1. THE LIVER

2. Objectives: Upon completion of this course, you should be able to: Discribe the pathophysiology, and diagnosis of specific pathologic conditions that affect the liver, including, hepatic failure, liver cirrhosis, portal hypertension, hepatitis, carcinoma, Wilson's disease, alpha 1- antitrypsin deficiency Recognize complications of liver decompensation, including, portal hypertension, esophageal varices, hepatic encephalopathy, and ascites. State measures to prevent food-borne and blood-borne hepatitis. Understand the etiology, risk factors, pathogenesis, morphology, clinical features, and outcome of pancreatic inflammation and neoplasms.

3. Normal adult liver wt. is 1400-1600 gm (2.5%) of body wt. Blood flow : 60-70% portal vein 30-40% hepatic artery

6. Microarchitecture: Vascular sinusoids are formed between hepatocyte cords. They are lined by discontinuous endothelial cells which demarcate an extrasinusoidal space of Disse. Vascular sinusoids are formed between hepatocyte cords. They are lined by discontinuous endothelial cells which demarcate an extrasinusoidal space of Disse. Ito cells (fat containing cells )of mesenchymal origin are found in the space of Disse. Ito cells (fat containing cells )of mesenchymal origin are found in the space of Disse. Kupffer cells are attached to the luminal surface of endothelial cells. Kupffer cells are attached to the luminal surface of endothelial cells. Bile canaliculi are formed by grooves in the plasma membrane of facing cells. These begin in the centrilobular regions & progressively join to drain into the canal of Hering which are the terminal parenchymal tributaries of the bile duct system. Bile canaliculi are formed by grooves in the plasma membrane of facing cells. These begin in the centrilobular regions & progressively join to drain into the canal of Hering which are the terminal parenchymal tributaries of the bile duct system.

7. HEPATIC FAILURE

8. This is the gravest consequence of liver disease. It should be noted that 80% of hepatic functional capacity must be damaged before failure ensues. In many cases decompensation arises as a result of intercurrent diseases that place further burden on an already sick liver; these include 1. Gastrointestinal bleeding 2. Systemic infection 3. Electrolyte disturbances 4. Severe stress such as major surgery or heart failure.

9. nknown) account for about one-third of the cases. Hepatitis C infection does not cause massive hepatic necrosis. The morphologic alterations that cause liver failure fall into three categories: 1.Massive hepatic necrosis;  most often drug-induced, as from paracetamol overdose, halothane & antituberculous drugs (rifampin, isoniazid).  Hepatitis A & hepatitis B infection, and other causes (including unknown) account for about one-third of the cases.  Hepatitis C infection does not cause massive hepatic necrosis.

10. 2. Chronic liver disease, which is the most common road to hepatic failure and is the endpoint of persistent chronic hepatitis ending in cirrhosis. 3. Hepatic dysfunction without overt necrosis: hepatocytes may be viable but unable to perform normal metabolic function, as with Reye syndrome, tetracycline toxicity, and acute fatty liver of pregnancy.

11. Two particular complications signal the gravest stages of hepatic failure 1.Hepatic encephalopathy, which is manifested:  disturbances of consciousness with rigidity, hyperreflexia, and tremor.  It is regarded as a disorder of neurotransmission in the central nervous system and neuromuscular system and appears to be associated with elevated blood ammonia levels, which impair neuronal function and promote generalized brain edema.

12. 2. Hepatorenal syndrome  Refers to the appearance of renal failure in patients with severe chronic liver disease, in whom there are no intrinsic morphologic or functional causes for the renal failure.  Sodium retention, impaired water excretion, and decreased renal perfusion and glomerular filtration rate are the main renal functional abnormalities.  There is oliguria associated with rising blood urea nitrogen and creatinine.  The prognosis is poor, with a median survival of only 2 weeks in the rapid-onset form and 6 months with the insidious-onset form.

13. Cirrhosis Among the top ten causes of death in the western world. Among the top ten causes of death in the western world. Characteristics : Bridging fibrosis Bridging fibrosis Regenerative nodules Regenerative nodules Small 3mm several cm (macro -nodules) Small 3mm several cm (macro -nodules)

14. Classification of cirrhosis  underlying etiology.  The descriptive terms "micronodular" and "macronodular" should not be used as primary classifications.

15. Cirrhosis Disruption of architecture of the entire liver Disruption of architecture of the entire liver parenchymal injury and fibrosis are diffuse parenchymal injury and fibrosis are diffuse nodularity is requisite for the diagnosis it reflects the balance between regeneration & scarring. nodularity is requisite for the diagnosis it reflects the balance between regeneration & scarring. fibrosis is irreversible. fibrosis is irreversible. vascular architecture is reorganized. vascular architecture is reorganized.

16. Etiology Alcoholic liver disease Alcoholic liver disease Viral hepatitis Viral hepatitis Biliary diseases Biliary diseases Primary hemochromatosis Primary hemochromatosis Wilson disease Wilson disease α 1 -antitrypsin deficiency α 1 -antitrypsin deficiency Cryptogenic cirrhosis. Cryptogenic cirrhosis. Infrequent forms including: Galactosemia & tyrosinosis Galactosemia & tyrosinosis Drug induced Drug induced Syphilis Syphilis Cardiac Cardiac

17. Pathogenesis In the normal liver interstitial collagens type I & III are concentrated in the portal tract & around central veins, occasional bundles are found in the space of Disse. Delicate type IV strands are also found in the space of Disse. In cirrhosis delicate or broad septal strands are formed by deposition of type I&III in the lobule. Hepatic vascular rearrangements shunt blood around parenchyma.

18. Pathogenesis There is loss of sinusoidal endothelial fenestration with impairment of hepatocellular secretion of proteins in continued fibrous deposition in the space of Disse within normal parenchyma. The major source of excess collagen is the peri- sinusoidal hepatic stellate cells (Ito cells) The normal function of these cells is vitamin-A fat – storing cells. In the development of cirrhosis they become activated, loose their retinyl ester stores & transform into myo-fibroblasts – like cells.

19. Pathogenesis Source of collagen synthesis stimulation inflammatory cytokines produced from chronic inflammation These include tumor necrosis factor TNF-α, transforming growth factor TGF – B & interleukin- 1. inflammatory cytokines produced from chronic inflammation These include tumor necrosis factor TNF-α, transforming growth factor TGF – B & interleukin- 1. cytokine production of stimulated endogenous cells (kupffer cells, endothelium, hepatocytes & Bile duct epithelial cells). cytokine production of stimulated endogenous cells (kupffer cells, endothelium, hepatocytes & Bile duct epithelial cells). Disruption of extra cellular matrix. Disruption of extra cellular matrix. Direct stimulation of stellate cells by toxins Direct stimulation of stellate cells by toxins

20. Pathogenesis  Constriction of sinusoidal channels by tonic contraction of myo-fibroblast stellate cells leads to increase vascular resistance within the liver. Blood delivery to hepatocytes is compromised.  Hepatocytes are stimulated to regeneration within spherical nodules.  Disruption of the interface between portal tracts & parenchyma obliterates the biliary channels leading to jaundice.

22. MicronodularMacronodular CirrhosisCirrhosis

23. Liver Cirrhosis (Gross)

24. Incomplete Septal Type Cirrhosis

25. Clinical features  Clinically silent.  Non-specific clinical signs & symptoms: anorexia, weight loss, weakness, osteoporosis & frank debilitation.  Hepatic failure is precipitated by superimposition of a hepatic metabolic load in systemic infection or GI bleeding.  Hepato pulmonary syndrome : imbalance of pulmonary blood flow.

26. Death is due to Progressive liver failure. Progressive liver failure. Portal hypertension & it’s complications. Portal hypertension & it’s complications. Hepatocellular carcinoma. Hepatocellular carcinoma.

27. Quiz Answer by T or F: Answer by T or F: The source of collagen in liver cirrhosis is the fibroblasts. The source of collagen in liver cirrhosis is the fibroblasts. In cirrhosis, fibrosis is requisite for diagnosis. In cirrhosis, fibrosis is requisite for diagnosis. Massive hepatic injury could be a cause for hepatic failure. Massive hepatic injury could be a cause for hepatic failure. Spider angiomas are indicative of hyperammonemia. Spider angiomas are indicative of hyperammonemia.

28. PORTAL HYPERTENSION

29. Causes Prehepatic conditions 1. Portal vein thrombosis & narrowing 1. Portal vein thrombosis & narrowing 2. Massive splenomegaly through shunting excessive blood into the splenic vein. 2. Massive splenomegaly through shunting excessive blood into the splenic vein. Posthepatic causes 1. Severe right-sided heart failure 1. Severe right-sided heart failure 2. Constrictive pericarditis 2. Constrictive pericarditis 3. Hepatic vein outflow obstruction. 3. Hepatic vein outflow obstruction.

30. Intrahepatic causes: 1. Cirrhosis is the dominant cause accounting for most cases of portal hypertension. 2. Schistosomiasis 3. Massive fatty change 4. Diffuse fibrosing granulomatous disease such as sarcoidosis and miliary tuberculosis 5. Diseases affecting the portal microcirculation, exemplified by nodular regenerative hyperplasia

31. The four major consequences of portal hypertension in the setting of cirrhosis are 1. Ascites 2. The formation of portosystemic venous shunts leading to esophageal varices & hemorrhoids 3. Congestive splenomegaly 4. Hepatic encephalopathy

32. Ascites refers to the collection of excess fluid in the peritoneal cavity The pathogenesis of ascites : 1- Sinusoidal hypertension, 2- Percolation of hepatic lymph into the peritoneal cavity: 3. Intestinal fluid leakage: 4. Renal retention of sodium and water

33. INFLAMMATORY & INFECTIOUS DISORDERS

34. VIRAL HEPATITIS

35. Unless otherwise specified, the term viral hepatitis is reserved for i.e. having a particular affinity for the liver. This group comprises Unless otherwise specified, the term viral hepatitis is reserved for “infection of the liver caused by a group of hepatotropic viruses” i.e. having a particular affinity for the liver. This group comprises 1. Hepatitis A virus (HAV) 2. Hepatitis B virus (HBV) 3. Hepatitis C virus (HCV) 4. Hepatitis D virus (HDV) 5. Hepatitis E virus (HEV)

36. Hepatitis A Virus (HAV) Acute viral hepatitis A (infectious H) Benign Self limiting disease Incubation period of 4 weeks HAV does not cause chronic hepatitis or a carrier state and only rarely causes fulminant hepatitis The viremia is short-lived, thus, blood-borne transmission of occurs rarely; therefore, donated blood is not screened for this virus.

37. Hepatitis B Virus (HBV) 1. Acute viral hepatitis B with recovery and clearance of the virus 2. Chronic viral hepatitis B, which is either a. Non-progressive or a. Non-progressive or b. Progressive ending in cirrhosis b. Progressive ending in cirrhosis 3. Fulminant hepatitis with massive liver necrosis 4. An asymptomatic carrier state.

38. Chronic viral hepatitis B Important precursor of hepatocellular carcinoma. Estimated carrier rate of 400 million. Incubation period 4-26 weeks It is also present in all physiologic and pathologic body fluids, with the exception of stool. In endemic regions, vertical transmission from mother to child during birth constitutes the main mode of transmission. The host immune response to the virus is the main determinant of the outcome of the infection.

39. Hepatitis C Virus (HCV) Carrier rate is estimated at 175 million persons. The major route of transmission is through blood inoculation, with low rates of sexual and vertical transmissions. HCV infection has a much higher rate (than HBV) of progression to chronic liver disease and eventual cirrhosis. The clinical course of acute viral hepatitis C is usually asymptomatic and is easily missed.

40. Persistent infection is the hallmark of HCV; in 80% of such cases it complicates subclinical acute infection. Persistent infection is the hallmark of HCV; in 80% of such cases it complicates subclinical acute infection. Cirrhosis develops in 20% of such patients. Cirrhosis develops in 20% of such patients. Fulminant hepatitis is rare. Fulminant hepatitis is rare.

41. Hepatitis D Virus (HDV) is a unique RNA virus in that it is replication defective, causing infection only when it is encapsulated by HBsAg i.e. HDV is absolutely dependent on HBV co-infection for multiplication. Delta hepatitis arises in two settings: 1. Acute coinfection 2. Superinfection

42. Hepatitis E Virus (HEV)  HEV is endemic in India (where it was first documented).  Epidemics have been reported from Asia and Africa.  HEV is not associated with chronic liver disease or persistent viremia.  A characteristic feature of the infection is the high mortality rate among pregnant women, approaching 20%.  Virus can be detected in stools, and anti-HEV IgG and IgM antibodies are detectable in serum.  Virus can be detected in stools, and anti-HEV IgG and IgM antibodies are detectable in serum.

43. Pathological features of Viral Hepatitis

44. Acute viral hepatitis The normal radial array of the lobules is lost. The normal radial array of the lobules is lost. There is diffuse ballooning degeneration of hepatocytes; the cells are swollen with clear, wispy cytoplasm. There is diffuse ballooning degeneration of hepatocytes; the cells are swollen with clear, wispy cytoplasm. Hepatocytes necrosis assume one of 3 morphologic types Hepatocytes necrosis assume one of 3 morphologic types 1. Cytolysis 2. Apoptosis 3. Confluent necrosis of hepatocytes,

45. Hepatocyte regeneration Hepatocyte regeneration Inflammation is usually a prominent feature of acute hepatitis.. Inflammation is usually a prominent feature of acute hepatitis.. Hypertrophy & hyperplasia of Kuppfer cells Hypertrophy & hyperplasia of Kuppfer cells Cholestasis may be present, both intracellular (brown pigmentation of hepatocytes) & canalicular (bile plugs in canaliculi). Cholestasis may be present, both intracellular (brown pigmentation of hepatocytes) & canalicular (bile plugs in canaliculi). HBV infection, acute or chronic, may produce two distinctive features of the infected hepatocytes. HBV infection, acute or chronic, may produce two distinctive features of the infected hepatocytes. a. Ground-glass" hepatocytes: a finely granular, eosinophilic cytoplasm due to massive quantities of HBsAg (as seen by electron microscopy). b. Sanded nuclei, resulting from abundant intranuclear HBcAg.

46. Acute viral hepatitis There is disruption of lobular architecture, inflammatory cells in the portal tracts & sinusoids, and hepatocellular apoptosis (arrow).

47. Acute viral hepatitis Portal inflammation with interface hepatitis (arrow)

48. Acute viral hepatitis B Acute viral hepatitis B. Centrolobular area of liver lobule, characterized by ballooning of hepatocytes, and mononuclear (mainly lymphocytic) inflammatory infiltration. (H&E)

49. Hepatocytes shrink, become intensely eosinophilic, and have fragmented or absent nuclei. Apoptotic cells are phagocytosed within hours by macrophages and hence may be difficult to find despite extensive apoptosis. Acute viral hepatitis: Acidophilic (apoptotic) bodies

50. Acute viral hepatitis B with confluent necrosis Severe necrotizing acute viral hepatitis B. Overview of liver lobule; mild to moderate mononuclear cell infiltration in portal tracts (lower left, top, and lower right). Bridging portal- central confluent lytic necrosis, creating a "star-shaped" area of necrosis with a centri- lobular vein at its center (arrow) and peripheral points reaching portal tracts. Inflammatory cells are scattered throughout the lobule. (H&E)

51. Chronic hepatitis The changes are of variable severity, ranging from very mild to severe. Hepatocyte necrosis may occur in all forms of chronic hepatitis. The inflammatory component consists mainly of lymphocytes, macrophages, and occasional plasma cells. In the mildest forms, significant inflammation is limited to portal tracts. Lymphoid aggregates in the portal tract are often seen in HCV infection. The liver architecture is usually well preserved Continued periportal necrosis (interface hepatitis) and bridging necrosis are forerunners of progressive liver damage.

52. The hallmark of serious liver damage is the deposition of. At first, at the portal tracts, but with time periportal fibrosis occurs. This is followed by bridging fibrosis that links fibrous septa between lobules. The hallmark of serious liver damage is the deposition of fibrous tissue. At first, at the portal tracts, but with time periportal fibrosis occurs. This is followed by bridging fibrosis that links fibrous septa between lobules. Continued loss of hepatocytes with fibrosis results in cirrhosis, with fibrous septa and hepatocyte regenerative nodules. Continued loss of hepatocytes with fibrosis results in cirrhosis, with fibrous septa and hepatocyte regenerative nodules. This pattern of cirrhosis is characterized by irregularly sized nodules separated by variable but mostly broad bands of fibrosis. This pattern of cirrhosis is characterized by irregularly sized nodules separated by variable but mostly broad bands of fibrosis. The nodules are typically greater than 0.3 cm in diameter; accordingly, the cirrhosis is by definition macronodular.

53. Interface hepatitis. Lymphocytic infiltrates extend from the portal tracts into acinar tissue with destruction of the limiting plate. Findings are consistent with autoimmune hepatitis, drug reaction, or viral infection. Chronic hepatitis showing interface hepatitis (formerly piecemeal necrosis)

54. Note inflamed portal tract (upper right) and wedge-like extension of necro-inflammation (towards lower left) and irregular interface between portal periphery and adjacent parenchyma. Interface hepatitis (piecemeal necrosis)

55. Severe chronic viral hepatitis B. Area of multilobular lytic necrosis in phase of postnecrotic collapse and early fibrosis, with several small islands of surviving hepatocytes, appearing swollen and pale, and sometimes arranged in tubular fashion (”hepatitic-type liver cell rosettes”). (H&E) Chronic hepatitis with hepatocytes regeneration (hepatitic-type liver cell rosettes)

56. Ground glass hepatocytes, characterized by more pale, eosinophilic, and homogeneous cytoplasm than surrounding normal (more granular) hepatocytes. Note (artifactual) cleft between "ground glass" cytoplasm and hepatocellular cell membrane. The change corresponds to extensive endoplasmic reticulum hyperplasia and massive accumulation of HBsAg. (H&E) Chronic viral hepatitis B showing ground glass hepatocytes

57. Portal lymphoid aggregates and minimal steatosis. The findings are consistent with a chronic hepatitis C infection. Chronic viral hepatitis C

58. This is a case of viral hepatitis C with extensive fibrosis and progression to macronodular cirrhosis, as evidenced by the large regenerative nodule at the center right. Chronic viral hepatitis C progressing to cirrhosis

59. Cirrhosis resulting from chronic viral hepatitis. Note the irregular nodularity of the liver surface resulting in a macronodular pattern of cirrhosis. Posthepatitic cirrhosis

60. Autoimmune Hepatitis is microscopically indistinguishable from chronic viral hepatitis but is associated with a set of immunologic abnormalities. This disease may run an indolent or severe course. Salient features include: Female predominance Absence of viral infection serologic markers Immunological abnormalities a. Elevated serum IgG (>2.5 g/dl) b. High titers of autoantibodies (80% of cases) c. Presence of other autoimmune diseases (in 2/3 of the patients), including rheumatoid arthritis, thyroiditis, Sjögren syndrome, and ulcerative colitis.

61. Pathogenesis Most patients have a variety of auto-antibodies such as antinuclear, anti-smooth muscle, liver kidney microsomal antibody, etc. The best characterized among these antibodies are smooth muscle antibodies directed against cytoskeletal proteins that include actin, and troponin, and liver kidney microsomal antibodies. The main effectors of cell damage are believed to be CD4+ helper cells. Response to immunosuppressive therapy is usually dramatic. The overall risk of cirrhosis, the main cause of death, is 5%.

62. PYOGENIC LIVER ABSCESSES

63. In developing countries most liver abscesses result from parasitic infections, such as amebic, echinococcal, etc. In developing countries most liver abscesses result from parasitic infections, such as amebic, echinococcal, etc. In the Western world, bacterial abscesses are more common, representing a complication of an infection elsewhere. In the Western world, bacterial abscesses are more common, representing a complication of an infection elsewhere. Gram-negative bacteria such as E. coli and Klebsiella sp. are the usual offenders. Gram-negative bacteria such as E. coli and Klebsiella sp. are the usual offenders.

64. The organisms reach the liver through one of the following pathways: The organisms reach the liver through one of the following pathways: 1. Ascending cholangitis 2. Vascular seeding, predominantly portal i.e. from the GIT 3. Direct invasion from a nearby focus 4. A penetrating injury. Debilitating disease with immune deficiency is a common background e.g. extreme old age, immunosuppression, or chemotherapy.

65. Gross features Pyogenic abscesses may be solitary or multiple, ranging from very small to massive lesions. Pyogenic abscesses may be solitary or multiple, ranging from very small to massive lesions. Bacteremic spread through the arterial or portal system tends to produce multiple small abscesses, whereas direct extension and trauma usually cause solitary large abscesses. Bacteremic spread through the arterial or portal system tends to produce multiple small abscesses, whereas direct extension and trauma usually cause solitary large abscesses.

66. Liver abscess Large liver abscess surrounded by a thick fibrous wall. It has liquefactive center. Multiple tan white nodules of varying size. Some have whiter, softer centers. Most are surrounded by a darker colored region which may represent hemorrhage.

67. Microscopic features These are identical to pyogenic abscesses elsewhere. These are identical to pyogenic abscesses elsewhere. Liver abscesses are associated with fever and right upper quadrant pain and tender hepatomegaly. Liver abscesses are associated with fever and right upper quadrant pain and tender hepatomegaly. Jaundice is often the result of extrahepatic biliary obstruction. Jaundice is often the result of extrahepatic biliary obstruction. Surgical drainage is often necessary. Surgical drainage is often necessary.

68. Abscesses in liver may also occur with hematogenous spread from other areas of the body with septicemia. Here are seen many microabscesses in the liver in a patient with Candida septicemia. Micro-abscesses liver A microabscess of liver contains numerous neutrophils in the center. The beginning of an organizing abscess wall with some pink fibrin is seen here.

69. AMEBIC LIVER ABSCESS AMEBIC LIVER ABSCESS is usually single, mostly right sided, & close to liver dome, but tends to be multicentric in immunocompromised patients. is usually single, mostly right sided, & close to liver dome, but tends to be multicentric in immunocompromised patients. Adults are mostly affected but can develop in infants & children. Adults are mostly affected but can develop in infants & children.

70. Gross features The necrotic center contains odorless, pasty, chocolate brown fluid.

71. Amebic abscess liver Abscesses may arise in liver when there is seeding of infection from the bowel, because the infectious agents are carried to the liver from the portal venous circulation. Amebic abscesses occupying most of the right lobe of the liver. Three distinct lobules are seen.

72. Microscopic Most of the lesion consists of necrotic debris. There few if any neutrophils. Most of the lesion consists of necrotic debris. There few if any neutrophils. This centre is surrounded by fibrin, macrophages, lymphocytes & a few fibroblasts with clusters of amebic trophozoites (up to 60 microns with small eccentric nucleus and cytoplasmic vacuoles that may contain red blood cells; resemble histiocytes). This centre is surrounded by fibrin, macrophages, lymphocytes & a few fibroblasts with clusters of amebic trophozoites (up to 60 microns with small eccentric nucleus and cytoplasmic vacuoles that may contain red blood cells; resemble histiocytes).

73. Amebic liver abscess in human. Trophozoites of Entamoeba histolytica are well observed (arrow). H&E, X400. Amebic abscess liver

74. Clusters of trophozoites Clusters of trophozoites Amebic abscess liver

75. Complications Complications 1. Bacterial super infection 2. Extension or perforation into the following 1. Pleuro-pulmonary structures 2. Subphrenic space 3. Peritoneal cavity, and pericardial sac, bile ducts 4. Kidney, mediastinum, chest wall, abdominal wall, and flank. Diagnosis: serology is 90% sensitive Diagnosis: serology is 90% sensitive

76. HYDATID DISEASE OF THE LIVER

77. Three quarters of infected individuals develop one or more hepatic cysts, which grow slowly. Three quarters of infected individuals develop one or more hepatic cysts, which grow slowly. The typical hydatid cyst is spherical and may measure up to more than 30 cm in diameter. The typical hydatid cyst is spherical and may measure up to more than 30 cm in diameter. The majority occur in the right lobe, but they may be multiple, involving all lobes. The majority occur in the right lobe, but they may be multiple, involving all lobes. A characteristic gross feature is the presence of the soft, whitish laminate membrane. A characteristic gross feature is the presence of the soft, whitish laminate membrane.

78. Hydatid cyst The characteristic laminated membrane is bile stained due to communication of the cyst with the biliary tree.

80. Histologic examination of the cyst wall shows an outer fibrous layer; a middle onionskin like laminated membrane, and an inner germinal layer. Histologic examination of the cyst wall shows an outer fibrous layer; a middle onionskin like laminated membrane, and an inner germinal layer. Calcification in the latter layer signifies that the cyst is dead. Calcification in the latter layer signifies that the cyst is dead. The adjacent liver parenchyma often shows pressure atrophy and a portal infiltrate in which eosinophils may be prominent. The adjacent liver parenchyma often shows pressure atrophy and a portal infiltrate in which eosinophils may be prominent. The viable cyst is filled with colorless fluid, which contains daughter cysts and brood capsules with scolices. The viable cyst is filled with colorless fluid, which contains daughter cysts and brood capsules with scolices.

83. Communication with the biliary tract and superimposed infection are frequent. Communication with the biliary tract and superimposed infection are frequent. Rupture of the cysts into the peritoneal cavity may result in a fatal anaphylactic reaction or in the formation of innumerable small granulomas grossly resembling peritoneal tuberculosis. Rupture of the cysts into the peritoneal cavity may result in a fatal anaphylactic reaction or in the formation of innumerable small granulomas grossly resembling peritoneal tuberculosis. Identification of fragments of germinal membrane or scolices in their center points to the diagnosis. Identification of fragments of germinal membrane or scolices in their center points to the diagnosis. Hepatic echinococcus cysts can also rupture inside the gallbladder or through the diaphragm into the pleural space and lung. Hepatic echinococcus cysts can also rupture inside the gallbladder or through the diaphragm into the pleural space and lung. The laboratory diagnosis can usually be made by hydatid serology and confirmed or established by ultrasound or computed tomograph The laboratory diagnosis can usually be made by hydatid serology and confirmed or established by ultrasound or computed tomograph