Trichrome stain of micrograph of liver tissue highlighting
bridging fibrosis surrounding regenerative liver nodules,
diagnostic of cirrhosis.Cirrhosis is the end result of liver
injury characterised by distortion of the hepatic architecture by
extensive fibrosis and the formation of regenerative nodules with
chronic inflammation of the liver tissues. Cirrhosis may result
from a variety of chronic liver injuries, including infectious,
autoimmune, toxic, and metabolic causes.
While earlier stages of cirrhosis may be potentially reversible with
treatment of the underlying cause, later stages of cirrhosis are
generally irreversible, with liver transplantation as the only option.
Here are the steps to help you recognize cirrhosis, based on symptoms,
signs, and tests.
!! Steps !!
Be aware of the various causes and risk factors that can cause or
lead to cirrhosis and chronic liver disease:
* _ Alcohol consumption is a major cause of cirrhosis.*Alcohol*:
Chronic alcohol consumption can result in alcoholic liver disease_
progressing to _alcoholic cirrhosis_ (also known as _Laennec's
cirrhosis_) in 10-20 percent of persons who drink excessively for
at least 10 years.[1] Alcohol causes liver injury by blocking
hepatic (liver-related) metabolism of carbohydrates, fats, and
proteins, which then build up within liver cells (hepatocytes) and
cause damage. The body may react to such damage by mounting an
inflammatory reaction, leading to hepatitis, or fibrosis
(excessive fibrous connective tissue), and cirrhosis.
* _ Ground glass hepatocytes as seen in a chronic hepatitis B
infection. Liver biopsy. H&E stain.*Chronic Hepatitis B*: An
infection by the hepatitis B virus results in chronic liver
inflammation and injury that can lead to cirrhosis over several
decades. Major risk factors include unprotected sexual contact,
blood transfusions, and injection drug use using contaminated
needles.
* Transmission electron micrograph of the hepatitis C
virus*Chronic Hepatitis C*: An infection by the hepatitis C virus
(the causative agent in most cases formerly known as "non-A, non-B
hepatitis") results in chronic liver inflammation and injury that
can lead to cirrhosis over several decades. Cirrhosis from
hepatitis C is the most common reason for a liver transplant.
Major risk factors for this includes infections from injection
drug use, blood transfusion, and body piercing and tattoos.
* Overview of the most significant symptoms of diabetes*Diabetes
mellitus*: As seen in 15-30 percent of persons with cirrhosis,
diabetes is a risk factor for developing non-alcoholic
steatohepatitis (NASH)_, and is common in chronic hepatitis C
infection, likely related to insulin resistance and inadequate
insulin secretion from beta cells of the pancreas.[2] Diabetes is
also seen in hemochromatosis, a cause of cirrhosis, characterized
by extensive iron depositions, leading to bronzed skin (iron
deposits in skin), diabetes (iron deposits in the pancreas),
restrictive cardiomyopathy and conduction abnormalities (iron
deposits in the heart), joint disease (iron deposits in joint),
etc.
* * _ Obesity is a risk factor for cirrhosis.Obesity*: Obesity is
a risk factor for non-alcoholic steatohepatitis – with fat in
the liver, causing inflammation and damage.
* A clandestine kit containing materials to inject illicit
drugs.*Injection drug use*: This is a risk factor for transmitting
hepatitis B and C viruses.
* * Blood transfusion is a risk factor for viral causes of
cirrhosis.Blood transfusions*: Hepatitis B and C viruses can
transmit via blood transfusion from an infected donor.
* *Family history of liver disease*: Certain causes of cirrhosis
have a genetic inheritance pattern. These include hereditary
haemosiderosis_, _Wilson's disease_, and _alpha-1 antitrypsin
(AAT) deficiency_, all with an autosomal recessive inheritance
pattern. Having a family member with liver disease increases one's
risk of cirrhosis.
* *Autoimmune diseases*: Having autoimmune diseases, such as
inflammatory bowel disease, rheumatoid arthritis, and thyroid
disease, increases the risk of complications of such disorders
leading to _autoimmune hepatitis_ and cirrhosis.
* _ The major signs and symptoms of heart failure*Heart disease*:
Heart disease is a risk factor for non-alcoholic steatohepatitis
leading to cirrhosis. In addition, heart disease associated with
right-sided heart failure can cause liver congestion (nutmeg
liver) and cardiac cirrhosis. Micrograph of congestive
hepatopathy, also known as nutmeg liver and cardiac cirrhosis.
Liver biopsy. Trichrome stain. Congestive hepatopathy is
characterized by perisinusoidal fibrosis, hepatic venule dilation,
and dilation of the sinusoids in zone III (centrilobular).
Feeling very tired could be a sign of cirrhosis.Recognize the
symptoms of cirrhosis. Note that these symptoms are variable,
not specific to cirrhosis, and some may not occur in all persons
with cirrhosis:
* Fatigue, or feeling tired
* Easy bruising
* Lower extremity edema (swelling)
* Fever
* Weight loss
* Diarrhea
* Intense itching (pruritus)
* Increase abdominal girth
* Confusion
* Sleep disturbance
Recognize the signs of cirrhosis. As noted before, these signs are
not specific to cirrhosis, nor do they occur in all cases of
cirrhosis:
* Spider angioma*Spider angiomata* or spider nevi, spider
telangiectasias: Vascular lesions consisting of a central
arteriole (the smallest branches of an artery, terminating in
capillaries) surrounded by many smaller vessels commonly found on
trunk, face, and upper limbs, due to an increase in estradiol to
free testosterone ratio.[3] These occur in about one third of
cases.[4] Verify this finding by compressing it with a glass
slide, and observe the pulsation of the central arteriole as blood
fills the central arteriole, then travels to the peripheral tips
with blanching. Spider angiomas may also be seen in pregnancy
(high estrogen state), severe malnutrition, or occasionally in
healthy individuals. Greater number and size of spider angioma are
associated with more severe liver cirrhosis and risk of bleeding
from varices (permanent abnormal dilation and lengthening of a
vein).[5][6]
* *Palmar erythema*: Exaggerations of normal speckled mottling of
the palm, due to altered sex hormone metabolism.[7] Palmar
erythema affects mainly the thenar and hypothenar prominences
while sparing the central palm. It is also seen in pregnancy,
rheumatoid arthritis, hyperthyroidism, and blood malignancies.
*Nail changes*:
* Muehrcke's lines*Muehrcke's nails*: Paired horizontal bands
separated by normal color due to hypoalbuminemia,[8] from
inadequate production of albumin, which is solely made by the
liver. Muehrcke's nails are seen in other conditions associated
with low serum albumin, such as malnutrition and nephrotic
syndrome (related to the kidney).
* Terry's nails: Proximal two-thirds of the nail plate appears white
and distal one-third red, also due to hypoalbuminemia.
* Clubbing of fingernails*Clubbing*: Angle between the nail
plate and proximal nail fold > 180 degrees, and may appear like a
drumstick when severe. This is more commonly seen with biliary
cirrhosis and is nonspecific.
* *Hypertrophic osteoarthropathy (HOA)*: Chronic proliferative
periostitis of the long bones, which can be very painful.[9] Note
that the most common cause of HOA is lung cancer, which must be
ruled out.
* Dupuytren's contracture of the fourth digit (ring
finger)*Dupuytren's contracture*: Thickening and shortening of
palmar fascia (connective tissue binding parts together) leading
to flexion deformities of the fingers. It results from fibroblast
proliferation and disorderly collagen deposition in the fascia,
likely due to free radical formation by oxidative metabolism of
hypoxanthine.[10] Dupuytren's contracture is common in alcoholic
cirrhosis, occurring in about one-third of cases.[11] A
nonspecific finding, it is also seen in diabetes mellitus,
cigarette smokers, alcohol users without cirrhosis, workers with
repetitive hand motions, and Peyronie's disease.
* Gynecomastia*Gynecomastia*: Benign proliferation of glandular
tissue of male breasts, presenting with a rubbery or firm mass
extending concentrically_ from the nipples. This results from
increased estradiol and is seen in up to two-third of cases.
Gynecomastia must be distinguished from pseudogynecomastia, fat
deposits without glandular proliferation, often seen in obese men.
To tell them apart, lie on the back, place thumb and forefinger on
each side of the breast, and slowly bring them together to
appreciate a concentric, rubbery-to-firm disk of tissue directly
under the nipple area in gynecomastia. No mass is felt in
pseudogynecomastia, and other mass disorders, such as cancer, tend
to be _eccentrically_ located (not centered).
* *Hypogonadism*: Manifested as impotence, infertility, loss of
sexual drive, and testicular atrophy, due to primary gonadal
injury or suppression of hypothalamic or pituitary function. It is
most often seen in alcoholic cirrhosis and hemochromatosis, likely
due to toxic effects of alcohol or iron, respectively.[12]
* *Change in liver size*: The liver can be enlarged (hepatomegaly),
or of normal size, or shrunken. When palpated, the cirrhotic liver
tends to feel firm and nodular.
* *Splenomegaly (increase in size of the spleen)*: Due to congestion
of the splenic red pulp as a result of _portal hypertension_
(increased pressure in the portal vein, as blood backs up from the
cirrhotic liver with extensive fibrosis impeding blood flow,
resulting in pressure buildup).
* _ Ultrasound scan showing ascites*Ascites*: Accumulation of
fluid in the peritoneal (abdominal) cavity giving rise to flank
dullness (needs about 1500 cc to detect flank dullness).
* *Caput medusa*: In portal hypertension, the umbilical vein may
open, to allow blood backing up the portal venous system to be
shunted through the periumbilical veins into the umbilical vein
and ultimately to the abdominal wall veins to the systemic venous
system. The increased prominence of the periumbilical veins
manifest as caput medusa, so called because it resembles the head
(caput) of Medusa.
* *Cruveilhier-Baumgarten murmur*: Venous hum heard in epigastric
region by auscultation with a stethoscope. Similar to caput
medusa, it results from collateral connections between the portal
system and the remnant of the umbilical vein in portal
hypertension. The murmur is augmented by the Valsalva maneuver
(increases intraabdominal pressure) and diminished by applying
pressure on the skin above the umbilicus (flattening the blood
vessels).[13]
* Dimethyl sulphide accounts for the smell of fetor
hepaticus.*Fetor hepaticus*: A musty odor in the breath due to
increased dimethyl sulfide in severe portal-systemic shunting from
portal hypertension.[14]
* Yellowing of the skin and conjunctiva overlying the sclera
caused by hepatitis.*Jaundice*: Yellow discolouring of the skin,
eye, and mucus membranes due to increased bilirubin (at least
2–3 mg/dL or 30 mmol/L). Urine may also appear darkened. Yellow
discolouration of the skin may also result from excessive
consumption of carotene (for example, in someone who eats lots of
carrots); this can be distinguished from jaundice by absence of
yellow discolouring of the sclera (white, external part of the
eye) in carotenemia and presence of icteric sclera in jaundice.
* *Asterixis*: Bilateral asynchronous flapping of outstretched,
dorsiflexed hands seen in hepatic encephalopathy (from buildup of
ammonia in liver failure that go to the brain). Asterixis is also
seen in uremia and severe heart failure.
Other:
* *Pigment gallstone*: May result from hemolysis[15]
* Location of the parotid gland*Enlarged parotid gland*: May
result from alcohol use leading to fatty infiltration, edema, and
fibrosis;[16]
Get tested. Some routine laboratory tests useful for recognizing
cirrhosis include:
* Complete blood count with differential: anemia, leukopenia and
neutropenia, and thrombocytopenia are all commonly seen in
cirrhosis, due to splenomegaly (hypersplenism) and sequestration
of red cells, white cells, and platelets. Gastrointestinal blood
loss, alcohol toxicity, folate deficiency (common in alcoholics),
anemia of chronic disease (from inflammation), and hemolysis
(breaking down of red blood cells) all contribute to anemia as
well. The enlarged spleen can sequester up to 90 percent of
circulating platelets, and platelet count may drop to less than
50,000/cc.
* Serum aminotransferases: Aspartate aminotransferase (AST) and
alanine aminotransferase (ALT) tend to be slightly elevated.
Alcoholic cirrhosis typically has AST/ALT ratio greater than 2.
Most forms of chronic hepatitis other than alcohol tend to have
AST/ALT ratio less than 1, although the ratio may reverse as
chronic hepatitis progresses to cirrhosis.[17][18]
* Total bilirubin: May be normal in compensated cirrhosis, but tends
to rise as cirrhosis worsens. Rising bilirubin is a poor
prognostic sign in primary biliary cirrhosis.[19]
* Albumin: Synthesised exclusively in the liver, albumin levels fall
as liver's synthetic function declines with progression of
cirrhosis. Low albumin is also seen in congestive heart failure,
nephrotic syndrome, protein losing enteropathy (intestinal
disease), and malnutrition.
Additional laboratory tests that may be helpful include:
* Alkaline phosphatase: Usually elevated but less than 2 to 3 times
the upper limit of normal. Higher levels may indicate biliary
causes of cirrhosis (sign of biliary obstruction), such as primary
sclerosing cholangitis (disease of bile duct) and primary
cirrhosis.
* Gamma-glutamyl transpeptidase (GGT): Liver specific enzyme that
correlates with alkaline phosphatase (which is nonspecific) in
liver disease.[20] GGT levels tend to be higher in alcoholic
cirrhosis than in other forms of cirrhosis, likely due to alcohol
induction of liver microsomal GGT[21] or causing GGT to leak from
hepatocytes.[22]
* Prothrombin time: Like albumin, this test reflects the liver's
synthetic functions. The liver is responsible for synthesis of
many proteins required for normal clotting time_, and impaired
synthesis of clotting factors will cause prolonged prothrombin
time.
* Globulins: Increased in cirrhosis, due to shunting of bacterial
antigens in portal venous blood away from the fibrotic liver to
lymphoid tissue, which induces immunoglobin production.[23] Very
high IgG levesl may indicate autoimmune hepatitis, while high
levels of IgM may indicate primary biliary cirrhosis.
* Serum sodium: Low sodium (hyponatremia) is common in cirrhosis
with ascites due to free water retention, as a result of high
anti-diuretic hormone levels.[24] Hyponatremia (deficiency of
sodium in the blood) tends to worsen as cirrhosis progresses to
end-stage liver disease.
Further testing may help identify specific causes of cirrhosis:
* Hepatitis serology (HCV Antibody, HBsAg, HBeAg) and viral RNA
molecular assays (to detect viral hepatitis).
* Antimitochondrial antibodies (positive in primary biliary
cirrhosis).
* Antinuclear, anti-smooth muscle, antiactin, anti-neutrophil
cytoplasmic antibody antibodies (positive in Type 1, or classic,
autoimmune hepatitis).
* Anti-LKM-1, anti-liver cytosol-1, anti-soluble liver antigen
(positive in Type 2 autoimmune hepatitis).
* Fasting transferrin saturation (total iron-binding capacity),
plasma ferritin (elevated in hereditary hemochromatosis).
* Serum ceruloplasmin (low in Wilson's disease).
* Serum alpha-1 antitrypsin (AAT) levels (low in AAT deficiency).
Imaging studies may help recognize cirrhosis, and are more useful to
detect complications of cirrhosis, including ascites, hepatocellular
carcinoma (hepatoma), and hepatic or portal vein thrombosis.
* Abdominal ultrasound (transverse sectioning) showing liver
cirrhosis with nodular formation in a 3 year old
child.*Ultrasound*: noninvasive, widely available, and
well-tolerated. Cirrhotic liver appears small and nodular. The
classic ultrasound finding in cirrhosis is atrophy of the right
lobe and hypertrophy (enlargement) of the caudate or left lobes.
Nodules seen on ultrasound may be benign or malignant and need
biopsy to evaluate. Findings of increased portal vein diameter or
presence of collateral veins suggest portal hypertension.[25]
Splenomegaly, ascites, and portal vein thrombosis are also readily
detected by ultrasonography.
* Abdominal computed tomography of a 3 year old child showing
liver cirrhosis in transverse section.*Computed tomography*: Not
routinely done for cirrhosis, as it provides the same information
as ultrasound, and involves radiation and contrast exposure.
* Magnetic resonance imaging: Its use is limited by cost and patient
intolerance. Low signal intensity on T1-weighted images suggests
iron overload from hereditary hemochromatosis.[26]
* Liver biopsy is needed to diagnose cirrhosis definitively.For
definitive diagnosis of cirrhosis, get a *liver biopsy*, in which
a sample of the liver is obtained and subsequently processed and
examined under the microscope.
!! Video !!
!! Tips !!
* The earlier stages of cirrhosis may be potentially reversible with
treatment of the underlying cause to: control diabetes, abstain
from alcohol, cure hepatitis, and reverse obesity to attain normal
weight.
!! Warnings !!
* The later stages of cirrhosis are generally irreversible -- and
the disease and complications are eventually fatal, leaving liver
transplantation as the only option for regaining health and to
save one's life.
!! Related WikiHows !!
* How to Recognize Iron Overload and Hemochromatosis Symptoms
* How to Prevent Kidney and Liver Failure at a Young Age
* How to Prevent Hepatitis B
* How to Overcome Hepatitis C
* How to Tell if You Have Diabetes
!! Sources And Citations !!
!! Article Tools !!
* Read on wikiHow
*
0 comments:
Post a Comment