Premium quality web hosting!
| View Our Guestbook | Sign Our Guestbook | Search Our Web Site |
| Chat Room | Discussion Forums | Free Classified Ads |
SURGICAL WEBSITES BREAST DISEASE LIVER ABSCESS Anatomy of liver SURGICAL WEBSITES KIDNEY SURGERY POSTGRADUATE SURGERY LINKS
BREAST DISEASE Breast cancer Breast lump Breast awareness Breast calcifications Breast cysts Breast pain Duct ectasia Fat necrosis Fibroadenoma Hyperplasia Intraductal papilloma Phyllodes tumour Sclerosing adenosis
LIVER ABSCESS Anatomy of liver Physiology of liver Method of examination of liver Haematology of liver disease. Amoebic liver abscess .Pyogenic liver abscess. Percutaneous needle aspiration of liver abscess. Case study. Result Result continued Discussion
CHOLECYSTECTOMY Introduction Historical Review Anatomy of Gallbladder Physiology of Gallbladder Physiologic effects of pneumoperitoneum Pathology of Gallbladder Investigations Pre- operative preparation of laparoscopic cholecystectomy Contraindications Treatment modalities for gallstones. Anaesthesia
INGUINAL HERNIA HOW SURGICAL OPERATION IS DONE THYROID EXAMINATION MANAGEMENT OF SEVERELY INJURED PATIENT SEPSIS AND MULTIPLE ORGAN FAILURE CHEST TRAUMA BRONCHOGENIC CARCINOMA TETANUS AND ANAEROBIC INFECTIONS
PATHOLOGY OF GALLBLADDER PATHOLOGY OF GALLBLADDER
INTRODUCTION:
Gallstones are the commonest biliary pathology. Interest in the formation and clinical management of gallstone disease date back to ancient times, as archaeological evidence suggest that members of the royal Egyptian family were affected with this disorder. The development and worldwide application of laparoscopic cholecystectomy has once again focused our attention to gallstone disease.
CHOLELITHIASIS [GALL STONES]
GENERAL CONSIDERATIONS
Gall stone disease continues to be a major health problem in the world. The major driving forces in lithogenesis are cholesterol saturation of the bile and haemolysis. It is important to note that both cholesterol and unconjugated bilirubin are virtually insoluble in water. The amount of cholesterol solubilised in the bile is about 2 million times greater than its aqueous solubility. This solubilisation is accomplished and dependent on the level of bile salts and to a lesser extent lecithin. Accordingly, any supersaturation of the bile by cholesterol relative to the bile salts and any increase in the unconjugated bilirubin content are lithogenic. Gallstones are shown in figure 10.
CLASSIFICATION OF GALL STONES:
There are three types of stones that are as follows.
(i) CHOLESTEROL STONES
(ii) PIGMENT STONES
(iii) MIXED STONES
INCIDENCE:
Cholesterol stones comprising of 6 percent and mixed stones accounts for 90 percent of gallstones seen in Western Hemisphere. Pigment stones are more common in the Far East than in West. At least 10 percent of the population in the United States have cholelithiasis. Autopsy studies documents an even higher prevalence of gallstones than studies using ultrasound and indicates that prevalence continues to rise with age and is higher in women. In 2,218 consecutive autopsies in Sweden gallstones were found in 33% of women and 4.5% of men aged 30 to 39, 53% of women and 27% of men aged 60 to 69 and 63% of women and 7% of men aged 90 to 99 at death 55.
RISK FACTORS:
Certain groups are far more prone than others to develop gallstones. The major risk factors are as follows,
i- ETHNIC-HEREDITY [GENETIC]:
Perhaps the most thoroughly examined population group is Pima tribe of the southern Arizona, which has the highest recorded prevalence of the gallstones in the world. Cholecystography surveys document gallstone prevalence over 70% for Pima women over age 25 56.
Cholesterol stones predominates in Northern Europe and North and South America, mixed pigments tend to occur in Orientals and pure pigment stones in Occidentals. In American Indian tribes the prevalence of cholesterol stones approaches 75%, but pigment stones are rare. This predisposition to cholesterol stone particularly among Indian women is believed to be the consequence of a racial (genetic) tendency to secrete excessive amounts of cholesterol, and concomitantly, inadequate amounts of bile acids.
ii- AGE: More common after forty years of age. The influence of age is attributed to increasing cholesterol secretion. Shaikh et al has reported it in a child of 7 year age 57.
iii- SEX:
Females are at least twice as “lithogenic” as males 58.
iv- MULTIPLE PREGNANCIES
Pregnancy may lead to formation of gallstones due to diminished gallbladder emptying and increased bile saturation with cholesterol 59.
v- DIET: Dietary habits have long been suspected but details have yet to be identified. Possibly related to diet, high serum triglyceride and low high density lipoproteins and cholesterol levels seems to be associated with increased gallstone formation 60. High-calorie diet may also be a causative factor.
vi- OBESITY:
Gallstones are associated with obesity.
vii- DRUGS- For example. Clofibrate, Oestrogen, Cholestramine therapy.
viii- DIABETES MELLITUS.
ix- POLYUNSATURATED FATS.
x- ILEAL DISEASE :
Abnormalities of the ileum play a significant role in the development of the gallstone in children. Gallstone can occur in diseases like Crohn’s disease, necrotising enterocolitis, antenatal volvulous, lymphoma of mesentery and radiation injury to the ileum 61.
xi- ILEAL RESECTION OR BY PASS:
Ileal disease or resection plays an important interferes in the enterohepatic circulation of bile salts, predisposing to lithogenic bile. Several disorders leading to ileal resection or dysfunction have been found as a cause of gallstone formation 62.
xii- CYSTIC FIBROSIS AND PANCREATIC INSUFFICIENCY.
xiii- ALCOHOLIC CIRRHOSIS.
xiv- BLOOD DYSCRASIAS:
Cholelithiasis in paediatric is associated with hereditary blood dyscrasias. It is well known that children with sickle cell anaemia 63, congenital spherocytosis, thalassaemia and glucose-6-phosphate dehydrogenase deficiency are at increased risk of gallstone formation secondary to haemolysis 64.
xv- E. COLI INFECTIONS OF THE BILIARY TRACT.
xvi- PARASITIC INFESTATIONS OF THE BILIARY TRACT [e. g. Ascaris Lumbricoides, Clonorchis Sinensis].
xvii- TRUNCAL VAGOTOMY.
xviii- PARTIAL OR COMPLETE GASTRECTOMIES.
xix- HEPATIC CIRRHOSIS.
PATHOGENESIS:
PATHOGENESIS OF CHOLESTEROL
Cholesterol gallstones were believed to occur as a result of altered hepatic metabolism. It is generally accepted that the pathogenesis of cholesterol gallstones is multifactorial and is a consequence of a series of a dynamic interaction between the gall bladder and liver. The solubilisation of cholesterol is critical to the formation of cholesterol gall stones and understanding the factors that regulate this process has provided new insights into gall stone disease.
Gallstone formation has three stages
i- Cholesterol saturation.
ii- Nucleation.
iii- Stone growth.
i- CHOLESTEROL SATURATION:
The hepatic secretion of cholesterol saturated bile is a prerequisite for the formation of cholesterol gallstones. Cholesterol supersaturation is due principally to excessive hepatic secretion of cholesterol into bile. There appears to be "biochemical mosaic" of several defects in most gall stone patients that results in an expansion of the hepatic cholesterol pool destined for biliary excretion 65. Maintenance of cholesterol in solution is dependent on the presence in the bile of sufficient amount of bile salt and phospholipids. Alteration in this balance that results in a relative increase in concentration of cholesterol compared with the other lipid component of bile may result in cholesterol saturation of bile and ultimately precipitation of cholesterol.
The major vehicle for transport and solubilisation of cholesterol in bile was micelles. If the micelles were saturated with cholesterol, then the excess would come out of solution and precipitate as crystals. This critical relationship between cholesterol, bile salts and phospholipids can be expressed by number of mathematical formulas.
More recent information indicates that perhaps no more than 30 percent of biliary cholesterol is transported in micelles, and that the majority is carried in a vesicular form. These vesicles are made up of lipid bilayers similar to those found in cell membranes. These vesicles are able to solubilise more cholesterol saturation and precipitation. Current theory suggests there is equilibrium between the physicochemical phase of these vesicles such that the formation of the liquid crystals may or may not result in actual gallstones.
ii- NUCLEATION:
Nucleation refers to the process by which cholesterol monohydrate crystals form and agglomerate to become macroscopic. There must be specific factors present (or absent) that promote or retard the process of nucleation. Although it is clear that, for bile from patients with cholesterol gallstones, the time required to nucleate is significantly shorter than that for bile from patients without gallstones, the factors responsible remain as yet unidentified. Data are conflicting regarding the status of anti nucleating factor in the bile of patients who fail to form gall stones - which factor may be absent in gallstone patients - as well as presence of pronucleating factors in gallstones patients.
Several specific heat labile glycoproteins in the bile of gallstone patients have been identified as potential pronucleating factors. It has been proposed that specific proteins within cholesterol-saturated bile induce vesicular aggregation and ultimately promote stone growth.
Gall bladder mucus secretion can serve as a nucleating factor and as a matrix on which crystals agglomerate and cluster. Other factors presumed to be important in the nucleation process include increased concentration of biliary calcium, alteration in gallbladder prostaglandin metabolism, gallbladder stasis and altered gall bladder absorption.
iii. STONE GROWTH: Once cholesterol crystals begin to agglomerate and form clusters the stones are inevitable.
PATHOGENESIS OF PIGMENT STONES:
Pigment stones can be further classified as either “brown” or “black” stones. Brown stones have a characteristic appearance and consistency and are typically found in Asia. These stones presumably occur as a result of infection and are quite similar to primary bile duct stones 66. By contrast black stones are not typically associated by infected bile. These stones are found in haemolytic disorder or cirrhosis. Altered solubilisation of unconjugated bilirubin with precipitation of calcium bilirubinate and insoluble salts is presumed to be the common final pathway for the formation of all pigment stones, regardless of the clinical setting. For many years b-glucroinadase released by the bacteria was thought to be the critical factor in the enzymatic hydrolysis of bilirubin glucronide into free bilirubin and glucronic acid. This free unconjugated bilirubin which is insoluble in water, then combined with calcium in the bile to produce a calcium bilirubinate matrix that is the predominant component of most pigment stones. The absence of bacteria from many patients with pigment stones suggests that other factors must be operational. A form of endogenous b-glucronidase has been identified in hepatic bile of humans.
MIXED STONES:
Between the “pure” cholesterol and “pure” pigment stones there is a broad spectrum of so called mixed stones in essence “deviant” cholesterol stones they are multiple and often faceted.
CLINICAL MANIFESTATIONS:
Patients having gallstones present in a number of different ways. Some patients remain asymptomatic.
i. ASYMPTOMATIC GALLSTONES:
It has been estimated that up to 50 percent of all patients with gall stones, regardless of the type, are asymptomatic.
ii. BILIARY COLIC:
Postprandial right upper quadrant pain precipitated by a fatty or protein rich meal, occurs 30 to 60 minutes after eating, lasts for several hours and then resolves. This constellation of symptoms is referred to as biliary colic. It is the most common presentation. The pain of biliary colic may be constant. The location of biliary colic may be constant. The location of the pain is generally in the right upper quadrant, but many patients will have pain referred to inferior medial aspect of scapula or shoulder or to the mid-epigastrium. The onset of pain is related to impaction of a stone in the cystic duct or Hartmann’s pouch, with obstruction to outflow of bile occurring secondarily.
This is a self-limited process and generally resolves within a few hours of onset. The frequency with which these attack occur is unpredictable and does not appear to be linked to either the size or the number of stones present within the gallbladder. Once people begin to have attacks of biliary colic they tend to increase in frequency and intensity.
iii. NAUSEA AND EMESIS:
They are frequently associated with attacks of biliary colic.
iv. GALL BLADDER DYSPEPSIA:
After fatty meal there is feeling of fullness associated with belching and heartburn, there may be epigastric discomfort, flatulence and episodic nausea.
COMPLICATIONS AND SEQUELAE OF GALL STONES:
It is as follows,
I. IN THE GALL BLADDER
a. Silent gall stones.
b. Acute cholecystitis.
c. Chronic cholecystitis.
d. Gangrene of gall bladder.
e. Perforation of gall bladder.
f. Mucocele of gall bladder.
g. Empyaema of gall bladder.
h. Emphysematous cholecystitis.
i. Hydrops of gall bladder.
j. Adenomyomatosis of gall bladder.
k. Cholesterosis of gall bladder.
l. Polyposis of gall bladder.
m. Cholecystitis glandularis proliferans.
n. Diverticulosis of gall bladder.
o. Thypoid gall bladder.
p. Carcinoma of gall bladder.
II. IN THE BILE DUCTS:
a. Obstructive jaundice.
b. Cholangitis.
c. Acute relapsing pancreatitis.
III. IN THE INTESTINE:
Gall stone ileus leading to acute intestinal obstruction.
DISEASES OF THE GALL BLADDER
i. SILENT GALL STONES:
It is possible for the calculus or calculi to be present in the gall bladder and to give rise to the symptoms during long lifetime. As 10% of the gallstones are radio-opaque they are discovered accidentally on radiograph for another condition, e.g. intravenous urogram. Some says there is no indication for the operation on the symptomless (silent stones); treatment should only be instituted when symptoms occurs and other say that of incidental finding of the gall stones is made at the operation cholecystectomy is indicated if the patients general condition is good.
ii. ACUTE CHOLECYSTITIS:
The primary event in acute cholecystitis is the destention of the gallbladder due to the obstruction of the cystic duct. 67. The bile may be sterile or it may become infected as a secondary event. E coli is commonest found organism in such cases. Other factors such as hydrolysis of lipids such as lecithin and reabsorption of the bile salts and prostaglandins may play an important role 68. Acute cholecystitis is in figure 11.
Acute biliary colic results in severe colicky abdominal pain usually accompanied by nausea and vomiting. The duration of the severe pain that makes the patient restless varies from 30 minutes to several hours. Biliary colic often merges into acute cholecystitis. However resolution of the severe colicky painful episode either spontaneously or as a result of analgesic medications/ antispasmodics without the development of acute cholecystitis. Much less commonly, acute cholecystitis is acalculous although the incidence of this complication in critically ill patient is diagnosed more frequently these days. The sonographic evaluation of the right upper quadrant will demonstrate gallstones in the majority of the patients but may not confirm the diagnosis of acute cholecystitis 69. Early cholecystectomy even in elderly patients suffering from acute cholecystitis could be quite safe 70, delay could lead to perforation, fistulas and abscess formation 71.
iii. ACUTE OBSTRUCTIVE [CALCULOUS] CHOLECYSTITIS
In 95% of the patient a gallstone is found impacted in the Hartman’s pouch or obstructing the cystic duct. Following obstruction of the cystic duct or the Hartman’s pouch, the gall bladder becomes hyperaemic, oedematous tense and distended. The initial inflammation is chemically induced and is not of bacterial origin although sepsis is an important features of the established disease and its complications. The exact cause of the initial chemical inflammation is not known but the release of mucosal phospholipase, which converts the lecithin in the bile to lysolecithin, is currently held responsible for the initiation of the inflammatory response, although bacterial lysozomal enzymes and more recently prostaglandins have been implicated. In the first few days bile appears macroscopically normal and is sterile but with the progress of the inflammation, absorption of the pigments and bile salts takes place and the contents than vary from a thin mucoid material to frank pus. The histological changes of the established condition involve the mucosa, fibromuscular wall and serosa and vary from mild acute inflammations with transmural oedema to severe disease with patches of necrosis usually in the fundal region of the gall bladder which becomes wrapped by the greater omentum. At the time of surgery carried during the same admission approximately 50% of the cultures of the gall bladder contents are sterile. Aerobic enteric organisms account for 94% of positive cultures and anaerobes for the remainder.
SYMPTOMS AND SIGNS:
These are as follows,
- Pyrexia
- Severe pain and tenderness in the right hypochondrium with rebound.
- Positive Murphy’s sign.
- Nausea
- Vomiting
- Ileus
- Mild abdominal distension
- Positive Boas’s sign.
- Toxicity in severe forms
- Jaundice in 20-25% of patients but common duct stones are found in only 12% of these patients.
- Reactive hepatitis.
- Oedema of the common bile duct
- Tender palpable mass in 25% of the cases and signifies one of the following
- Empyaema of the gall bladder
- Omental phlegmon
- Abscess due to localised perforation carcinoma of the gall bladder if the patient is elderly
- Leucocytosis
- Slight elevation of the serum transaminases
- Serum bilirubin and alkaline phosphatase may be elevated.
iv. ACUTE ACALCULOUS CHOLECYSTITIS:
The incidence of it is 2-8%. Socava et al had reported a high mortality rate of 6% 72. It is usually encountered in critically ill elderly patients but acute acalculous cholecystitis is also encountered in children. The disorder usually occurs during the course of prolonged serious illness e.g. multiple trauma, following major surgical intervention in patient with extensive burn, severe sepsis and drug overdose. The risk factors which predispose to the development of the acute acalculous cholecystitis are
- Blood volume depletion
- Prolonged ileus
- Morphine administration exceeding 6 days
- Intra venous hyperalimentation
- Multiple blood transfusion
- Sepsis
- Starvation
The inflammation is predominantly chemical in origin. In the fully developed condition, the gall bladder shows marked oedema of the seromuscular layer, mucosal ulceration and sloughing and focal necrotic are, substantial gangrene occurs in 25%.
The early manifestation includes fever leucocytosis, tenderness in the right hypochondrium.
v. ACUTE EMPHYSEMATOUS CHOLECYSTITIS:
It is caused by mixed polymicrobial infection which includes gas forming bacteria (E. coli, Clostridium welchii, aerobic and anaerobic streptococci). The gall bladder may or may not contain stones. Acute emphysematous cholecystitis occurs predominantly in males (70%) and is specially found in the diabetic patients. Thrombosis of the cystic artery has been implicated in the development of acute cholecystitis. Xray is shown in figure 12.
The presence of air within the gall bladder lumen its wall or the biliary tree is characteristic of the condition which often leads to gangrene and perforation by the time diagnosis is made.
CLINICAL PICTURE
It includes,
- Severe rapidly oncoming upper abdominal peritonitis
- Prostration.
- Marked toxicity.
COMPLICATIONS OF ACUTE CHOLECYSTITIS:
The important forms of all forms of acute cholecystitis are,
- Empyaema.
- Perforation.
- Gangrene.
vi. EMPYAEMA OF THE GALL BLADDER OR PYOCELE:
It may be a sequel of acute cholecystitis or the result of the mucocele becoming infected. It has incidence of 2-3%. It presents as a tender mass in the right hypochondrium and usually effects elderly patients in whom systemic signs, including pyrexia and leucocytosis are minimal. Cultures of the gall bladder contents are positive in 80% of the patients. Empyaema of the gall bladder doubles the mortality figures of the cholecystectomy.
vii. GANGRENE OF THE GALL BLADDER:
Patchy gangrene of the gall bladder is encountered in 5-7% of patients with obstructive cholecystitis. It is more commonly encountered in elderly patients diabetics and in patients with empyaema of the gall bladder, acute acalculous cholecystitis, and especially emphysematous cholecystitis. It may lead to localised or free perforation of the gall bladder.
viii. PERFORATION OF THE GALL BLADDER:
The site of perforation is either at the fundus which is farthest away from the blood supply or less commonly at the neck from the pressure necrosis of an impacted calculus. The sequelae are as follows,
- Local abscess
On account of the present and probably the past attacks of the cholecystitis, there are adhesion of the gall bladder the greater omentum and the parietal peritoneum. Consequently when an infected obstructed gall bladder perforates the usual out come is the local abscess.
- Perforation into the general peritoneal cavity
It occurs only in the 0.5% of the patients undergoing conservative treatment for acute cholecystitis, and the patient is usually a man. If the bile is infected diffuse peritonitis supervenes readily and rapidly and the mortality is about 50%.
The perforation may involve the duodenum and the development of the cholecystoduodenal fistula and resolution of the inflammatory episode. However this bilioenteric fistula persists and the passage of large stone through this fistula may cause gallstone ileus.
ix. CHRONIC CHOLECYSTITIS.
Chronic inflammation of the gall bladder is most commonly due to stones and the term chronic cholecystitis should be restricted to the gall bladders containing gall stones with varying degree of inflammation from mild mucosal / sub mucosal changes to gross transmural fibrosis encasement of the biliary calculi.
SYMPTOMS AND SIGNS
It includes,
- Recurrent attacks of the epigastric or right hypochondrial pain, often radiating to the right side of the back or to the shoulder blade.
- Pain is persistent than intermittent.
- Episodes of biliary colic with severe intermittent peaks of pain lasting for a few minutes to several hours may subside spontaneously or progress to cystic duct obstruction and acute cholecystitis.
- Nausea and vomiting.
- Jaundice and dark urine indicates common bile duct obstruction by a calculus.
- Indigestion.
- Dyspepsia
- Flatulance.
- Intolerance to fatty foods.
- Abdominal distension.
x. ACALCULOUS CHRONIC GALL BLADDER DISEASE:
Chronic inflammation of the gall bladder in the absence of the gallstones is due to adenomyomatosis or cholesterolosis of the gall bladder and these may be conveniently grouped as acalculous chronic gall bladder disease. It has vague symptoms not dissimilar to those of chronic cholecystitis. Oral cholecystography shows no abnormality of the gall bladder in 50% of the patients. In many instances the diagnosis is made on pathological examination of the excised gall bladder.
THE CHOLECYSTOSIS:
This includes,
- Adenomyomatosis of gall bladder.
- Cholesterolosis.
- Polyposis.
- Cholecystitis glandularis proliferance.
This is not uncommon group of condition affecting the gall bladder in which there is no chronic inflammatory change with hyperplasia of all tissue elements.
xi. ADENOMYOMATOSIS OF THE GALL BLADDER:
It is also known as adenomatous hyperplasia. It is also thought to represent a development defect, which results in hyperplasia of the smooth muscle bundles with sacculations or diverticulum formation of the epithelial lining [Rokitansky-Aschoff sinuses]. The cholecystogram may be normal or the late film taken after a fatty may demonstrate either the mural diverticula or a concentric narrowing of the fundus. Xray is shown in figure 13.
xii. CHOLESTEROLOSIS OF THE GALL BLADDER (STRAWBERRY GALL BLADDER):
In the fresh state interior of the gall bladder looks something like a strawberry; the yellow specks (submucous aggregation of the cholesterol and cholesterol esters) corresponds to the seeds. It may be associated with the cholesterol stones.
xiii. CHOLESTEROL POLYPOSIS OF THE GALL BLADDER:
Cholecystography shows negative shadows in a functioning gall bladder. The shadows which are adjacent to the wall of the gall bladder, remain constant in position and in relation to one another in all films of the series. Histologically, cholesterol polyposis is similar to the cholesterol laden projections of the strawberry gall bladder, but the lesions are much less numerous and are relatively gigantic. The treatment is cholecystectomy.
xiv. CHOLECYSTITIS GLANDULARIS PROLIFERANS:
A polyp of the mucous membrane is fleshy and granulomatous. All layers of the gall bladder wall may be thickened but sometimes, an incomplete septum forms which separates hyperplastic from the normal. Intraperital mixed calculi may be present. These can be complicated by an intramural and later an extramural abscess.
xv. DIVERTICULOSIS OF THE GALL BLADDER:
It manifests as black pigment stones impacted in the out-pouching of the lacunae of Lushka. Diverticulosis of the gall bladder may be demonstrated by cholecystography, especially when the gall bladder contracts after a fatty meal: there are small dots of contrast medium just outside the gall bladder. A septum may also be present. Treatment is cholecystectomy
xvi. TYPHOID GALL BLADDER:
Occasionally , Salmonella typhimurium can infect the gall bladder. Acute cholecystitis can occur. More frequently, chronic cholecystitis occurs the patient being a typhoid carrier excreting the bacteria in the bile. Gallstone may be presents. It is detectable whether the stones are secondary to Salmonella cholecystitis or whether pre-existing stones predispose the gall bladder to chronic infection. Salmonellae can however frequently cultures from stones. Ampicillin and cholecystectomy are indicated.
xvii. MUCOCELE OF THE GALL BLADDER:
This is often confused with empyaema. The grossly distended gall bladder associated with cystic duct obstruction, usually by a stone, not inflamed and is filled with mucoid material. The bile is absorbed and replaced by mucous secreted by the gall bladder epithelium. The gall bladder may be palpable. Enormous sizes and shapes are encountered. A mucocele also occurs in those case of malignancy which occlude the cystic duct. The treatment is cholecystectomy which can be performed safely by laparoscopic approach.
xviii. HYDROPS OF THE GALL BLADDER:
It is due to chronic obstruction of the gall bladder. The gall bladder is thick walled, distended, full of mucoid material.
xix. PORCELAIN GALL BLADDER:
The dystrophic calcification in the wall gall bladder.
xx. XANTHOMATOUS CHOLECYSTITIS:
` It is rare benign destructive inflammatory process of the gall bladder. It is a variant of chronic cholecystitis. The gall bladder wall is thickened and the serosa is often covered with dense fibrous adhesions. Gallstones are present in most instances, mucosal surface may be superficially involved, ulcerated and haemorrhagic.
Xanthogranulomatous foci are composed of abundant lipid laden histiocytes, inflammatory cells, fibroblasts, cholesterol clefts, foreign body giant cells, haemosedrin, extravasated bile is also seen.
Females are more prone for this disease and patients tend to present tend to present this disease in 6th and 7th decades of life. There are right upper quadrant pain and gallstones. Xanthogranulomatous cholecystitis. Mimics with adenocarcinoma of gall bladder.
xxi. TUMOURS OF THE GALL BLADDER:
These consist of the benign lesions and carcinoma of gall bladder.
BENIGN TUMOURS
These include adenomas and papillomas. Most are discovered in clinical practice following pathological examination of the excised gall bladder although some are identified as fixed isolated shadow seen on oral cholecystogram or gall bladder ultrasound scan in patient with unexplained right hypochondirial discomfort or pain. There is some evidence that adenomas may progress to carcinoma. When diagnosed, a cholecystectomy is considered advisable because of the uncertainty of the diagnosis and possibility of malignant change.
CARCINOMA OF GALL BLADDER:
Carcinoma of the gall bladder is not uncommon in Pakistan, but there are areas of world where the incidence is high (Indiana). Incidence increases if the chronic cholecystitis is left untreated. An increased incidence is found in chronic typhoid carries, patients with porcelain (calcified) gall bladder, obese individuals. It is found in less than 1 percent of gall bladder operations. In over 90 percent of the cases gallstones are present. The patients are mostly in their 70s. The female: male ratio is 5:1. The majority of the tumours are adenocarcinomas with papillary, undifferentiated, squamous and adenoacanthoma constituting a minority. Rare tumours include carcinoid, melanoma and ACTH- secreting apudomas. The staging of the gall bladder cancer is based on the depth of invasion as follows:
Stage I Confined to the mucosa / Sub mucosa.
Stage II Involvement of the muscle layer.
Stage III Serosal involvement.
Stage IV Spread to the cystic node.
Stage V Invasion of the liver and adjacent organs.
Spread is by direct invasion of the liver and porta hepatis, by lymphatics to hilar lymph nodes and by veins to the liver. Distant metastases are uncommon.
CLINICAL FEATURES:
The disease is either discovered accidentally during cholecystectomy or presents with non-specific symptoms. The non-specific symptoms includes,
- Inflammatory mass in the right hypochondrium.
- Anorexia
- Nausea and vomiting.
- Weight loss
- Patient may be jaundiced [due to involvement of the common hepatic duct].
- Enlarged liver
- Palpable gall bladder
- Ascites – in advanced stage.
- Anaemia in 50% of the patients due to chronic haemobilia.
- Normal serum bilirubin.
- Elevated alkaline phosphatase.
Ultrasound examination of the gall bladder may miss the early potentially curable lesion. Oral cholecystography may show a non functioning gall bladder or a filling defect projecting into the lumen. A coeliac axis angiogram may demonstrate an enlarged cystic artery or tumour circulation into the gall bladder area.
Washington, DC Registry
Last modified: Monday, 29-Nov-2004 07:11:52 EST |
