A liver biopsy is the only definitive test that actually indicates whether or not you have cirrhosis [irreversible scaring of the liver]. So, what exactly is your doctor looking for when he/she does a physical exam? Are there actually some physical clues that suggest that you have cirrhosis? The answer to this question is yes.

The following is a list of clues that indicate that you may already have cirrhosis. These are listed alphabetically by their common medical name. It is important to remember that, although helpful, each of these physical manifestations do not indicate the actual cause of one's liver disease, and, in fact, are not specific only to liver disease. They can be due to other disorders as well.

ASCITES

An accumulation of excess fluid in the abdomen. Causes abdominal distention. Can be treated with a low sodium diet, and the use of diuretics, i.e. water pills.

Ascites:
The two most important factors in the development of ascites are failure of the liver to synthesize albumin and portal venous hypertension.
The abdomen is distended with fluid and by air in the dilated intestines.
The fullness is more conspicuous in the flanks. The umbilicus is flattened.
The intra-abdominal hypertension favours the protrusion of hernias. Scrotal edema is frequent.
The raised diaphragm may cause dyspnea.

In about 5% of cirrhotic patients a pleural effusion may be found, usually to the right side. It is due to defects in the diaphragm allowing ascites to pass into the pleural cavity. Right pleural effusion may be seen in the absence of ascites due to the negative intrathoracic pressure during breathing, drawing the peritoneal fluid through the diaphragmatic defects into the pleural cavity.

Click Photo To Enlarge

ASTERIXIS

An uncontrollable flapping of the hands that becomes noticeable when patients stretch out their arms, palms out, as if stopping traffic. Is associated with mental confusion, i.e. encephalopathy.

To Test For Asterixis:

Extend the arms, spread the fingers, dorsiflex the wrist and observe for the abnormal “flapping” tremor at the wrist. If not immediately apparent, this tremor may be accentuated by asking the patient to keep the arms straight while the examiner gently hyperextends the patient’s wrist with a sweeping motion.

An alternate method of testing for asterixis involves having the patient relax his legs while he lies supine with his knees bent. The feet should be kept flat on the table and as the legs fall to the sides, watch for flapping of the legs at the hip joint. This repetitively brings the knees back together.

"Ascites":
Metabolic encephalopathies, especially hepatic and renal, are the most common causes of bilateral asterixis. Those caused specifically by hepatic failure are known as “liver (or hepatic) flap”.

Other causes of asterixis include cardiac and respiratory disease, electrolyte abnormalities and drug intoxication.
Electrolyte abnormalities known to cause asterixis include hypoglycaemia, hypokalaemia and hypomagnesaemia.
Drug intoxications include barbiturate intoxication, alcoholism, phenytoin intoxication (“phenytoin flap”) and primidone intoxication. Wilson’s disease and focal brain lesions in the rostral midbrain tegmentum may also cause asterixis.

2000 Trinity Student Medical Journal

(Photo of how to test for Asterixis: )

CAPUT MEDUSA

Enlarged blood vessels that snake out from the belly button in a patient with ascites.

Caput Medusae

The term Caput Medusae describes the appearance of distended and engorged umbilical veins which are seen radiating from the umbilicus across the abdomen to join systemic veins. It is a sign of severe portal hypertension with portal-systemic shunting through the umbilical veins.
The name originates from the apparent similarity to Medusa's hair once Minerva had turned it into snakes.

Caput Medusae is distinguished from inferior vena cava obstruction by determining the direction of flow in the veins below the umbilicus; it is towards the legs in the former, and towards the head in the latter (as abdominal collaterals develop to bypass the blocked inferior vena cava and permit venous return from the legs).

GP Notebook 2001 Oxbridge Solutions
http://www.gpnotebook.co.uk/simplepage.cfm?ID=328859648

Click on Image To Enlarge

DUPUYTREN'S CONTRACTURE

A puckering of the palms that prevents people from totally straightening out their hand. Usually associated with alcoholic liver disease.

EDEMA

Fluid accumulation in the legs, especially the ankles. Usually associated with ascites.

Edema

Why do patients with liver disease develop ascites and edema?

In patients with chronic diseases of the liver, fibrosis (scarring) of the liver often occurs. When the scarring becomes advanced, the condition is called cirrhosis of the liver. "Ascites" is fluid that accumulates in the abdominal (peritoneal) cavity. It is a complication of cirrhosis and appears as an abdominal bulge. The peritoneum is the inner lining of the abdominal cavity, which also folds over to cover the organs inside the abdomen such as the liver, gallbladder, spleen, pancreas, and intestines.

Ascites develops because of a combination of two factors: (1) increased pressure in the vein system that carries blood from the stomach, intestines, and spleen to the liver (portal hypertension); and (2) a low level of albumin in the blood (hypoalbuminemia). Albumin, which is the predominant protein in the blood and which helps maintain blood volume, is reduced in cirrhosis primarily because the damaged liver is not able to produce enough albumin.

Other consequences of portal hypertension include dilated veins in the esophagus (varices), prominent veins on the abdomen, and an enlarged spleen. Each of these conditions is due primarily to the increased pressure and accumulation of blood in the abdominal blood vessels.

Other signs of chronic liver disease are spider nevi (distinctive vascular malformations)

Spider Nevi

on the skin, certain characteristic changes in the nails, gynecomastia (enlarged breasts), and shrinkage of the testicles (testicular atrophy).

The fluid of ascites can be removed from the abdominal cavity by using a syringe and a long needle. This procedure is called paracentesis. Analysis of the fluid can help differentiate ascites that is caused by cirrhosis from other causes of ascites, such as cancer, tuberculosis, congestive heart failure, and nephrosis. Sometimes, when ascites does not respond to treatment with diuretics, paracentesis can be used to remove large amounts of the ascitic fluid.

Peripheral edema, which is usually seen as pitting edema of the legs and feet, also occurs in cirrhosis.

Click on Image

The edema is a consequence of the hypoalbuminemia and activation of the renin-angiotensin- aldosterone hormonal system, which prompt the kidneys to retain salt and water.

The presence or absence of edema in patients with cirrhosis and ascites is an important consideration in the treatment of the ascites.

In patients with ascites without edema, diuretics must be given with extra caution. The reason for this is that a diuresis (induced increased volume of urine) that is too depleting or rapid in these patients can lead to a low blood volume (hypovolemia), which can possibly be followed by kidney and liver failure.

In contrast, when patients who have both edema and ascites undergo diuresis, the edema fluid in the interstitial space serves as somewhat of a buffer against the development of low blood volume. The excess interstitial fluid moves into the blood vessel spaces to rapidly replenish the depleted blood volume.

ENCEPHALOPATHY

An altered mental status leading to coma. Can be treated with animal protein restriction and a poorly absorbed sugar called Lactulose.

Encephalopathy is an altered or impaired mental status, typically leading to coma, that can occur in people with cirrhosis. It is often referred to as "brain fog". Encephalopathy is often associated with poor coordination, fetor hepaticus (foul-smelling breath), and asterixis (uncontrollable flapping of the hands). The exact cause of encephalopathy is not known, but is probably due to a combination of factors. Most researchers believe that it mainly has something to do with the ailing liver’s inability to clear toxins—primarily ammonia—from the body. In fact, elevated blood levels of ammonia are found in approximately 90 percent of people with encephalopathy. When ammonia and other poisons begin to accumulate in the brain, a variety of mental disturbances occur.

In mild cases – known as minimal hepatic encephalopathy, a person will develop subtle personality changes, such as irritability, a change in sleeping patterns, or short-term memory loss. A person may have a shortened attention span or appear to be apathetic toward life. Movements may appear poorly coordinated and clumsy. People suffering from encephalopathy will commonly lose their tempers over minor incidents or have mood swings for no apparent reason. Or a person may repeatedly enter a room, forgetting what he needed from the room in the first place. Or he may continually misplace common objects, such as reading glasses, only to find that they were on top of his head the whole time! These people may also have an increased incidence of automobile accidents, as their reaction time may be somewhat impaired.

In more severe cases, total confusion, associated with inappropriate behavior, will occur. A person may become outright violent or may be so confused that he cannot properly identify the current year, season, or even his own family members. Sometimes, a person will sleep all day and can only be partially aroused. This, obviously, is a more serious condition and requires hospitalization.

In most cases, encephalopathy is easily detected on a physical examination in a patient known to have cirrhosis. Whenever there is a question about the diagnosis, an imaging study, such as CT scan or MRI, of the brain should be performed in order to eliminate other potential causes - such as a brain tumor, blood clot, or meningitis (brain infection). The factors that can precipitate encephalopathy in the cirrhotic patient should be searched for and immediately addressed by the doctor. These factors as well as the treatment of encephalopathy will be discussed below.

Grading of hepatic encephalopathy

Grade: 1
Level of consciousness: Lack of awareness, Personality change, Day/night reversal
Intellectual function: Short attention
Neurological findings: Incoordination, Mild asterixis
EEG: Slowing (5-6 cps) Triphasic

Grade: 2
Level of consciousness: Lethargic, Inappropriate behavior
Intellectual function: Disoriented
Neurological findings: Asterixis, Abnormal reflexes
EEG: Slowing Triphasic

Grade: 3
Level of consciousness: Asleep, Rousable
Intellectual function: Loss of meaningful communication
Neurological findings: Asterixis, Abnormal reflex
EEG: Slowing Triphasic

Grade: 4
Level of consciousness: Unrousable
Intellectual function: Absent
Neurological findings: Decerebrate
EEG: Very slow (2-3 cps), delta

FETOR HEPATICUS

A particularly foul "dead mouse" smell found on the breath. Frequently precedes coma.

Portal-Systemic Encephalopathy (PSE)

Fetor hepaticus is caused by the mercaptans dimethyl sulfide and methanethiol and may follow the administration of a known precipitant of PSE (Portal-Systemic Encephalopathy), methionine.

Fetor hepaticus is a sweetish odor reminiscent of garlic and has been described as "fruity" or "musty".

It is commonly but inconsistently detected on the breath or urine of PSE patients, but can be difficult to differentiate from other odors. Therefore, fetor hepaticus has limited usefulness in physical diagnosis.

taken from:
Portal-Systemic Encephalopathy by Sanjay Sandhir, MD, Frederick L. Weber, Jr, MD,
Current Practice of Medicine 1999 Jan.

GYNECOMASTIA

Enlarged, tender breasts in men. Commonly associated with alcoholic cirrhosis, but may also be due to Aldactone, a drug used to control ascites.

HAIR LOSS

Hair becomes sparse in men from the face, chest and pubis, and under the arms in women.

Hepatic hydrothorax.

Cirrhosis can cause fluid to build up between the lungs and the chest (Pleural Effusion) and press on the lungs. Treatment can include taking medicines such as diuretics, restricting salt in the diet, and using procedures to remove the fluid.

Pleural effusion

Pleural effusion occurs when fluid collects in the pleural cavity-the area between the lungs and the chest. Fluid buildup may cause abnormal pressure on the lungs.

Hepatorenal syndrome.

Kidney (renal) failure can occur in cases of advanced liver disease stemming from cirrhosis. Usually, liver failure is the condition that threatens a person's life. But in some cases the liver disease may be stable, while kidney problems are life-threatening. A liver transplant may be necessary to cure renal failure caused by cirrhosis

Hepatopulmonary syndrome.

Portal hypertension caused by cirrhosis can cause lung (pulmonary) problems, such as widening of the blood vessels in the lungs. This widening causes the blood to move too swiftly through the lungs to pick up enough oxygen. Liver transplantation is the most effective treatment for this condition.

JAUNDICE

A yellow discoloration of the skin due to an elevated bilirubin level.

Click to Enlarge

JAUNDICE

The normal level of bilirubin in the blood is 1 mg/dL. If the concentration increases to 2 mg/dL, yellowing of the skin, sclera, and mucous membranes will become evident. Yellowing due to increased levels of bilirubin in the blood (hyperbilirubinemia), which then deposits in the tissues of the body, is called jaundice or icterus. Depending on the site of the problem, hyperbilirubinemia is usually dominated by either the unconjugated or conjugated type. Jaundice can be classified according to the mechanism that produced it:

1. Hemolytic (prehepatic) jaundice: occurs when the liver cells are normal, but so much bilirubin is present that the capacity of the liver to take it up and/or conjugate it is exceeded. A typical cause is excessive breakdown of red blood cells (i.e., hemolytic anemia). In prehepatic jaundice, the type of bilirubin seen in the blood is largely unconjugated.

2. Hepatocellular jaundice: usually occurs when production of bilirubin is normal, but damage to the liver cells interferes with uptake, conjugation, or excretion of bilirubin. Depending on which factors predominate, bilirubin may be conjugated or unconjugated.

3. Posthepatic (obstructive): is due to obstruction in the biliary drainage system, rather than to any problem with the hepatocytes themselves. Strictures or stones in the extrahepatic biliary tract, as well as tumors, may produce this type of jaundice. This "backed-up" bilirubin, which is conjugated, can get into the blood.

In young people, jaundice is most frequently due to viral hepatitis or alcohol abuse. In older people, malignancies are a more common cause. Premature infants may develop jaundice due to increased hemolysis and immature liver cells that contain insufficient enzymes to process bilirubin properly. Jaundice itself is not toxic except in newborns. Since their blood-brain barrier is not fully functional, bilirubin can pass into the brain and cause damage.

Low Blood Pressure

Many patients with cirrhosis or scarring of the liver develop abnormalities in their cardiovascular system as a result of their liver disease. All diseases that result in cirrhosis can lead to these cardiovascular changes but they occur more frequently in patients with more advanced disease.

It is believed that substances circulating in the blood that are normally cleared by a healthy liver can cause a generalized dilatation of the blood vessels throughout the body (except in the kidney where they are intensely constricted) .

The generalized vasodilatation then results in a low blood pressure. Most patients with this form of low blood pressure are asymptomatic because of its very gradual onset and because of a compensatory increased blood flow from the heart.

There is no specific treatment for the development of low blood pressure in patients with cirrhosis other than general, supportive care. The blood pressure will normalize after removal of the diseased liver and transplantation of a healthy liver.

Robert Fontana, MD (internal medicine), University of Michigan

http://www.transweb.org/qa/asktw/answers/answers9511/TIPSprocedure.html

MUSCLE WASTING

Loss of muscle mass, seen in end-stage cirrhosis when the liver can no longer manufacture proteins.

Nails

Clubbing
Bulbous uniform swelling of the soft tissue of the terminal phalanx of a digit with subsequent loss of the normal angle between the nail and the nail bed.

Due to chronic cardiopulmonary disease, liver or bowel disease, thyroid disease (acropachy):

Clubbing

Click on Image To Enlarge

PALMAR ERYTHEMA

Bright red coloring of the palms, particularly at the base of the thumb and little finger. May be due to excess estrogen.

Clinical findings of liver diseases

Palmar erythema:
The palms are red in colour, especially the thenar and hypothenar eminences and pulps of the fingers. The soles of the feet may be also affected. Palmar erythema blanches with pressure. As vascular spiders, palmar erythema may be seen in normal persons, during pregnancy and in other pathologic conditions.

Click to See picture in full-size image.

Palmar erythema:

PAPER MONEY SKIN

Numerous small blood vessels that resemble the silk threads in a U.S. dollar bill. Commonly cover the upper body, often in association with spider naevi.

PAROTID GLAND ENLARGEMENT

Enlargement of a gland on the face located under the ear. Causes an unusual appearance of the protrusion of the earlobes straight out from the jaw.

(Pleural Effusion)

SCLERAL ICTERUS

Yellow discoloration of the whites of the eyes [sclera], due to an elevated bilirubin level.

PHOTO http://www-medlib.med.utah.edu/WebPath/CINJHTML/CINJ049.html

SPIDER ANGIOMATA

Enlarged blood vessels that resemble little spiders. Usually found on the upper chest,back, face, and arms. Turn white when their center is touched [blanches]. More common in alcoholic cirrhosis.

Spider angioma

Spider angioma is so named because of its appearance: a central, red, elevated area with surrounding broken blood vessels radiating outward like a spider's legs. Many children and adults have a spider angioma.

Causes
Spider angiomas are associated with childhood, pregnancy, liver disease, birth control pills, estrogen treatment, and they develop for unknown reasons as well.

Signs & Symptoms
Spider angiomas classically appear as small, centrally raised bumps (papules) caused by a dilated arteriole (small artery).
A network of dilated capillaries (tiny blood vessels) radiate from the arteriole.
Pressing on the lesion causes the redness to disappear briefly, and there is a rapid return of redness once the pressure is lifted.

SPONTANEOUS BACTERIAL PERITONITIS

Fever, and abdominal pain in a patient with ascites.

Spontaneous Bacterial Peritonitis (SBP)

General Information:

Most patients with peritonitis will have abdominal pain and a fever.
Also, they usually already have Ascites (a build-up of fluid within their stomach) and a distended stomach. Peritonitis may or may not cause the stomach to be more distended than normal.
Some patients will have nausea, vomiting, loss of appetite, and weight loss. Which of these symptoms are present depends on the cause of the problem.
Many patients with Ascites also have liver problems. When these patients develop peritonitis, they often experience deterioration in mental status because of the build-up of toxic substances in their blood.
Examination by a doctor usually reveals tenderness of the abdomen, and fever.

A. SBP is a common complication in patients with cirrhosis and ascites, and occurs mostly in the setting of low ascitic fluid total protein level (<1 g/dl).
B. Pathogenesis involves bacterial translocation from the gut to the systemic circulation and then to ascitic fluid.
C. E. coli, Klebseilla pneumoniae, and pneumococcus are the three most common isolates.
D. Renal [kidney] failure occurs in approximately one-third of the patients despite treatment of the infection.

Presentation and Diagnosis:

A. Abdominal pain and fever are the most characteristic symptoms, but hepatic encephalopathy, gastrointestinal bleeding, vomiting, diarrhea, shock, or hypothermia may be the presenting symptom(s) in a large number of patients.

B. It can also be totally asymptomatic. Therefore one must have a low threshold for performing a paracentesis to obtain ascitic fluid for analysis.

C. SBP is diagnosed when there is a positive ascitic fluid culture or when the ascitic fluid PMN count is >250 cells/mm3 in the absence of an identifiable intraabdominal source of infection.

D. Ascitic fluid culture must be placed directly into blood culture preferably at bedside to increase the sensitivity of culture.

E. Secondary peritonitis due to perforated viscus usually results in PMN count in the thousands, multiple organisms on gram stain and culture, and at least 2 of the following: total protein >1 g/dl, LDH > the upper limit of normal for serum, and glucose <50 mg/dl.

Treatment:

A. Empiric antibiotic treatment should be begun before the culture results become available to prevent demise of the patient.

B. A broad-spectrum therapy is recommended in suspected ascitic fluid infection until culture results and susceptibility are available. Cefotamine 2 g IV Q8h or a comparable third-generation cephalosporin is the treatment of choice. Five days of treatment is appropriate. A repeat paracentesis can be performed after completion of 5 days of therapy with IV antibiotics to ensure efficacy of the treatment especially in patients with atypical presentation or response.

C. Intravenous albumin at a dose of 1.5 g per kilogram body weight on day 1 and 1 g per kilogram on day 3 has been shown to reduce significantly the incidence of renal impairment and death in comparison with treatment with antibiotics alone.

D. Subsequently, these patients should be placed on SBP prophylaxis therapy (norfloxacin 400 mg QD or levofloxacin 250 mg QD) for the remaining part of their hospital stay.

http://www.vh.org/Providers/ClinRef/FPHandbook/Chapter05/18-5.html

TERRY'S NAILS

The normal pinkish color of the nails turns completely white, with the disappearance of the half-moon circles at the base of the nails.

Clinical findings of liver diseases
White nails. White nails are commonly seen in patients with cirrhosis and rarely in other diseases. They are due to opacity of the nail bed. Nails appear white and a pink zone is seen only at the tip of the nail. The lunula may be not distinguished.
PHOTO:

Thrombocytopenia

Definition
Thrombocytopenia is an abnormal drop in the number of blood cells involved in forming blood clots. These cells are called platelets.

Description
The normal amount of platelets is usually between 150,000 and 450,000 cells per microliter of blood. A microliter is an amount equal to one one-millionth of a liter (a liter is almost equal to a quart). Platelet numbers are counted by having a blood sample collected and placing a measured amount of blood in a machine called a cell counter.
When the platelet number drops below 150,000 cells per microliter of blood, this person is said to be thrombocytopenic.

Causes & symptoms
Abnormal reductions in the number of platelets are caused when abnormalities occur in any of the following three processes: decreased platelet production by the bone marrow; increased trapping of platelets by the spleen; or a more rapid than normal destruction of platelets.
Persons with this condition easily bruise and can have episodes of excess bleeding (a hemorrhage).

Platelets come from megakaryocytes, which are produced in the material located within the center cavity of the bones (bone marrow). When abnormalities develop in the marrow, the marrow cells can lose their ability to produce platelets in correct amounts. The result is a lower than normal level of platelets in the blood. Drugs used in cancer chemotherapy can cause the marrow to malfunction in this way, as can the presence of tumor cells in the marrow itself.

Normally, the spleen holds about one-third of the body's platelets as part of this organ's function to recycle aging or damaged red blood cells (the cells that carry oxygen in the blood).
When liver disease or cancer of the spleen is present, the spleen can enlarge, resulting in a greater number of platelets staying in the organ. This condition results in abnormally low numbers of platelets in the blood.

Platelets can breakdown in unusually high amounts in persons with abnormalities in their blood vessel walls, with blood clots, or with man-made replacement heart valves. Devices placed inside blood vessels to keep them from closing (stents) due to weakened walls or fat build-up can also cause platelets to breakdown.
In addition, infections and other changes in the immune system can speed up the removal of platelets from the circulation.

Diagnosis
Thrombocytopenia is diagnosed by having a blood sample taken and counting the platelets present in the sample. However, accurately determining the medical reason for this conditions is complex.

Once a low platelet count is verified, a careful evaluation of the function of the bone marrow and spleen are necessary. Improper functioning of either or both of these organs can cause thrombocytopenia.
In addition, the causes for the abnormal spleen or marrow function must be investigated since different cancers, blood disorders, or liver disease can be the true cause for the drop in platelets found in the blood.

Treatment
If low platelet counts are caused by an enlarged spleen, removal of the spleen can help raise the platelet level, since the spleen is no longer there to capture the platelets. However, proper treatment for what causes the enlarged spleen is necessary as well.

Low platelet counts can indicate more serious conditions. If a dysfunctional immune system is found to be the cause for this condition, drugs like steroids or gamma globulin can be used to help maintain platelet levels in certain cases.

If low platelet levels are due to an abnormally low level of platelet production, transfusions of platelets can be given as well.

Prognosis
Thrombocytopenia can result in fatal bleeding, but it also can indicate various other, more serious, cancers and disorders that affect the blood cells. This condition requires thorough medical evaluation.

Prevention
There is no known way to prevent thrombocytopenia.

Key Terms to know:

Gamma globulin: One of a group of proteins found in the blood that is involved in helping the body fight infections.
Stent: A man-made surgical device, usually tube-shaped, that is placed into a blood vessel to keep it from closing.
Transfusion: The transfer of blood from one person to another. Transfusions can be direct, in which blood is transferred from the donor to the recipient; or indirect, in which the blood is taken from the donor, stored in a container, and then given to the recipient.

http://www.findarticles.com/cf_0/g2601/0013/2601001350/p1/article.jhtml?term=%2B%22Blood+tests%22

UMBILICAL HERNIA

Patients with massive ascites may experience abdominal discomfort, depressed appetite, and decreased oral intake. Diaphragmatic elevation may lead to symptoms of dyspnea. Pleural effusions may result from the passage of ascitic fluid across channels in the diaphragm.

Umbilical and inguinal hernias are common in patients with moderate and massive ascites.
The use of an elastic abdominal binder may protect the skin overlying a protruding umbilical hernia from maceration and may help prevent rupture and subsequent infection.
Timely large-volume paracentesis also may help to prevent this disastrous complication.

Umbilical hernias should not undergo elective repair unless patients are significantly symptomatic or their hernias are irreducible.

As with all other surgeries in patients with cirrhosis, herniorrhaphy carries multiple potential risks such as intraoperative bleeding, postoperative infection, and liver failure because of anesthesia-induced reductions in hepatic blood flow.

However, these risks become acceptable in patients with severe symptoms from their hernia. Urgent surgery is necessary in the patient whose hernia has been complicated by bowel incarceration.

http://www.emedicine.com/med/topic3183.htm#section~portal_hypertension

Umbilical Hernia

Click on Photo to Enlarge

Liver/Cirrhosis

Page updated Jan 2010