distended and bile diffuses into the liver cells (where dystrophic processes develop) and passes into the lymph and the blood. Moreover, due to increased pressure inside fine bile capillaries, communications are formed at the periphery of the lobules between the capillaries and the lymph spaces, through which bile enters the blood vessels.
Skin and mucosa of patients with obstructive jaundice are yellow. Later, as bilirubin is oxidized to biliverdin, the skin and mucosa turn green and dark-olive. The bound bilirubin content in the blood with direct van der Bergh test is as high as 250-340 mmol/1 or 15-20 mg/100 ml, and more. In protracted jaundice associated with liver dysfunction, free bilirubin content increases as well. Bound bilirubin can be found in the urine (the presence of bile pigments is determined by urinalysis) to give it brown colour and brightyellow foaming. Feces are colourless either periodically (in incomplete obstruction, usually by a stone), or for lengthy periods of time (in compression of the bile duct by a tumour). Jaundice in-creases progressively in such cases; the skin and mucosa gradually turn greenish-brown; cachexia of the patient increases. In complete obstruction of the bile ducts, feces become colourless (acholic); their colour is clayish and grey-white; stercobilin is absent from feces.
Bound bilirubin and also bile acids produced by the hepatocytes in ample quantity (cholemia) are delivered to the blood in this type of jaundice. Some symptoms associated with toxicosis develop: pronounced skin itching, which intensifies by night, and bradycardia (bile acids increase the tone of the vagus nerve by reflex). The nervous system is also affected: the patient develops rapid fatigue, general weakness, adynamia, irritability, headache, and insomnia. If it is impossible to remove the cause of impatency of the common bile duct (stones or a tumour) the liver is gradually affected to add symptoms of hepatic insufficiency.
Enlargement of the abdomen (sometimes rapid) can be due to accumulation of ascitic fluid in the abdominal cavity (in obstructed blood outflow from the intestine via the portal vein), in considerable meteorism (due to deranged digestion in the intestine in upset bile excretory function), or in pronounced hepatoor splenomegaly.
Many chronic diseases of the liver and biliary tracts are attended by general weakness, non-motivated fatigue, and decreased work capacity.
History of the present disease
When collecting anamnesis, it is necessary to find out if the patient had in his past history jaundice or acute diseases of the liver or the gall bladder (Botkin's disease, acute cholecystitis, cholangitis), attacks of hepatic colics, enlargement of the liver or the spleen, which might be an early symptom of the present disease (chronic hepatitis, liver cirrhosis, chronic cholecystitis, cholangitis, cholelithiasis).
135
Life history of patient
When inquiring the patient it is necessary to establish factors that might be important for the etiology of the present disease of the liver or bile ducts: liking for fat and meat foods, exposure to chemical and vegetable poisons (alcohol, carbon tetrachloride, compounds of phosphorus, copper, lead, arsenic, dichloroethane, etc.), poisoning with mushrooms containing strong hepatotropic poisons (e.g. helvellic acid, amanitotoxin, etc.), some infectious diseases (Botkin's disease, lambliosis, typhoid fever, malaria, syphilis, etc.), diseases of the gastro-intestinal tract (gastritis, colitis), and diabetes mellitus. Familial predisposition is also important in the development of some liver diseases (e.g. congenital benign hyperbilirubinemia) and diseases of the gallbladder (cholelithiasis).
Physical Examination
General inspection (survey)
The general condition of the patient is first assessed. In the presence of marked functional hepatic insufficiency of various etiology (liver cirrhosis, cancer, prolonged obstructive jaundice, etc.), the patients's condition can be grave because of pronounced poisoning (hepatic coma). The patient's condition may be grave in acute inflammatory diseases of the liver (abscess), gallbladder (acute cholecystitis), or bile ducts (acute cholangitis). But in many chronic diseases of the liver and the bile ducts, the general condition of the patient may remain satisfactory for long periods of time. Patients with hepatic colics are restless, they toss in bed, try to find (without success) a position in which the pain might be relieved. Hepatic coma is characterized by deranged consciousness in the form of pronounced euphoria or inhibition to complete loss of consciousness.
The general appearance (habitus) of the patient usually does not change. At the same time, hypersthenic constitution with predisposition to obesity is often characteristic of patients with cholelithiasis. Quite the reverse, significant wasting (to cachexia) occurs in cirrhosis or malignant tumour of the liver or the bile ducts. If the disease of the liver begins in childhood or adolescence, the patient may look infantile.
An important diagnostic sign is jaundice of varying intensity. In order to assess correctly the colour of the skin, the patient should be inspected in daylight or in the light of the luminescent lamp. A subicteric symptom is jaundice of the sclera, the lower surface of the tongue, and the soft palate; next coloured are the palms, soles, and finally the entire skin. Inspection of the sclera helps differentiate between true (bilirubinogenic) and exogenic jaundice. Prolonged use of quinacrine, ethacridine lactate (rivanol), carotin (carrots), excess tangerines and oranges, exposure to trinitrotoluene and picric acid can cause slight jaundice of the skin (false jaundice) but the sclera
136
is not coloured in such cases. Hepatic jaundice is usually attended by itching and scratching of the skin.
Icteric skin can be of various hues. The skin is orange-yellow (rubinicterus) due to accumulation of bilirubin in the skin; it is usually characteristic of the early stages of the disease. Lemon-yellow colour of the skin (flavinicterus) is characteristic of hemolytic jaundice. Greenish-yellow colour (verdinicterus) is due to accumulation of biliverdin (the product of gradual oxidation of bilirubin); it is mostly due to obstructive jaundice. In long-standing mechanical jaundice the skin becomes dark bronzy (melasicterus).
In certain cases the skin becomes pallid due to anemization (hemorrhage from varicose esophageal or hemorrhoidal veins in portal cirrhosis); the skin may be greyish ("dirty") in patients with some hepatic diseases. Greyish-brown or brown skin is characteristic of hemochromatosis (bronzed diabetes or pigmentary cirrhosis of the liver), the disease associated with primary or secondary excessive absorption of iron in the intestine and accumulation of hemosiderin in various organs and tissues (in the first instance in the liver and the pancreas). Local hyperpigmentation of the skin in the right hypochondrium can be due to frequent application of a hot-water bottle, which indicates persistent pain in this region (in chronic diseases of the gallbladder).
Inspection of the skin (especially in obstructive and less frequently in parenchymatous jaundice) can reveal scratches due to severe itching. The scratches are often infected and purulent. Jaundice of this type can be attended by hemorrhagic diathesis - petechial eruption and hemorrhage into the skin (ecchymosis).
In patients with cirrhosis of the liver associated with disordered cholesterol metabolism, cholesterol is deposited intracutaneously in the form of yellow plaques (xanthomatosis) which are often located on the eyelids (xanthelasma) and less frequently on the hands, elbows and soles (xanthomas). Xanthomatosis occurs also in other diseases attended by cholesterol metabolic defect (atherosclerosis, diabetes mellitus, essential hyperlipemia, etc.).
An important symptom for diagnosis of chronic diseases of the liver is spider angiomata. These are slightly elevated pulsating angiomata with fine vessels radiating from the centre. Their size varies from that of a pin head to 0.5-1 cm in diameter. The angiomata are often found on the neck, face, shoulders, hands, and the back; less frequently they are practically absent from the lower part of the body. The spider angiomata may disappear with improvement of the liver function. In addition to these angiomata, patients with chronic diseases of the liver may have specifically coloured palms and soles - liver palms; symmetrical reddening is especially characteristic in the thenar and hypothenar region. When pressed, the reddened site becomes pale
137
but when the pressure is removed, the redness is quickly restored. The mechanism of development of the spider angiomata and liver palms is believed to be connected with the grave hepatic dysfunction of the liver during which estrogens are destroyed incompletely and therefore act as a vasodilatory agent on the skin vessels.
Excess estrogens in the blood are also associated with other symptoms that may be revealed on inspection. Patients with chronic diseases of the liver have a glassy crimson tongue (raspberry tongue). Unior bilateral enlargement of the mammary glands often occurs in men (gynecomastia) along with defective growth of hair on the chin, chest, and the abdomen. Hair growth is decreased in the armpits and on the pubis in women. When the, hepatic condition improves, the hair growth is restored. Drum (Hippocratic) fingers, sometimes with white nails, occur in patients with chronic diseases of the liver. It is believed to depend on excess estrogens and serotonin in the blood.
A greenish-brown Kayser-Fleischer ring round the outer edge of the cornea is characteristic of the Konovalov-Wilson disease (congenital disease characterized by decreased synthesis in the liver of ceruloplasmin, the copper transport protein, and its increased deposition in tissues).
Inspection of the mouth can repeal angular stomatitis (inflammation of the mucosa and skin in the mouth angles) characteristic of group B hypovitaminosis occurring amongst patients with chronic liver diseases.
Inspection of the abdomen
Inspection of the abdomen should be done with the patient in vertical and horizontal position.
Important diagnostic symptoms can be found during inspection of the abdomen. The abdomen may be enlarged significantly due to accumulation of free fluid (ascites). This occurs in liver cirrhosis concurrent with portal hypertension. The abdomen may be enlarged due to pronounced hepatoor splenomegaly. When the patient with ascites stands erect, his abdomen becomes pendulous due to the downward flow of fluid; in the lying position the abdomen is flattened (“frog belly”). The navel often becomes protruded in ascites when the patient stands erect. It is due to increased infra-abdominal pressure. This sign can be used to differentiate between enlargement of the abdomen in ascites (also large intraabdominal tumours) and pronounced obesity (the navel is retracted).
Inspection of the abdomen can reveal another important symptom of portal hypertension, the presence of dilated venous network on the anterior abdominal wall. This network is formed by anastomoses of the portal and both vena cava systems. The superior vena cava and portal vein are anastomosed above the navel, while the portal and inferior vena cava are anastomosed below the navel; cavocaval anastomoses are located on the sides
138
of the abdomen. Anastomoses may develop in obstructed blood flow in the inferior vena cava (thrombosis, compression, etc.). Dilated, swollen and twisted venous collaterals, found round the navel and radiating from it, form the so-called Medusa head. These symptoms are characteristic of the portal hypertension syndrome occurring in cirrhosis of the liver, thrombosis and compression of the portal vein. Establishing the direction of the blood flow in the collaterals helps determine the type of anastomosis and hence locate the vessel where the blood flow is obstructed in the system of the portal vein or the inferior vena cava. To that end a small area of the dilated venous branch is pressed between two fingers (with an attempt to empty this area from the blood). In a short lapse of time the pressure of the upper finger is released. If blood fills the vessel to the level of the other finger, the blood flows from the portal vein system to the inferior vena cava (i.e. in the downward direction). If the vessel remains empty, the blood flows upwards, i.e. from the vena cava inferior-system to the superior vena cava.
In patients with cachexia and pronounced enlargement of the liver, the right hypochondrium and epigastrium are protruded. If the abdominal wall is thin, the protruded surface is uneven and tuberous (in tumours or cysts of the liver). Only significantly enlarged gallbladder can be responsible for protrusion of the abdomen, especially in cachectic patients (in hydrops of the gallbladder, cancer of the common bile duct, or cancer of the pancreas head which compresses the common bile duct). The left hypochondrium is protruded in cases with considerably enlarged spleen attending cirrhosis of the liver (hepatolienal syndrome).
Percussion of abdomen
Percussion of abdomen in a vertical position of the patient is used for revealing a free fluid in the abdominal cavity and definitions of its level. By percussion on midline and lateral flanks from top to down, it is possible to differentiate the tympanic sound above intestines and the dull sound lower than fluid level.
In a horizontal position of the patient percussion of an abdomen is performed on midline from umbilicus to epigastrium and hypogastrium, and in lateral directions from umbilicus to flanks. With the purpose of differentiation a dull sound originated from free fluid and contents of intestines the physician can repeat percussion in lateral directions from umbilicus to flanks in position on one side of the patient’s body. In the presence of ascites the level of dull sound is changed in this position of patient.
139