Peritonitis treatment

First make diagnosis for appropriate treatment

A diagnosis of rubor is based primarily on the clinical manifestations described above. If rubor is strongly suspected, then surgery is performed without further retard for another investigations. Leukocytosis, hypokalemia, hypernatremia and acidosis haw be present, but they are not specific findings. Abdominal X-rays haw expose dilated, edematous intestines, though such X-rays are mainly multipurpose to countenance for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under think and is likely to expand in the future. Computed tomography (CT or CAT scanning) haw be multipurpose in differentiating causes of abdominal pain. If reasonable uncertainty ease persists, an exploratory peritoneal lavage or laparoscopy haw be performed. In patients with ascites, a diagnosis of rubor is prefabricated via paracentesis (abdominal tap) more than 250 polymorphonucleate cells per μL is considered diagnostic. In addition, Gram bactericide and culture of the peritoneal fluid can watch the microrganism responsible and watch their sensibility to antimicrobial agents.

GENERAL CARE OF PATIENT

INTRAVENOUS FLUIDS restoration of ECF volume. rebuke of ECF electrolyte balance.correction of ECF protien depletion.Hyperalimentation ( IV intake ) , if patient's recovery is delayed for more than 7 - 10 life .

NASOGASTRIC ASPIRATION intermittent aspiration is maintained ,until paralytic ileus has recovered.If the cavum is soft and non-tender and bowel-sounds return ,oral intake haw be progressively introduced.

ANTIBIOTICS paraenteral Polycillin ,gentamycin ,and antiprotozoal haw be given.

ANALGESICS narcotic analgesics haw be presented ,e.g dextropropoxyphene ,nalbuphine and diminutive dose continuing for 48 hours.

FLUID BALANCE CHARTING

VITAL SIGN MONITORING

NEUTRALIZATION OF LOCAL SOURCE
BY SURGERY this is indicated in cut appendicitis , cut diverticulitis ,perforated peptic lesion ,perforated or unhealthy cholecystitis.
BY CONSERVATIVE TREATMENT this is done in rubor due to pancreatic salpingitis , or in case of primary rubor of streptococcal or pneumococcal lineage .

PERITONEAL LAVAGE if surgery has been undertaken ,then whole peritoneal cavity should be explored with sucker and mopped dry .Through improvement of peritoneal cavity can be achieved by work with upto 10 litres of armed normal saline.Last some litres should contain a broad-spectrum antibiotic ( e.g antibacterial ).


COMPLICATIONS OF PERITONITIS these may be either systemic or local.

Local complications allow :intraperitoneal abcess e.g subphrenic and pelvic ,Wound infection ,Anastomotic breakdown ,Fistula formaton ,adhesions .
Systemic complications allow : hypovolemic damper ,septic damper ,adult respiratory disress syndrome ,disseminated intravascular coagulation ,immunological unfortunate ,multiorgan unfortunate .

PROGNOSIS

The coverall mortality in generalized rubor ,especially if it is unhealthful ,is broad .Factor affecting mortality allow :
Age __ old patients with soiled rubor hit an exceptionally broad mortality.
causation __ unhealthful causes hit a higher mortality than chemical.
Duration of symptoms.
Degree of bacterial contamination.
Concomitant disease processes e.g cardiac ,renal , and hepatic organ failure.......read more

Acute peritonitis and peritonitis symptoms

A SERIOUS CONDITION IN WHICH THE INSIDE WALL OF THE BODY BECOMES SWOLLEN AND INFECTED 

ACUTE PERITONITIS 

Peritonitis is an inflammatory or suppurative response of the peritoneal lining to direct irritation.It haw be decentralised or unspecialised bacterial or chemical.Localized peritonitis is due to transmural inflammation of aviscus ,e.g. accent appendicitis ,acute cholecystitis .acute diverticulitis .It haw remain decentralised by being contained by omentalwrapping or adhesion of conterminous structures .In some cases ,however ,it becomes unspecialised ,spreading to involve the whole peritoneum .Sudden perforation of a viscus usually results in unspecialised peritonitis.

In this case , the patient is usually seriosly ill .Hypovolemia results from large oozing into the peritoneal decay and septicemia haw result if the cause is infective .eg faecal peritonitis due to perforated diverticulitis.Chemical peritonitis results from viscus or pancreatic juice ,bile ,urine ,or blood in the peritoneal decay .Bile causes lowercase reaction if it is sterile ,but can cause a nonindulgent peritonitis if it is infected or mixed with pancreatic juice.Blood and urine ,again ,cause lowercase raction if sterile ,but a nonindulgent reaction usually results if thy are infected.

CAUSES OF PERITONITIS 

It haw be ACUTE OR CHRONIC

In Acute cases we crapper categarize BACTERIAL and CHEMICAL and we boost cypher in PRIMARY And SECONDARY. 

Primary are rare but crapper due to streptococcus ,Pneumococcus ,haematogenous spread occurs in young girls ,ascites ,nephrotic syndrome and post-splenectomy .

Secondary is common related to perforation ,infection ,inflammation or anaemia of the GIT or GU tract. In chemical culprits are  Gastric juice e.g cut gastric ulcer.
Pancreatic juice e.g accent pancreatitis .
Bile e.g cut gall bladder.
Blood e.g damaged spleen.
Urine e.g intraperitoneal break of the bladder.

In CHRONIC cases allow Tuberculosis and Starch ( medicine activity )

CLINICAL FEATURES

Most patients with rubor module hit abdominal pain and a fever. Also, they commonly already hit Ascites (a build-up of changeful within their stomach) and a distended stomach.  Peritonitis haw or haw not drive the breadbasket to be more distended than normal.

Some patients module hit nausea, vomiting, expiration of appetite, and coefficient loss.  Which of these symptoms are inform depends on the drive of the problem. Many patients with Ascites also hit liver problems.  When these patients develop peritonitis, they often undergo deterioration in mental status because of the build-up of toxic substances in their blood.

Patients with tuberculous rubor hit low-grade fever, expiration of appetite, and coefficient loss. Often, their Ascites module develop slowly.

In patients with cancer, the cancer crapper spread to the peritoneum (the abdominal cavity).  If this happens, it triggers a activity and causes the accumulation of fluid.  This crapper drive an abnormal increase in the size of the abdomen, expiration of appetite, and lack of energy. If there is a large amount of changeful within the breadbasket cavity, the enduring haw hit trouble breathing because the lungs cannot expand normally.  Also, changeful haw country the intestine and not allow food to pass through.Examination by a doctor commonly reveals compassionateness of the abdomen, and fever.

DIAGNOSTIC INVESTIGATIONS 

A diagnosis of rubor is based primarily on the clinical manifestations described above. If rubor is strongly suspected, then surgery is performed without further retard for another investigations. Leukocytosis, hypokalemia, hypernatremia and acidosis haw be present, but they are not specific findings. Abdominal X-rays haw expose dilated, edematous intestines, though such X-rays are mainly multipurpose to countenance for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under think and is likely to expand in the future. Computed tomography (CT or CAT scanning) haw be multipurpose in differentiating causes of abdominal pain. If reasonable uncertainty ease persists, an exploratory peritoneal lavage or laparoscopy haw be performed. In patients with ascites, a diagnosis of rubor is prefabricated via paracentesis (abdominal tap): more than 250 polymorphonucleate cells per μL is considered diagnostic. In addition, Gram bactericide and culture of the peritoneal fluid can watch the microrganism responsible and watch their sensibility to antimicrobial agents........ read more

70% adult cases of chronic pancreatitis are caused by chronic alcohol use

Main culprits are heavy alcohol consumption and gallstones for chronic pancreatitis

CHRONIC PANCREATITIS 

is a relapsing disorder which may arise  insidiously or following repeated attacks of acute pancreatitis .The most commonest cause is chronic alcohol consumption and accompanied by a protien and fat rich diet .Other causes include cystic fibrosis ,hypercalcemia ,hyperlipidemiaand a rare familial pancreatitis .Pathological changes include parenchymal destruction ,fibrosis ,loss of acini ,calculi and duct stenosis with dilatation behind the stenosis.At operation the gland feels hard and irregular and may be mistaken for carcinoma .Calcification is often seen on plain abdominal X-ray.This is thought to be due to calcification of protien precipitates in ducts .

 Pancreatic duct obstruction : due to Stricture e.g.after trauma or acute pancreatitis.Occlusion by pancreatic cancer.

 Hyperparathyroidism ,cystic fibrosis ,Hereditory pancreatitis ,Infantile malnutrition ,Idiopathic ,Stenosis of ampulla of vater . In 12 % of adults ,etiology is unknown.

 Initially pancreas may appear normal.Later pancreas enlarges and becomes hard due to sclerosis ,while the ducts become distorted and dilated with areas of ectasia .Calcified stones ,weighing from a few mg 200 g ,may form within ducts .Ducts become occluded with gelatinous protein-rich fluid and debris ,to form cysts.

Lesions affect a particular lobule producing ,Ductular metaplasia and hyperplasia ,Atrophy of acini ,Interlobular fibrosis .

In clinical features there is symptom of discompose in epigastrium ,which alter to left and correct hypochondrium and finished to back .boring discompose to biliary colic in character .duration about 3-4 days ,and exacerbated by beverage consumption.Vomiting ,anorexia ,Steatorrhea ,and Weight loss ( results from anorexia ,malabsorption steatorrhea and vomiting .It can cause some symptoms of diabetes mellitus ,these are late feature and includes polyuria ,polydipsia ,weight loss and imperfectness.

Signs of jaundice haw be present ( due to narrowing of retropancreatic bile duct ) A protective ,hard epigastric mass haw indicate formation of a sac . ( best way to palpate pancreas is to invoke the enduring to correct and hips and knees are flexed .Left costal margin is deeply palpated.This will evoke tendrness in accent and habitual pancreatitis ( Mallet-Guy's sign ).

DIAGNOSTIC INVESTIGATIONS

The identification of habitual pancreatitis is typically based on tests on pancreatic structure and function, as direct biopsy of the pancreas is thoughtful excessively risky. Serum amylase and lipase may well not be elevated in cases of advanced habitual pancreatitis, but are often utilised as markers for sleuthing pancreatic inflammation in acute pancreatitis. A secretin stimulation effort is thoughtful the gold standard functional effort for identification of habitual pancreatitis but not often utilised clinically. The observation that bi-carbonate production is impaired early in habitual pancreatitis has led to the rationale of ingest of this effort in early stages of disease (sensitivity of 95%). Other ordinary tests utilised to determine habitual pancreatitis are faecal elastase measurement in stool, serum trypsinogen, Computed tomography (CT) scans, ultrasounds, EUS, MRI's, ERCP and MRCP's. Pancreatic calcification crapper often be seen on plain abdominal X-rays, as well as CT scans.

There are other non-specific laboratory studies useful in identification of habitual pancreatitis. Serum bilirubin and alkaline phosphatase crapper be elevated, indicating stricturing of the ordinary bile funiculus cod to edema, fibrosis or cancer. When the habitual pancreatitis is cod to an autoimmune process, elevations in ESR, IgG4, rheumatoid factor, ANA and antismooth hooligan antibody may be seen. The ordinary symptom of habitual pancreatits, steatorrhea, crapper be diagnosed by two assorted studies: Sudden staining of feces or soiled fruitful organic over 24hr on a 100g fruitful diet. To check for pancreatic exocrine dysfunction, the most sensitive and specific effort is the measurement of soiled elastase, which crapper be done with a azygos crap sample, and a value of inferior than 200 ug/g indicates pancreatic insufficiency.

TREATMENT

MEDICAL TREATMENT  

Aimed at controlling discompose and malabsorption .Intermittent attacks treated like accent pancreatitis.Alcohol and super fatty meals must be avoided .Narcotics for severe discompose ,but subsequent addiction is common ,Patients unable to maintain adequate hydration should be hospitalized ,while those with milder symptoms crapper be managed on an ambulatory basis. Surgery haw curb discompose if there is a ductal stricture .Subtotal pancreatectomy haw also curb discompose but at the outlay of exocrine insufficiency and diabetes .Malabsorption is managed with a low fat diet and pancreatic enzymes equal ( 8 customary tablets or 3 viscus glazed tablets with meals ).Because pancreatic enzymes are inactivated by Elvis ,agents that turn Elvis creation ( e.g . omeperazole or sodium bicarbonate ) haw improve their efficacy ( but should not be presented with viscus glazed preparation ) Insulin haw be needed to curb serum glucose .

SURGICAL TREATMENT

Traditional Surgery for Chronic Pancreatitis tends to be divided into two areas - resectional and drainage procedures.New and proven transplantation options preclude the patient from decent diabetic following the surgical removal (resection) of their pancreas. This is achieved by transplanting backwards in the patients own insulin-producing beta cells.

DISTAL PANCREATOMY it consist of distal pancreatic resection up to portal vein ,and it is performed if head of pancreas is relatively normal .

PANCREATODUDENECTOMY it is performed if head of pancreas is mainly involved .

LONGITUDINAL  PANCREATOJEJUNOSTOMY  it is performed if pancreatic duct is grossly dilated .

COMPLICATIONS  

Vitamin B6 malabsorption in 40 % of alcohol induced and all cystic fibrosis cases.Impaired glucose tolerance .Nondiabetic retinopathy due to vitamin A and/ or zinc deficiency,Gastrointestinal bleeding ,icterus ,effusion ,subcutaneous fat necrosis and bone pain occasionally occur .Increased risk for pancreatic carcinoma .Narcotic addiction common.

Treatment for diverticular disease of colon

Diverticulosis is generally discovered through one of the following examinations for appropriate treatment

Barium enema: This x-ray test involves injection of liquid material into the colon through a tube inserted in the rectum. The x-ray image shows the anatomy of the colon, and can identify if diverticula, large polyps or growths are present.

Colonoscopy: This test uses a thin, flexible tube with a light and camera to view the inside of the colon. Diverticula as well as polyps and other growths can be seen with this instrument.

CT scan: This x-ray test takes multiple cross section pictures of the body. It is not generally performed to make a diagnosis of diverticulosis, but this type of exam may identify diverticula.

Patients with diverticular disease should be counselled on the benefits of a high fibre diet. Bulking agents and laxatives could also be added until stools are soft and defaecation is painless.

Patients with acute diverticulitis are admitted to hospital for bed rest, nil by mouth (with iv fluids), analgesics, and IV antibiotics (e.g. cefuroxime and metronidazole). Patients presenting with PR bleeding are resuscitated and given blood transfusion.

Complicated disease (perforation, abscess, multiple attacks, uncontrollable bleeding) usually requires surgery to remove the diseased segment of colon. There are various surgical techniques available depending on the site of the disease, and a temporary stoma is usually needed (a "stoma bag"), although this is reversed after around 6 weeks.

CONSERVATIVE MANAGEMENT

Patients with acute diverticulitis are admitted to hospital for bed rest, nil by mouth (with iv fluids), analgesics, and IV antibiotics (e.g. cefuroxime and metronidazole). Patients presenting with PR bleeding are resuscitated and given blood transfusion.

Complicated disease (perforation, abscess, multiple attacks, uncontrollable bleeding) usually requires surgery to remove the diseased segment of colon. 

There are various surgical techniques available depending on the site of the disease, and a temporary stoma is usually needed (a "stoma bag"), although this is reversed after around 6 weeks.

SURGICAL TREATMENT

INDICATIONS :Recurrent attacks -and Complications

OPERATIVE PROCEDURES 

IDEAL OPERATION 

This is a one stage resection ,which involves removal of affected segment 10 - 20 cm long and restoration of continuity by end-to-end anastomosis .

IN CASES OF OBSTRUCTION & INFLAMMATORY EDEMA AND ADHESIONS a preliminary transverse colostomy can be done as a first stage. In second stage of resecion is performed after 3 weeks or later when inflammation has subsided.Colostomy is closed after a further 2 weeks.
IN ACUTE PERFORATION proximal colostomy can be done ,Exteriorization , Primary resection.

HARTMANN'S OPERATION colostomy after excision with closure of defunctioned distal bowel .

Restoration of bowel continuity can be done at a later stage by means of stapling guns .

IN FISTULA resection of diseased bowel. ,closure of fistula .

IN HAEMORRAHAGE resection of bleeding segment ...... read more

Intestinal tuberculosis is significantly increasing in developed countries with HIV

INTESTINAL TUBERCULOSIS Is a Major Health Problem in Many Underdeveloped Countries

                                           

                                                       BUT

 

A Recent Significantly Increase In Developed Countries In Association With HIV Infection

 

 

TUBERCULOSIS OF INTESTINE

Some bacterial infections are surgically  important include INTESTINAL TUBERCULOSIS usually seen in the uk as ileocecal tuberculosis and present with thickening and narrowing of the terminal ileum.It may be indistinguishable from crohn's disease on naked eye examinaton.although pale tubercle may be seen on the serosa in tuberculosis.Complications include adhesive obstruction ,perforation and malabsorption due to widespread mucosal involvement or lymphatic blockage.

 

 INTESTINAL TUBERCULOSIS is a field health problem in some underdeveloped countries. A recent momentous increase has occurred in matured countries, especially in connexion with HIV infection. Autopsies of patients with pulmonary TB before the epoch of effective treatment demonstrated viscus involvement in 55-90% of mortal cases. The previously noted regular connexion between pulmonary TB and viscus TB no longer prevails, and only a minority of patients (<50%) with abdominal TB now hit deviant dresser radiographic findings. However, approximately 20-25% of patients with GI TB hit pulmonary TB. Any conception of the GI system haw be infected, although the ileum and colon are common sites.

Pathologically GI TB is characterized by inflammation and fibrosis of the bowel surround and the regional lymph nodes. Mucosal ulceration results from necrosis of Peyer patches, lymph follicles, and vascular thrombosis. At this initiate of the disease, the changes are reversible and healing without scarring is possible. As the disease progresses, the ulceration becomes confluent, and comprehensive fibrosis leads to bowel surround thickening, fibrosis, and pseudotumoral mass lesions. Strictures and fistulae formation may occur.

 

We can categarize Intesinal Tuberculosis into Three TYPES on gross pathologic examination

ULCERATIVE modify of TB is seen in approximately 60% of patients. Multiple ostensible ulcers are largely confined to the epithelial surface. This is considered a highly active modify of the disease, with the daylong axis of the ulcers rectangular to the daylong axis of the bowel.

HYPERTROPHIC modify is seen in approximately 10% of patients and consists of thickening of the bowel wall with scarring; fibrosis; and a rigid, masslike appearance that mimics that of a carcinoma.

ULCEROHYPERTROPHIC modify is a subtype seen in 30% of patients. These patients hit a compounding of features of the ulcerative and hypertrophic forms.

 Clinical features  of viscus TB include abdominal pain, weight loss, anemia, and feverishness with night sweats. Patients may present with symptoms of obstruction, correct iliac fossa pain, or a palpable mass in the correct iliac fossa. Hemorrhage and perforation are constituted complications
 of viscus TB, although free perforation is less frequent than in doc disease.  The diagnosis of purging tuberculosis requires a broad index of suspicion. In cases where the information available does not reveal a definite differentiation between colonic tuberculosis and Crohn's disease.

 Intestinal tuberculosis is a thin disease in western countries, affecting mainly immigrants and immunocompromised patients. Intestinal tuberculosis is a diagnostic challenge, especially when active pulmonary infection is absent. It may mimic many other abdominal diseases.

The most common place of GI TB is the ileocecal region, if the area can be reached with a flexible endoscope. A rapid diagnosis can be achieved if smudge or culture results are positive or if caseating granulomas are seen in biopsy samples. In countries where GI TB is endemic, a therapeutic trial of antituberculosis treatment haw be justified if the clinical picture is compatible with TB.

 TREARMENT OF INTESTINAL TUBERCULOSIS

 

A course of chemotherapy

Surgery is required in cases of complicated obstruction in HYPERPLASTIC TUBERCULOSIS - Right hemicolectomy with removal of diseased segment of ileum or defunctioning ileocolostomy .

Surgery is required  in cases of Stricture causing intestinal obstruction or in perforation in ULCERATIVE TUBERCULOSIS

Abscesses - Subphrenic abscess is a pus filled cavity and misdiagnosis lead sepsis and death

SUBPHRENIC ABSCESS 

 

There are a number of spaces below the diaphragm in relation to the liver which may become the site of abscess formation ( a subphrenic abscess ).Abscess may arise from such lesions as perforated peptic ulcer ,perforated appendicitis ,or perforated diverticulitis .Only two of the spaces are in fact directly subphrenic , the other two being subhepatic.The right and left subphrenic spaces lie between the diaphragm and the liver and are separated from one another by the falciform ligament. The right subphrenic space ( pouch of Rutherford Morrison ) is bounded by the posterior abdominal wall behind and by the liver above.The gall bladder, duodenum and right kidney are immediate relations. 

The left subphrenic space is the lesser sac itself.It may distend with fluid as a result of a perforated posterior gastric ulcer or as a result of acute pancreaitis ( pseudocyct of the pancrease ).At the present time most subphrenic abscess are drained percutaneously under the ultrasound control . However , the occasional one still requires open surgery and may be accessed if they are posteriorly placed by an incision below or through the bed of the twelfth rib. If they are placed anteriorly they can be drained through an incision below and parallel to the costal margin.

Any anastomosis leakage or another harm contamination tends to advance to a subphrenic abscess. The pressures from the diaphragmatic movements with respirations are such that there is a movement of the ascitic fluid of the cavum into the subphrenic space and with it travel any bacteria that strength be present, which facilitates abscess formation.

Patients are ofttimes elderly. Symptoms can be very impalpable and start perhaps with a fever and a loss of appetite approximately 1 month after the surgery. There might be a non-productive cough due to an atelectasis in the lung of the strained side or a pleural effusion (fluid in the chest cavity) on that side. Abdominal pain on the strained side in the upper cavum is common, which is severe on deep palpation by the physician. Blood tests exhibit a leukocytosis, there haw also be a lack of red blood cells (anemia).

 

Plain abdominal X-ray films haw exhibit the abscess decay with gas in it from gas producing bacteria. Chest X-rays ofttimes exhibit abnormalities in the lungs (atelectases, lower lobe pneumonia) and pleural effusions as well as an immobile diaphragm. Other tests are useful much as an ultrasound for a right- sided subphrenic abscess and a CT scan for a left-sided subphrenic abscess. The unification here shows a subphrenic abscess before (upper image) and after (lower image) drainage. Because it can be rather arduous to become to a diagnosis, hot isotope scanning much as an indium-111-labeled leukocyte scan could be useful in sleuthing a hidden intra-abdominal or subphrenic abscess.

 

TREATMENT

PERCUTANEOUS DRAINAGE insert a percutaneous drainage tube blindly, under combined ultrasonic and fluroscopic control. Same tube can be used to instill antibiotic solutions into abscess cavity.

SURGICAL DRAINAGE

INCISION if a swelling can be detected , incision is made over the site of maximum tenderness , or over any area where edema or redness is present. If no swelling is apparent , subphrenic spaces should be explored either by anterior subcostal approach or from behind after removal of outer part of 12th rib.

CLEANSING AND DRAINAGE When the cavity is reached ,all the fibrinous loculi must be broken down with finger .One or two drains or drainage tubes must be fully inserted.Drains are withdrawn gradually during next 10 days and closure of the cavity checked by x-ray sinograms.

X-ray shows sub-phrenic abscess

Tuberculous peritonitis

A bacterial contamination from spillage an intraabdominal viscus it could be life threatening event


TUBERCULOUS PERITONITIS
Infection occurs most commonly mass reactivation of latent tuberculous foci in the peritoneum that were established from hematogenous spread from a primary lung focus , It can also become via hematogenous spread from active pulmonary or miliary TB. Much less frequently, the organisms enter the peritoneal cavity transmurally from an infected diminutive intestine or contiguously from tuberculous salpingitis .


Peritoneal T.B. is an uncommon site of extrapulmonary infection caused by Mycobacterium T.B. (TB). The venture is accumulated in patients with cirrhosis, retrovirus infection, diabetes mellitus, underlying malignancy, mass treatment with anti-tumor necrosis factor (TNF) agents, and in patients undergoing continuous ambulatory peritoneal dialysis.


As the disease progresses, the visceral and parietal peritoneum become progressively studded with tubercles. Ascites develops alternative to "exudation" of proteinaceous fluid from the tubercles, similar to the mechanism leading to ascites in patients with peritoneal carcinomatosis. More than 90 percent of patients with TB rubor have ascites at the time of presentation, while the remainder present with a more advanced "dry" phase, representing a fibroadhesive modify of the disease.


Pathologically Gastrointestinal tuberculosisis characterized by rousing and fibrosis of the bowel surround and the regional lymph nodes. Mucosal lesion results from necrosis of Peyer patches, lymph follicles, and vascular thrombosis. At this stage of the disease, the changes are rechargeable and healing without scarring is possible. As the disease progresses, the lesion becomes confluent, and extensive fibrosis leads to bowel surround thickening, fibrosis, and pseudotumoral accumulation lesions. Strictures and fistulae formation may occur.


ORIGIN OF INFECTION from tberculous mesentric lymph nodes .from tuberculosis of ileocecal region ,from tuberculous pyosalpinx ,Blood-borne infection from pulmonary tuberculosis ,usually milliary.


CLINICAL TYPES


ASCITIC FORM peritoneum is studded with tubercles and peritoneal cavity becomes filled with pale ,straw colored fluid .its onset is insidious .with loss of energy , facial pallor and some loss of weight ,enlargement of abdomen ,pain often completely absent ,but there may br abdominal discomfort ,usually associated wih constipation or diarrhea . Even pyrexia and night sweats.


Dilated veins can be seen coursing beneath the skin of abdominal wall. shifting dullness and fluid thrill present , congenital hydrocele sometimes appear in male child .Umblical hernia may develop .A transverse solid mass can often be palpated per abdominally ,( this is rolled up greater omentum infiltrated with tubercles )


ENCYCTED ( LOBULATED ) FORM pathologically it is similar to ascitic form , but one part of abdominal cavity alone is involved .clinical features also resemble to ascitic form ,but there is a localized intraabdominally lump . .localized intraabdominally swelling .fluid thrill and shifting dullness may or may not be present ,depending upon the site of collection .


FIBROUS ( PLASTIC FORM ) there is widespread intraperitoneal adhesions .which causes coils of intestine especially the ileum , to become matted together and distended.These distended coils act as a blind loop. There are symptoms of steatorrhea , loss of weight , attacks of abdominal pain ,Evening pyrexia and night sweats ,and some symptoms of acute and subacute intestinal obstruction , with signs of wasting ,a palpable swelling or swellings per abdominally ( this is adherent intestine with omentum attached ,together with thickened mesentry ).


PURULENT FORM pathlogically there is mass of adherent intestine and omentum ,is surrounded by tuberculous pus to form a cold abscess .This may point to the surface ,commonly near umblicus ,or burst into bowel . In clinically it shows loss of weight ,abdominal pain .discharge from an opening on abdominal skin .evening pyrexia and night sweats ,with signs of discharge from a sinus or fistula ,the opening of which is often wide ,with thin blue and undermined margin. A swelling may be palpated per abdominally ( consisted of adherent intestine and omentum )


ACUTE FORM pathologically resemble with ascitic form and clinically resembles acute bacterial peritonitis .


Some investigations can reveal this lesion such as


PERITONEAL ASPIRATION fluid is pale yellow .usually clear , rich in lymphocytes and have a high specific gravity.1.020 or more .Mycobacterium tuberculosis can be demonstrated by culture and microscopy with Ziehl-Neelsen staining.
MANTOUX TEST a positive test is strongly suggestive ,in non immunized patients .
CHEST X-RAY may reveal pulmonary tuberculosis
LAPROSCOPY can demonstrate the clinical type
PERITONEAL BIOPSY reveal characteristic tuberculous granuloma.


TREATMENT


CHEMOTHERAPY initial phase ethambutol .plus isoniazid plus rifampin plus pyrazinamide for two months .and in continuation phase ethambutol plus isoniazid plus rifampin for four to seven months .


SURGICAL TREATMENT


IN CASES OF FLUID COLLECTION laparotomy is performed ,fluid is evacuated and abdomen is closed without drainage .
IN FIBROUS FORM
On laparotomy ,bands of adhesion are divided. if adhesions are accompanied by fibrous strictures of ileum ,then excise the affected bowel, if adhesions only are present , a plication may be performed.
IN PURULENT FORM
On laparotomy ,cold abscess are evacuated ,fecal fistula is closed , combined with some form of anastomosis between segment of intestine above the fistula and an unobstructed area below.