LIVER CIRRHOSIS-causes-signs-symptoms and treatment



Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.

  • Many forms of liver injury are marked by fibrosis.
  • Fibrosis is defined as an excess deposition of the components of extracellular matrix (i.e. collagens, glycoproteins, proteoglycans) within the liver.
  • This response to liver injury potentially is reversible.
  • In contrast, in most patients, cirrhosis is not a reversible process
  • The progression of liver injury to cirrhosis may occur over weeks to years
  • Some patients with cirrhosis are completely asymptomatic and have a reasonably normal life expectancy.
  • Other individuals have a multitude of the most severe symptoms of end-stage liver disease and have a limited chance for survival.
  • Common signs and symptoms may stem from decreased hepatic synthetic function (e.g. coagulopathy), decreased detoxification capabilities of the liver (e.g. hepatic encephalopathy), or portal hypertension (e.g. variceal bleeding).


  • Many patients die from the disease in their fifth or sixth decade of life.


 Excessive chronic alcohol use can cause several different types of chronic liver disease, including alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis.

  • Alcoholic liver disease once was considered to be the predominant cause of cirrhosis in the United States.
  • Hepatitis C has emerged as the nation’s leading cause of both chronic hepatitis and cirrhosis
  • Many cases of cryptogenic cirrhosis appear to have resulted from nonalcoholic fatty liver disease (NAFLD).
  • When cases of cryptogenic cirrhosis are reviewed, many patients have one or more of the classical risk factors for NAFLD: obesity, diabetes, and hypertriglyceridemia
  • Up to one third of Americans have NAFLD.
  • About 2-3% of Americans have nonalcoholic steatohepatitis (NASH), where fat deposition in the hepatocyte is complicated by liver inflammation and fibrosis.
  • It is estimated that 10% of patients with NASH will ultimately develop cirrhosis
  • Most common causes of cirrhosis in the United States
  • Hepatitis C (26%)
  • Alcoholic liver disease (21%)
  • Hepatitis C plus alcoholic liver disease (15%)
  • Cryptogenic causes (18%)
  • Hepatitis B, which may be coincident with hepatitis D (15%)
  • Miscellaneous (5%)
  • Miscellaneous causes of chronic liver disease and cirrhosis
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Secondary biliary cirrhosis (associated with chronic extrahepatic bile duct obstruction)
  • Primary sclerosing cholangitis
  • Hemochromatosis
  • Wilson disease
  • Alpha-1 antitrypsin deficiency
  • Granulomatous disease (e.g. sarcoidosis)
  • Type IV glycogen storage disease
  • Drug-induced liver disease (e.g. methotrexate, alpha methyldopa, amiodarone)
  • Venous outflow obstruction (e.g. Budd-Chiari syndrome, veno-occlusive disease)
  • Chronic right-sided heart failure
  • Tricuspid regurgitation


  • Ethanol is mainly absorbed by the small intestine and, to a lesser degree, through the stomach.
  • Gastric alcohol dehydrogenase (ADH) initiates alcohol metabolism.
  • Three enzyme systems account for metabolism of alcohol in the liver.
  • These include cytosolic ADH, the microsomal-oxidizing system (MEOS), and peroxisomal catalase.
  • The majority of ethanol oxidation occurs via ADH to form acetaldehyde, which is a highly reactive molecule that may have multiple effects.
  • Ultimately, acetaldehyde is metabolized to acetate by aldehyde dehydrogenase (ALDH).
  • Intake of ethanol increases intracellular accumulation of triglycerides by increasing fatty acid uptake and by reducing fatty acid oxidation and lipoprotein secretion.
  • Protein synthesis, glycosylation, and secretion are impaired.
  • Oxidative damage to hepatocyte membranes occurs due to the formation of reactive oxygen species; acetaldehyde is a highly reactive molecule that combines with proteins to form protein-acetaldehyde adducts.
  • These adducts may interfere with specific enzyme activities, including microtubular formation and hepatic protein trafficking.
  • With acetaldehyde-mediated hepatocyte damage, certain reactive oxygen species can result in Kupffer cell activation.
  • As a result, profibrogenic cytokines are produced that initiate and perpetuate stellate cell activation, with the resultant production of excess collagen and extracellular matrix.
  • Connective tissue appears in both periportal and pericentral zones and eventually connects portal triads with central veins forming regenerative nodules.
  • Hepatocyte loss occurs, and with increased collagen production and deposition, together with continuing hepatocyte destruction, the liver contracts and shrinks in size.
  • This process generally takes from years to decades to occur and requires repeated insults


Hepatic fibrosis

  • The development of hepatic fibrosis reflects an alteration in the normally balanced processes of extracellular matrix production and degradation.
  • Extracellular matrix, the normal scaffolding for hepatocytes, is composed of collagens (especially types I, III, and V), glycoproteins, and proteoglycans.
  • Stellate cells, located in the perisinusoidal space, are essential for the production of extracellular matrix.
  • Stellate cells, which were once known as Ito cells, lipocytes, or perisinusoidal cells, may become activated into collagen-forming cells by a variety of paracrine factors.
  • Such factors may be released by hepatocytes, Kupffer cells, and sinusoidal endothelium following liver injury.
  • Increased collagen deposition in the space of Disse (the space between hepatocytes and sinusoids) and the diminution of the size of endothelial fenestrae lead to the capillarization of sinusoids
  • Activated stellate cells also have contractile properties.
  • Both capillarization and constriction of sinusoids by stellate cells contribute to the development of portal hypertension

Portal hypertension

Definition: Elevation of the hepatic venous pressure gradient (HVPG) to >5 mmHg

  • Causes: Portal hypertension results from a combination of increased portal venous inflow and increased resistance to portal blood flow
  • Portal hypertension is directly responsible for the two major complications of cirrhosis, variceal hemorrhage and ascites
  • Pathophysiology: Patients with cirrhosis demonstrate increased splanchnic arterial flow and, accordingly, increased splanchnic venous inflow into the liver.
  • Increased splanchnic arterial flow is explained partly by decreased peripheral vascular resistance and increased cardiac output in the patient with cirrhosis.
  • Nitric oxide appears to be the major driving force for this phenomenon
  • Dynamic factors account for one third of intrahepatic vascular resistance.
  • Stellate cells serve as contractile cells for adjacent hepatic endothelial cells.
  • The nitric oxide produced by the endothelial cells, in turn, controls the relative degree of vasodilation or vasoconstriction produced by the stellate cells.
  • In cirrhosis, decreased local production of nitric oxide by endothelial cells permits stellate cell contraction, with resulting vasoconstriction of the hepatic sinusoid.
  • (This contrasts with the peripheral circulation where there are high circulating levels of nitric oxide in cirrhosis.)
  • Increased local levels of vasoconstricting chemicals, like endothelin, may also contribute to sinusoidal vasoconstriction
  • The portal hypertension of cirrhosis is caused by the disruption of hepatic sinusoids.
  • However, portal hypertension may be observed in a variety of noncirrhotic conditions.
  • Prehepatic causes include splenic vein thrombosis and portal vein thrombosis
  • Intrahepatic causes of portal hypertension are divided into presinusoidal, sinusoidal, and postsinusoidal conditions
  • The classic form of presinusoidal disease is caused by the deposition of Schistosoma oocytes in presinusoidal portal venules, with the subsequent development of granulomata and portal fibrosis.
  • Schistosomiasis is the most common noncirrhotic cause of variceal bleeding worldwide
  • The classic sinusoidal cause of portal hypertension is cirrhosis
  • The classic postsinusoidal condition is an entity known as veno-occlusive disease
  • Posthepatic causes of portal hypertension may include chronic right-sided heart failure and tricuspid regurgitation and obstructing lesions of the hepatic veins and inferior vena cava.
  • These latter conditions, and the symptoms they produce, are termed Budd-Chiari syndrome.
  • Symptoms of Budd-Chiari syndrome are attributed to decreased outflow of blood from the liver, with resulting hepatic congestion and portal hypertension.
  • These symptoms include hepatomegaly, abdominal pain, and ascites


  • Definition: Ascites is defined as an accumulation of excessive fluid within the peritoneal cavity and may be a complication of both hepatic and nonhepatic diseases.
  • Etiology: The 4 most common causes of ascites in North America and Europe are cirrhosis, neoplasm, congestive heart failure, and tuberculous peritonitis
  • Classification: In the past, ascites was classified as being a transudate or an exudate.
  • In transudative ascites, fluid was said to cross the liver capsule because of an imbalance in Starling forces.
  • In general, ascites protein was less than 2.5 g/dL.
  • Classic causes of transudative ascites are portal hypertension secondary to cirrhosis and congestive heart failure
  • In exudative ascites, fluid was said to weep from an inflamed or tumor-laden peritoneum.
  • In general, ascites protein was greater than 2.5 g/dL.
  • Examples included peritoneal carcinomatosis and tuberculous peritonitis
  • Attributing ascites to diseases of nonperitoneal or peritoneal origin is more useful.
  • Investigations: Serum-ascites albumin gradient (SAAG) has come into common clinical use for differentiating these conditions.
  • Nonperitoneal diseases produce ascites with a SAAG greater than 1.1 g/dL
  • Pathophysiology: Patients with cirrhosis are observed to have increased hepatic lymphatic flow
  • Fluid and plasma proteins diffuse freely across the highly permeable sinusoidal endothelium into the space of Disse.
  • Fluid in the space of Disse, in turn, enters the lymphatic channels that run within the portal and central venous areas of the liver
  • Because the transsinusoidal oncotic gradient is approximately zero, the increased sinusoidal pressure that develops in portal hypertension increases the amount of fluid entering the space of Disse.
  • When the increased hepatic lymph production observed in portal hypertension exceeds the ability of the cisterna chyli and thoracic duct to clear the lymph, fluid crosses into the liver interstitium.
  • Fluid may then extravasate across the liver capsule into the peritoneal cavity
  • Treatment: Patients with small amounts of ascites can usually be managed with dietary sodium restriction alone.
  • Often, a simple recommendation is to eat fresh or frozen foods, avoiding canned or processed foods, which are usually preserved with sodium.
  • When a moderate amount of ascites is present, diuretic therapy is usually necessary.
  • Traditionally, spironolactone at 100–200 mg/d as a single dose is started, and furosemide may be added at 40–80 mg/d, particularly in patients who have peripheral edema.
  • If compliance is confirmed and ascitic fluid is not being mobilized, spironolactone can be increased to 400–600 mg/d and furosemide increased to 120–160 mg/d.
  • If ascites is still present with these dosages of diuretics in patients who are compliant with a low-sodium diet, then they are defined as having refractory ascites, and alternative treatment modalities including repeated large-volume paracentesis, or a TIPS (transjugular intrahepatic portosystemic shunt) procedure should be considered
  • The prognosis for patients with cirrhosis with ascites is poor, and some studies have shown that <50% of patients survive 2 years after the onset of ascites.
  • Thus, there should be consideration for liver transplantation in patients with the onset of ascites

Hepatorenal syndrome

  • This syndrome represents a continuum of renal dysfunction that may be observed in patients with cirrhosis and is caused by the vasoconstriction of large and small renal arteries and the impaired renal perfusion that results.
  • The syndrome may represent an imbalance between renal vasoconstrictors and vasodilators.
  • Plasma levels of a number of vasoconstricting substances are elevated in patients with cirrhosis and include angiotensin, antidiuretic hormone, and norepinephrine.
  • Hepatorenal syndrome progression may be slow (type II) or rapid (type I).
  • Type I disease frequently is accompanied by rapidly progressive liver failure.
  • In type II hepatorenal syndrome, patients may have stable or slowly progressive renal insufficiency
  • Hepatorenal syndrome is diagnosed when a creatinine clearance less than 40 mL/min is present or when a serum creatinine greater than 1.5 mg/dL, urine volume less than 500 mL/d, and urine sodium less than 10 mEq/L are present.
  • Urine osmolality is greater than plasma osmolality
  • Treatment: HRS is often seen in patients with refractory ascites and requires exclusion of other causes of acute renal failure.
  • Treatment has unfortunately been difficult, and in the past, dopamine or prostaglandin analogs were used as renal vasodilating medications.
  • Carefully performed studies have failed to show clear-cut benefit from these therapeutic approaches.
  • Currently, patients are treated with midodrine, an -agonist, along with octreotide and intravenous albumin.
  • The best therapy for HRS is liver transplantation; recovery of renal function is typical in this setting.
  • In patients with either type 1 or type 2 HRS, the prognosis is poor unless transplant can be achieved within a short period of time

Spontaneous bacterial peritonitis

  • SBP is observed in 15-26% of patients hospitalized with ascites.
  • The syndrome arises most commonly in patients whose low-protein ascites (<1 g/dL) contains low levels of complement, resulting in decreased opsonic activity.
  • SBP appears to be caused by the translocation of GI tract bacteria across the gut wall and also by the hematogenous spread of bacteria.
  • The most common causative organisms are Escherichia coli, Streptococcus pneumoniae, Klebsiella species, and other gram-negative enteric organisms
  • Diagnosis: Classic SBP is diagnosed by the presence of neutrocytosis, which is defined as greater than 250 polymorphonuclear (PMN) cells per mm3 of ascites, in the setting of a positive ascites culture
  • Treatment: Treatment is with a second-generation cephalosporin, with cefotaxime being the most commonly used antibiotic.
  • In patients with variceal hemorrhage, the frequency of SBP is significantly increased, and prophylaxis against SBP is recommended when a patient presents with upper GI bleeding.
  • Furthermore, in patients who have had an episode(s) of SBP and recovered, once-weekly administration of antibiotics is used as prophylaxis for recurrent SBP

Hepatic encephalopathy

  • Definition: It is broadly defined as an alteration in mental status and cognitive function occurring in the presence of liver failure
  • Hepatic encephalopathy is a syndrome observed in some patients with cirrhosis that is marked by personality changes, intellectual impairment, and a depressed level of consciousness
  • Pathophysiology: Patients may have altered brain energy metabolism and increased permeability of the blood-brain barrier.
  • The latter may facilitate the passage of neurotoxins into the brain.
  • Putative neurotoxins include short-chain fatty acids, mercaptans, false neurotransmitters (e.g. tyramine, octopamine, and beta-phenylethanolamines), ammonia, and gamma-aminobutyric acid (GABA).
  • Ammonia is produced in the GI tract by bacterial degradation of amines, amino acids, purines, and urea.
  • Normally, ammonia is detoxified in the liver by conversion to urea and glutamine.
  • In liver disease or portosystemic shunting, portal blood ammonia is not converted efficiently to urea.
  • Increased levels of ammonia may enter the systemic circulation because of portosystemic shunting
  • Ammonia has multiple neurotoxic effects, including altering the transit of amino acids, water, and electrolytes across the neuronal membrane.
  • Ammonia also can inhibit the generation of both excitatory and inhibitory postsynaptic potentials.
  • Clinical features: The symptoms of hepatic encephalopathy may range from mild to severe and may be observed in as many as 70% of patients with cirrhosis.
  • Symptoms are graded on the following scale:
  • Grade 0: Subclinical; normal mental status, but minimal changes in memory, concentration, intellectual function, coordination
  • Grade 1: Mild confusion, euphoria or depression, decreased attention, slowing of ability to perform mental tasks, irritability, disorder of sleep pattern (i.e. inverted sleep cycle)
  • Grade 2: Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, intermittent disorientation (usually for time)
  • Grade 3: Somnolent but arousable, unable to perform mental tasks, disorientation to time and place, marked confusion, amnesia, occasional fits of rage, speech is present but incomprehensible
  • Grade 4: Coma, with or without response to painful stimuli
  • Patients with mild and moderate hepatic encephalopathy demonstrate decreased short-term memory and concentration on mental status testing.
  • Findings upon physical examination include asterixis and fetor hepaticus.
  • Treatment: Treatment is multifactorial and includes management of the above-mentioned precipitating factors.
  • Sometimes hydration and correction of electrolyte imbalance is all that is necessary
  • The mainstay of treatment for encephalopathy, in addition to correcting precipitating factors, is to use lactulose, a nonabsorbable disaccharide, which results in colonic acidification.
  • Catharsis ensues, contributing to the elimination of nitrogenous products in the gut that are responsible for the development of encephalopathy
  • Poorly absorbed antibiotics are often used as adjunctive therapies for patients who have had a difficult time with lactulose.
  • The alternating administration of neomycin and metronidazole has commonly been employed to reduce the individual side effects of each: neomycin for renal insufficiency and ototoxicity and metronidazole for peripheral neuropathy.
  • More recently, rifaximin has been very effective in treating encephalopathy without the known side effects of neomycin or metronidazole.
  • Zinc supplementation is sometimes helpful in patients with encephalopathy and is relatively harmless.
  • The development of encephalopathy in patients with chronic liver disease is a poor prognostic sign, but this complication can be managed in the vast majority of patients

Clinical features

  • Patients with alcoholic liver disease can present with nonspecific symptoms such as vague right upper quadrant pain, fever, nausea and vomiting, diarrhea, anorexia, and malaise.
  • Alternatively, they may present with more specific complications of chronic liver disease, including ascites, edema, or upper gastrointestinal (GI) hemorrhage.
  • Other clinical manifestations include the development of jaundice or encephalopathy.
  • On physical examination, the liver and spleen may be enlarged, with the liver edge being firm and nodular.
  • Other frequent findings include scleral icterus, palmar erythema, spider angiomas, parotid gland enlargement, digital clubbing, muscle wasting, or the development of edema and ascites.
  • Men may have decreased body hair and gynecomastia as well as testicular atrophy, which may be a consequence of hormonal abnormalities or a direct toxic effect of alcohol on the testes.
  • In women with advanced alcoholic cirrhosis, menstrual irregularities usually occur, and some women may be amenorrheic.
  • These changes are often reversible following cessation of alcohol


  • Abstinence is the cornerstone of therapy for patients with alcoholic liver disease
  • In addition, patients require good nutrition and long-term medical supervision in order to manage underlying complications that may develop.
  • Complications such as the development of ascites and edema, variceal hemorrhage, or portosystemic encephalopathy all require specific management and treatment.
  • Glucocorticoids are occasionally used in patients with severe alcoholic hepatitis in the absence of infection
  • Management of complications of cirrhosis revolves around specific therapy for treatment of whatever complications occur, whether they be esophageal variceal hemorrhage, development of ascites and edema, or encephalopathy.
  • In patients with chronic hepatitis B, numerous studies have shown beneficial effects of antiviral therapy, which is effective at viral suppression, as evidenced by reducing aminotransferase levels and HBV DNA levels, and improving histology by reducing inflammation and fibrosis.
  • Currently available therapy includes lamivudine, adefovir, entecavir, and tenofovir.
  • Interferon α can also be used for treating hepatitis B, but it should not be used in cirrhotics


  • These include portal hypertension and its consequences of gastroesophageal variceal hemorrhage, splenomegaly, ascites, hepatic encephalopathy, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, and hepatocellular carcinoma

Portal hypertension


  • Portal hypertension is defined as the elevation of the hepatic venous pressure gradient (HVPG) to >5 mmHg.


  • Portal hypertension is caused by a combination of two simultaneously occurring hemodynamic processes: (1) increased intrahepatic resistance to the passage of blood flow through the liver due to cirrhosis and regenerative nodules, and (2) increased splanchnic blood flow secondary to vasodilatation within the splanchnic vascular bed.
  • Portal hypertension is directly responsible for the two major complications of cirrhosis, variceal hemorrhage and ascites
  • The causes of portal hypertension are usually subcategorized as prehepatic, intrahepatic, and posthepatic
  • Prehepatic causes of portal hypertension are those affecting the portal venous system before it enters the liver; they include portal vein thrombosis and splenic vein thrombosis.
  • Posthepatic causes encompass those affecting the hepatic veins and venous drainage to the heart; they include BCS, venoocclusive disease, and chronic right-sided cardiac congestion.
  • Intrahepatic causes account for over 95% of cases of portal hypertension and are represented by the major forms of cirrhosis.
  • Intrahepatic causes of portal hypertension can be further subdivided into presinusoidal, sinusoidal, and postsinusoidal causes.
  • Postsinusoidal causes include venoocclusive disease, while presinusoidal causes include congenital hepatic fibrosis and schistosomiasis.
  • Sinusoidal causes are related to cirrhosis from various causes
  • Cirrhosis is the most common cause of portal hypertension in the United States, and clinically significant portal hypertension is present in >60% of patients with cirrhosis.
  • Portal vein obstruction may be idiopathic or can occur in association with cirrhosis or with infection, pancreatitis, or abdominal trauma
  • Coagulation disorders that can lead to the development of portal vein thrombosis include polycythemia vera; essential thrombocytosis; deficiencies in protein C, protein S, antithrombin 3, and factor V Leiden; and abnormalities in the gene regulating prothrombin production.
  • Some patients may have a subclinical myeloproliferative disorder

Clinical features

  • The three primary complications of portal hypertension are gastroesophageal varices with hemorrhage, ascites, and hypersplenism.
  • Thus, patients may present with upper GI bleeding


  • Varices should be identified by endoscopy
  • If necessary, interventional radiologic procedures can be performed to determine wedged and free hepatic vein pressures that will allow for the calculation of a wedged-to-free gradient, which is equivalent to the portal pressure.
  • The average normal wedged-to-free gradient is 5 mmHg, and patients with a gradient >12 mmHg are at risk for variceal hemorrhage


  • Treatment for variceal hemorrhage as a complication of portal hypertension is divided into two main categories: (1) primary prophylaxis and (2) prevention of re-bleeding once there has been an initial variceal hemorrhage.

Primary prophylaxis

  • Primary prophylaxis requires routine screening by endoscopy of all patients with cirrhosis.
  • Once varices that are at increased risk for bleeding are identified, then primary prophylaxis can be achieved either through nonselective beta blockade or by variceal band ligation.
  • Patients treated with beta blockers have a lower risk of variceal hemorrhage than those treated with placebo over 1 and 2 years of follow-up.
  • Endoscopic variceal ligation (EVL) has achieved a level of success and comfort with most gastroenterologists who see patients with these complications of portal hypertension.
  • Thus, in patients with cirrhosis who are screened for portal hypertension and are found to have large varices, it is recommended that they receive either beta blockade or primary prophylaxis with EVL
  • The approach to patients once they have had a variceal bleed is first to treat the acute bleed, which can be life-threatening, and then to prevent further bleeding.
  • Prevention of further bleeding is usually accomplished with repeated variceal band ligation until varices are obliterated.
  • Treatment of acute bleeding requires both fluid and blood product replacement as well as prevention of subsequent bleeding with EVL
  • The medical management of acute variceal hemorrhage includes the use of vasoconstricting agents, usually somatostatin or Octreotide.
  • Balloon tamponade (Sengstaken-Blakemore tube or Minnesota tube) can be used in patients who cannot get endoscopic therapy immediately or who need stabilization prior to endoscopic therapy
  • Octreotide, a direct splanchnic vasoconstrictor, is given at dosages of 50–100 ug/h by continuous infusion.
  • Endoscopic intervention is employed as first-line treatment to control bleeding acutely.
  • Variceal band ligation is used to control acute bleeding in over 90% of cases and should be repeated until obliteration of all varices is accomplished.
  • When esophageal varices extend into the proximal stomach, band ligation is less successful.
  • In these situations, when bleeding continues from gastric varices, consideration for transjugular intrahepatic portosystemic shunt (TIPS) should be made

Prevention of Recurrent Bleeding

  • This usually requires repeated variceal band ligation until varices are obliterated.
  • Beta blockade may be of adjunctive benefit in patients who are having recurrent variceal band ligation; however, once varices have been obliterated, the need for beta blockade is lessened

Splenomegaly and Hypersplenism

  • Congestive splenomegaly is common in patients with portal hypertension.
  • Clinical features include the presence of an enlarged spleen on physical examination and the development of thrombocytopenia and leukopenia in patients who have cirrhosis.
  • Some patients will have fairly significant left-sided and left upper quadrant abdominal pain related to an enlarged and engorged spleen.
  • Splenomegaly itself usually requires no specific treatment, although splenectomy can be successfully performed under very special circumstances.
  • Hypersplenism with the development of thrombocytopenia is a common feature of patients with cirrhosis and is usually the first indication of portal hypertension

Malnutrition in Cirrhosis

  • Because the liver is principally involved in the regulation of protein and energy metabolism in the body, it is not surprising that patients with advanced liver disease are commonly malnourished.
  • Once patients become cirrhotic, they are more catabolic, and muscle protein is metabolized.
  • There are multiple factors that contribute to the malnutrition of cirrhosis, including poor dietary intake, alterations in gut nutrient absorption, and alterations in protein metabolism.
  • Dietary supplementation for patients with cirrhosis is helpful in preventing patients from becoming catabolic.

Abnormalities in Coagulation

  • Coagulopathy is almost universal in patients with cirrhosis.
  • There is decreased synthesis of clotting factors and impaired clearance of anticoagulants.
  • In addition, patients may have thrombocytopenia from hypersplenism due to portal hypertension. Vitamin K–dependent clotting factors are Factors II, VII, IX, and X. Vitamin K requires biliary excretion for its subsequent absorption; thus, in patients with chronic cholestatic syndromes, vitamin K absorption is frequently diminished.
  • Intravenous or intramuscular vitamin K can quickly correct this abnormality.
  • More commonly, the synthesis of vitamin K–dependent clotting factors is diminished because of a decrease in hepatic mass, and under these circumstances administration of parenteral vitamin K does not improve the clotting factors or the prothrombin time.
  • Platelet function is often abnormal in patients with chronic liver disease, in addition to decreases in platelet levels due to hypersplenism.

Bone Disease in Cirrhosis

  • Osteoporosis is common in patients with chronic cholestatic liver disease because of malabsorption of vitamin D and decreased calcium ingestion.
  • The rate of bone resorption exceeds that of new bone formation in patients with cirrhosis resulting in bone loss.
  • Dual x-ray absorptiometry (DEXA) is a useful method for determining osteoporosis or osteopenia in patients with chronic liver disease.
  • When a DEXA scan shows decreased bone mass, treatment should be administered with bisphosphonates that are effective at inhibiting resorption of bone and efficacious in the treatment of osteoporosis.

Hematologic Abnormalities in Cirrhosis

  • Numerous hematologic manifestations of cirrhosis are present, including anemia from a variety of causes including hypersplenism, hemolysis, iron deficiency, and perhaps folate deficiency from malnutrition.
  • Macrocytosis is a common abnormality in red blood cell morphology seen in patients with chronic liver disease, and neutropenia may be seen as a result of hypersplenism


One Comment on “LIVER CIRRHOSIS-causes-signs-symptoms and treatment”

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