Friday, 18 May 2012

approach to patient with liver disease


APPROACH TO  PATIENT WITH LIVER DISEASE

The many causes of liver disease present clinically in a few distinct patterns either
a)        Hepatocellular diseases-Features of injury, inflammation and necrosis.
b)       Cholestatic (obstructive)-Feature of obstruction of bile flow predominate.
-Typical presenting symptoms of liver disease include
    -Jaundice
    -Generalized Fatigue
    -Itching
    -Right upper quadrant pain,
    -Abdominal distention
    -Intestinal bleeding.
-However, some patients with liver disease are found to have abnormalities in biochemical liver tests as a part of a routine biochemical tests.
Evaluation of patients with liver disease should be directed at
(1) Establishing the etiologic diagnosis
Hepatocellular versus cholestatic injury, as well as on the specific etiologic diagnosis
(2) Estimating the disease severity (grading)
Assessing the severity or activity of disease-active or inactive, and mild, moderate, or severe.
(3) Establishing the disease stage (staging).
Estimating the place in the course of the natural history of the disease, whether acute or chronic; early or late; pre-cirrhotic, cirrhotic, or end-stage.
CLINICAL HISTORY
-Follow symptoms of liver disease
ü  Their nature
ü  pattern of onset
ü  progression
- Liver-specific symptoms of jaundice, dark urine, light stools, itching, abdominal pain, and bloating.
-Itching occur early in obstructive jaundice (from biliary obstruction or drug-induced cholestasis)
Itching also occurs in chronic liver diseases, typically the cholestatic forms such as primary biliary cirrhosis and sclerosing cholangitis where it is often the presenting symptom, occurring before the onset of jaundice.
-RUQ pain or ache ("liver pain") occurs in many liver diseases and is usually marked by tenderness over the liver area.
-The pain arises from stretching or irritation of Glisson's capsule, which surrounds the liver.
-Severe pain is most typical of gall bladder disease, liver abscess, and severe venoocclusive disease but is an occasional accompaniment of acute hepatitis.
-Jaundice is the hallmark symptom of liver disease.
Patients usually report darkening of the urine before they notice scleral icterus.
Rarely detectable with a bilirubin level less than 51 umol/L. With severe cholestasis there will also be lightening of the color of the stools and steatorrhea. Jaundice without dark urine usually indicates indirect (unconjugated) hyperbilirubinemia and is typical of hemolytic anemia eg malaria and sickle cell and the genetic disorders of bilirubin conjugation eg Gilbert's syndrome, Crigler-Najjar syndrome..


Symptoms suggestive of complications of stage of liver disease:
ü  Haematemesis-varices or portal HTN
ü  Hemoptysis-chronic heart failure and cardiac cirrhosis.
ü  Any other bleeding diasthesis-liver failure.
ü  Swelling of legs-low albumin.
ü  Abnormal behaviour, confusion or drowsiness

PHYSICAL EXAMINATION
-In many patients, the physical examination is normal unless the disease is acute or severe and advanced.
-The physical examination can reveal signs that point to a specific diagnosis, either in risk factors or in associated diseases.
-Typical physical findings in liver disease
-General condition
-The patient may be wasted because of chronic illness, confused-encephalopathy, dehydrated etc
Hands-6 items
-Leuconychia-chronic liver disease with hypoalbuminaemia
-Finger clubbing
-Asterexis
-Dupytrens contracture
-Palmar erythema
-Palmar parlor

Others general exam
-Spider angiomata
-Excoriations
-Jaundice
-Gynecomastia, scrotal atrophy, parotid enlargement
-Edema
-Hepatic fetor  

Per Abdomen
-Prominent veins over the abdomen, and caput medusa
-Ascites
-Hepatomegaly- Careful assessment of the liver edge may also demonstrate unusual firmness, irregularity of the surface, or frank nodules.
-Hepatic tenderness
-Splenomegaly
-Pulsatile liver-Chronic CCF with Tricuspid regurgitation.
-Hepatic bruit-hepatoma, hepatic hemangioma


Signs of advanced disease include
-Dilated abdominal veins
-Asterixis
-Mental confusion
-Stupor or Coma.

A helpful measure of hepatic encephalopathy is a careful mental status examination and use of the trail-making test, which consists of a series of 25 numbered circles that the patient is asked to connect as rapidly as possible using a pencil. The normal range for the connect-the-dot test is 15 to 30 s; it is considerably delayed in patients with early hepatic encephalopathy.

INVESTIAGTIONS
1. FHG- Anaemia of chronic illness may be seen.
Lymphocytosis-Viral hepatitis.
2. LFT
-Liver parenchyma- ALT and AST)
-Cholestasis-alkaline phosphatase, γ-glutamyl transpeptidase (GGT) to define whether alkaline phosphatase elevations are due to liver disease
-Direct and total serum bilirubin
-Synthetic Function of the liver-albumin and prothrombin time.
3.Viral hepatitis serology to define the type of viral hepatitis-Commonly HBV and HBV plus
HIV ELISA
Hepatitis B
Acute- HBsAg and anti-HBc IgM
Chronic- HBsAg and HBeAg and/or HBV DNA
Hepatitis C
Anti-HCV IgG
HCV RNA
Other hepatitis
HAV- Anti HAV IgM
HDV- HBsAg and anti-HDV
HEV-Anti-HEV IgM
4.RFT’s esp those presenting with ascitis
5.Autoimmune markers –If indicated
-Primary biliary cirrhosis (antimitochondrial antibody; AMA, elevated IgM levels, and compatible histology
-Sclerosing cholangitis (peripheral antineutrophil cytoplasmic antibody; P-ANCA), cholangiography
-Autoimmune hepatitis – ANA-antinuclear antibodies; SMA-smooth-muscle antibody, elevated IgG levels, and compatible histology
6.Familial liver diseases
i)α1 Antitrypsin disease- Reduced α1 antitrypsin levels, phenotypes PiZZ or PiSZ
ii) Wilsons disease-Decreased serum ceruloplasmin and increased urinary copper; increased hepatic copper level
iii) Haemachromatosis-Elevated iron saturation and serum ferritin; genetic testing for HFE gene mutations
7.Tumour markers
Elevated α-fetoprotein level >500; ultrasound or CT image of mass

 Staging of Liver disease
Reliable staging system is the modified Child-Pugh classification with a scoring system of 5 to 15:
§  scores of 5 and 6 being Child-Pugh class A (consistent with “compensated cirrhosis”),
§  scores of 7 to 9 indicating class B
§  10 to 15 class C
-This scoring system was initially devised to stratify patients into risk groups prior to undergoing portal decompressive surgery.
-The Child-Pugh score is a reasonably reliable predictor of survival in many liver diseases and predicts the likelihood of major complications of cirrhosis such as bleeding from varices and spontaneous bacterial peritonitis.
-It was used to assess prognosis in cirrhosis and to provide the standard criteria for listing for liver transplantation (Child-Pugh class B).
Child Pugh Classification
Factor

       
1
2
3

Serum bilirubin   µmol/L


  <34

34–51

>51

Serum albumin  g/L


  >35

30–35

<30

Prothrombin time INR


<1.7
1.7–2.3
>2.3
Ascites

None

Easily
controlled
Poorly controlled
Hepatic
encephalopathy

None
Minimal
Advanced


Long term follow up for liver disease patients
1.Abstinence from alcohol should be encouraged for all patients with alcohol-related liver disease and in patients with cirrhosis and those receiving interferon-based therapy for hepatitis B or C.
2.Regarding vaccinations, all patients with liver disease should receive hepatitis A vaccine and those with risk factors should receive hepatitis B vaccination as well. Influenza and pneumococcal vaccination should also be encouraged.
3. Patients with liver disease should be careful in use of any medications, other than the most necessary. Drug-induced hepatotoxicity can mimic many forms of liver disease and can cause exacerbations of chronic hepatitis and cirrhosis; drugs should be suspected in any situation where the cause of exacerbation is unknown.
4. Surveillance for complications of chronic liver disease such as variceal hemorrhage and hepatocellular carcinoma.
Upper endoscopy to assess the presence of varices and should be given chronic therapy with beta blockers if large varices are found.
Patients with cirrhosis also screening and long-term surveillance for development of hepatocellular carcinoma. Eg  US of the liver at 6- to 12-month intervals
Constitutional symptoms such as fatigue, weakness, nausea, poor appetite, and malaise.
Nausea - may accompany fatigue or be provoked by odors of food or eating fatty foods.
Vomiting -rarely persistent or prominent.
Anorexia with weight loss occurs commonly in acute liver diseases but is rare in chronic disease, except when cirrhosis is present and advanced.
 Diarrhea -uncommon in liver disease, except with severe jaundice, with malabsorption leading to steatorrhea.
-Major risk factors for liver disease
ü  Detailed history of alcohol use- more than two drinks (22 to 30 g) per day in women and three drinks (33 to 45 g) in men. Increased risk. Most patients with alcoholic cirrhosis have a much higher daily intake and have drunk excessively for 10 years or more before onset of liver disease.
ü  Previous history of yellowness of eyes-viral hepatitis, aflatoxicosis.
ü  Medications (including herbal compounds, birth control pills, and over-the-counter medications).
ü  History of pulmonary TB treatment or chronic cough-Dessimnated TB .Also adverse effects of anti-TB.
ü  Sexual History- For assessing the risk of viral hepatitis should include life-time number of sexual partners. Sexual exposure is a common mode of spread of hepatitis B but is rare for hepatitis C
ü  Methods of grain storage and history of other family members having similar symptoms.
ü  Exposure to jaundiced or other high-risk persons
ü  A history of injection drug use, even in the remote past, is of great importance in assessing the risk for hepatitis B and C. Injection drug use is now the single most common risk factor for hepatitis C.
ü  Recent surgery
ü  Remote or recent transfusion with blood and blood products .Transfusion with blood or blood products is no longer an important risk factor for acute viral hepatitis. However, blood transfusions received before the introduction of sensitive enzyme immunoassays for antibody to hepatitis C virus (anti-HCV) in 1992 is an important risk factor for chronic hepatitis C. Blood transfusion before 1986, when screening for antibody to hepatitis B core antigen (anti-HBc) was introduced, is also a risk factor for hepatitis B
ü  Occupation-schistosomiasis, chemical exposure
ü  Accidental exposure to blood or needlestick
ü   familial history of liver disease -Wilson's disease; hemochromatosis and a1-antitrypsin (a1AT) deficiency
ü  Suggestive of heart failure-orthopnea , paroxysmal nocturnal dysnea-Cardiac cirrhosis

-Spider angiomata and palmar erythema occur in both acute and chronic liver disease and may be especially prominent in persons with cirrhosis, during pregnancy.
-Spider angiomata are superficial, tortuous arterioles and, unlike simple telangiectases, typically fill from the center outwards.
-Occur arms, face, and upper torso; they can be pulsatile and may be difficult to detect in dark-skinned individuals.
-Hepatic failure is defined as the occurrence of signs or symptoms of hepatic encephalopathy in a person with severe acute or chronic liver disease.
-The first signs of hepatic encephalopathy can be subtle and nonspecific-change in sleep patterns, change in personality, irritability, and mental dullness. Thereafter, confusion, disorientation, stupor, and eventually coma supervene. Physical findings include asterixis and flapping tremors of the body and tongue.
-Fetor hepaticus refers to the slightly sweet, ammoniacal odor that is common in patients with liver failure, particularly if there is portal-venous shunting of blood around the liver.
-Other causes of coma and confusion should be excluded, mainly electrolyte imbalances, sedative use, and renal or respiratory failure.
-Widened pulse pressure and signs of a hyper dynamic circulation can occur in patients with cirrhosis as a result of fluid and sodium retention, increased cardiac output, and reduced peripheral resistance.
-Patients with long-standing cirrhosis are prone to develop the hepatopulmonary syndrome with hypoxemia due to pulmonary arteriovenous shunting, characterized by hypoxia that worsens when lying flat.
Several skin disorders and changes occur commonly in liver disease.
-Hyper pigmentation -chronic cholestatic diseases such as primary biliary cirrhosis and sclerosing cholangitis.
-Xanthelasma and tendon xanthomata occur as a result of retention and high serum levels of lipids and cholesterol. A slate-gray pigmentation to the skin also occurs with hemochromatosis if iron levels are high for a prolonged period.
-Mucocutaneous vasculitis with palpable purpura, especially on the lower extremities, is typical of cryoglobulinemia of chronic hepatitis C but can also occur in chronic hepatitis B.
-Some physical signs point to specific liver diseases. Kayser-Fleischer rings occur in Wilson's disease and consist of a golden-brown copper pigment deposited at the periphery of the cornea; they are best seen by slit-lamp examination.

 DIAGNOSTIC IMAGING
1. Ultrasonography-have a high sensitivity for detecting biliary duct dilatation and are the first-line options for investigating the patient with suspected obstructive jaundice.
2. (CT-scan)
3. (MRI)
CT and MRI are indicated for the identification and evaluation of hepatic masses, staging of liver tumors, and preoperative assessment.
4.. Magnetic resonance cholangiopancreatography (MRCP
5.ERCP
-(MRCP) and (ERCP) are the procedures of choice for visualization of the biliary tree.
-MRCP offers several advantages over ERCP; there is no need for contrast media or ionizing radiation, images can be acquired faster, it is less operator dependent, and it carries no risk of pancreatitis.
-MRCP is superior to US and CT for detecting choledocholithiasis but less specific.
-It is useful in the diagnosis of bile duct obstruction and congenital biliary abnormalities, but ERCP is more valuable in evaluating ampullary lesions and primary sclerosing cholangitis.
-ERCP allows for biopsy, direct visualization of the ampulla and common bile duct, and intraductal ultrasonography.
-It also provides several therapeutic options in patients with obstructive jaundice, such as sphincterotomy, stone extraction, and placement of nasobiliary catheters and biliary stents.
-Doppler US and MRI are used to assess hepatic vasculature and hemodynamics and to monitor surgically or radiologically placed vascular shunts such as transjugular intrahepatic portosystemic shunts (TIPS).
- Finally, interventional radiologic techniques allow the biopsy of solitary lesions, insertion of drains into hepatic abscesses, and creation of vascular shunts in patients with portal hypertension.
 Liver biopsy
Check preparation and the performance of liver biopsy






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