How to Recognize Cirrhosis (with pictures)
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.
- Be aware of the various causes and risk factors that can cause or lead to cirrhosis and chronic liver disease:
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. 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.
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.
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.
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. 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 : Obesity is a risk factor for non-alcoholic steatohepatitis – with fat in the liver, causing inflammation and damage.
Injection drug use: This is a risk factor for transmitting hepatitis B and C viruses.
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.
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)
- Weight loss
- Intense itching (pruritus)
- Increase abdominal girth
- 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 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. These occur in about one third of cases. 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).
- Palmar erythema: Exaggerations of normal speckled mottling of the palm, due to altered sex hormone metabolism. 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 nails: Paired horizontal bands separated by normal color due to hypoalbuminemia, 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: 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. Note that the most common cause of HOA is lung cancer, which must be ruled out.
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. Dupuytren’s contracture is common in alcoholic cirrhosis, occurring in about one-third of cases. 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: 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.
- 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).
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).
- Fetor hepaticus: A musty odor in the breath due to increased dimethyl sulfide in severe portal-systemic shunting from portal hypertension.
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.
- 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.
- 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.
- 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. GGT levels tend to be higher in alcoholic cirrhosis than in other forms of cirrhosis, likely due to alcohol induction of liver microsomal GGT or causing GGT to leak from hepatocytes.
- 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. 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. 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.
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. Splenomegaly, ascites, and portal vein thrombosis are also readily detected by ultrasonography.
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.
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.
- Earlier stages of cirrhosis may be potentially reversible with treatment of the underlying cause, such as controlling diabetes, abstaining from alcohol, curing hepatitis, and reversing obesity to attain normal weight.
- Don’t use any medicine until and unless doctor prescribe. Keep active by taking vitamines/juice/fruits.
- 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 saving one’s life.
- ↑ Alcohol-Induced Liver Disease, http://www.liverfoundation.org/education/info/alcohol/
- ↑ Petrides AS, Vogt C, Schulze-Berge D, et al. Prognostic significance of diabetes in patients with cirrhosis. Hepatology 1994; 20:119.
- ↑ Pirovino M, Linder R, Boss C, et al. Cutaneous spider nevi in liver cirrhosis: Capillary microscopic and hormonal investigations. Klin Wochenschr 1988; 66:298.
- ↑ Li CP, Lee FY, Hwang SJ, et al. (1999). “Spider angiomas in patients with liver cirrhosis: role of alcoholism and impaired liver function”. Scand. J. Gastroenterol. 34 (5): 520–3.
- ↑ Zaman, A, Hapke, R, Flora, K, et al. Factors predicting the presence of esophageal or gastric varices in patients with advanced liver disease. Am J Gastroenterol 1999; 94:3292.
- ↑ Foutch, PG, Sullivan, JA, Gaines, JA, Sanowski, RA. Cutaneous vascular spiders in cirrhotic patients: correlation with hemorrhage from esophageal varices. Am J Gastroenterol 1988; 83:723.
- ↑ Erlinger, S, Benhamou, J. Cirrhosis: Clinical aspects. In: Oxford Textbook of Clinical Hepatology, Mcintyre, N, Benhamou, J, Rizzetto, M, Rodes, J (Eds), University Press, Oxford 1991. p.380.
- ↑ Fitzpatrick, T, Johnson, R, Polano, M, et al. Color Atlas and Synopsis of Clinical Dermatology: Common and Serious Diseases, Second edition, McGraw Hill, Inc. New York 1994.
- ↑ Epstein, O, Dick, R, Sherlock, S. Prospective study of periostitis (inflammation of the dense fibrous membrane covering the surface of bones) and finger clubbing in primary biliary cirrhosis and other forms of chronic liver disease. Gut 1981; 22:203.
- ↑ Murrell, GA, Francis, MJ, Bromley, L. Free radicals and Dupuytren’s contracture. Br Med J (Clin Res Ed) 1987; 295:1373.
- ↑ Attali, P, Ink, O, Pelletier, G, et al. Dupuytren’s contracture, alcohol consumption, and chronic liver disease. Arch Intern Med 1987; 147:1065.
- ↑ Van Thiel, DH, Gavaler, JS, Spero, JA, et al. Patterns of hypothalamic-pituitary-gonadal dysfunction in men with liver disease due to differing etiologies. Hepatology 1981; 1:39.
- ↑ Groszmann, R, Franchis, R. Portal Hypertension. In: Schiff’s Diseases of the Liver, Eighth Edition, Schiff, E, Sorrell, M, Maddrey, W (Eds), Lippincott Williams & Wilkens, Philadelphia 1999. p.415.
- ↑ Tangerman, A, Meuwese-Arends, MT, Jansen, JB. Cause and composition of foetor hepaticus. Lancet 1994; 343:483.
- ↑ Bouchier, IA. Postmortem study of the frequency of gallstones in patients with cirrhosis of the liver. Gut 1969; 10:705.
- ↑ Dutta, SK, Dukehart, M, Narang, A, Latham, PS. Functional and structural changes in parotid glands of alcoholic cirrhotic patients. Gastroenterology 1989; 96:510.
- ↑ Sheth, SG, Flamm, SL, Gordon, FD, Chopra, S. AST/ALT ratio predicts cirrhosis in patients with chronic hepatitis C virus infection. Am J Gastroenterol 1998; 93:44.
- ↑ Williams, AL, Hoofnagle, JH. Ratio of serum aspartate to alanine aminotransferase in chronic hepatitis. Relationship to cirrhosis. Gastroenterology 1988; 95:734.
- ↑ Krzeski, P, Zych, W, Kraszewska, E, et al. Is serum bilirubin concentration the only valid prognostic marker in primary biliary cirrhosis?. Hepatology 1999; 30:865.
- ↑ Pratt, D, Kaplan, M. Evaluation of the Liver A: Laboratory Tests. In: Schiff’s Diseases of the Liver, Eighth Edition, Schiff, E, Sorrell, M, Maddrey, W (Eds), Lippincott Williams & Wilkens, Philadelphia 1999. p.205.
- ↑ Goldberg, DM. Structural, functional, and clinical aspects of gamma-glutamyltransferase. CRC Crit Rev Clin Lab Sci 1980; 12:1.
- ↑ Barouki, R, Chobert, MN, Finidori, J, et al. Ethanol effects in a rat hepatoma cell line: Induction of gamma-glutamyltransferase. Hepatology 1983; 3:323.
- ↑ Triger, DR, Wright, R. Hyperglobulinaemia in liver disease. Lancet 1973; 1:1494.
- ↑ Asbert, M, Gines, A, Gines, P, et al. Circulating levels of endothelin in cirrhosis. Gastroenterology 1993; 104:1485.
- ↑ Zwiebel, WJ. Sonographic diagnosis of hepatic vascular disorders. Semin Ultrasound CT MR 1995; 16:34.
- ↑ Ernst, O, Sergent, G, Bonvarlet, P, et al. Hepatic iron overload: Diagnosis and quantification with MR imaging. AJR Am J Roentgenol 1997; 168:1205.