Cirrhosis of the liver: symptoms of hypertension
Patients with cirrhosis develop symptoms that are both a consequence of portal hypertension and metabolic failure of the liver, or both. Typical symptoms of portal hypertension are spleen enlargement, ascites, peripheral edema, dilated veins in the abdominal wall, bleeding esophageal varices, and oliguria. In turn, the classic symptoms of liver metabolic decompensation are yellowing of the skin integuments and hemorrhagic diathesis; the first is due to increased levels of bilirubin in the blood and skin, and the second is due to a deficit of clotting factors produced in the liver and a low platelet count (enlarged spleen!). Encephalopathy is an example of a symptom caused by both a decrease in the effective weight of the liver and the presence of a portal-systemic collateral circulation. The metabolic failure of the liver also causes a number of endocrine disorders, the best known consequences of which are gynecomastia and atrophy.
Ascites
Ascites (ascites) means the accumulation of free fluid in the peritoneal cavity, regardless of the mechanism of this phenomenon. In patients with cirrhosis of the liver, ascites is caused by the effusion of plasma from the sinus vessels of the liver, in which there is increased hydrostatic pressure and decreased oncotic pressure (low albumin concentration!). In patients with cirrhosis, ascites is a sign of severe portal hypertension. Its presence is associated with 50% mortality over 2 years of follow-up. Ascites usually precede the appearance of peripheral edema, but this is not always the case. In patients with a strongly developed collateral portal systemic circulation, peripheral edema may occur in the absence of ascites. Ascites is sometimes preceded by a nagging distension of the intestines (“first wind, then rain”). Large ascites makes breathing difficult due to reduced diaphragm mobility. Approximately 6% of patients with ascites also have fluid in the pleural cavity (hydrothorax hepaticus), and 2/3 on the right side. The cause is most likely congenital or acquired cavities in the diaphragmatic muscle. The fluid can cause a troublesome, dry cough.
Ascites is not just a symptom of cirrhosis of the liver. The accumulation of fluid in the peritoneal cavity may be a consequence of the transudation mechanisms in Buddha-Chiari syndrome, portal vein thrombosis, fibrosing pericarditis, heart failure or nephrotic syndrome, and exudative mechanisms in cancerous or tuberculous peritonitis. Moreover, ascites can be misdiagnosed in conditions associated with high elevation of the abdominal integuments, which are associated with functional bloating and mechanical intestinal obstruction, obesity, giant ovarian tumor or cyst, and pregnancy. In these states, the highest point of the abdominal wall is the navel, which does not bulge. In patients with ascites, the navel is arched and sometimes inverted. Due to the caudal shift of the navel, the umbilicus-pubic symphysis section is shortened, and the navel-xiphoid section of the sternum is enlarged. Large ascites keeps the skin of the abdomen tight and shiny. Long-term ascites is responsible for the skin’s stretch marks (striae distensae). The increase in pressure in the peritoneal cavity causes the formation of hernias: inguinal, umbilical or in postoperative scars. In men, the fluid through the inguinal hernia enters the scrotum, sometimes causing monstrous perineal swelling.
There are several methods for detecting free fluid in the peritoneal cavity. The first involves tapping the abdominal wall while changing the patient’s body position. In a patient lying on his back, free fluid is distributed to the sides of the peritoneal cavity, creating an image of the so-called frog belly. The fluid lifts the intestines filled with air, so in a patient lying on his back, the character of the arch in the middle of the abdominal cavity is tympanic, while it is muffled on both sides. If the sick person is placed on one side, all the fluid flows to that side according to gravity (puffed convexity). On the other side, the convexity is tympanic because of the air-filled intestines.
The second physical symptom of ascites is gagging. This symptom is caused by a quick, repeated hitting of the lateral surface of the abdomen of the patient with the pads of 3-4 fingers of the right hand, with the movement of the hand being derived from the wrist. This activity induces a wave in the free fluid that hits the opposite wall of the abdominal wall. This phenomenon is recorded by the left hand resting flat on the sheaths of the lower abdomen on the right side of the patient. In obese patients, people with flabby integuments or with a small amount of fluid in the pelvis, the bubbling symptom may not be present. In patients without ascites, the phenomenon of alleged gagging may develop as a result of vibrations transmitted through the subcutaneous tissue. To eliminate this possibility, the patient or the attending nurse is asked to apply pressure with the edge of the hand to the abdominal wall in the midline (Fig. 24).
DIG. 24. Induction of bubbling fluid in the abdominal cavity with compression of the abdominal wall in order to eliminate pseudo-bubbling.
The third symptom of ascites is the so-called puddle symptom. In order to find it out, after a few minutes’ rest in the supine position, the patient is asked to assume the knee-elbow position. This method allows the detection of smaller amounts of fluid by means of a bow test than in the previously described tests, but none of these methods can detect fluid with a volume of less than 1000 ml. The diagnostic sensitivity of physical methods is estimated at 60% compared to ultrasound, which detects smaller volumes of fluid. The volume of ascites is a dynamic phenomenon, and the commonly used methods of recording changes in the amount of fluid are the measurements of body weight and the circumference of the abdomen at the level of the navel.
Spontaneous bacterial infection of the ascites fluid with subsequent peritonitis (peritonitis bacterialis spontanea) is one of the most serious complications of liver cirrhosis. In addition to laboratory tests that determine the diagnosis of this complication, an important symptom is the tenderness of the abdominal wall to pressure.
Edema peripheral
In patients with portal hypertension, the renal mechanisms responsible for sodium and water retention are activated, and consequently, the volume of circulating blood and extracellular water increase. The exudation is also favored by the low concentration of albumin (low oncotic pressure!). One-kilogram increase in body weight due to water retention in the tissues is invisible, however, after 1,5-2 liters of water accumulate, swelling of the feet and ankles appears. Swellings can be of considerable size (anasarca). Often there is a painful swelling of the penis. In conditions of fluid leakage, bacterial inflammation of the subcutaneous tissue (cellulitis) can easily occur, the symptom of which is redness and swelling of the skin, most often in the lower extremities.
Spleen enlargement
Spleen enlargement is a constant symptom of portal hypertension and results from blood stagnation in the red pulp of the spleen. An enlarged spleen can cause pain or discomfort in the left hypochondrium. Due to congestion in the spleen, it may cause the feeling of early postprandial satiety. An infarction of an enlarged spleen causes severe pain. The enlarged spleen is a pathological resistance found on palpation of the left superior abdominal quadrant. In patients with portal hypertension, the spleen is usually neither as large nor as hard as in hematological diseases associated with splenomegaly.
Dilated veins of the abdominal integuments
Usually, in healthy people, the abdominal veins are invisible. In a patient with cirrhosis of the liver, dilated veins of the abdominal integuments are part of the collateral portal-systemic circulation resulting from portal hypertension. In these vessels, blood flows downwards (towards the lower extremities). Usually, the venous vessels are clearly visible through the atrophic skin, sometimes they take the form of convex varicose cords (Fig. 25 A, B). A special type of collateral circulation is the so-called Medusa’s head (caput Medusae), the central part of which is located at the level of the navel, from which tortuous venous vessels radiate outward. The name refers to the beautiful hair of the mythological Medusa, which the goddess Athena turned into crawling snakes in an act of revenge (fig. 26). The condition for the formation of the Medusa head is the recanalization of the umbilical vein, which plays an important role in fetal life, but undergoes permanent obliteration during individual development. The patency of the umbilical vein is secondary to portal hypertension (Cruveilhier-Baumgarten syndrome). This vessel significantly decomposes the vascular portal system, protecting the patient against the development of ascites (decrease in portal blood pressure), however, due to impaired portal blood flow, the liver becomes atrophied. If the cause of a patent umbilical vein is not portal hypertension, but a defect in its obliteration in the postnatal life, then it is called Cruveilhier-Baumgarten disease. The umbilical vein originates intrahepatic from the left branch of the portal vein and then runs along the posterior surface of the abdominal wall towards the navel. Unblocking the umbilical vein causes the widening of the umbilical veins with the formation of numerous collaterals in their vicinity (Sappey’s veins), which drain blood to the inferior epigastric vein (systemic circulation). In radial vessels, blood flows from the center to the periphery in many directions, both cranially (outflow of the superior vena cava) and caudally (outflow of the inferior vena cava). In portal hypertension caused by thrombosis of the portal or splenic vein, Medusa’s head is absent because the vascular block is located proximally to the umbilical vein.
A
B
DIG. 25. Dilated veins of the abdominal integuments (A); cords of varicose veins in the skin (B).
The widening of the veins in the abdominal skin is not an exclusive feature of portal hypertension; they are also a consequence of obstruction of the inferior vena cava, caused by a tumor or blood clot. The veins of the abdominal integuments then allow the venous blood to return from the lower extremities to the heart, so unlike portal hypertension, the blood flows from the bottom up (towards the head). A physical examination can determine the direction of blood flow in dilated veins (see Figure 27).
DIG. 26. The hair of the mythological Medusa.
DIG. 27. Methods for determining the direction of blood flow in cutaneous collaterals.
The diagram shows dilated venous vessels with the direction of blood flow marked in a patient with portal hypertension. After squeezing the vessel with 2 fingers spaced several centimeters apart, the vessel will empty of blood in the section between the fingers. In the case of bottom-up blood flow, releasing the pressure on the lower finger will cause the vessel to fill, while after releasing the pressure on the upper finger, the vessel will remain collapsed.
Source: Abdominal PHYSICAL TEST WITH ELEMENTS OF DIFFERENTIAL DIAGNOSTICS; Czelej Publishing House