Definition: Is thin layer of endothelial cells lies over a basement membrane. It usually lines the whole peritoneal cavity including: Interior of the whole abdominal wall ( parietal peritoneum). Whole viscera (visceral peritoneum) . During embryonic development numerous compartment are developed.At the end 2 main compartments are developed: Greater sac Supracolic compartment left subphrenic space. Right subphrenic space Right sub hepatic space Infracolic compartment pelvic space Lesser sac. Behind the stomach.
Endothelial surface is characteristically smooth , glistening & it is normally lubricated by small amount of fluids. In its deeper layers there is rich net work of capillaries and lymphatics. Peritoneum is characteristically quite resistant to infection. F.B can reduce resistance to infection significantly. Bacteria injected in to the peritoneal cavity can be rapidly phagocytized and eliminated ,while the same quantity of bacteria if it is injected subcutaneously or retroperitonealy it can cause spreading cellulitis or abscess. So bacterial peritonitis can only occur in: Continuous or persistent contamination. Contamination with unusually virulent bacterial strain or species. Omentum : Is double fold of peritoneum usually loaded with fat and hanged from the stomach and transverse colon as an apron over the small bowel. It is very mobile. Highly specialized tissue. Play active role in control of suppurative inflammation & infection within peritoneal cavity.
Is an acute inflammation of peritoneum. It could be divided into 2 major types: 1.Primary peritonitis. 2. Secondary peritonitis.
Result from direct hematogenous invasion of peritoneal cavity. Mainly caused by pneumococcal and streptococcal microorganisms in healthy individuals. Now it usually involve debilitated patients with ---- Nephrosis . Cirrhosis . Ascites of any cause.
Is mainly due to secondary infection from near by structure like (bacterial peritonitis) : Inflamed organ like- Appendicitis, Diverticulitis. Perforated viscus ( perforated colon ,Penetrating abdominal wounds). It can occur due to irritation with chemical substances in the secretions that are produced by different intra- abdominal structures like stomach, small bowel ,liver & pancreas (chemical peritonitis).
This can results from gastric , bile, pancreatic juices, blood and urine. These substances can cause severe peritoneal irritation . The body will respond by exudation of large amount of fluid into the peritoneal cavity to dilute these irritant material. This will results in massive loss of fluids resulting in hypovolemia & shock.
Gastric juice Gastric acid secretion will contaminate the general peritoneal cavity results in severe chemical peritonitis with severe abdominal signs and symptoms.
Pancreatic secretions can produce very severe peritonitis as it contain digestive enzymes.
Bile if not gets infected or mixed with other secretion is remarkably innocuous. but once it gets infected or mixed with gastric and pancreatic secretion it produce very profound irritation & can cause progressive type of ascites with little abdominal signs and symptoms.
Blood usually produce very mild irritation to the peritoneum but once the RBC hemolyse and hemoglobin is released into the peritoneum it causes severe irritation specially if it is contaminated with bacteria.
Sterile urine causes very mild irritation . But infected urine can cause severe irritation and urinary peritonitis.
Perforated colon causes severe peritonitis as it is loaded with bacteria which might lead septicemia and overwhelming sepsis due to mixed bacterial infection often gas forming organism.
chemical peritonitis is almost always changed into bacterial peritonitis
Localization depends on --Nature of primary disease. Natural defense mechanism. Virulence of microorganism. Liver : play an important role in defense mechanism. It picks up bacteria through lymphatics & portal circulation. It destroy bacteria. In the presence of hepatic insufficiency as in liver cirrhosis generalized septicemia might developed very rapidly. e.g Appendicitis , Appendicular abscess.Symptoms: Signs: Severe abdominal pain. Palpation: Tenderness all over Board like rigidity Nausea. Percussion : Tenderness Vomiting. Auscultation: Silent abdomen Constipation. Abdominal distension. in very young & very old patients peritonitis develop insidiously so that marked ileus and abdominal distension are present when the patients were first seen. Without treatment hypotension ,toxemia and multi-system organ dysfunction and organ failure will develop . ( Respiratory , renal and cardiac).
WBC count : Leukocytosis , leukopenia. Serum electrolytes measurement : varies . 3. Acid base imbalance : increase in the BMR a. Metabolic acidosis . PH b. Respiratory alkalosis. Increase the depth and rate of respiration PCo2 4. Plain abdominal X-ray findings: Gaseous distension of small and large bowel with multiple air fluid levels. Thick bowel loops and fluid in between bowel loops can be seen as (appearance of white lines between bowel loops which are distended with gas). Crescentic shadow of gas under diaphragm : In perforated viscus ( perforated DU, Perforated colon ) mainly under the right dome of diaphragm. large crescent of gas under the left dome of diaphragm is characteristic for colonic perforation.
Abdominal paracentesis:
4 quadrant peritoneal tap.Peritoneal lavage
Particularly helpful in Non-penetrating abdominal injuries. Aged patients. Signs and symptoms are equivocal.
Differential diagnosis is related to the primary cause: 1. If it occur rapidly: Perforated Du. Acute pancreatitis. Mesenteric thrombosis. 2. If it occur more slowly: Acute appendicitis. Acute cholecystitis. Diverticulitis
Many systemic conditions can produce abdominal pain, distension resembling cases of intestinal obstruction,and peritonitis: 1. Pneumonia: Old people can presents with abdominal distension. 2. Diaphragmatic pleurisy: Abdominal pain. simulate Acute cholecystitis,Perforated DU. 3. Uremia: Presents with abdominal distension&ileus. Uremic pt. is more prone to develop intra abdominal diseases making differentiation more difficult: Appendicitis. Perforated DU. 4 Quadrant peritoneal tape is done. Significant only if positive
*Rare condition. * Can produce all the signs of acute peritonitis without identifiable cause. * Characteristically present with: 1. History: Recurrent episodes of abdominal pain . 2. O/E: Tenderness & rebound tenderness. *Fever ( 38-390 C ) . *Leukocytosis. *Colchicine is capable of preventing attacks. *Familial tendency in Mediterranean sea (Turk,Arab &Italian). *Laparotomy is usually done for the first attack. a. Inflamed peritoneal surfaces. b. Free fluid with negative culture. c. Even with normal appendix appendicectomy should be done to rule out the diagnosis of the recurrent episode.
Could be divided into: 1. Early complications: a. Shock. b. Respiratory failure. c. Acute tubular necrosis. d. Hepatic failure---------------Liver abscess. Pyelphlebitis. 2. Late complications: a. Intra-abdominal abscesses: 1. Pelvic abscess. 2. Subphrenic abscess. b. Intra-peritoneal adhesions ---Intestinal obstruction.
Early peritonitis:A.Removal of the cause by operation:Appendicectomy.Closure of perforated DU.Cholecystectomy.Resection of gangrenous bowel……….etc.B.Antibiotic therapy.C.Early operation has negligible mortality from peritonitis.
A. Surgery is needed to control the source of contamination in most cases. In localized peritonitis: in some cases continuous observation and non surgical treatment may be attempted. In patients with severe peritonitis in debilitated patients when condition deteriorate so anesthesia can not be given. Surgery might be lethal. The only hope will be: Antibiotics. Supportive therapy. This will permit localization & formation of abscess which can be drained later.
1.Nothing per oral. 2.Nasogastric suction. 3.Intravenous fluids: a. Started immediately. b. Ringer lactate or balanced salt solution. c. Potassium should not be given unless renal function is normal after good resuscitation if it is needed. 4. Laboratory investigations: It should be done in emergency room at the time of fluid therapy. a. Blood should be aspirated for: CBP,S.Na,S.K+ ,s.chloride,Urea,s.creatinine,amylase,bicarbonate b. In critically ill patients: Blood gas analysis (PO2,PCO2 PH )
5. Urinary catheter: Early & moderately advanced peritonitis should be avoided as it can be a port of entry for bacteria. In severe cases catheter is advisable to determine : 1. Hourly urine output. 2. Estimate fluid requirement. 6. CVP (central venous pressure): in circulatory instability: It should be used a. Critically ill patients. b. Moderately ill elderly patient. C. Patient with cardiac disease. 7.Analgesia: a. Narcotics and sedatives like morphine should be given in a dose of (10-15 mg) intramuscularly if the patient is not shocked. B. If the patient is shocked Morphine should be given intravenously (1-3 mg) and repeated if necessary. 8. Antibiotics: Is the mainstay treatment. 3rd generation cephalosporins ( cefotaxime) is given which acts on Gram(+VE), Gram(-VE) and anaerobes mainly bacteroids fragilis. It should be given according to culture and sensitivity.
9.Oxygen Patients with peritonitis shows remarkable increase in metabolic demands accompanied with increase in oxygenation and ventilation because of : Marked abdominal distension. Elevation of dome of diaphragm. Associated with pulmonary insufficiency from emphysema. Determination of arterial blood gas is essential. Oxygen therapy: is done. Assisted ventilation. Tracheostomy might be needed. Decompression of bowel by ---------- Nasogastric suction , operative decompression. be used).
a. Peritoneal toilet. B. Intestinal decompression. C. Peritoneal irrigation. D. Drainage. 1. Drainage of general peritoneal cavity is unnecessary ,ineffective and undesirable. 2. Drainage Should be done in localized masses of necrotic material and debris which can not be removed. 3. In localized abscess. 4. Prophylactic drainage will not prevent abscess formation. 5. The principle indications for drainage: Presence of possible source of contamination. Wounds and inflamed disorders of pancreas and biliary tree. When an opened viscus can not be surely closed .( Sump drain should be left in the peritoneal cavity. 6.BINDERS Should be avoided as it restrict respiratory .movement Adhesive tap will provide excellent support to the wound & not restrict rep movement.
1. All preoperative measurements should continue. 2. N.P.O 3. NG suction. 4. Intravenous fluids. 5. Electrolyte balance should be carefully monitored. 6. Narcotic analgesics (Meperidine or pethidine) might be needed. 7. Antibiotics should be given according to culture and sensitivity. 8. Blood might be given: a. if anemia is present. b. Intra-operative transfusion of whole blood or packed RBCs might be required.
: Depends mainly on: 1. Cause. 2. Age --------Very young. Very old. 3. Duration of illness before surgery. The earlier the better.
They presents with very characteristic features: The patient does not look ill. Severe abdominal pain. Right hypochondrial pain can simulate acute cholecystitis. Fever. Peritoneal signs of rigidity and tenderness. No tachycardia. No hypotension. No shock. Unique feature is the extent of inflammation through out the peritoneal cavity with the formation of adhesions between liver and diaphragm.
Is a chronic glaucomatous lesion of peritoneal cavity. Often it is Primary infection. History: Hx. Of generalized weakness of (2-4 months). Loss of appetite, loss of weight, night sweating and abdominal distension. On Examination: Doughy abdomen Free peritoneal fluid (Ascites) may be the only positive finding. Distinct mass in the right iliac fossa. Investigations: Paracentesis: Shows straw color fluid. (exudate) High protein (3 gm /L i.e. exudates), low sugar, Chronic lymphocytic infiltration with lymphocytes. 1.Smear: Acid fast bacilli are rarely identified. 2. Culture: is positive in 80% of cases. b. Percutaneous needle biopsy can be diagnostic. c. Laparoscopic or open biopsy may be necessary if percutaneous biopsy is negative. 4. Treatment: Anti-Tuberculous therapy can give excellent results. Steroid may be added to decrease the incidence of intra-peritoneal adhesions and band ormation.
Chronic type of peritonitis. Caused by presence of chyle fluid in the peritoneal cavity. Could be: Congenital-- Childhood (Chronic abdominal swelling). Acquired --- Adult due to malignant tumors- Upper abdomen. Thorax. Pancreatic tumor No cause ----50% of cases. Congenital type: Is due to obstruction of intestinal lymphatic channels which will remarkably enlarged and communicate freely with peritoneal cavity. It may also involve the extremities so that chyle appears in the skin (Cutaneous chylous reflux). If Ascites is minimal chylous cutaneous reflux can be treated by surgery by dividing incompetent large lymphatic channel between the lymphatics of skin and that of intestinal mesentery. If it is discovered during surgery retroperitoneal dissection is not needed to locate the rupture of lymphatic vessels. DXT (deep x-ray therapy) results in dramatic improvement in cases of lymphoma.
Is peculiar type of acute or chronic peritonitis secondary to a varieties of substances used in preparation of surgical gloves like: 1. Talc. 2. Starch (Corn, Rice). It can produce a peculiar syndrome. Develop within (2-3 weeks) after uncomplicated abdominal operation. Severe abdominal pain. Fever. Marked peritoneal irritation. Normal WBC. If the condition is diagnosed, operation should be avoided. Symptoms might be so severe that immediate laparotomy might be taken. This might aggravate the condition due to dissemination of causative agent and reactivation of the pathological process. The cause of such reaction is unknown as it is restricted to a very small number of patients who react in hypersensitive manner to the presence of foreign body. Treatment: Corticosteroids: can give good immediate results. Prevention: Washing all surgical gloves from foreign material.
large defects in the peritoneum in the absence of trauma, hemorrhage or infection can very rapidly heal by the process of metamorphosis of in situ mesenchymal cells. Is commonest after operation for localized or generalized peritonitis and not due to simple defect in peritoneal coverage and new peritoneal surfaces arises from the raw surfaces. It can occur without operation following peritonitis as in Gonococcal peritonitis as severe adhesions occurs between liver and diaphragm. In low grade peritonitis as in tuberculous peritonitis. Can follow operation without any clinical signs of peritonitis. Short fatty females are more prone to develop postoperative adhesions.
1. Mechanical injury.2. Ischemia.3. Bacterial contamination.4. Venous stasis.5. Presence of blood.6. Foreign body of any type. (Talc, cellulose, fabrics….from disposable surgical gloves). Clinical features:Symptomless …in most cases.Pain…………...In severe adhesions.Intestinal obstruction.Prevention:Meticulous surgical technique is the only way of avoiding adhesions with or without peritonitis.Traumatized areas of peritoneum should be protected by interposing omentum between the area and bowel loops.All foreign materials and blood should be carefully aspirated completely at the end of operation.
Peritoneum could be involved by varieties of tumors:Primary tumors: Mesothelioma. …..present as one massSecondary tumors: from secondary cancerous implants… Ovarian, gastric, colonic….etc. presents as multiple masses that simulate chronic peritonitis.
Is the only primary tumor of the peritoneum.It has increasing tendency.Following latent period of (30-40 years) after exposure to asbestos the tumor appears. 65% …………..pleura.25%.................peritoneum.10%.................both. Exposure to asbestos is responsible in 50% of cases.Clinical features:Bulky mass -------Epigastric mainly in 15% of cases.Diffuse involvement of peritoneum.Abdominal pain, abdominal distension, marked weight loss and Ascites.Metastasis to the liver, lungs are rareDifferential diagnosis:TB.Carcinomatosis.Diagnosis:Thrombocytosis.Increase in fibrin degradation products.Cytological examination of ascetic fluid.Treatment:No treatment was found to be beneficial.Patients were usually died within 12 months after diagnosis.
Is an obscure disease that begins as intraperitoneal dissemination of mucus and implantation of mucus secreting cells from mucocele of appendix or mucinous cystadenoma of ovary. The abdomen will be filled with masses of gelatinous material (jelly like fluid) partially encysted with mucins. Patients may present with abdominal pain , ascites and low grade intestinal obstruction. Explorative laparotomy shows huge masses of jelly like material which is easily evacuated from peritoneal cavity. It runs chronic course which may be palliated by period operations to remove the mucinous material and relieve the obstruction. Treatment with alkylating agents like Thiotepa into the peritoneal cavity after removal of muciod masses appear to be beneficial. With time the disease assume low grade diffuse peritoneal malignancy but with no distant metastasis (neither by blood or by lymphatics). DXT and chemotherapy is not beneficial. Death occurs from malnutrition and recurrent obstruction
Is rare developmental lesion. Is of variable sizes filled with straw color fluid and has very little blood supply. Most are benign. Can be removed by enucleation without injury to the mesenteric blood vessels or intestine. Masses are characteristically move from side to side perpendicular to the level of attachment of the mesentery. If fixed it should be differentiated from retroperitoneal sarcoma. Excisional biopsy through laparotomy is essential for diagnosis.
Large no. of varieties is present usually of connective tissue type. It include: Fibrosarcoma, Leiomyosarcoma, liposarcoma, lymphosarcoma. Usually presents with HX : Low grade pain, fever. O/E : Palpable mass (fixed mass). X-ray : shows displacement of bowel and ureters. They are rarely benign or of low grade malignancy. These give good results following surgical excision. Malignant tumors apart from lymphosarcoma treatment are not satisfactory. Palliation could be achieved by aggressive but incomplete removal of liposarcoma and Leiomyosarcoma. Abdominal exploration and biopsy is essential as response to irradiation is gratifying if lymphoma is discovered.
Is rare condition. Usually affects the urinary tract (most commonly ureters) but it can involve small and large bowel or their mesenteries. It is thought to be----- hypersensitivity to drugs like (Methysergide, protocol). Auto-immune process. Clinically: Presents with signs and symptoms of low grade small or large bowel obstruction. Diagnosis is established by biopsy. Treatment: Lysis of constricting band. Use of steroids.
Is walled -off collection of pus containing leukocytes,necrotic debris and microorganism
Intraperitoneal abscess. Retroperitoneal abscesses. Visceral abscesses.Are mainly caused by secondary peritonitis i.e by direct spread from ( GIT, Genitourinary, Biliary tract ). Most are poly microbial .(rarely sterile) Single or multiple. It is a major cause of mortality and morbidity in general surgical population (20% ). Mortality is highest in immunocompramized patients especially in patients with significant chronic organ failure (cirrhosis). Mortality is highest in very old and very young patients. Early diagnosis: high index of suspicion. proper clinical investigations (U/s and CT scan). Prompt adequate drainage. Antibiotics should be given ( against gram negative & anaerobes).
Many are caused by monomicrobial microorganism. Are mainly results from hematogenous spread. Less commonly to secondary peritonitis.
1. Does the patient have intra-abdominal abscess. 2. Where is it and is there more than one. 3.What cause it ( Bacteriology and pathophysiology) 4. How should the abscess (es) be drained. 5. Is it necessary to do more than drain.
History & clinical examination: Fever. Tachycardia. Localized abdominal or rectal tenderness ( with or without mass) . Punch percussion signs in subphrenic and sub hepatic abscesses. Gut dysfunction ( abdominal distension, paralytic ileus ). Abdominal symptoms and signs may be minimal or absent in the setting of large upper abdominal or pelvic specially in obese people. Persistent gastric ileus & respiratory symptoms in upper abdominal abscesses ( Subphrenic, sub hepatic ,lesser sac). Urinary symptoms , diarrhea , tenismus in pelvic abscess.
Investigations: leukocytosis (sensitive but not specific). Increasing glucose intolerance (increasing blood sugar level). Blood cultures: ( +ve) for anaerobic or multiple microorganism indicates intra-abdominal infection. Chest X-ray Elevated dome of diaphragm, Pleural effusion, Persistent atelactasis. U/S of abdomen. CT scan. Gastrograffin meal (lesser sac abscess). Gastrograffin rectal enema (pelvic abscess
Localization of abscess depends on the cause.(usually near by the organ which is involved by disease. Upper abdominal surgery ( pancreatitis, biliary tract, peptic ulcer disease (subphrenic and sub hepatic &lesser sac abscesses ). Acute appendicitis---- (R . iliac fossa , pelvic ). The single best technique for localizing intra-abdominal abscesses is : ( 90) % CT scan with oral or intravenous contrast ) Site,size and number--- it gives clue in planning effective treatment ( operative and percutaneous drainage ). operation is chosen if it is multiple Contrast in the abscess cavity indicates a hole in the gastrointestinal tract. ( operative drainage and closure or diversion). Ultrasound study could be done in not too ill patient especially (upper abdomen and pelvis) . CT and U/S could be done in severely ill patient in intensive care unit. Gallium 67scan and indium111 had no place in diagnosis.
Pathogenesis: It can be caused by: 1.Perforated viscous ( GIT ): ( spontaneous, anastamotic and traumatic ) . 2.Pelvic inflammatory disease. 3.Visceral; abscess can result from : local infections. Hematogenous spread. Infarction with subsequent super infection. Bacteriology: Bacteriology depends on whether it results from : Direct contamination ( Secondary peritonitis) Hematogenous spread . Rather than the localization of abscess or its viscous of origin.
The priorities of treatment includes: 1. Supportive care. 2. Adequate drainage. 3. Appropriate antibiotics. * Resuscitation measures should be started before surgery. * Resolution will depends heavily on Drainage which should be done within 24 hours . * Antibiotics should be given empirically preoperatively.
Is a disease cause by tapeworm (Echinococcus granulosus).Dogs and foxes harbor the adult worm in their intestine.Human being is intermediate host that harbor the larval cyst in his tissues.Life cycle:Dog intestine (adult worm) ------------Excrete OVA in FECESIngestion of contaminated material by intermediate host ( Sheep , cattle, man, rodents) ----OVA----penetrate the intestinal wall---via portal circulation—Liver-------Lung-----Other tissues.In tissues-----OVA will develop into Cyst ( Filled with crystal clear fluid which contain Hydatid sand) ------Ruptured into peritoneum or pleura ---another cysts.Cyst :Is composed of:pseudo cyst: Adventitious fibrous tissues which surrounds the cyst.Ectocyst: composed of whitish laminated layer called laminated membrane on its inner side it contain broad capsules which if the cyst is ingested by definitive host it will form adult worm..
Local symptoms (pressure symptoms). Systemic allergic reaction. Eosinophilia is present in 40% of cases. Liver and lung account for 90% of cases, but it can affect any tissue. Usually solitary. 25% of cysts will die and calcify so therapy is not needed. Diagnosis can be substantiated by serological tests: Skin tests are inaccurate. Haemagglutination test for Hydatid disease and complement fixation test is accurate and specific and it tend to be negative when the cyst is eradicated or die. Treatment: Is usually surgical. Medical treatment with antihelmenthics can be given in: Small cysts In cases of rupture into endothelial lining serous cavities like peritoneum and pleura. Pre and post operatively to decrease the incidence of recurrence if spillage occurs during surgery.
Liver is the most common organ involved by disease. Presentation: Chronic upper abdominal pain. Hepatomegaly. Intrabiliary rupture of Hydatid cyst can results in: Biliary colic. Jaundice. Intraperitoneal and intrapleural rupture can result in anaphylactic reaction. Liver U/S Can outline cyst or cysts. > 2 cysts is present in 15% of cases. Selective Angiogram can also be obtained if hepatic resection is planned to be done.
Surgery is the only effective treatment. Aspiration of cyst fluid Injection of scolicidal agents is usually done such as hypertonic sodium chloride solution (20-30%) or sodium hypochlorite solution (0.5%). Formaldehyde and phenol is not recommended as it can result in sclerosing cholangitis especially in the presence of communication between cyst cavity and billiary tree. Ectocyst can be shelled out intact through the line of cleavage. In intrabiliary rupture : exploration of CBD can be done debris are removed. Remaining cavity can be dealt with by either: Drained by tube drain. Filled with normal saline and closed Filled by omentum (omentoplasty). Excision of part of the ectocyst and macipilization was done.