Gone are the days when it was a common sight to see a patient of jaundice being left undiagnosed for months together. Now-a-days, with the help of the above investigations it is very easy to diagnose surgical causes of jaundice which are all operable.


Acute Drug Hepatitis :
In more than 90% ofthe patients, this drug hepatitis seen in private practice is only in TB patients who are on anti-TB drugs. (All the male and female hormones including oral contraceptives can cause only mild cholestatic jaundice with marked itching but no clinical picture of viral hepatitis). The diagnosis is very easy. The major culprit is rifampicin. The next in order is isoniazid. Pyrazinamide in a dose of more than 15 mg/kg can also cause jaundice, with the result that the best and the cheapest first line of drugs can all cause jaundice. Although, the incidence of this is high in a HIV positive patient, generally 1 out of 100 patients develops significant hepatitis to produce clinical jaundice. However, the blood test for SGPT may be done after 10-15 days. Often it will be found to be slightly elevated. If the elevation is more than 3 times the normal level the patient is going to develop drug hepatitis. All the drugs should be stopped and the patient should be put on streptomycin injections and ethambutol. After the liver function tests become normal and the hepatitis subsides, pyrazinamide is the first drug to be started and then isoniazid may be added but the blood test for SGPT should be asked for every week. The commonest culprit rifampicin if at all should be very cautiously tried again and only under the specialistís advise (because rarely rifampicin hepatitis can be fatal). Such patients will often need second line of drugs for tuberculosis. If the patient has a positive family history of jaundice at that time in the family or the patient happens to be a student having exams or an important executive, blood test for anti HEV may be done to confirm the presence of virus E hepatitis in a patient of anti-TB drugs. Even in such patients, till the jaundice subsides, rifampicin and isoniazid will have to be omitted.


Amoebic Liver Abscess: (ALA) should be thought of only when the patient complains of pain and tenderness in the liver area with or without fever which may be high or low.


The definition of "liver area" is - the area of the gall bladder (anterior surface of the right lobe), area of the right kidney (posterior surface of the right lobe), lateral aspect of the chest and the shoulder areas of the trapezius muscle (superior surface of the rt lobe) and the epigastrium (left lobe). Rarely the fever is present before the pain starts and the high WBC count and sonography of the liver done routinely can pick up the liver abscess. IHA blood test for amoebiasis must be done in every case to confirm the illness and to exclude a pyogenic liver absce ss.


Treatment of Amoebic Liver Abscess : Prescribe them metronidazole 400 - 600 mgm three times a day for 1 week (can cause nausea and coated tongue) along with or without chloroquine tablets 2 twice a day for 2 days followed by 1 tablet twice a day for 3 weeks. Tinidazole in a dose of 600 mg three times a day is equally effective and has similar side effects. Both the drugs could be used as a single dose of 2G after breakfast for a period of 3 days. Inj. Emetine is hardly ever required nowadays. However, the patient will need tapping of the abscess in case:
  1. Pain and tenderness or fever persists after 2-3 days
  2. If the patient has an obvious lump seen in the liver area.
Chronic illness - Cirrhosis of the liver and malignancy of the liver (hepatoma).

Cirrhosis of the liver - the commonest cause of liver cirrhosis is alcohol or virus B or C. In short, if the patient is not alcoholic and his blood test is negative for HBs Ag or anti HCV, the chances of his having cirrhosis are very remote. Doctors who are not confident of palpating an enlarged liver can take advantage of this fact.


Unfortunately cirrhosis is a silent disease and by the time the symptoms start, cirrhosis is already advanced and the patient, with or without treatment can die in 5 years. Therefore, such patients should always be referred to a Gastroenterologist. The patients complain either of upper GI bleed (either haematemesis or melaena or an acute attack of fainting with sweating, severe pallor and routine aspiration with Ryles tube shows black blood in the stomach). They should always be admitted in the hospital where endoscopy will exclude associated peptic ulcer and where the gastroenterologist can inject the oesophageal varices (the cause of bleeding) which may be fatal. The patient might need multiple blood transfusions.


Later on, gastroenterologist will call his patient on a couple of occasions to inject sclerosing solutions into oesophageal varices (piles) to prevent the future fatal bleed. These patients are kept on betablockers and long acting nitrates for life time to keep the portal hypertension controlled. An isotope liver scan done on such patients can also confirm the diagnosis of both cirrhosis and portal hypertension.


Liver function tests (liver profile) have very little role to play in the diagnosis and remain nearly normal unless the patient develops ascites.


Ascites is the second presentation of advanced cirrhosis. The presence of fluid can be confirmed easily on sonography. By tapping the fluid - peritoneal tuberculosis can be excluded by doing adenosine de-aminase test of the aspirated fluid. Malignancy can be excluded by cytological examination of the fluid for malignant cells. These cirrhotic patients always have low albumin levels in the blood and prothrombin time is abnormal. They should always be under the care of a gastroenterologist because, off and on they can go into hepatic coma during their life span of about 5 years, by the end of which most of them will die. The gastroenterologists give them a combination of high protein, absolutely salt free diet with very high doses of spironolactone diuretics. Every time they develop a complication of upper GI bleed or early hepatic coma (abnormal behaviour) or any infection (which they are very prone to because of the immunosuppression) they should be admitted in the hospital and should never be treated in private practice.


Malignancy of the liver (hepatoma) - First of all we must remember that in a patient having any cancer in the body, any enlargement of the liver or abnormal liver function tests (specially elevated alkaline phosphatase or Gama GT) should be diagnosed as secondary malignant deposits in the liver.


To diagnose "primary" cancer of the liver (hepatoma), the following requirements should be fulfilled :-
    1. A sonography or CT Scan must show a space occupying lesion which may be fluid or
      solid or both.
    2. Serum alpha feto protein levels should be markedly raised.
    3. Blood test for HBs Ag must be positive. It is worth noting that IHA blood test for
      amoebiasis should be done in every case because very rarely a "chronic ALA" can
      present like a hepatoma but is 100% curable.
Incidentally, primary cancer of the liver is one of the commonest cancers specially in a male patient next to only prostate (and lungs in smokers). Thus it is common in private practice to come across primary cancer of the liver.

ALCOHOL AND LIVER

Even a layman knows that alcohol is bad for liver. Most of the alcoholics have palpable fatty liver. This does not produce any signs or symptoms and therefore has no significance except that, if the patient stops drinking, the liver can become absolutely normal. Once this stage has progressed farther, alcoholic livers cannot return to normal completely.


Last stage of alcoholic liver damage is cirrhosis, which has already been discussed, where the patient one day either develops haematemesis or ascites.

There is a third interesting disease of livercaused by alcohol which is known as Alcoholic Hepatitis. I have no intention of writing details about this disease. But I would only like to warn the GPs, that this condition can mimic all liver diseases. These patients may develop typical symptoms and signs of Viral Hepatitis e.g. loss of appetite with jaundice or signs of cirrhosis with ascites or a picture of hepatic amoebiasis or a combination of all above symptoms and signs. If these patients stop drinking even at this stage (there is no specific treatment), about 50 per cent may be cured, 10 to 30 per cent die and others develop permanent cirrhosis. This condition should be thought of only in heavy drunkards.

Congestive Hepatomegaly due to Cardiac conditions and disease of the major veins (hepatic veins and IVC).

Day by day such patients are becoming rare because of the new drugs in the market and advances in the medical and the surgical treatment of the heart disease and cardiac failure. Even then, off and on one sees patients having painful and tender enlarged liver due to atrial fibrillation which is often associated with rheumatic heart disease but which can occur in either patients having IHD or those who are alcoholics. Rare cases of thrombosis of hepatic veins or IVC (Budd Chiari) can mimic cirrhosis. A clever sonographer with the help of doppler studies can make an accurate diagnosis and a modern interventional specialist can do angioplasty or stenting which can result in cure.


Finally, all young non-alcoholics having chronic liver disease and having negative blood tests for virus B and C and a negative ANA disease should be sent to ophthalmologist for a slit lamp examination to exclude Wilsonís disease - a rare disease.



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