A surgery had not progressed to the stage


Peritonitis is defined as inflammation of the serosal membrane that lines the abdominal cavity and the organs contained therein. Peritonitis usually occurs secondary to contamination of the peritoneal cavity by the gastro intestinal contents, either due to perforation of the hollow viscera or due to translocation of bacteria through the wall of ischemic gut.
Acute generalized peritonitis is considered as a surgical emergency, which is very challenging to manage .The rate of secondary infection is higher as majority of patients being from rural areas, present late to the hospital due to low awareness, local beliefs and faith in native medicine. This study aims to compare the efficacy of povidone iodine in normal saline and normal saline in peritoneal lavage and to ensure adequate control of infection and to decrease the chances of post operative wound infection thereby preventing prolonged hospital stay
The early treatment of peritonitis had to be medical since surgery had not progressed to the stage where the abdomen was entered intentionally. The generally accepted treatment for peritonitis at the beginning of the nineteenth century was absolute rest, purgatives-especially magnesium sulphate, abstention of food, cold applied to the abdomen, bloodletting in acute cases, and opium very sparingly.
Peritonitis was first recognized as a disease entity in 1815, that the pathology was in the peritoneum itself in contradistinction to the commonly held view that all abdominal inflammation were infections of various organs.
In 1881, opening the abdomen as soon as the condition was diagnosed, and the so called toilette of the peritoneum using a 2% thymol solution in sponging the soiled intestines and the use of drainage tubes.
Later filling the abdomen with blood warm water and washing all organs repeatedly until the water came off clear. Early Surgeons reported a case of peritonitis following herniotomy treated by irrigation of the abdominal cavity with 1 in 5000 bichloride of mercury solution through a ten inch metal tube passed up through the operative wound. After four days he changed to a 1% carbolic acid solution. Morphine was given for pain and milk only diet was instituted, the patient was able to go home on the fourteenth day.
After closure of perforation, peritoneum is cleaned through saline lavage and aspiration. Intraoperative peritoneal lavage is a standard procedure in the operative management of peritonitis Lavage reduces the bacterial load, thereby reducing the incidence of postoperative surgical site infection and sepsis.
Different types of fluids have been used for peritoneal lavage in peritonitis patients. These include,

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• Sterile water

• Warm saline

• Aqueous povidone iodine

• Saline with antibiotics

Peritoneal lavage reduces the bacterial load, thereby reducing the incidence of post operative surgical site infection and sepsis .Saline lavage reduces significantly counts in peritoneal fluid of aerobic and anaerobic bacteria in peritoneal fluid and gives us the idea of amount of debris present in the peritoneal fluid. Povidone iodine is a stable chemical complex of poly vinyl pyrrolidone and elemental iodine. It contains 9% to 12% available iodine. It is an effective bactericide and is safe when used as peritoneal lavage solution.
Addition of antibiotics to the fluid does not have distinct advantage over warm saline lavage. Experimental studies have shown that adequate therapeutic levels of antibiotics are attained in the peritoneal fluid with IV injections.
In this study peritonitis patients are divided into two groups randomly. In the first group of patients, 20 ml of betadine in 2 liters of warm saline is used for intraoperative peritoneal lavage. In the second group, 2 liters of warm saline is used.


1. To study the clinical outcome of patients with peritonitis who have received peritoneal lavage with povidone iodine in normal saline.

2. To study the clinical outcome of the patients with peritonitis who have received peritoneal lavage with normal saline.

3. To compare the clinical outcome between two sets of patients.

The earliest descriptions of a peritoneal infection was provided by Hippocrates.
He described the patient’s appearance as sick and wasted, with his face expressing fear called Hippocratic facies.
During that time, little was known about the normal physiologic process and effective treatments for peritonitis did not exist.
As a result, these infections were associated with significant morbidity and mortality.
Morbidity of the peritonitis is realized when one appreciates that it involves 22000 sq cm of serosa, which is equivalent to 70 to 100% body surface area burns.
The surgical treatment of peritonitis started with the first laparotomy for an infected ovarian cyst by McDowell in the beginning of the 19(th) century.
In the last decade of the 19th century Mikulicz advocated that laparotomy was indicated in all patients with purulent peritonitis.
In the beginning of the 20th century Korte and Kirschner defined the principles of surgery for peritonitis that are valid up to this day: early surgical intervention, elimination of the source of infection, and peritoneal toilet.
Intra operative peritoneal lavage, first performed by Gynaecologist Joseph Price in 1905 using sterile water.
After closure of the perforation, the peritoneum is cleaned through peritoneal lavage and aspiration.
Intra operative peritoneal lavage is the standard procedure in the operative management of peritonitis.
Different fluids have been used for lavage like sterile water, warm saline, aqueous povidone iodine, saline with antibiotics.
Lavage reduces the bacterial load thereby reducing the surgical site infection and and sepsis. It has also shown to reduce the mortality in experimental studies.
Addition of antibiotic to saline does not have distinct advantage over warm saline lavage. It has been shown by experimental studies that adequate levels of antibiotics are attained in the peritoneal fluid with IV injections.


The anatomic relationship within the abdomen are important in determining possible source and routes of spread of infection.
The peritoneal cavity extends from the under surface of the diaphragm to the floor of the pelvis.
In man, the peritoneal cavity is a closed space. In women, it is perforated by the free ends of the fallopian tubes.
Anteriority the peritoneal cavity reflects onto the posterior aspect of the anterior abdominal musculature.
Posteriorly, the peritoneal lining lies superficial to the retro peritoneal viscera, including aorta, venacava, ureters and kidneys.
The anterior and posterior peritoneal layers are described collectively as the parietal peritoneum.
The visceral peritoneum represents the mesothelial lining cells that are reflected onto the surface of the viscera. The peritoneum covering the intestine is the serosa of the bowel.


The peritoneal reflections and the mesenteric attachments compartmentalize the intraperitoneal space and route, spreading exudates to sites that are often distant from the source.
The transverse mesocolon divides the peritoneal cavity horizontally into an upper and a lower space.
The greater omentum, extending from the transverse mesocolon and the lower border of the stomach, covers the lower peritoneal cavity.
The peritoneal cavity has several recesses into which exudates may become loculated. The most dependent recess of the peritoneal cavity in the supine position is in the pelvis. Between the rectum and bladder in men is a pouch of peritoneal cavity that extends slightly below the level of the seminal vesicles.
In women, the uterus and fallopian tubes project into the pelvic recess. Between the rectum and the body of the uterus is the pouch of Douglas, which lies above the posterior fornix of the vagina. On either side of the rectum and bladder are the pararectal and paravesical fossae. The pelvic recess is continuous with both the right and left paracolic gutters. The phrenicocolic ligament, which fixes the splenic flexure of the colon to the diaphragm, partially bridges the junction between the left paracolic gutter and the left perihepatic space.
In contrast, the right paracolic gutter is continuous with the right subhepatic space and the right subphrenic space. A posterior extension of the right subhepatic sac, Morrison’s pouch, is the most dependent portion of the supine position of the right paravertebral groove and lies just above the beginning of the transverse mesocolon.
The horizontal posterior reflection of the serosal surface of the liver onto the diaphragm, (the right triangular and coronary ligaments), and the vertical reflection (falciform ligaments) divide the right perihepatic space, into right subphrenic and right subhepatic spaces. The left subphrenic and subhepatic spaces communicate freely around the smaller left lobe of the liver, and it is more superiorly placed to left triangular ligament.
The right and left subphrenic spaces are separated by the falciform ligament, which probably prevents the spread of pus to the opposite side and explains why only about 5 to 15% of subphrenic abscess are bilateral.
The left subhepatic space is divided by the gastro-hepatic omentum into an anterior space and the lesser sac. Abscesses within the perihepatic spaces become localized by pyogenic membranes.
In the right subphrenic space, they lie anteriorly or posteriorly and in the subhepatic space, superiorly or inferiorly. Abscesses of the left perihepatic space are either in the single left subphrenic or in the lesser sac.
The lesser sac, the largest recess of the peritoneal cavity, is connected to the main peritoneal space by the foramen of Winslow, an opening situated between the free border of the gastro-hepatic omentum and the posterior parietal peritoneum.
The lesser sac is surrounded posteriorly by the pancreas and kidneys, anteriorly by the stomach and laterally by the liver and spleen. It may also extend to variable extent between the folds of the greater omentum.
Because of limited communication from the lesser sac to the major cavity via foramen of Winslow, suppuration in the lesser sac lie between the stomach and pancreas but may spread to the right and lie anterior to the right kidney and inferior to liver.
After intraperitoneal injection of water soluble contrast material, selectively into various intraperitoneal spaces, Autio demonstrated that right paracolic gutter is the main communication between the upper and lower peritoneal cavities.
Fluid introduced into the right upper peritoneal space gravitates towards Morrison’s pouch and then into the right subphrenic space and along the right paracolic gutter into the pelvic recess.
Flow of fluid in the left upper peritoneal space is mainly into the left subphrenic space. The phrenicocolic ligament limits flow inferiorly into the left paracolic gutter.
Fluid introduced into the lowerperitoneal cavity first gravitates to the pelvic recess and then ascends, whether in supine or erect position, along the right paracolic gutter into the right subhepatic space, especially into Morrison’s pouch and into the right subphrenic space.
Ascension of fluid from the pelvic space along the left paracolic gutter is minimal and is limited by phrenicocolic ligament. Although gravity would account for the pooling of fluid in the dependent peritoneal recesses, such as the pelvic recess, ascension of fluid from the pelvis to the subphrenic space is probably caused by hydrostatic pressure differences between the upper and lower peritoneal cavities created by diaphragmatic motion.
Normal intestinal and abdominal wall motion would also account for some spread of intraperitoneal fluid.
The anterior retro-peritoneal space between the peritoneum and anterior renal fascia contain the ascending and descending colons, duodenum and pancreas. The kidneys and ureters lie within the posterior retro peritoneal (perinephric) space. The renal fascia encloses the kidneys and adrenal superiorly and laterally, but not inferiorly, favouring spread of infection in this space inferior.

Innervation of the peritoneal lining figures prominently in clinical recognition of peritonitis. The nerve supply of visceral peritoneum is poor and arises from the visceral structures beneath the lining. Therefore, it’s stretching produces nausea and poorly localized pain. Pain is usually localized to the dermatome distribution of the associated visceral organ eg. Irritation of the peripheral diaphragmatic peritoneum is felt as pain near the adjacent body wall, and irritation of the central portion is felt as a pain referred to shoulder or neck.
The nerve supply of the parietal peritoneum, the somatic afferents, arises from branches of cutaneous nerves in the anterior abdominal wall. The parietal peritoneum is exquisitely pain sensitive to stretch as well as light touch and cutting, particularly anterior, pain thus produced can be very precisely localized by patients and is the basis for the clinical findings of “peritoneal sign”. Pain may be associated with tenderness and involuntary muscle spasm (guarding).
Organ / Structure Dermatome Innervation
Esophagus Vagus (brainstream)
Stomach T5-7
Small Intestine T8-10
Colon T10-L1
Liver T6-8
Gallbladder T6-8
Uterus T10-L1
Kidney T10-L1
Bladder S2-4
Diaphragm C4-8

The blood and lymphatic supply of the peritoneum generally follow the distribution of the innervations.
The blood supply of the visceral peritoneum arises from the adjacent visceral organs.


The peritoneal cavity is lined by a serous membrane. The surface area of this membrane approximate that of skin i.e. 1.8 m2.
It is semipermeable membrane. Each of these layers comprises of a layer of flattened mesothelial cells, a basement membrane and a layer of loose vascular connective tissue containing collagen bundles, lymphatics and macrophages.
The mesothelial cells contain microvilli 1.5 to 3.00 mm in length, which greatly increase the surface area of the mesothelial cells. As the peritoneum covers the abdominal surface of the diaphragm, the basement membrane disappears and large intercellular gaps stomata become obvious.
These measure from 8 to 500 angstroms in diameter which vary according to the contraction of diaphragm.


The peritoneum is a single layer of mesothelial cells, with a basement membrane supported by an underlying layer of highly vascularised connective tissue.
The surface area of the peritoneum is extensive, averaging 1.8m2 (adult male) and is comparable to the surface area of the skin.
It has been estimated that a 1mm increase in the thickness of the peritoneum can result in the sequestration of 18 liters of fluid, a fact relevant to the massive fluid shifts associated with diffuse peritonitis.
Under normal condition, 11,000 cells / mm3) with a shift to the immature forms on the differential cell count.
But patients who are immunocompromised and patients with certain types of infection (e.g. typhoid) may demonstrate absence of leukocytosis and may even demonstrate leucopenia.
Serum amylase and lipase levels in patients with possible diagnosis of pancreatitis. Urine analysis is essential to rule out urinary tract diseases (E.g. pyelonephritis may mimic peritonitis).
However patients with lower abdominal and pelvic infection often demonstrate WBC in the urine and microhematuria. The presence of frank pyuria, large number of red blood cells and bacteria in the specimen suggest a urinary source of patient’s symptoms.
This is a test for the measurement of H and O agglutinins in the patient’s sera for typhoid infection. The results are interpreted according to the agglutination titre.
The test is taken to be positive if titre is greater than 1/100 for O agglutinin and 1/200 or more for H agglutinin or rise in titre is demonstrated .
If positive, ileal perforation should be suspected as the cause of peritonitis.

A peritoneal fluid should be evaluated for glucose, protein, and lactate dehydrogenase, and gram stain, aerobic and anaerobic culture.
A peritoneal fluid amylase should be done if pancreatitis or pancreatic leak is suspected; creatinine level when a urinary leak is suspected.
The peritoneal levels should be compared with serum levels.


The presence of free, intraabdominal gas almost always indicates perforation of a hollow viscus.
The commonest cause is perforation of peptic ulcer; other much less common causes are diverticulitis and malignant tumors. About 70% of perforated ulcers will demonstrate free gas, a phenomenon that is almost never seen in cases of a perforated appendix.
As little as 1 ml of free gas can be demonstrated on a radiograph, either an erect chest, or a left lateral decubitus abdominal film. Radiographic techniques are important and the patient should remain in position for 5-10 minutes.
The clinical condition of the patient will determine the radiographic technique used. Chest films taken with the patient in an upright position are ideal for demonstrating free air because the x-ray beam strikes the hemi diaphragms tangentially at their highest point.
A lateral decubitus or even a supine radiograph is used in patients who are too ill to be moved. Left lateral decubitus views of the abdomen are also sensitive for detecting small amount of free air interposed between the free edge of the liver and the lateral wall of the peritoneal cavity.
Care should be taken to include the upper abdomen, because air rises to the highest point in the abdomen, which frequently is beneath the lower ribs. Films obtained with the patient in the right lateral decubitus position are also helpful, but gas in the stomach or colon may obscure small amounts of the free air.
Pneumoperitoneum can be detected in 76% of cases using an erect film only, but when a left lateral decubitus projection is included, a pneumoperitoneum can be demonstrated in nearly 90% of cases.
Reasons suggested for only 76% perforations manifesting as free gas in peritoneum are sealing of perforation, lack of gas at the site of perforation or adhesions around the site of perforation.


A number of conditions have been described which simulate free air in the peritoneal cavity i.e. pseudopneumoperitoneum. These are important because failure to recognize them may lead to an unnecessary laparotomy in search of a perforated viscus.
These are
1. Chilaiditi syndrome: is distended bowel, usually hepatic flexure of the colon,
2. Interposed between the liver and the diaphragm.
3. Sub diaphragmatic fat
4. Curvilinear pulmonary collapse.
5. Uneven diaphragm
6. Subphrenic abscess.

Occasionally, asymptomatic patients or those with very minimal signs and symptoms are found to have a pneumoperitoneum.
Causes of pneumoperitoneum without peritonitis are –
1. Silent perforation of a viscus which has sealed itself.
2. Postoperative setting.
3. Peritoneal dialysis .
4. Perforated jejunal diverticulosis .
5. Laparoscopy

Not infrequently, a patient presenting with severe upper abdominal pain has equivocal clinical signs and no free gas is demonstrable on plain radiographs.
Water soluble contrast medium (about 50 ml) is given by mouth or injected through a nasogastric tube, with the patient lying on his/her right side.
The patient can be examined fluoroscopically or the abdominal radiographs can be repeated after the patient has remained in this position for 5 minutes.
Duodenal ulcers which have perforated but show no free gas will normally demonstrate evidence of a leak of contrast medium. Patients with pancreatitis may have an oedematous stretched duodenal loop.
Ionic water soluble contrast medium should not be given if the patient’s clinical state is such that there is risk of it being inhaled and causing pulmonary oedema.

Ultrasound examination allows very rapid screening in suspected patients. Visualization of an interference echo with a shifting phenomenon is a very strong indication of the presence of free air in the abdominal cavity.
This interference echo can be defined as the interruption of echo transmission due to the space between the parietal peritoneum and the surface of the liver. This free air within the peritoneal cavity can be shifted by changing the patient’s position.
Since the distal stomach and proximal duodenum are the most frequent sites of peptic ulcer disease, focal peritonitis due to perforation usually is located in the right upper quadrant. Unlike free peritoneal fluid, this localised exudate doesn’t change shape or location when the patient’s position is altered .
Other findings are subphrenic or subhepatic collections. Moreover ultrasound can detect ascitic fluid as little as 10 ml.


The Computed tomography diagnosis of perforation was based on the direct findings of extraluminal air or gastrograffin. Indirect findings are an abscess or inflammatory mass surrounding an enterolith in the region of appendix or a bowel wall related phlegmon or abscess with fluid in the mesentery or surrounding radiopaque foreign body.
Computed tomography is a valuable method in the diagnosis of alimentary tract perforation .The diagnosis can be established rapidly without patient preparation and with a high sensitivity.


The mainstay of success is timely surgical intervention to stop delivery of bacteria and adjuvants into the peritoneal cavity.
Management of peritonitis can be broadly divided into supportive and surgical treatment.

Principles of Supportive measures are

A. To combat hypovolemia and shock
B. To treat bacteria, not eliminated by surgery, with antibiotics
C. To support failing organ systems
D. To provide adequate nutrition

In all cases of peritonitis, some degree of hypovolemia is present. This is owing to the “third spacing” of extracellular fluid within the periodical cavity, which can be sometimes immense.
The rate and rapidity at which resuscitation is instituted, depends on the severity and acuity of the condition. If a patient is young and surgically fit and has presented early, the duration of resuscitation, may have to be curtained in favour of early surgery.
In contrast, in elderly patients who present late, the resuscitation takes predominance and surgery may have to be considered after reassessing the patient after resuscitation.
The effectiveness of fluid replacement efforts can be judged by pulse rate, blood pressure and mental status. Monitoring of accurate urine output is essential to find out about adequate resuscitation.
Invasive procedures like peripheral arterial and central cardiac pressure – monitoring catheters are usually reserved for high risk patients. Supplementary oxygen and positive ventilation may be required in some cases.
Recent studies have shown that institution of IPPV causes decreased incidence of sepsis syndrome by blocking diaphragmatic stomata, thereby preventing flooding of circulation with bacteria.
Nasogastric decompression is necessary to reduce abdominal distension and to prevent pulmonary aspiration. Antacid therapy like H2 blockers should be administered to prevent stress gastric ulceration.


Empiric antibiotic therapy should be initiated, as soon as diagnosis of peritonitis is made. The antibiotic used depend on the presumed bacteria present. E. coli and B. fragilis are the main target organisms for therapy.


Principle 1 (Repair) :
Control the source of infection
Principle 2 (Purge) :
Evacuate bacterial inoculum, pus (peritoneal ‘toilet”)
Principle 3 (Decompress):
Treat abdominal compartment syndrome
Principle 4 (Control)
:Prevent or treat persistent and recurrent infection or verify both repair and purge

Eliminating the source of infections may include procedures extending from simple perforation closure to major resections.
If extensive bowel is gangrenous, exteriorization may be preferred. The perforation can be closed with pedicle or free omental grafts also.
The choice of the procedure, and whether the ends of resected bowel are anastomosed, exteriorized, or simply closed depends on the anatomic source of infection, the degree of peritoneal inflammation and generalized septic response, and the patient’s premorbid conditions.


All the infectious peritoneal fluid, pus, should be removed. Necrotic peritoneal tissue should be debrided – an aggressive debridement should be avoided to prevent excessive blood toss or bowel injury.
Peritoneal irrigation or lavage should be done thoroughly with adequate amount of normal saline which is warmed. Addition of antibiotic to the solution may be helpful.
Experimental studies using rabbit models have shown that addition of antibiotic into the lavage fluid, reduced mortality and incidence of intra abdominal abscess formation.

During acute peritonitis, the peritoneum and its submesothelial loose connective tissue may absorb more than 10 liters of inflammatory oedema.
Draining the peritoneal fluid reduces the abdominal compartment pressure in most cases. However coexistent ileus, visceral and perietal oedema may increase intraabdominal pressure to levels producing compartment syndrome.
The closure of abdominal wall with tension will add to this. Laparostomy or staged abdominal repair techniques will obviate the increase in intra abdominal pressure.

Complications that may arise during post operative period should be anticipated by the surgeon. This will result in early diagnosis and re-exploration when indicated.
Whenever needed, planned re-laparotomy should be done if surgeon is not convinced of eradication of septic focus.
The surgical options have been classified into the following groups
1. Open abdomen / laparostomy (OPA)
2. Covered laparostomy (COLA)
3. Planned re-laparotomy (PR)
4. Staged abdominal repair (STAR)

The open abdominal techniques (OPA and COLA) avert deleterious effects of increased intraabdominal pressure. OPA includes laparotomy without approximation and suture closure of abdominal fascia and skin.
Disadvantages :
The exposed intestines perforate easily since, augmented intraluminal pressure is not countered by abdominal wall. Definitive closure of abdominal wall becomes impossible because of fascia retracts and huge incisional hernia result.
COLA includes same principle as above but fascial gap is closed using a mesh or ethizip in order to protect the exposed viscera. This may give rise to raised intra-abdominal pressure, occurrence of large incisional hernia is not obviated.
Planned relaparotomy includes “leaving the abdomen open” following the initial operation to allow the reexploration and irrigation, debridement or fistula closure, either in OT or ICU.
Re-exploration intervals range from 12 to 48 hours or longer as situation demands. The initial laparotomy wound may be temporarily closed by using retention sutures or ethizip.
STAR is a series of abdominal operations with staged re-approximations and final suture closure of the abdominal fascia. The abdomen is closed temporarily and controlled tension is exerted to the fascia, avoiding the consequences of increased intraabdominal pressure.


?Critical patient’s condition (hemodynamic instability) precluding definitive repair
?Excessive peritoneal oedema (abdominal compartment syndrome: pulmonary, cardiac, renal, or hepatic dysfunction, and decreased visceral perfusion) preventing abdominal closure without undue tension, intra-abdominal pressure > 15 mmHg
1. Massive abdominal wall loss.
2. Impossibility to eliminate or to control the source of infection.
3. Incomplete debridement of necrotic tissue.
4. Uncertainty of viability of remaining bowel.
5. Uncontrolled bleeding.(the need for “packing”)


?Acute renal failure
?Cardio respiratory failure
?Pulmonary oedema
?Thrombo- embolic phenomena
?Systemic inflammatory response syndrome
?Multi organ dysfunction

? Subphrenic abscess
? Pelvic abscess
? Leak at site of perforation closure
? Anastamotic leak
? Enterocuteneous fistula
? Wound infection
? Wound failure including burst abdomen
? Intestinal obstruction due to adhesions
? Incisional hernia


The data will be collected from R.L. JALAPPA HOSPITAL, TAMAKA, KOLAR, in between the study period of December 2016 to June 2018.

All patients undergoing surgeries for peritonitis admitted under different surgical units.
Number to be studied: 172-divided as 86 in each group comprising of odd and even serial numbers.

This number was chosen keeping in mind the time restrictions of the study, the feasibility and ease of calculations.

The preoperative preparation of each case consists of correction of shock, electrolyte imbalance, dehydration, gastric aspiration, parenteral broad spectrum antibiotic coverage and tetanus prophylaxis.
Operative details such as date of surgery, hospital no, will be noted. Operative findings such as the site of perforation, degree of peritoneal contamination will be noted. At laparotomy a definitive procedure for underlying pathology followed by peritoneal lavage with either normal saline or normal saline with povidone iodine is done.
Available forms of, betadine scrub 7.5% w/v in 50 ml, betadine microbial solution 10% w/v in 100ml ,betadine ointment 10% w/v in 15 g.
2 liters of warm saline and 20 ml of betadine in 2 liters of warm saline is used in the groups to give peritoneal lavage 1%wt/volume. Abdomen is closed in layers after keeping flank drain.
Samples of peritoneal fluid collected before and after the procedure are labeled and sent immediately for isolation of organism and bacterial colony count.
Semi quantitative bacterial count of the peritoneal fluid collected before wash and the peritoneal fluid collected after wash will be performed by plating on blood agar.
Povidone iodine rarely lead to thyroid disorders, so patient is advised to undergo thyroid profile before and after peritoneal lavage.
Post operative progress is assessed by comparing the development of surgical site infection (SSI), duration of hospital stay, pre wash and post wash bacterial colony count in both the groups.

The treatment to be adopted in each case was decided by the attending surgeon .Post operative fluid and electrolyte balance was maintained by input and output charts and adequacy of replacement was judged mainly on the basis of clinical features.
In most of the cases empirical broad spectrum antibiotics were started pre-operatively. The drainage tubes were removed between 3rd to 5th post operative day and gastric aspiration was discontinued as soon as the patient passes flatus and appearances of normal bowel sounds.
The post operative complications, especially SSI were studied in the immediate follow up period.

All patients with peritonitis of age >20yrs and


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