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The post-hepatic jaundice report

  • Category: Health
  • Subcategory: Medicine
  • Pages: 3
  • Words: 1478
  • Published: 23 October 2018
  • Downloads: 43
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In this case, the most likely diagnosis of the patient has post-hepatic jaundice which might due to the presence of gallstone blocking the bile duct known as extra-hepatic obstruction. Another cause is carcinoma of the head of the pancreas. The elevation of bilirubin level which is 250 µmol/l will give rise to severe, painless and deep jaundice. The post-hepatic jaundice is characterized by high alkaline phosphatase (ALP) activity that is more than seven times the upper limit of the reference range. In the given case, the aspartate and alanine aminotransferase activities do not indicate severe hepatocellular damage.

An elevated level of bilirubin is ten times higher than the reference range, so it often indicates that an obstruction of bile flow or a defect in the processing of bile by the liver. Biliary obstruction signs and symptoms include light color stool, dark urine, nausea, vomiting, and jaundice. Other possible causes elevation of bilirubin are red blood cell breakdown destruction (anemia), liver scarring, liver inflammation and cancer of pancreas or gallbladder. Several diseases are associated with hyperbilirubinemia. Hemolytic jaundice is one of the diseases because more bilirubin is conjugated and excreted than normally, but the conjugation mechanism is overwhelmed, and an abnormally large amount of unconjugated bilirubin is found in the blood. Gilbert’s disease may be caused by an inability of the hepatocytes to take up bilirubin from the blood. As a result, unconjugated bilirubin accumulates. Physiological jaundice and Crigler-Najjar syndrome are conditions in which conjugation is impaired. Unconjugated bilirubin is retained by the body. Dubin-Johnson syndrome is associated with the inability of the hepatocytes to secrete conjugated bilirubin after it has been formed. Conjugated bilirubin returns to the blood. The given result showed that the AST is exceeded the reference range value. AST levels increase when there’s damage to the tissues and cells where the enzyme is found. Elevated levels indicate that there is a certain amount of damage in that area. AST is less specific for liver disease than ALT. It elevated in other conditions such as myocardial infarction. The sensitive indicator of liver cell injury is aminotransferase. They are most useful in helping to recognize the acute hepatocellular diseases such as hepatitis and cirrhosis. ALT is more specific for liver damage than AST. ALT usually increased more than AST in liver damage. Usually, the aminotransferases are present in the serum with a low concentration. When there is damage to the liver cell membrane resulting in increased permeability, these enzymes will release into the bloodstream in a greater amount. The activities of two enzymes include alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT) are normally increases in obstructive liver disease which also known as cholestasis. The elevation of the alkaline phosphatase in serum is more specific than GGT. GGT estimation is done to identify the patients with occult alcohol use. The normal serum alkaline phosphatase consists of many distinct isoenzymes found in the liver, bone, placenta and less common is a small intestine. There is not totally specific for cholestasis in the elevation of liver-derived alkaline phosphatase. A less threefold elevation can be seen in almost any type of liver disease. An elevation greater than four times normal of alkaline phosphatase occur in patients indicate that cholestatic liver disorder, infiltrative liver disease such as cancer and bone conditions characterized by rapid bone turnover (eg. Paget’s disease). This elevation is due to increased amount of bone isoenzymes in bone disease whereas the elevation is due to increased amount of liver isoenzymes in liver disease. In intrahepatic obstruction, the values increased as in drug-induced hepatitis and primary biliary cirrhosis. The values are found in extra-hepatic obstructive is very high due to cancer, common duct stone or bile duct structure. The increased of the level of serum alkaline phosphatase is not helpful to differentiate between intrahepatic and extra-hepatic cholestasis. Values are also greatly elevated in hepatobiliary disorders seen in patients with AIDS. Other than biochemical testing, certain parameters are needed to be used to confirm it is post-hepatic jaundice.

Surgical history:

The surgical history of the patients whether recent or past need to understand because it may be implicated in the cause of post-hepatic jaundice. It may be due to a variety of problems within the first three postoperative weeks. Levels of bilirubin increased related to hemolysis of transfused erythrocytes (especially stored blood), resorption of hematomas or hemoperitoneum and rarely to hemolysis of the patient’s erythrocytes due to G-6PD deficiency or malarial parasites in the transfused blood. Administration of halogenated anesthesia agents, exposure to other hepatotoxic drugs, sepsis, or hepatic ischemia associated with preoperative or intraoperative hypotension or hypoxia may cause the impaired hepatocellular function. It is very important to examine the operative record for transfusion, anesthesia, x-rays, drugs, and potential hypotension or hypoxia, as well as the surgeon’s dictated note of intraoperative events and his visual and palpation impression of the patient’s liver, biliary tree, and pancreas when a case of jaundice potentially related to surgery needed to be investigated.

Family history:

A family history of jaundice, liver disease, or anemia (especially when requiring splenectomy) should be sought. A positive family history of the liver disease may implicate the genetically transmitted non-hemolytic hyperbilirubinemias (Crigler–Najjar, Gilbert’s, Dubin–Johnson, or Rotor’s syndromes), benign recurrent intrahepatic cholestasis, Wilson’s disease, hemochromatosis, alpha-1 antitrypsin deficiency or hereditary spherocytosis in the differential diagnosis.

Imaging evaluation:

To investigate jaundice, some advanced techniques and equipment are really useful such as high-resolution ultrasound, computerized tomography (CT), percutaneous transhepatic cholangiography (PTC), endoscopic retrograde cholangiopancreatography (ERCP) and hepatobiliary scintigraphy (HBS). A valuable screening test in the jaundiced patient is abdominal sonography. The demonstration of biliary ductal dilation, gallstones, hepatic mass lesion, or an enlarged or abnormally shaped pancreas directs further investigation or therapy. Computerized tomography has the advantage of surveying the entire abdomen as well as the hepatobiliary-pancreatic axis. Furthermore, to reliably detecting ductal dilation, CT is superior to sonography in determining the level and cause of obstruction. The pancreas is displayed more reliably and accurately by CT than by sonography.

Liver biopsy:

Percutaneous needle liver biopsy is a safe procedure in experienced hands provided that the patient’s coagulation mechanism is normal. The individual factor deficiencies can be corrected by needle biopsy even if the clotting process is abnormal. It is very helpful in jaundiced patients to determine the cause of hepatomegaly, differentiate between intrahepatic and extra-hepatic obstruction (patients with drug-induced jaundice, primary biliary cirrhosis, and intrahepatic neoplasm may present with jaundice and defy diagnosis until liver tissue is obtained), follow chronic liver disease to determine progression of the natural process or the effects of therapy and provide liver tissue for special investigations such as culture, chemical analysis (hemochromatosis, Wilson’s disease), enzyme assay (glycogen storage disease) or immunologic studies (hepatitis B virus, delta agent).

Treatment for post-hepatic jaundice:

The treatment for post-hepatic jaundice entirely depends on the causes. Once a diagnosis has been established, the appropriate course of treatment can then be initiated. Patients can request for hospitalization or manage at home as outpatients. Alcohol cessation is necessary for patients with cirrhosis, alcoholic hepatitis, or acute pancreatitis secondary to alcohol use. Anti-viral medications may be used for liver damage caused by an infection such as viral hepatitis or glandular fever to prevent further damage. In general ways, surgery to unblock the bile duct system is recommended. During surgery, it may need to remove the gallbladder, a section of the bile duct system or pancreas to prevent further blockage. Liver transplant is another possible option in severe cases of liver disease. Prevention is better than cure in certain condition leading to post-hepatic jaundice. In fact, there are certain measures that can be taken in order to decrease the risk of developing jaundice. To decrease the risk of developing Hepatitis B or C, high-risk behaviors such as unprotected intercourse or intravenous drug use, and implement universal precautions when working with blood products and needles must be avoided. Vaccination of Hepatitis A or B can be considered. When traveling to areas where malaria is endemic, take the recommended precautions and prophylactic medications in order to prevent the development of malaria. Reduce alcohol consumption is also important to prevent liver diseases such as alcoholic hepatitis, alcoholic cirrhosis, and pancreatitis. Smoking behavior should be avoided as well because it is the risk factor for the development of pancreatic cancer and many other malignancies’.

In conclusion, the 65 years old man patient, in this case, study having post-hepatic jaundice (obstructive jaundice) after diagnosis. The prognosis for patients with post-hepatic jaundice is depended on the underlying causes. Diagnostic test and certain ways can be used to find out the best solutions to treat the disease. Appropriate treatment advised by doctors must be taken in order to cure or prevent the conditions became worse. However, more serious causes of jaundice can sometimes be fatal despite medical or surgical intervention.

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