INTRODUCTION

Despite of our better understanding of pathophysiology and advances in surgery and antimicrobial therapy peritonitis remains a potentially fatal affliction. Peritonitis refers to an inflammatory response of peritoneum of abdominal cavity in terms of activation of local mediator cascades by different stimuli. Therefore bacterial, viral and chemical agents may cause inflammation of peritoneal layer.1 Gastrointestinal perforations have been surgical problem since the time immortal. Scientists have found evidence of gastrointestinal perforations in Egyptian mummies (167 B.C). Perforation is said to occur once a pathology which extends through the full thickness of the hollow viscous leading to peritoneal contamination with intraluminal contents. Gastrointestinal perforation in our region generally occurs as a result of chronic inflammation due to Helicobacter pylori, NSAIDs like aspirin, stress, excessive smoking, alcohol, or coffee consumption. Other causes include appendicitis, diverticulitis, typhoid, malignancy. Crohn's disease and less commonly ulcerative colitis are rare causes of perforation and if untreated, it leads to bacteremia, generalized sepsis, multiorgan failure, shock and abdominal abscess formation. The first successful surgical management for any gastrointestinal perforation was done for perforated gastric ulcer by Ludwig Heusner in Germany in 1892 in the form of partial gastrectomy . Gastrointestinal perforation is a
1

serious surgical problem in developing nations with substantial morbidity and mortality and is one of the most common cause of emergency surgery.2 Rapid diagnosis and treatment of these conditions is essential to reduce the high morbidity and mortality of late-stage presentation. Successful treatment requires a thorough understanding of the anatomy, microbiology, and pathophysiology of this disease process and in-depth knowledge of the therapy, including resuscitation, antibiotics, source control, and physiologic support.3 In this study peritonitis cases were analyzed with respect to etiology, clinical features and management strategies.

AIMS AND OBJECTIVES 1) In this study non traumatic hollow viscus perforation is evaluated in detail with reference age group and sex incidence. 2) Analysis of various signs and symptoms with reference to their diagnostic value. 3) Evaluation of reliability of investigation like plain X Ray abdomen. 4) Study of operative findings and proceure undertaken for each patient.

REVIEW OF LITERATURE
Rajender singh jobta et al (2000-2005) conducted a study to highlight the spectrum of perforation peritonitis as encountered at GMCH Chandigarh 504 cases of perforation peritonitis over period of 5 years were reviewed in terms of clinical presentation operative findings postoperative course retrospectively at GMCH Chandigarh and concluded that most common of perforation was duodenal ulcer

perforation followed by appendicular perforation . Mean age was 36.8 yrs with majority being males. 251 cases of 504 incurred postoperative complication. The mortality rate was 10% with septicemia associated with multiorgan failure being most common cause.4 Sanjay Gupta et al(2006) dept of surgery GMC Chandigarh conducted study dealing with over all spectrum of perforative peritonitis in India . Simple closure of perforation using pedicled omental patch give good results even in large perforation, aggressive

resuscitation, antibiotics, early surgery has reduced mortality.5 Shyam Kumar Gupta et al (2006-2008) studied 400 hundred patients who presented in the emergency of GMC Jammu as a case of perforation peritonitis over a period of two years. The overall mortality was 6% and morbidity in the form of wound infection, fever, respiratory complication, residual abscess, dyselectrolytemia, burst abdomen, jaundice, sepsis, were present.2

SURGICAL ANATOMY OF PERITONEUM:

The peritoneum is a smooth, thin lustrous, translucent membrane lines the

abdomen, the largest cavity of body. Investing the abdominal viscera it presents a very complex topography and surface area of enormous extent of 1.2m, approximately equal to that of skin.6 Development of peritoneum: Peritoneal cavity is formed from two limbs of horse-shoe shaped intraembryonic coelom. The two parts are at first separate but fuse to form one cavity as result of lateral folding of embryonic disc. The two halves of peritoneal cavity remain separate in cranial part of abdomen. The attachment of mesentery of the primitive gut on posterior abdominal wall is at first in midline. As a result of changes involving rotation of gut and as result of some part of gut becoming retroperitoneal the line of attachment of mesentery becomes complicated. The peritoneal cavity therefore comes to be divided into number of pockets that are partially separated by folds of peritoneum.7 Peritoneum: The peritoneum is the largest serous membrane in body and its arrangements are complex. In males it forms a closed sac but in females it is open at lateral ends of uterine tubes. It consists of single layer of flat mesothelial cells lying on layer of loose connective tissue. The mesothelium usually forms a continuous surface but in some areas may be fenestrated. Neighboring cells are joined by junctional complexes but probably
5

permit the passage of macrophages. Peritoneal cavity is potential space between parietal peritoneum which lines the abdominal wall and in folding of visceral peritoneum which suspends the abdominal viscera within cavity.8 The peritoneal cavity is subdivided further into greater sac and omental bursa or lesser sac. The greater sac accounts for most of space in the peritoneal cavity beginning superiorly at diaphragm and continues inferiorly into pelvic cavity . Omental bursa is smaller sub division of peritoneal cavity posterior to stomach and liver and is continuous with greater sac through an opening , the omental foramen. Throughout peritoneal cavity numerous folds connects organs to each other or to the

abdominal wall. These folds develop from original dorsal and ventral mesenteries. Omentum: The omenta consist of two layers of peritoneum which pass from stomach and first part of duodenum to other viscera. There are two, 1) Greater omentum is large apron like peritoneal fold that attach to greater

curvature of stomach and first part of duodenum. It drapes inferiorly over the transverse colon and coils of jejunum and ileum. Turning to posteriorly, it ascends to associate with but remains separate from the peritoneum on the superior surface of transverse colon and mesocolon. 2) Lesser omentum extends from lesser curvature of stomach and first part of

duodenum to inferior surface of liver. Enclosed in the free edge of lesser omentum are the

hepatic artery proper, the bile duct, and the portal vein. Additionally the right and left gastric vessels are between the layer of lesser omentum near lesser curvature of stomach.9 Subphrenic spaces: Six spaces may be defined in relation to periphery of liver they are of surgical importance because pus may collect in them forming abscess. The ligaments of liver take a large part in delineating these spaces. Of these six spaces three are on right and three are on left. They are named 1) 2) 3) 4) 5) 6) Right anterior intraperitoneal compartment. Right posterior intraperitoneal compartment. Right extraperitoneal compartment. Left anterior intraperitoneal compartment. Left posterior intraperitoneal compartment. Left extraperitoneal compartment.

Right anterior intraperitoneal compartment: It is bounded anteriorly by diaphragm and anterior abdominal wall. Posteriorly by anterior surface of liver. left side by right side of falciform ligament. Right side fossa communicates with the right posterior intraperitoneal compartment by potential space between diaphragm and right lateral surface of liver, below fossa is open to general peritoneal cavity. Right anterior intraperitoneal compartment is continuous with right posterior intraperitoneal compartment round the anterior sharp margin of liver. In cases where an
7

abscess forms in one of compartment it is usually prevented from extending round this sharp margin by the formation of adhesion between transverse colon and greater omentum to anterior border of the liver which serves to limit the abscess to one compartment. Right posterior intraperitoneal compartment (morrisons pouch or the hepatorenal pouch): It is bounded anteriorly by inferior surface of liver and posteriorly by peritoneum covering the diaphragm and upper pole of the right kidney. Above by coronary ligament and below the pouch is open to the general peritoneal cavity. Left anterior intraperitoneal compartment: It is bounded anteriorly by abdominal wall, posteriorly by liver, above by left triangular ligament, on right side by falcifarm ligament and fossa is open to left and below. Left posterior intraperitoneal compartment: This is lesser sac of peritoneum which is open into main peritoneal cavity through epiploic foramen. Right extraperitoneal compartment: This is area between bare area of liver and diaphragm. It is bounded anteriorly by superior layer of the coronary ligament, posteriorly by inferior layer of the coronary ligament, on left by inferior vena cava, right side by fusion of two layers of coronary
8

ligament to form right triangular ligament, above by diaphragm and below by posterior surface of liver. Left extraperitoneal compartment is merely connective tissue around upper pole of left kidney.10 Vascular supply and lymphatic drainage: Parietal and visceral peritoneum develops from the somatopleural and splanchnopleural layers of lateral plate mesoderm. Parietal peritoneum therefore supplied by somatic blood vessels of abdominal wall and pelvis and its lymphatics join those in body wall and drain to parietal lymph nodes. Visceral peritoneum is best considered as an integral part of viscera which it overlies it derives blood supply from the viscera and its lymphatic joins the visceral vessels. Innervation: The parietal peritoneum is innervated by branches from somatic efferent and afferent nerves that also supply the muscles and skin respectively of the overlying body wall. The visceral peritoneum is innervated by branches of visceral afferent nerves which travel with autonomic supply to underlying viscera. The sensation from parietal peritoneum is usually confined to one or two dermatome for each area of peritoneum stimulated and is both lateralized and well localized. The visceral peritoneum is supplied by visceral afferent innervations provides much more limited discomfort. Pain is less severe, with no significant localization.9
9

PHYSIOLOGY OF PERITONEUM
Peritoneal fluid exchange: The mesothelial lining cells of peritoneum secrete serous fluid that circulates within peritoneal cavity. The peritoneal cavity normally contains 50 to 100 ml of fluid with solute concentration nearly identical to that of plasma. Fluid is absorbed by peritoneal mesothelial lining cells and sub diaphragmatic lymphatics. Mesothelial cells also absorb solutes by continuous process of endocytosis. Splanchnic blood flow affects the efficiency of fluid exchange. Peritoneal permeability is markedly increased by intraperitoneal inflammation. Peritoneal fluid movement: The routes of normal fluid movement within peritoneum have been defined by injection of water soluble contrast material into normal individuals .The right paracolic gutter is the main conduit between upper and lower peritoneal cavities because left gutter is obstructed by phrenicocolic and splenorenal ligaments. Two primary forces govern the movement of fluid within the peritoneal cavity 1) 2) Gravity Negative pressure created beneath diaphragm with each normal respiratory cycle. Fluid flux within peritoneal cavity is dramatically altered by presence of adhesions, fibrin, paralytic ileus or mechanical ventilation. Movement of fluid into pelvis
10

was in past an important component of surgical treatment of intraabdominal infections. Earlier generation of surgeons routinely positioned the patients in fowler position, almost sitting position to facilitate dependent movement of purulent material and formation of pelvic abscess which would then be drained transrectaly without laparatomy. Subphrenic purulent fluid collection occurs because a relatively negative pressure is created beneath the diaphragm with each exhalation. Intra peritoneal pressure measurement shows that pressure is lowest beneath the diaphragm during expiration. The diaphragm rises during exhalation producing a transiently larger space in upper abdomen. With positive pressure mechanical ventilation there is significantly impaired capacity of peritoneal cavity to clear particulate debris.11 Mesothelial cells (PMC): The peritoneal cell population consists mainly of mesothelial cells. It is now clear that in addition to its structural function this cell layer plays an important role in peritoneal inflammatory response. To mount an effective immune response against invading pathogens a large number of leukocytes are recruited to peritoneum from the blood by a process in which human PMC play an important role. 12 Ultra structural features, such as the presence of microvilli and a prominent rough endoplasmic reticulum with abundant intracytoplasmic lipid inclusions, reflect the active role of the mesothelial cells in the intercellular communication and secretion of protein and lipid mediators to their surroundings.13

11

The uneven distribution of stomata within the abdomen indicates that peritoneal mesothelium is morphologically and functionally heterogeneous for example PMC covering the liver and spleen are more substantial than those overlying the intestines and omentum and parietal regions. The former are cubic cells with a cytoplasm rich in organelles, dense microvilli coat and elaborate intercellular contacts. The latter have scant cytoplasm, few organelles and sparsely distributed microvilli. Hence mesothelium overlying paenchymal organs have strong structural integrity as well as inherent ability to promote flow of fluid within peritoneum by the action of microvilli. It is evident that peritoneal mesothelium contains machinery to adapt to peritonitis that aimed at enhancing peritoneal clearance. The fluid within the peritoneal cavity is battleground in which effector mechanism meet the contaminants. The result is mix of cascading process that have evolved to protect life in absence of surgery.14 Macrophages: Macrophage forms the first line of innate defense against bacteria in peritoneum along with natural killer cells (NK). E coli injected into the peritoneum are cleared initially via translymphatic clearance and phogocytosis by resident macrophages. Macrophages can be activated in several ways. IFN-Y is main activator of

macrophages during sepsis and NK cells have shown to be major producer of IFN-Y in polymicrobial sepsis. Through direct cell-cell interaction and cytokine production, NK cells influence macrophage activity and ability to clear bacteria.15

12

Milky spots in omentum: Aggregations of cells within omentum known as milky spots are source of PMNs, macrophages and lymphocytes. Milky spots composed of these mesenchymal cells are found surrounding capillary convolution that have been termed omental glomeruli. They appear as tiny cotton wool spots to naked eye. Milky spots were first described in rabbit omentum by Van Recklinghausen in 1863 and were not demonstrated in humans until 1921. Milky spot lymphocytes are able to enter and exit the peritoneal cavity via the overlying mesothelial stomas. Cross link between lymphocytes and phagocytes: A complex relationship exists between cytokines adhesions molecules and leucocytes, all of which participate in adhesion cascade. Adult mammals respond to tissue damage by implementing the acute phase response, which comprises a series of specific physiological reactions involving cytokines and adhesion molecules. The result of this cascade of events is the emigration of leucocytes from the periphery to an inflammation site where the production of oxygen radicals, nitrogen radicals and protease may lead to tissue injury. Macrophages are able to modify their behavior in response to diverse signals from other cells and the extra cellular matrix.16

13

Defense mechanism in peritoneum: Macrophages have been implicated in host defense against infection and to contribute to instigation of the initial inflammatory response. Macrophages participate in both innate and specific immunity and have numerous functions including phagocytosis, and antigen processing/presentation and secretion of pro and anti-inflammatory cytokines. Previous investigations have documented that, during the early phase of peritonitis, residential macrophages and the lymphatic system (that drains to the thoracic lymphatic ducts and subsequently into the bloodstream) are important for containing the infection. Dunn et al. showed that the first line of host defense during peritonitis caused by Escherichia coli is determined by the capacity of peritoneal macrophages and the diaphragmatic lymphatic system to inactivate and eliminate invading microorganisms. These authors instilled radiolabelled dead E. coli and found that one-half of the bacteria were mechanically cleared and one-third were engulfed by macrophages within minutes.17 The role of fibrin seems to be ambivalent. Fibrin deposits help to wall off the perforated viscous from the peritoneal cavity as well as to sequester bacteria. This slows spread within the confines of peritoneal cavity and reduces bacteremia associated with the bacterial spill. The fibrin mesh is further stabilized by a reduction in the release of fibrinolytic enzymes by the mesothelial lining cells. In essence the final resolution of the infecting focus would seem to depend on the critical interaction between the phagocyte and the bacterium within a fibrin-laden microenvironment.18

14

Peritoneal healing: Peritoneal injury due to surgery, infection or irritation initiates an inflammatory reactionthat increases peritoneal fluid including proteins and cells. This fibrinous exudates later leads to formation of fibrin. The fibrinous exudates and fibrin deposition is an essential part of normal tissue repair, but its complete resolution is required for normal healing. The degradation of fibrin is regulated by the plasminogen system. The balance between fibrin deposition and degradation is critical in determining normal peritoneal healing or adhesion formation .19 Cellular components of peritoneal healing:20 The kinetics of cellular infiltration in response to inflammation is as follows. The earliest cells to appear in the damaged peritoneum are mainly polymorpho nuclear neutrophils which persist for 1-2 days. This is followed by entry of monocytes which later differentiates into macrophages and becomes adherent to wound surface. By day 3 mesothelial cells begin to cover the peritoneal macrophages at the wound surface. On day 4-7 the predominant cells on peritoneal surface are mesothelial cells. These mesothelial cells then proliferate throughout the wound base and form multiple islands of cells. Confluence of these islands of cells allows larger wounds to heal in the same amount of time as smaller wounds. This form of healing contrasts with that of skin in which healing takes place from skin edge.

15

Biochemical and cellular cascade occurring after peritoneal injury21 Fig 1

16

PERITONITIS:
Primary peritonitis is a monomicrobial infection in which the integrity of the gastrointestinal tract has not been violated. The most common manifestation is spontaneous bacterial peritonitis, and is typically identified in patients who have ascites due to end-stage liver disease. Peritonitis may also develop in conjunction with the use of indwelling peritoneal catheters, such as peritoneal dialysis catheters. This type of peritonitis is sometimes considered a form of primary peritonitis, or may be described as a separate entity. Primary and catheter-associated peritonitis are usually monomicrobial infections treated medically.22

Secondary peritonitis, the most common form of peritonitis, is an acute peritoneal infection resulting from loss of integrity of the gastrointestinal tract or from infected

viscera. It is caused by perforation of the gastrointestinal tract (e.g. perforated duodenal ulcer) by direct invasion from infected intra-abdominal viscera (e.g. gangrenous appendicitis). Secondary peritonitis resulting from the perforation of a hollow viscous is the most common type of complicated intra-abdominal infection managed by surgeons.23 Tertiary peritonitis is a poorly defined entity. At a minimum, it is a diffuse infection developing after the failure of initial management of secondary peritonitis. Many of these patients have impaired host defenses because of ongoing infection or pre-existing co morbid conditions.23

17

PATHOPHYSIOLOGY OF PERTONITIS Perforation, and the bacterial inoculation that ensues, causes an inflammatory response that acts locally to contain the infection; but, in the setting of overwhelming contamination, it can spread to cause systemic inflammation. Several mechanisms act locally to contain or destroy infection. Tissue injury stimulates mast cell degranulation. Mast cell degranulation releases histamine, kinins, leukotrienes, prostacyclines, and free radicals. These factors increase vascular and peritoneal permeability allowing for local influx of complement and coagulation cascade factors. Influx of complement at the site of contamination allows for bacterial opsonization via C3b. Diaphragmatic motion, described above then leads to absorption of bacteria laden peritoneal fluid into the lymphatic system. Opsonised organisms in the lymph are transported to the reticuloendothelial system, where they are destroyed. In addition to bacterial destruction via opsonization, complement also attracts neutrophils to the site of injury via chemotactic factors C3a and C5a. Neutrophils attack bacteria by three mechanisms, first they express and release more cytokines further propagating the inflammatory response; second, they phagocytose and destroy bacteria via respiratory burst; third they secrete neutrophil extracellular traps (NETs). NETs are composed of DNA, chromatin and serine proteases. NETs act as a physical barrier to prevent the further spread of pathogens. Finally tissue factor expressed by injured tissue leads to

18

activation of the coagulation cascade. This results in increased fibrin production necessary to contain bacteria by abscess formation.24 In the abdominal cavity of patients with bacterial peritonitis both coagulation cascade and fibrinolytic system are stimulated. The markedly raised concentration of thrombin - antithrombin complex in peritoneal fluid of all patients with peritonitis demonstrates intraperitoneal stimulation of coagulation.25 The response to intra abdominal infection depends on 5 key factors. 1) 2) 3) 4) 5) Inoculum size. Virulence of contaminating organism. The presence of adjuvants within peritoneal cavity. Adequate local, regional and systemic host responses. The adequacy of initial treatment.

Inflammation within the peritoneal cavity evokes a series of secondary changes that produce clinical syndrome of peritonitis. 26 Peritonitis physiological alterations systemically affecting system. the both produces profound also

locally within the abdominal cavity and

cardiovascular, respiratory, renal and

neuro-endocrine

19

Fluid Shifts: The peritoneum reacts to inflammation by vascular dilatation, hyperemia and exudation of fluid from the vascular space into the free peritoneal cavity. This translocation of water, electrolytes and protein into the sequestrated third space effectively removes fluid from the body economy. The rate of fluid loss is proportional to the surface area of peritoneum involved in the inflammatory process and with extensive peritonitis, may reach upto 4-6 L in 24 hours. Ileus : Generalized peritonitis produces an inhibition of intestinal motility with resultant dynamic ileus. Distention of the bowel with unabsorbed fluid and gas, aggravated by

relative mural ischemia if intraluminal pressure exceeds capillary perfusion pressure, permits bacteria to penetrate the mucosal barrier and enter Endocrine Response: Peritonitis results in a major systemic stress producing a vigorous response from the pituitary-adrenal axis. Adrenal medullary secretion of catecholamine is in large part responsible for the vasoconstriction, tachycardia and sweating accompanying the the vascular compartment.

initial response to peritonitis. Aldosterone secretion increases as a response to hypovolaemia and further aggravates potassium loss and sodium retention. Release of antidiuretic hormone results in renal conservation of water which may exceed sodium retention with consequent dilutional hypotonicity of plasma sodium.
20

Cardiovascular System: Loss of extracellular fluid volume depletes central venous return, lowering cardiac output and increasing the heart rate. Compensatory vasoconstriction results in an increased total peripheral resistance to maintain blood pressure and cardiac and cerebral perfusion pressures. Decreased perfusion and oxygenation to the splanchnic bed, kidneys and inactive muscles result in anaerobic glycolysis with progressive accumulation in

lactic acid. Metabolic acidosis is aggravated by decreased renal clearance, secondary to reduced renal perfusion. If acidosis progresses, depression of cardiac contractility further decreases cardiac output.

Respiratory System: Demands on the respiratory system increase significantly in peritonitis with a decrease in total respiratory capacity. Abdominal distention secondary to ileus causes an elevation and restriction of diaphragmatic movement. Respiratory restriction, fatigue and inefficient respiratory effort diminish ventilatory volume with ensuing atelectasis which may progress to ventilation-perfusion imbalance, intrapulmonary arteriovenous shunting and peripheral hypoxaemia.

21

Kidneys: Renal changes induced by peritonitis are primarily a reflection of hypovolaemia, reduced cardiac output and increased secretion of aldosterone and antidiuretic hormone. Renal blood flow, glomerular filtration and urine volume are reduced. Aldosterone promotes sodium retention and antidiuretic hormone results in increased reabsorption of water from the distal tubules with a further decrease in urine output. Protein catabolism progresses during the duration of peritonitis and serum albumen concentrations decrease with further loss into the peritoneal cavity. Hepatic glycogen stores are depleted. The net effect of these metabolic changes in the body results in a significant energy deficit.27 Factors that favour development of generalized peritonitis: Speed of peritoneal contamination is prime factor in the spread of peritonitis. If an inflammed appendix or other hallow viscous perforates before localization has taken place there is gush of contents into the peritoneal cavity is associated with severe generalized peritonitis and high mortality. Stimulation of peristalsis by ingestion of food or even water hinders localization, violent peristalsis by the administration of purgative enema may cause the wide spread distribution of an infection that would otherwise have remain localized. The virulence of the influencing organism may be so great as to render

localization of infection difficult or impossible. Young children have small omentum disruption of localized collection may occur with injudicious and rough handling.28

22

Factors influencing peritonitis: The degree of bacterial contamination or inoculum is dependent primarily upon the site of the perforation. Gastric perforations are frequently sterile initially and result in a chemical peritonitis, excecpt in achlorhydrics. Bacterial concentrations increase as perforation occurs more distally in the gut. Bacterial concentration in the sigmoid colon reaches 1010 to 1011 bacteria per gram. Also, more distal perforations are associated with a higher concentration of anaerobes, particularly Bacteroids fragilis. Aerobes represent less than 0.1 percent of distal colonic flora. Solid debris, devitalized tissue, foreign bodies, and blood all increase the virulence of peritoneal contamination.29

TABLE 1 -- FACTORS INFLUENCING PERITONITIS Factors Promoting Infection Bacterial inoculums Local adjuvant factors Hematoma Foreign body Devitalized tissue Systemic adjuvant factors Hypoxemia Shock Steroids Malnutrition Comorbid medical conditions
23

Host Defense Factors Dissemination of contaminant Clearance of peritoneal fluid Complement activation Fibrin deposition Phagocytosis by macrophages and neutrophils Loculation of bacterial collections

Factors influencing peritoneal inflammation and infection:

Bacterial virulence: The virulence of contaminating bacteria is influenced by a number of factors. Several organisms are well recognized for their innate ability to produce intra abdominal infection in humans. Despite massive contamination and complexity of microbial spectrum that occurs with feacal perforation within24 to 48 hours only few isolates are recovered in peritoneal fluid culture. Weinstein demonstrated that E.coli and Enterococcus were the predominant organism during peritonitis phase while B .fragilis predominated during abscess phase. Another example of unique pathogenicity is remarkable ability of encapsulated anaerobic bacteria to produce abscess formation. A characterstic attributed to capsular polysaccharide.30 The ability to adhere to the mesothelial surface may also enhance the virulence of some organism such as the Enterobactriaece and Bacteroids fragilis. Encapsulated B. Fragilis adheres well to rat peritoneal mesothelial cells in contrast to other unencapsulated bacteroids species.31 Adjuvant factors: The ability of adjuvant substance to promote infection has been well demonstrated in number of studies. The susceptibility of human tissues to infection that largely or entirely depends on availability of freely available iron for bacteria. Natural resistance to infection operates in an environment where the amount of freely available
24

iron is extremely low. This depends very much on physical condition in tissue fluids where eh and ph govern the binding of iron to unsaturated iron binding proteins transferrin and lactoferrin. The eh is inturn depends on degree of tissue oxygenation and therefore hypoxia is of greatest importance since it produces fall in tissue eh which can result in production of free ferrous iron and huge stimulus to bacterial growth..32 Adjuvant substances such as heamoglobin , bile ,or necrotic debris are thought to exirt their detrimental effects in part by increasing bacterial proliferation within peritoneal cavity , to counteract their effect many surgeons irrigate the peritoneal cavity during or just prior to closure of laparotomy to dilute out adjuvant substances and microbes which are present even during clean case. Although irrigation of peritoneal cavity with crystalloid solution would seem prudent during laparotomy in order to remove debris, bacteria and adjuvant substances, these substances must be removed prior to closure to prevent interference with normal host defense of peritoneal cavity.33

BACTERIALOGY OF PERITONITIS:
Breach of the gastrointestinal wall causes intra-abdominal contamination with peritonitis or abscess formation. The type and degree of peritoneal contamination depends on the site, size, and duration of the perforation and on the physiologic state, including the time from the last meal, administration of a mechanical bowel preparation before the perforation, coexistent diseases, and the presence or absence of an ileus or bowel obstruction with accompanying bacterial overgrowth. These factors affect the
25

relative degree and type of bacterial and fungal contamination from perforation. The anatomic site of perforation significantly affects the type and burden of enteric contamination. The composition of the microflora of the gastrointestinal tract varies greatly. 3 The stomach in fasting state contains sparse microflora of few relatively more acid resistant species eg; lactobacilli or candida species. Similarly the duodenum and proximal bowel contain sparse micro flora in fasting state. 34 Gastric anaerobes outnumber aerobes by about 1000-fold. The relative frequency of aerobes progressively increases along the small bowel, with gram-negative aerobes becoming the predominant organisms in the terminal ileum. The microfloral load and composition dramatically and abruptly changes between the terminal ileum and the colon. Colonic anaerobes outnumber aerobes by up to 1000-fold, with the predominant genera consisting of Bacteroides, Bifidobacterium, Eubacterium, Clostridium, Lactobacillus, Fusobacterium, and a limited variety of gram-positive anaerobes. Understanding the

characteristic microflora of each gastrointestinal organ is clinically important in selecting antibiotics for secondary peritonitis and potential sepsis.
3

A number of studies have been performed in an attempt to mimic clinical peritonitis and to ascertain importance of microbial pathology involved.How these microbes interact and how best to direct antimicrobial therapy. Necrosis or perforation of the hollow viscous allows these organisms to enter the peritoneum. Because perforation of obstructed small bowel, appendix and colon all involve spillage of polymicrobial
26

aerobic and anaerobic microflora, it is not surprising that eventual infection involve these organisms as well. But what is of interest is that bowel microflora contains many many different microbial species yet only a small number come to be present in established infection. Experimental studies have attempted to define this simplification process and have concomitantly led to conclusion that pathogens that escape host defense are frequently aerobes such as E.coli and anaerobes such as Bacteroids fragilis that are

capable of acting in concert to produce synergistic severe type of infection..34 Microbial synergy may increase the net pathogenic effect and hence the severity of infection in several ways, 1) Oxygen consumption by aerobic bacteria produces tissue hypoxia results in lowering of redox potential which favours the growth of anaerobic bacteria. 2) Specific nutrients produced by one bacteria may encourage the growth of . fastidious and potentially pathogenic co habiting microorganism.

3) Some anaerobes are able to impair host immune function and provide competitive advantage for themselves as well as for other co habituating microorganisms.35 Common pathogens isolated from complicated intraabdominal infection Gram negative E .coli , Enterobacter , Klebsiella , Proteus , Pseudomonas aerogenous, Acinetobacter .

27

Gram positive Streptococci, Enterococci , Coagulase negative staphylococci, Staphylococcus aureus. .Anaerobic bacteria; Bacteroids species, Clostridium species.36

Definitions:
1. SIRS (Systematic inflammatory response syndrome); Two or more of following clinical sign indicates Temperature >38C or <36 Heart rate >90/ min Respiratory rate >20/min or PaCO2<32 mm Hg WBC count >12x109 cells / m3 2) SEPSIS; SIRS + documented infection. 3) SEVERE SEPSIS; SIRS+ SEPSIS + Heamodynamic compromise. 4) MODS; This is a physiological derangements in which organ functions are capable of maintaining homeostasis. not

28

Mediators of SIRS: When the inflammatory response is initiated a wide variety of chemical mediators are released into systemic circulation but clearly implicated in pathogenesis of abnormality in MODS is an abnormal generalized and persistent response to injury. When the normal response to injury becomes unregulated abnormal activation of multiple inflammatory cascades leads to diffuse cellular injury and dysfunction of endothelium. This leads to procoagulant state with micro vascular thrombosis, which results in local and regional organ hypoxia. If oxygen delivery is inadequate to meet this increase in demand, diffuse cellular ischemia results. Ischemia exacerbates cellular injury and leads to further release of stress hormone and inflammatory mediators. In this manner a

vicious cycle is established that if uncorrected eventually leads wide spread organ damage.37 Clinical features of peritonitis: The signs and symptoms produced by the perforation vary according to the time which has elapsed since rupture has occurred. There are three stages in pathological process which can usually be recognized easily. First stage -(stage of chemical peritonitis). The initial symptoms are those due to pain. Pain is most constant symptom. It may be confined to local area of inflammation or reffered more generally over abdomen. Vomiting common at the onset of peritonitis but is usually infrequent until late in case. The later vomiting is usually obstructive character. This stage may last for few minutes or
29

persist for an hour or two. Its length depends to certain extent on the size of perforation and degree to which general peritoneal cavity is flooded. In cases where the perforation is very small and soon sealed up by fibrinous exudates, the symptoms of onset are correspondingly less severe. Pulse temporarily is small and feeble, the face is livid, with pain and anxiety. Intermediate stage- 2 to12 hours (stage of reaction). The intensity of initial pain subsides and pt then looks better and feels more comfortable. The circulatory system recovers to such an extent that the limbs may become warm and pulse normal in frequency and strength. The improvement in symptom doesnt imply stoppage of the pathological process. The patients chance of recovery depends on the appreciation of this dangerous latent period by practioner. There are in addition observations, some or all of which give valuable indication of the serious inraabdominal mischief. The abdominal wall may be rigid and tender. Respiration costal and shallow. Pelvic peritoneum may be tender. There may be free fluid and free gas in peritoneal cavity. The rigidity of abdominal wall is an almost constant feature. The muscles are flat and board like. Pressure on any part of abdominal wall causes pain and retching, tenderness is often greater in right iliac fosssa in case of ruptured duodenal and pyloric ulcer. The rigid muscles dont move on respiration and the movement of diaphragm is also considerably inhibited, so that breathing is shallow and costal type.

30

The tenderness in pelvic peritoneum is most important sign, this can be determined by rectal or in female by vaginal examination. Movable dullness in flanks due to free fluid in the peritoneal cavity should usually be determinable. The diminution or absence of liver dullness is the sign produced by free gas in peritoneum. It is often easily demonstrated but frequently ambiguous. Percussion over the front of liver may produce resonant note even when no free gas is present in peritoneum. It may result from distended intestine which is sometime pushed up in cases of intestinal obstruction or peritonitis of any other cause. If there is no abdominal distension however diminution of liver dullness anteriorly is significant. It is always of significance to obtain resonance on percussion over the liver in the mid axillary line. If in any acute abdominal case distinct resonance is obtained over liver in midaxillary line about two or more inches above coastal border, one is certainly dealing with perforation of duodenal or gastric ulcer. It is in only minority of cases that the sign is positive however.

An additional symptom which may be helpful is occurrence of pain on tip of shoulder in the supraspinous fossa, that is in region of distribution of cutaneous branch 4th cervical nerve. This symptom if present has to be considered carefully because diaphragmatic pleurisy causes similar pain.

31

Late stage after 12 hours (stage of bacterial peritonitis). This follows quickly after previous stage. Locally the extensive peritonitis clearly is shown by increasing distension of abdomen. Distension of abdomen is not sign of perforation, It is an indication that the peritonitis is advanced and condition has been allowed to proceed too far. The other effects of extensive peritonitis are increasing and persisting vomiting, gradual increase in rate and depreciation in force and volume of pulse. Decrease in temperature of extremities and body. Generally the abdomen remains tender but late in peritonitis the rigidity frequently lessens as a result of vomiting and depressed circulation. The face becomes pinched and anxious; the cheecks hollow, and eyes dim and beringed with dark circles so called facies hippocratica. It is not difficult to diagnose a flagent case of peritonitis for pain, vomiting, local tenderness and muscular rigidity with fever sufficiently indicate the condition. The early symptoms are slight and deceptive when part primarily affected lies in pelvis or some other silent area of abdomen. They are often atypical in patients who are old, debilitated or very fat.38

Investigations: A number of investigations may elucidate a doubtful diagnosis, but the importance of a careful history and repeated examination must not be forgotten. leucocytosis is usually seen in peritonitis but is often delayed for many hours. Peritoneal diagnostic aspiration may be helpful but is usually unnecessary. After infiltrating the skin of the abdomen with local anesthesia, the peritoneum is entered in one or more
32

quadrants with a sterile needle or an intravenous cannula attached to a syringe into which is sucked any free fluid. Bile stained fluid indicates perforated peptic ulcer or gall bladder, the presence of pus indicates bacterial peritonitis. Blood is aspirated in a high proportion of patients with intraperitoneal bleeding, when aspiration fails, the introduction of small quantity of sterile physiological saline, followed after a few minutes by peritoneal aspiration may produce a diagnostic value. Microscopy of the fluid may show neutrophil and bacteria. A radiograph of the abdomen may confirm the presence of dilated gas filled bowel loops (consistent with paralytic ileus) or show free gas, although the later is best shown on an erect chest radiograph. If the patient is too ill for an erect film to demonstrate free air collecting under the diaphragm, a lateral decubitus film is just as useful, showing gas beneath the abdominal wall. Serum amylase estimation may uphold the diagnosis of acute pancreatitis provided it is remembered that moderately raised values are frequently found following other abdominal catastrophes and operation e.g., perforated duodenal ulcer. Ultrasound and CT scanning, when available may also be helpful in some patients by identifying a cause of peritonitis e.g., perforated appendicitis, acute pancreatitis.39

33

MANAGEMENT OF PERITONITIS
Kirschner in 1926 formulated two surgical principles for management of peritonitis which later have become the gold standard. 1) 2) Plugging the source of infection. Purging the peritoneal cavity of bacteria, toxins, and adjuvant substances.

The sine qua non of success is timely surgical intervention to stop delivery of bacteria and adjuvants into the peritoneal cavity. All other measures are of little use if the operation does not successfully abort the infective source and quantitatively reduce the inoculum of micro-organisms and adjuvants of infection so that they can be effectively handled by the patient's defenses, supported by antibiotic therapy.40

Management principles of 1.

peritonitis:

Supportive measures A. To combat hypovolemia and shock and maintain adequate tissue oxygenation. B. To treat bacteria, not eliminated by surgery, with antibiotics. C. To support failing organ systems. D. To provide adequate nutrition.
34

II. Operative treatment: Principle 1 (Repair) - Control the source of infection. Principle 2 (Purge) ,Evacuate bacterial inoculum, pus, and adjuvants . Principle 3 (Decompress), Treat abdominal compartment syndrome. Principle 4 (Control), Prevent or treat persistent and recurrent infection . or verify both ,Repair and purge .41

Hemodynamic resuscitation: The mainstay of resuscitation is the rapid administration of adequate amounts of fluid to restore adequate intravascular volume, and so to optimize oxygen delivery to the tissues. There is no compelling evidence of the superiority of one type of fluid over another. Resuscitation should be guided by frequent assessment of heart rate and blood pressure. Urinary output is a simple and sensitive measure of intravascular volume filling and organ function; an hourly output of 3050 ml/kg should be the minimal objective of therapy. Patients who have significant co-morbidities, who present with more profound hemodynamic instability, or who fail to respond rapidly to fluid replacement should be managed in an ICU setting. The amount of fluid required to achieve hemodynamic stability is variable, and frequently substantial, because of unappreciated third space losses into the focus of infection and into the GI tract as a consequence of ileus.42
35

Use of antibiotics: The antibiotic treatment of intra-abdominal infection has evolved over the past 30 years and is based on solid experimental and class 1 clinical data. The original experiments of Weinstein et al(1975) demonstrated that a combination of antibiotics directed against aerobes and anaerobes proved optimal regarding survival and minimal residual abscess formation. Meat-fed rats given an intraperitoneal fecal capsule were treated with gentamicin, clindamycin, both, or placebo. Therapy directed against aerobes decreased the mortality rate, but the survivors had abscesses. On the other hand, when therapy was directed against anaerobes, it had little effect on the mortality rate but the survivors had very few abscesses. Combination therapy produced increased survival without abscess formation and was the basis for clinical treatment with ampicillin, gentamicin, and clindamycin. As newer agents are developed that cover both types of gram-negative infections, monotherapy has become the preference of most surgeons for the treatment of secondary bacterial peritonitis. Literally scores of prospective randomized trials have been conducted for antibiotic treatment of intra-abdominal infection. In fact, most cases of peritonitis are community-acquired infections, and extended-spectrum antibiotics are unnecessary. Mosdell et al(1991) have shown that obtaining cultures from such patients is probably unimportant as long as appropriate antimicrobial therapy is administered. Inappropriate antimicrobial therapy was associated with increased mortality, as it has been shown in other infections as well.

36

Surgical Infection Society guidelines for antibiotic treatment of peritonitis. Single agents Ampicillin-sulbactam Cefotetan Cefoxitin Imipenem-cilastatin Meropenem Piperacillin-tazobactam Ticarcillin-clavulanic acid Combination regimens Aminoglycoside plus antianaerobe
Aztreonam

plus clinadamycin

Cefuroxime plus metronidazole Ciprofloxacin plus metronidazole Third- and fourth-generation cephalosporin plus antianaerobe.43 Surgical management of severe secondary peritonitis Based on three principles. 1) 2) 3) Elimination of source of infection. Reduction of bacterial contamination of peritoneal cavity. Prevention of persistent or recurrent intra abdominal infection.

37

Source control In general the operative approach and surgical strategy depends on the source of infection, the degree of contamination of peritoneal cavity. The current condition of patient and his or her premorbid health status. Traditionally severe secondary peritonitis has been approached by performing midline laporotomy to identify and eliminate the source of peritonitis. This midline approach permits surgeon to perform a thorough and complete cleaning of the peritoneal cavity in order to reduce bacterial contamination. Ongoing contamination is controlled by closure, exclusion, or resection of infection focus. The generally held concept is that primary anastomoses in a strongly contaminated peritoneal cavity is at high risk of dehiscence and therefore be avoided. However this general concept has been challenged more than once and further testing in controlled clinical trial is being undertaken to define those patient more likely to benefit from primary anastomoses.44

Clinical factors predicting failure of source control for intraabdominal infections. 1) 2) 3) 4) 5) 6) 7) 8) Delay in initial intervention. High severity of illness ( Acute physiology and chronic health evaluation) Advanced age. Co morbidity and degree of organ dysfunction. Low albumin. Poor nutritional status. Degree of peritoneal involvement and diffuse peritonitis. Inability to achieve adequate debridement or control of drainage.45
38

Reduction of bacterial contamination: The second goal of surgical management of severe secondary peritonitis is achieved by aspiration of all gross purulent exudates and removal of feacal debris or food particles. Pelvic region paracolic gutter subphrenic spaces must be opened and debrided. Radical peritoneal debridement as described by Hudspeth 1975 including removal of fibrinous exudates from parietal and visceral peritoneal surfaces lived upto early expectation. In 1980 a randomized trial in which this technique was compared with standard method demonstrated no advantage; on the contrary radical mechanical debridement caused excessive bleeding and probably endangered integrity of intestines. Intra operative peritoneal lavage with saline on other hand is performed regularly by most surgeons to reduce the degree of bacterial contamination and remove blood, feacal material and necrotic tissue. Its efficacy is however is not well documented. There is no evidence that intraoperative peritoneal lavage reduce mortality rate or incidence of septic complications. In patient receiving adequate systemic antibacterial therapy the addition of antibiotics to lavage solution appears to be without clear benefit. The addition of antiseptics may even produce toxic effect. In view of lack of clear benefit Nathens and Rothstien(1990) have recommended that lavage fluid be completely aspirated before closure of abdomen .

39

Prevention of recurrent or persistent infection: Post operative peritoneal lavage, intraabdominal drains and relaporatomy have all been used to prevent persistent or recurrent infection. The role of continuous post operative peritoneal lavage is questionable. In early 1980s such lavage received much attention was installed frequently to reduce postoperative septic complication. At the end of laparotomy intraabdominal drains were left in place and the peritoneal cavity was lavaged continuously until the affluent becomes clear. Antibiotics as well as low dose heparin were added to the lavage solution to reduce further the risk of persistent or recurrent infection and to prevent adhesion formation. In 1987 however leiboff and soroff concluded that clinical value of continuous post operative peritoneal lavage remained unclear. Furthermore postoperative peritoneal lavage is extremely labour intensive and can lead to complications related to the use of intraabdominal drains such as visceral or vascular erosions with fistula formation or bleeding . Besides drains may act as route for retrograde spread of infection into an otherwise sterile environment. Ideally an intraabdominal infection should be cured with single operation. Unfortunately intraabdominal infection often persists or reccurs in case of severe secondary peritonitis. This led in 1980s to concept of the relaporotomy. Reoperations are performed at fixed intervals irrespective of patient clinical condition thereby preventing the development of new septic fluid collections and so precluding their deleterious systemic effects. In this belief relaporotomies and open management of abdomen were introduced.44

40

New operative methods: With the entire above complex and interesting knowledge, we can now concentrate on the new operative methods evolved for the treatment of severe intra

abdominal sepsis. In 1993, the International society of surgery called several experts in this field to the International surgical week held at Hongkong and decide on four basically different methods. OPA-Open abdomen (Laparostomy) COLA-Covered Laparostomy PR-Planned relaparotomy STAR-Staged abdominal repair Open abdomen (laparostomy): This is defined as laparotomy without reapproximation and suture abdominal fascia and skin. Abdominal cavity is left open like an closure of

open wound and

dressed and finally heals by granulation. This method takes care of principles- repair, purge and decompression. The disadvantages are, there is no control over

intraabdominal process, exposed viscera may perforate

and huge ventral hernia results

since definitive closure is not possible. Hence it has lost is popularity.

41

Covered laparostomy (cola): This is defined as laparotomy without reapproximation and suture closure of abdominal fasciae and covering the fascial gap with materials like marlex or vicryl

mesh. The viscera may also be covered with skin with relaxing incision. Planned relaparotomy (pr): In this approach abdomen is left open initially and re-explored at an interval of 12-24 hours for irrigation, debridement etc. Devices used to ease re-exploration include commercially available Zipper, Ethizip, Velcro, artificial burr, PTFE mech (Gortex)

etc. this procedure allows for having control over intra-abdominal process. Staged abdominal repair (star): This is a series of planned abdominal operations with staged reapproximation and final suture closure of the abdominal fasciae. It is first operation called Index Star. The planned either before or during the

abdomen is closed temporarily with devices like

Zip, Velcro etc and controlled tension is exerted to the fascia avoiding the intra abdominal pressure effects. Relaparotomies are performed at 24 hours intervals at operating room. Once problem is solved abdominal cavity is formally closed.

42

Indications for star: It is Indicated in the following conditions: 1. Diffuse peritonitis in critical patient condition. 2. Severe peritoneal edema. 3. Source of infection is not controlled. 4. Incomplete debridement of necrotic tissue. 5. When viability of bowel is uncertain, anastomosis/ repair needs reinspection. 6. Uncontrolled bleeding with packing. 7. Infected pancreatic necrosis. 8. Massive abdominal wall loss. 9. Any intra abdominal problem that is difficult or impossible to manage with a single operation.

43

Advantage of star: Staged abdominal repair technique allows for complete repair, debridement and purge. Anastomotic healing is monitored and any complications are diagnosed early & corrected. Intraabdominal compartment syndrome and its consequences are prevented. With the STAR technique colostomies may be avoided in favor of anastomosis, abdominal drains with their disadvantages are avoided and finally this technique allows for suture closure of abdomen with sound healing.41 PR evolved in the 1980s, is based on the finding that relaparotomy may be futile once multiple organ failure (MOF) has developed. 46 In recent years the on-demand strategy has been strengthened by the availability of improved imaging techniques with which to select patients who may benefit from relaparotomy.46 The planned relaporatomy strategy required decision to be made during the initial operation for secondary peritonitis to perform one or more relaporotomies every 1-3 days until no residual infection found. The on demand strategy required laporatomy performance after initial laporotomy only when clinical condition of patient deteriorated or failed to improve. The index operation was defined as initial laparotomy of a patient for secondary peritonitis.47 Opponents of ROD argue that a wait and see strategy introduces a delay, increasing the risk that the patient will reach a point of no return in the cascade of generalized inflammatory responses. The rationale for this approach is to anticipate the formation of infectious collections and to preclude their systemic effects; some authors consider it to be the cornerstone of aggressive management of peritonitis. Opponents of
44

PR argue that performing multiple relaparotomies for peritoneal lavage does not change the course of the disease and may even increase the risk of complications. Furthermore, although this approach has gained popularity for severe peritonitis, substantial data confirming a reduction in mortality rate are lacking. One claimed advantage of the PR strategy is a surgically more accessible abdomen, whereas any delay in relaparotomy with the on-demand strategy may increase the risk of surgical complications owing to a less accessible abdomen. On the other hand, frequent laparotomies may lead to complications such as fistula, hemorrhage and incisional hernia.46

Unnecessary relaparotomies and open abdomens should be avoided, always remembering that any delay in intervention for an ongoing intra-abdominal infectious source may well prove deleterious. The correct and timely selection of patients for relaparotomy on demand is feasible by combining clinical criteria with multi-slice helical CT data. An on-demand strategy also provides a time window for resolution of remnant infection, mediated by host defence systems, and the formation of more or less walled-off fluid collections or abscesses. These may be suitable for percutaneous drainage, which is often successful and which avoids an invasive surgical procedure.48 In the present series, differences in in-hospital and long term mortality rates showed a benefit for the ROD over the PR strategy for treatment of secondary peritonitis. The risk of death among patients treated according to a ROD policy was 69 percent of that among patients subjected to a PR policy factors such as age, sex, co-morbidity and severity of disease (APACHE II), as well as anatomical origin of peritonitis and intervention, were
45

analysed in this study, and were comparable between the two groups. Patients with more severe peritonitis (MPI score more than 25) who were treated by the ROD strategy showed improved survival compared with those who had PR. Patients with faecal contamination, which is regarded as a risk factor for adverse patient outcome and often an important reason for performing a planned relaparotomy, were equally distributed between the treatment groups. Important in this respect is the finding that patients with faecal peritonitis who were treated by the PR strategy had a significantly higher mortality rate than similar patients with comparable APACHE II scores in the ROD group. Hau et al.(1995) found that postoperative MOF was more common in patients treated with PR than in those treated with an on-demand strategy.46

A more recent prospective randomized clinical trial has also favored

the on-

demand concept, predominantly as a result of a substantial reduction in relaparotomies, health care utilization and associated medical costs. Contrary to long-standing dogma, the evidence exists that the on-demand strategy can be applied safely in even the most severe disease, in patients with Acute Physiology And Chronic Health Evaluation (APACHE)

II scores greater than 20. Adherence to the on-demand philosophy will mean a change in surgical attitude. It must be emphasized that this does not imply a passive wait and see attitude, but rather a vigilant observation of the postoperative patient with peritonitis, with round the- clock monitoring and decision making. For as long as objective, well defined and validated criteria for the selection of patients for relaparotomy within an ondemand strategy do not exist, the surgeon should be prepared to initiate frequent CT
46

imaging. Percutaneous interventions, when necessary during the course of disease, play a substantial role in the nonsurgical treatment of patients with secondary peritonitis. A multidisciplinary approach with close collaboration between surgeons, interventional radiologists, intensivists and microbiologists is essential.48

Laparoscopic approach for peritonitis: Laparoscopy has gained widespread acceptance in common surgical practice as a diagnostic and therapeutic tool. Abdominal emergencies often pose a diagnostic challenge to the general surgeon. A correct diagnosis is crucial because of the various

diseases that may be responsible for the same symptoms, in order to plan the appropriate procedure or to avoid unnecessary Laparotomies. Non-invasive diagnostic procedures . Laparoscopy is the

are expensive, not always conclusive and available in all settings

only minimally invasive technique to allow at the same time for adequate diagnosis, appropriate treatment and/or the best abdominal approach. Indications: the absolute and relative contraindications to Laparoscopy in the treatment of abdominal emergencies are the same as for elective procedures . As for peritonitis, there is a theoretical concern that the CO2 pneumoperitoneum may enhance bacteremia and endotoxemia due to the increased intraperitoneal pressure most clinical and experimental studies support the idea that Laparoscopy appears to produce a less

inflammatory response with a less trauma and less tissue damage than the open one.

47

The high diagnostic yield of LAPS is important especially in patients with pelvic disease suspected appendicitis, where LAPS allows for a better thorough exploration of the abdominal cavity and identification of concomitant diseases procedure) Treatment options: LAPS allows to perform the same surgical procedures as open surgery, or even to schedule the appropriate medical therapy in the presence of concomitant diseases. Another main advantages of Laparoscopic management of generalized peritonitis are a better quality of peritoneal washing and an easy cleaning in the deep abdominal areas (such as Douglas recessus). As consequence, there is an evergrowing request from the lay public. LAPS in the treatment of abdominal emergencies due to peritonitis is possible, simple and reproducible, effective without any specific complications in experienced hands.49 Disadvantages of laparoscopy Learning curve is more. Length of procedure is more compared to open surgery Theoretical risk of enhanced bacteremia and endotoxeamia due to than OP.(open

pneumoperitoneum49.

48

PEPTIC ULCER
Peptic ulcer are focal defect in gastric or duodenal mucosa that extend into submucosa or deeper. They may be acute or chronic and ultimately are caused by imbalance between mucosal defense and peptic injury. Pathophysiology: A variety of factors may contribute to the development of PUD. Although it is now recognized that large majority of duodenal and gastric ulcer are caused by H,pylori and NSAIDS. The final common pathway to ulcer formation is acid peptic injury to gastroduodenal mucosal barrier. Thus the adage no acid no ulcer remains true even today. H .pylori infection. with specialized flagella and rich supply of urease, H pylori is uniquely equipped for survival in hostile environment of stomach. 55% world population is infected with H pylori. One of mechanism by which H pylori cause gastric injury may be through disturbance in gastric acid secretion.50 Until discovery of role of H pylori in gastric and peptic ulcer by Bary j marshall and Robin warren in 1982, stress and life style factors were believed to be the most important factors contributing to PUD . H pylori infection can be held responsible in more than 90% duodenal ulcer and in upto 80% gastric ulcer. H pylori infection and accompanying inflammation disrupts the inhibitory control of gastrin release by decreasing antral somatostatin and this is more marked if infecting organism is CAG A positive strain. The resulting increase in gastrin
49

release and gastric acid secretion is key mechanism by which the H pylori induces PUD.51

infection

.Infection predominantly in antral area leads to hypergastrinemia and characterstic increase in acid production. Acid injury in duodenum is thought to promote the

development of gastric metaplasia allowing the organism to colonise these areas and leading to duodenal ulcer. NSAIDS promote ulcer formation primarily through their inhibition of prostaglandin synthesis. Prostaglandins play a pivotal role in protecting the gastric

mucosa from injurious effects of acid through the stimulation of mucous and bicarbonate secretion and enhancement of surface hydrophobicity and increase of mucosal blood flow. There is evidence to suggest that NSAIDS and aspirin may stimulate gastric acid secretion. The systemic effect of prostaglandin inhibition leads to impairment of heamostasis and to platelet aggregation and direct interference on ulcer healing , both of which promote ulcer complication. The risks of smoking, alcohol and diet on the development of PUD have been extensively evaluated .The impact of smoking in ulcer risk has become less clear over time .Multiple studies performed before the recognisation of role of H pylori suggested a two fold increased risk in smokers compared to non smokers for PUD development but more recent studies have cast doubt on increased risk in smokers . This suggest that prior observations reflected the higher H pylori infection rate among smokers. Overall the evidence suggest that smoking may augment
50

the

risk

of PUD

and ulcer

complications by impairing healing and that much of the negative impact of smoking is associated with H pylori infection . Some studies have suggested that alcohol may increase the risk of ulcer

complication in NSAIDS users but its overall effect in patients without concomitant liver disease is unclear . There are several chronic illnesses associated with increased risk of PUD which may contribute to the increased risk ulcer complication among elderly patients. Epidemiologic data indicate an increased risk of duodenal ulcer in patient with COPD , hepatic cirrhosis CRF , cystic fibrosis , Finally there is increased incidence of PUD in families. This finding is most likely due to the familial clustering of H pylori infection and inherited genetic factors reflecting response to organism likely to play a secondary role in pathogenesis.52 Perforated peptic ulcer Perforation occurs in 210% of patients with PUD and accounts for more than 70% of deaths associated with PUD. Perforation is often the first clinical presentation of PUD. The perforation site usually involves the anterior wall of the duodenum (60%), although it might occur in antral (20%) and lesser-curvature gastric ulcers (20%). Duodenal ulcer is the predominant lesion of the western population, whereas gastric ulcers are more frequent in oriental countries, particularly in Japan. Gastric ulcers have a higher associated mortality and a greater morbidity resulting from hemorrhage, perforation and obstruction. PPU used to be a disorder mainly of younger patients (predominantly males), but recently the age of PPU patients is increasing (predominantly females). The current
51

peak age is 4060 years. The need for surgery

for PPU has remained stable or even

increased and the mortality of peptic ulcer surgery has not decreased since the introduction of H2 receptor antagonists. This may be due to an increase in use of aspirin and/or NSAIDS.51

Current Management Perforated Peptic Ulcer:

Non operative management Conservative treatment is known as the Taylor method and consists of nasogastric aspiration, antibiotics, intravenous fluids and nowadays H. pylori triple therapy. In 1946, Taylor presented the first series of successful outcome of conservatively treated patients with PPU, based on the theory that effective gastric decompression and continuous drainage will enhance self-healing. The fundamental idea for conservative treatment came from Crisp who in 1843 noted that perforations of the stomach were filled up by adhesions to the surrounding viscera which prevented leakage from the stomach into the peritoneum. Since then, many reports have been published on this topic, with different success rates. But still there is an ongoing debate whether PPU generally needs to be operated on or not. It has been estimated that about 4080% of the perforations will seal spontaneously and overall morbidity and mortality are comparable. However, delaying the time point of operation beyond 12 hours after the onset of clinical symptoms will worsen the outcome in PPU. Also in patients with 70 years of age conservative treatment is unsuccessful with a failure rate as high as 67%. Shocks at admission and conservative treatment were associated with a high mortality rate (64%). Patients likely to respond
52

well to conservative treatment can be selected by performing a gastroduodenogram as described by Donovan et al (1998). Nonsurgical treatment in these patients, who had proven sealing of their perforation site was safe, only resulting in 3% intra-abdominal abscess formation and 2% repeat leak. The advantages of conservative treatment are avoidance of operation with associated morbidity caused by surgery and anesthesia, reduction in formation of intra-abdominal adhesion induced by surgery which makes elective surgery for PUD or for other indications in a later phase less complicated and hospital stay perhaps shorter. However, there are also studies that showed a prolonged hospital stay after conservative treatment. Disadvantages are a higher mortality rate in case conservative treatment fails. Another disadvantage is the lack of the benefit of laparoscopy or laparotomy as a diagnostic tool in case the patient was misdiagnosed. Finally, one always has to bear in mind that PPU can be a symptom of gastric cancer, so if conservative treatment has been chosen after a few weeks endoscopy should be performed. In conclusion, one can say that nonoperative treatment is limited to patients, 70 years of age who are not eligible for surgical repair due to associated morbidity, with documented contrast studies showing that the perforation has sealed completely. When the patient is in shock or when the time point between perforation and start of treatment is 12 hours, simple closure should be the first treatment of choice.51

53

Operative treatment of perforated duodenal ulcer: Local excision of ulcers was first described by Czerny in 1882. Based on the early experience of high recurrence rates for local gastric ulcer and duodenal ulcer excisions, these lesser procedures were largely abandoned. In the modern era of pharmacologic control of acid secretion and eradication of H pylori, these procedures have not been reevaluated.53 Simple suture: In conventional surgery, an upper midline incision is performed. Identification of the site of perforation is not always easy. Sometimes a perforation has occurred at the dorsal site of the stomach, only to be detected after opening of the lesser sac through the gastrocolic ligament. Also, double perforations can occur. Cellan-Jones published an article in 1929 entitled A rapid method of treatment in perforated duodenal ulcers.

Treatment of choice at that time was, after excision of friable edges if indicated, the application of purse string sutures and on top an omental graft. An encountered problem was narrowing of the duodenum. To avoid this, he suggested omentoplasty without primary closure of the defect. His technique consisted of placing 46 sutures, selecting a long omental strand passing a fine suture through it, the tip of the strand is then

anchored in the region of the perforation and finally the sutures are tied off. It was not until 1937 that Graham published his results with a free omental graft. He placed three sutures with a piece of free omentum laid over these sutures, which are then tied. No

54

attempt is made to actually close the perforation. The omental graft provides the stimulus for fibrin formation. His approach has been the golden standard since.51 Definitive treatment: Controversy has continued over the merits of simple closure versus those of definitive therapy, which deals with the emergency and also attempts to prevent persistent or recurrent ulcers. Many surgeons do not accept definitive surgery as initial treatment for perforated pyloroduodenal because of their concern for increased morbidity and mortality in some patients who might never require definitive ulcer therapy. The ideal operation, if definitive treatment of perforated pyloroduodenal ulcers is to be accepted, should have negligible mortality, provide protection against recurrent ulcer, and cause no morbidity for patients who would not have required definitive therapy for recurrent ulcers. The excellent results obtained with PCV for elective treatment of duodenal ulcer suggest that it might fulfill our requirements for the definitive treatment of perforated ulcers.54 Types of definitive surgery: 1) 2) 3) 4) 5) Truncal vagotomy with gastrojejunostomy. Antrectomy with vagotomy. Pyloroplasty and vagotomy. Partial gastrectomy with vagotomy. Highly selective vagotomy with simple closure.

55

Indications 1) 2) 3) 4) When patient has had previous perforation treated by simple closure. When perforation and bleeding occur together. Presence of synchronous second ulcer complication. Perforation of ulcer during medical treatment.

Contraindication 1) 2) 3) 4) More than 24 hours of presentation. Gross abdominal contamination. Concurrent medical illness. Poor risk patient like preoperative shock.

Perforated gastric ulcer: In perforated gastric ulcer the main option include simple closure after 4 quadrant biopsy, excision and primary closure or gastric resection. Factors influencing operative choice include, patient age and general condition, the location of ulcer and the degree of peritoneal contamination and the presence of malignancy on frozen section. For ulcers located in the distal stomach antrectomy both removes ulcer and provides definitive therapy. Benign ulcers in unstable or elderly patient may be treated with Excision and closure or closure with omental patch. If excision is not possible ulcer margin should be biopsied before closure with omental patch.55
56

Laparoscopic approach to perforated ulcers: Since the advent of H2-antagonists, the usefulness of simple closure of a perforated peptic ulcer is increasing, and improvements in laparoscopic surgery have made possible minimally invasive surgery for perforated ulcer. Surgical technique of laparoscopic omental patch repair; The patients were placed in the supine position with legs spread apart. The operating surgeon stood at the patients right side, with an assistant stationed at the patients left side and a second assistant positioned between the patient's legs. Intraperitoneal pressure was maintained at or below 12 mm Hg. The abdominal cavity was first explored by video laparoscope assisted by the atraumatic retractor, to determine the degree of peritoneal soiling and the perforation site. Soiled ascitic fluid usually is present in the upper right quadrant and the pelvis. Acute duodenal perforations usually were covered by the undersurface of the liver and were identified easily with upward displacement of liver using retracter. The peritoneal cavity was irrigated with 3 to 5 liters of warm saline, and any increase of intraperitoneal pressure was noted. Pulling and maneuvering the omentum to the perforation site without tension, the perforation was then closed. Tate et al presented a sutureless method using a gelatin sponge plug. Preliminary experience suggests that laparoscopic omental patch repair followed by administration H2 antagonist is minimally invasive surgery for perforated peptic ulcer and offers an attractive alternatrive to open surgery.56

57

SMALL BOWEL PERFORATIONS:

Before the 1980s duodenal perforation due to PUD was the most common form of small bowel perforation today itraogenic injury occurred during upper gastrointestinal endoscopy is the most common cause of small bowel perforation , other etiology of small bowel perforations include infections , TB, Typhoid, and CMV, IBD, Ischemia, Drugs ( Pottassium and NSAIDS induced ulcers.), Radiation injury, Meckels and acquired diverticula Neoplasm ( lymphoma , adenocarcinoma and melanoma ).57 Typhoid enteric perforations: Typhoid fever is predominant cause of nontraumatic perforation in developing countries. Typhoid fever, a severe febrile infectious disease caused primarily by Salmonella typhi occurs in areas where poor socioeconomic levels and unsanitary environmental conditions prevail. After ingesting contaminated food, multiplication of bacteria occurs in the reticuloendothelial system during an incubation period of 114 days; clinical manifestations start with bacterimia. Later the bacteria become localized in Peyers patches. These undergo swelling and ulceration that can progress to capillary thrombosis and subsequent necrosis. These ulcerations are always located on the antimesenteric border of the intestine and may perforate, usually in 3rd week of disease. There may be one or several perforations and many other impending perforations, which makes the surgery difficult. Nonspecific inflammation of the terminal ileum was another predominant cause. In such cases, the operative findings were similar to that of typhoid fever but no laboratory evidence of the disease was found.58
58

Perforations are predominantly in the terminal ileum, over 80% being within 60 cm of the ileoceacal valve. Eighty-five per cent of typhoid perforations are solitary. Cultures of peritoneal fluid are rarely positive for Salmonella typhi and disclose only the usual intestinal flora. Ileal perforation secondary to tuberculosis is extremely rare in the western hemisphere. Of patients with tuberculosis, less than 1% will have G.I. involvement and of these perhaps 10% will perforate leading to peritonitis. The most common site of G.I. involvement is the ileum, and operative differentiation from Crohn's disease may be difficult and this can be a clue to the etiology of the acute abdominal process. Free perforation of the intestine is rare in Crohn's disease, because of the chronic nature of the condition and the tendency to form abscesses and fistulae if full thickness penetration of the bowel occurs. The reported incidence of this complication is 1% to 2% of all cases of Crohn's disease. Perforation may occur in an area of active inflammation or through normal bowel proximal to an obstructing lesion.

Perforation of the intestine secondary to malignant disease is becoming more frequent as the numbers of patients undergoing successful initial treatment is increasing. Perforation may occur in an area of cancerous involvement, often secondary to a partial or complete distal obstruction. Additionally, patients with infiltrating malignancies of the bowel such as lymphoma may perforate during chemotherapy due to rapid lysis of the tumor.59
59

Management of ileal perforations: Bontecou, in 1887, performed the first surgical intervention in a patient affected by intestinal perforation caused by typhoid fever in America. The patient died in recovery room. Although surgery for the management of ileal perforation caused by S. typhi has been used since the end of the last century, it did not become routine until the work of Finney, Keen, and Cushing. All these series have proposed diverse surgical treatments, including primary closure of perforations, resection with anastomosis, and ileostomy and ileotransverse anastomosis. Despite this great variety in treatments, mortality resulting from this complication is approximately 30%.60 Most surgeons agree that treatment of typhoid perforation should be surgery as there is peritoneal soiling and endotoxaemia. There is however no uniformity of opinion as to extent of surgery. Some surgeons recommend that simple closure should be reserved for single perforation while others have found wedge excision to be effective for fewer than three perforation. Segmental resection and resection and anastomoses recommended if three or more than three perforation found. Others have found no relation between type of procedure and complication or mortality rate.61

60

Tubercular intestinal perforations: Infection by mycobacterium tuberculosis is common in tropics but increasingly being seen in UK mostly among immigrants. Two types are recognized Ulcerative and hyperplastic The ulcerative type occurs when the virulence of the organism is greater than the host defence. The opposite occurs in hyperplastic type. Small bowel stricture are common in the hyperplastic type mainly affecting the ileoceacal area. In ulcerative type bowel serosa is studded with tubercles. Clinical features : Intestinal tuberculosis should be suspected in any patient from endemic area who presents with weight loss, malaise, evening fever. The abdomen has doughy feel. The emergency patient present with features of distal small bowel obstruction or features of peritonitis from a perforated tuberculous ulcer in small bowel.28 Treatment : All though bypass of affected segment has been recommended, the result are so poor that resection should be considered as preferred treatment in tubercular perforation. The decision whether to exteriorize or anastomose will depend on degree of peritonitis and other individual circumstances. ATT is mandatory after operation. With knowledge of common causes of small bowel perforation and adherence to these principles the current excessive mortality rates noted in this condition should be reduced in future.60
61

LARGE BOWEL PERFORATIONS:

Non-traumatic perforation of colon is a fatal surgical emergency that confronts with serious risks and high mortality influenced by leakage of several types of virulent bacteria inside the colon. This condition has various etiologies, which is difficult for accurate preoperative diagnosis, causing a problem for surgical decision. Etiologies of colonic perforation 1) 2) 3) 4) 5) 6) Diverticulitis. Colonic ulcer. Carcinoma colon. Incarcerated groin hernia. Intususception . Colonic ischemia.

The common etiologies were complicated diverticulitis, cancer and benign ulcer with mortality rate of 14-19%. In one report perforated carcinoma was common cause with overall mortality 26.6%.

62

Management: The accurate pre-operative diagnosis is beneficial in the operative plan i.e. postoperative colostomy status. Plain abdominal radiography and USG scan was also proved to be useful in diagnosing various causes in non-traumatic colorectal perforation, especially in suspected diverticulitis. CT scan has a higher sensitivity than ultrasonography in the cases with gaseous dilated bowel or obesity and was helpful in suspected cases. 62 The appropriate surgical management of colonic perforation has always been a controversial issue and one that continues to evolve. The differences in patients characteristics, due to their medical problems, general conditions, peritonitis grade, or causes of perforation, influence both the surgical decision and the outcome.63 The operative procedure decisions were dependent on the intra-abdominal conditions and patient status. Whenever the bowel looked compromised and patients condition is unstable, malnourished or immunocompromised, resection and diversion should be performed.62 Diverticular disease of the colon is common in the western world with a prevalence of approximately 33% in pts over age 60yrs. Surgical treatment has evolved from a three-stage procedure to two-stage procedure of primary resection of the perforated segment and end colostomy (Hartmanns procedure -HP) with subsequent restoration of intestinal continuity, HP has been accepted as the gold standard for perforated diverticular disease by the great majority of colorectal surgeons in the United States and the United Kingdom. However, there is a growing body of evidence reporting
63

on high complication rates with end stoma reversal procedures. Primary resection and anastomosis (PRA) has been proposed as an alternative to HP in the setting of peritonitis secondary to diverticular disease. Several published studies have reported on comparable morbidity and mortality rates after PRA when compared with HP for perforated

diverticular disease. Based upon the best available data, it is our recommendation that PADS may be performed when the risk of morbidity and mortality is not excessive to obviate the need for a complicated reversal operation and a high risk of permanent stoma. HP should be reserved for patients with a high risk of complications after appropriate counseling regarding the long-term implications.64 About 15% patient with carcinoma large intestine present with surgical emergencies such as obstruction and perforation. The incidence of PCC ranges from 3% to 10. Perforated colorectal carcinoma is generally reported to have a low survival rate and high operative mortality. Factors contributing to the unfavorable prognosis in this group include: high operative mortality due to sepsis, locally advanced malignancy, and a higher incidence of distant metastasis at presentation. Perforation in colorectal carcinoma occurs due to direct perforation from tumor necrosis or due to proximal colon blow-out from an obstructed tumor and a competent ileocaecal valve producing a closed-loop. Both of these types of perforations had a similar long-term survival. More patients with right and transverse colon perforations underwent resection and primary anastomosis . Traditionally, Hartmanns procedure or resection and double barrel colostomy were the surgical procedures of choice, but at

present, one-staged procedures are often performed with significant survival advantage.65
64

METHODOLOGY
Study Setting: This study was carried at Karnataka Institute of Medical Sciences Hubli. Study Duration: The study was carried out for a period of 1 year from November 2009 to October 2010. Study Design: A 1 years prospective study was carried out in Karnataka Institute of Medical Sciences Hubli. Source of Data: Data was collected through a prescribed proforma from among the patients admitted in Department of Surgery, KIMS, Hubli with diagnosis of perforative peritonitis from November 2009 to October 2010. Method of collection of Data: Data will be collected in prescribed proforma where in it contain, history, clinical findings, investigations and surgical procedures done. Patients were followed up in the postoperative period to know the postoperative complications, morbidity and mortality rates. After satisfactory improvement, patients were discharged from the hospital. Inclusion Criteria: All patients admitted with perforative peritonitis. Both males and females more than 12 years are included in study.

65

Exclusion Criteria: Children less than 12 years of age. Patients with perforation of esophagus, biliary tree, bladder and reproductive organs and post operative anastomotic leak. All traumatic cases. Patients not undergoing surgery.

66

RESULTS
In this study 100 cases of non traumatic perforation peritonitis were studied with reference age group of presentation, diagnosis, management and complications.

Table2: Age distribution Age (yrs) 13-19 20-29 30-39 40-49 50-59 60-69 70-80 No. Of cases (n=100) 09 17 25 14 14 16 05

The most common age group affected in this study was 30-39 yrs of age.

67

Graph 1: Age distribution

30 25 25

20 17 15 9 5 5 14 14 16 Series 1

10

0 13-19 20-29 30-39 40-49 50-59 60-69 70-80

68

Table 3 : Sex distribution

Sex Male Female

No. Of cases 79 21

Graph no 2:Sex distribution

90 80 70 60 50 40 30 20 10 0 MALE FEMALE 21 Sex distrubition 79

. In this study total 100 cases were studied and 79 were males and 21 were females with male to female ratio of 3.76. Males are affected more may be because of presence of risk factors like alcoholism and smoking more common in men.

69

Table 4: Distribution according to age and etiology

Site of perforation 10-19 20-29 Duodenal perforation Gastric perforartion Ileal perforation Appendicular perforation Total 04 00 02 03 09 06 01 04 06 17

Age in years 30-39 40-49 50-59 13 01 05 06 25 10 01 02 01 14 10 01 00 03 14

60-69 11 05 00 00 16

70-79 04 01 00 00 05

Graph 3: Distribution according to age and etiology

14 12

13 11 10 10 Duodenal perforation 6 6 5 4 4 3 2 2 1 0 1 1 1 1 0 20-29 30-39 40-49 50-59 00 60-69 1 00 70-79 3 6 5 4 Gastric perforartion Ileal perforation Appendicular perforation

10 8 6 4 2 0 13-19

70

In this study duodenal perforations were seen more common in 30-40 age group although 4 cases were of below 20 yrs age. Gastric perforations were common in older age group of 60-70 yrs. One of the reason for increased morbidity and mortality in gastric ulcer patients. Ileal and Appendicular perforations were common in 30-40 yrs of age group. Appendicular perforations were also commonly seen in younger ages from 20-29 yrs as appendicitis is disease of younger age group.

Table 5 : Distribution according to etiology and sex

Site of perforation duodenal ulcer perforation

Male

Female

Total

47

11

58

Gastric ulcer perforation

07

03

10

Ileal perforation

12

01

13

Appendicular perforation

13

06

19

79
71

21

100

Graph 4: Distribution according etiology and sex

50 45 40 35 30 25 20 15 10 5 0

47

Male Female 11 7 3 1 Ileal perforation Appendicular perforation 12 13 6

Duodenal perforation

Gastric perforation

In this study total male were 79 and female were 21. In duodenal ulcer group 47 were males and 11 were females. Gastric ulcer group 07 were males and 03 were females and in ileal perforation group 12 were males and 1 was female. In appendicular perforation 13 were males and 06 were females.

72

Table 6: Distribution according to risk factors No of patients Use of NSAIDS Alcoholic Smoker 15 13 15

Graph 5: Distribution according to risk factors

15.5 15 15 14.5 14 13.5 13 13 12.5 12 NSAIDS Alcohol Smoking No of pts 15

15 Patients of gastroduodenal perforation gave history of NSAIDS intake in last month of perforation and equal no of patients were smokers and 13 patients were

alcoholics out of total 68 gastroduodenal perforations. 9 patients had multiple risk factors with 3 patients having all three risk factors one of three died and one had prolonged recovery. 4 patients were both alcoholic and smokers. and 2 patients had history of NSAIDS use and were smokers
73

Table 7 : Distribution according to symptoms

Symptoms Pain Vomiting Abdominal distension Fever Loose stools

No.of cases 98 48 36 29 08

Graph 6 : Distribution according to symptoms

120 100 80 60 40 20 0 Pain Vomiting Abdomen distension Fever loose stools 48 36 29 8 98

symptom

In this study most common presenting symptom was pain abdomen of varying duration ranging from hours to weeks with 98 patients presenting as pain abdomen. 48 patients had vomiting and abdomen was distended in 36 patients. Fever was present in 29 cases and loose stools in 8 patients.
74

Table 8: Distribution according to symptom complex of peritonitis Symptom complex Pain abdomen alone. Pain abdomen and vomiting. Pain abdomen, vomiting and distension abdomen Pain abdomen, vomting and fever. 09 09 29 29 No. of cases 22 47 Percentage 22 47

Graph 7: Distribution according to symptom complex of peritonitis

50 45 40 35 30 25 20 15 10 5 0 47

29 22 9

no of patients

Pain abdomen alone Pain abdomen and vomiting

Pain abdomen vomint and distension of abdomen

Pain abdomen vomiting and fever

Patients presented with combinations of above mentioned symptoms. 22 patients had pain abdomen alone and 47 had both pain abdomen along with vomiting. 21 of these patients had associated distension of abdomen and 9 of these patients had fever.
75

Table 9 : Distribution according to duration of symptoms Duration of symptoms (days) 0-2 3-5 6-10 More than 10 No. of patients 51 38 10 01

Graph 8 : Distribution according to duration of symptoms

60 51 50 40 30 No of patients 20 10 10 1 0 0-2 Days 3-5 Days 6-10 Days More than 10 days 38

51 patients presented within 48 hours of onset of symptoms and another 38 patients presented in next 3- 5 days of symptoms. One patient presented with 15 days symptoms.

76

Table 9: Distribution according to signs Signs Tachycardia Guarding Rigidity Tenderness Distension Obliteration of liver dullness No.of cases 54 91 71 98 36 41 Percent 54 91 71 98 36 41

Absent Sluggish Present Bowel sounds 29 45 26

Graph 9: Distribution according to signs

120 100 80 60 40 20 0 No of patients 54 41 91 71 98

64

54 patients had tachycardia, 98 patients had tenderness and 91 patient

had

guarding. Board like rigidity was felt in 71 patients and obliteration of liver dullness was found in 41 cases. Bowel sounds were absent in 29 cases and sluggish in 45 cases.
77

Table 11: Clinical signs of peritonitis in patients Clinical signs Tenderness and guarding Tenderness, guarding and rigidity Tenderness, guarding, rigidity and obliteration of liver dullness 36 36 No.of patients 86 70 Percentage 86 70

Graph10: Clinical signs of peritonitis in patients

100 90 80 70 60 50 40 30 20 10 0

86 70

36 Series 1

Tenderness and guarding

Tenderness, guarding Tenderness , guarding , and rigidity rigidity and obliteration of liver dullness

Most common signs of peritonitis were abdominal guarding and tenderness which were present in 86 cases,of these 70 cases had rigidity also. Only 36 cases presented with classical signs of peritonitis guarding, rigidity, tenderness and obliteration of liver dullness so detailed clinical examination of patient is essential to diagnose peritonitis in a patient.
78

Table 12: Distribution according to presence of pneumoperitoneum Presence of Site of perforation Peptic ulcer perforation Ileal perforation Appendicular perforation pneumoperitoneum 65 10 00

Graph 11: Distribution according to presence of pneumoperitoneum

70 60 50 40 30 20

65

No of patients 10

10 0 0 Pepti ulcer perforation Ileal perforation Appendicular perforation

Out of 68 peptic ulcer perforations 65 had air under diaphragm and out 13 ileal perforations 10 had pneumoperitoneum. None of appendicular perforations had pneumoperitoneum.

79

Table 13: Distribution according to procedure and cause

Cause Duodenal Per perforation Gastric perforation Appendicular perforation Ileal perforation

Omental patch closure 58 10

Resection Anastomoses

Appendectomy Wedge Primery resection closure

00 00 07

19 01 05

Graph 12: Distribution according to procedure and cause

70 60 50 40 30 20 10 0

Duodenal perforation Gastric perforation Ileal perforation Appendicular perforation

In this study 68 cases underwent omental patch closure and 7 patients of ileal perforation were managed with resection and anastomoses. Wedge resection was done in one case and primary closure of ileal perforation in 5 cases. Appendectomy was done in 19 cases.
80

Table 14: distribution according to duration of hospital stay No.of days 00-05 06-10 11-15 16-20 21-25 26-30 More than 30 days No.of patients 12 41 30 08 06 01 02

Graph 13: Distribution according to duration of hospital stay

45 40 35

41

30 30 25 20 15 10 5 0 00-05 Days 06-10 Days 11-15 Days 16-20 21-25 26-30 more than 30 days 12 8 6 1 2 No of patients

Most patients were discharged between 6th to 10th post operative day and 30 patients were discharged between 11th to 15th post operative day. Only two patients stayed for more than 30 days.
81

Table 15 : Distribution according to complications

Complication Wound infection

No.of cases 26 02

Graph 14 : Distribution according to complications Post operative leak Septicemia Electrolyte imbalance Respiratory complication

09

03
08

30 26 25 20 15 10 5 0 Wound infection Septicemia Electrolyte imbalance Respiratory complication Post op leak 9 8 3

82

In this study wound infection was most common complication seen in 26 cases followed by respiratory complication in 8 patients and septicemia seen in 09 patients. Two patients developed postoperative leak. Table16: Histopathology of main causes of perforation

Site of perforation Stomach Appendix

Total number of cases.

Inflammtion

Malignancy

Tuberculosis

10 19 13

09 19

01 00 00

00 00 04

Ileum

A four quadrant biopsy should be taken from all gastric ulcers as it was done in this study since malignancy should be ruled out. Histopathological examination and reports were analysed there was one case of adenocarcinoma of stomach and rest were inflammatory ulcers. Hisopathological examinations of specimens of appendix and ileum revealed 4 cases of tubercular perforation of ileum and all appendicular specimens were reported as inflammatory.

83

Table 17: Distribution of complications with procedure

Complication

Omental patch closure

Resection with Appendectomy anastomoses 05 02 09

Primery Closure 03

Wound infection Septicemia Electrolyte Imbalance Respiratory complication Post operative Leak

09 07 03 06 02

02

Graph 15: Distribution of complications with procedure

84

10 9 8 7 6 5 4 3 2 1 0 Primary closure Res with E-E anastomoses Appendectomy Simple closure

Simple closure with omental is safest procedure with minimal complications with only 09 having wound infection and septicemia in 07 cases. Resection and anastomoses had 5 wound infections and 2 septicemia. Appendectomy was safe with only 9 wound infection.

Table18 : Incidence of mortality

Mortality Site of perforation Total no of patients No.of deaths Gastro Duodenal Ileal 68 13
85

Mortality rates 13.23 15.38

09 02

Appendicular

19

00

00

Graph 16: Incidence of mortality

10 9 9 8 7 6 5 4 3 2 2 1 0 0 Gastroduodenal Ileal Appendicular No of deaths

86

Total 11% mortality was recorded in this study. 09 cases were gastroduodenal perforations and two were ileal perforation with no mortality in appendicular perforation. Septicemia was important cause of mortality with 09 cases went into post op septicemia and age was important factor with only three patients below 50 yrs in mortality group. Other factors responsible for mortality were shock at presentation and delayed presentation. 4 patients presented with shock at the time of admission and seven patients presented with symptoms of more than 3 days. 2 patients were asthamatics on irregular treatment. Though diabetis is common important co morbid condition none of the non survivors in present study were diabetics.

DISCUSSION
Secondary peritonitis caused by intraabdominal lesions such as perforation of hollow viscus is still a severe disease with high mortality and mandates surgical intervention. The results of present study were compared with similar studies in past and comparable results were obtained.

Table 19 : Comparison of age groups

87

Study Mathikere lingaiah ramachandra et al1 Rajendrasingh jobta et al4 Nitin agarwal et al66

Age group affected(yrs)

20-30

30-40

20-40

Present study

30-40

Most common age group affected in this study was 30-40 yrs and similar results were obtained in studies by Rajendrasingh jobta et al and Nitin agarwal et al may be because peak age affected by peptic ulcer is same.

Table 20 : Comparison of sex ratio

Study Shahida parveen afridi et al67 Shyam kumar gupta et al 2 Nuhu ali et al68 Present study

Male to female ratio 2.1 : 1 3.25 : 1 2.73 : 1 3.76 : 1

Male to female ratio waa 3.76 and it was comparable with other similar
88

Studies done by Shahida parveen et al and Nuhu ali

Table 21: Comparison of sex ratio in different perforations

Male Site of perforation Latit Present Latit

Female Present

Sharma et al69 study Duodenal perforations Appendicular perforations 44 17 47 13

Sharma et al69 study 01 06 11 06

89

Ileal perforations

44

12

10

01

In this study total males were 79 and female were 21. In duodenal ulcer group 47 were males and 11 were females. Gastric ulcer group 07 were males and 03 were females and in ileal perforation group 12 were were males and 1 was female. In appendicular perforation 13 were males and 06 were females The increase in ratio of females in present study may be due to increased risk factors in females like NSAIDS use..

Table 22 : Comparison of symptoms

Symptom

Mathikere lingaiah et al1

Rajedersing jobta et al4

Shahida parveen afridi67 78 21 45

Present study

Pain Vomiting Distension of abdomen

100 64 100

98 59 44
90

98 48 36

Fever Loose stools

42 04

25 07

20 26

29 08

Presenting symotoms in this study were compared with other studies done by Shahida parveen et al and Mathikere Lingaiah et al and results were similar with pain being most common symptom present in 98 patients. Vomiting and distension of abdomen being present in less than half patients. These were present in late cases. Fever was more common in appendicular and ileal perforations.

Table 23: Comparison of duration of symptoms

Duration of symptoms >3days Survivors Raju singh et al70 Non survivors Survivors
91

< 3days 51(73.91%) 00 47(52%)

18(26.08%) 15(100%) 42(47%)

Present study

Non survivors

7(63%)

4(36%)

In this study 51 patients presented within three days of symptoms and there were only four deaths in this group and 49 patients presented after three days or more of symptoms and there were seven deaths in this group so delayed presentation was a poor prognostic factor. The results were compared with study done by Raju singh et al .

Table 24 : Comparison of signs of peritonitis

Study

Mathikere lingaiah1

S.V. Punekar et al71

Present study

Tachycardia Guarding Rigidity Tenderness 100 100 100

92

90 50 50 100

54 91 71 98

Obliteration of liver dullness Bowel sounds absent/diminshed

72

50

34

80

74

Examination finding of patients were compared with similar studies by S .V Punekar and Mathikere Lingaiah and results showed that more than half patients were tachycardiac. Guarding, tenderness present in all most all cases and rigidity was late

onset and felt in 71 cases in this study. Obliteration of liver dullness was felt in 34 cases and bowel sounds were not well heard in 74 cases. Though all signs of peritonitis may be seen in late classical case of peritonitis initial signs of peritonitis, systemic as wel as local eg. Tachycardia, Tenderness should be carefully looked for and interpreted so that surgical intervention can be done early to improve prognosis.

Table 25 : Comparison of complications

Complications

Shyam kumar gupta et al2 16 3 4

Shahida parveen afridi et al67 42 20 -

Present study

Wound infection Septicemia Electrolyte imbalance Respiratory complication

26 09 03

6
93

20

08

Post operative leak

1.6

02

Complications in this were compared with study done by Shahida parveen afridi et al Karachi There were less number of complication in present study. Adequate

resuscitation, proper antibiotic use and source control resulted in less complication. Wound infection was treated with adequate antibiotics according to culture sensitivity. Septicemia was dreaded complication leading to mortality in 09 cases most of them were elderly persons with delayed presentation and gross peritoneal contamination leading to inadequate source control. Respiratory complications were more in elderly smokers and two had mortality due to ARDS. Two developed post operative leak both were hypoprotienemic one was treated conservatively and other was managed with jejunal serosal patch. When study done by Shyam kumar et al was compared similar results were obtained.

Table 26: Comparison of mortality

Site of perforation

Nitin agarwal et al66

Present study

Gastroduodenal

8.2

13.23

Ileal

12

15.38

94

Appendicular

00

00

There were total 11 deaths in this study 09 were gastroduodenal

amounting to

13.23 percent mortality and 02 were ileal perforation amounting to 15.38 percent mortality and it was comparable with study done by Nitin agarwal et al . Old age was major predictor of mortality with only three patients who died were below 50 yrs of age and all remaining 8 patient were above 50 yrs. Other factors contributing to mortality were shock at admission. Four of our cases in mortality group were in septiceamic shock. Delayed presentation is important prognostic factor because seven patients of non survivors presented after three days of symptoms. Various scoring system like APACHEII has

been evaluated in many studies to stratify the patients according prognosis so that high risk patients can be treated with intensive care to improve prognosis.

CONCLUSION
Peritonitis is one of the most important emergency surgical condition. Pain abdomen is the most important and common presenting symptom in non-traumatic perforation peritonitis followed by vomiting, fever, distension of abdomen and loose stools. Erect abdomen X-ray and USG abdomen are very useful investigation for diagnosis in non-traumatic perforation peritonitis. Scoring system like APACHE-II can be used to
95

stratify patients into high risk of mortality so as to treat them with intensive care to improve prognosis. Omental patch closure of perforation was the most common procedure employed. Resection and anastomosis is also done for bowel perforation. With the available effective acid reducing drugs, definitive surgery is not mandatory for peptic ulcer perforation. The most common cause of perforation peritonitis is due to peptic ulcer perforation 68% followed by appendicular(19%) and ileal perforation(13%). All cases were treated surgically according to site of perforation .Elderly patients with delayed presentation and gross contamination of peritoneal cavity and shock at presentation were poor prognostic indicators with higher motality. Adequate resuscitation , Early surgical intervention and source contol ,and proper antibiotic therapy resulted in lower mortality and morbidity in this study.

SUMMARY
Non traumatic perforation of hallow viscous forms important part emergency surgical admissions. Incidence is more in 3rd and 4th decade. Pain abdomen is most common and important presenting complaint followed by vomiting distension of abdomen, fever and loose stools. It is possible to make a fairly accurate diagnosis by the symptoms and signs of
96

presentation. In our study the most common cause of perforation peritonitis was peptic ulcer perforation followed by appendicular and ileal perforations. Investigative modalities including plain erect X-ray of abdomen, USG abdomen, are very useful in diagnosing this condition with accuracy. All peptic ulcer perforations in our study underwent only simple omental closure of perforation. No definitive acid reductive procedure was done for any of the cases. Small bowel perforations were treated depending on the number and size of perforations and condition of the bowel. Resection and anastamosis was the commonly done procedure. Specific viscus perforation like appendix treated accordingly Postoperatively the most common complication was wound infection and systemic complications. Mortality rate in the present study was 11% Delay in the presentation, shock at the time of presentation old age and extensive peritonitis were associated with high mortality.

97

Fig 2: Duodenal ulcer

Fig 3:

Duodenal ulcer

98

Fig 4: Closure of Duodenal ulcer

Fig 5: Closure of Duodenal ulcer

99

Fig 6: Omental patch closure of Duodenal ulcer

Fig 7 : Ileal Perforation

100

Fig 8: Primary closure of Ileal perforation

Fig 9: Perforated appendix

101

Fig 10: Appendicectomy done

102

BIBLIOGRAPHY
1) Mathikere Lingaiah Ramachandra,Bellary Jagadish, Sathees B.C.Chandra. Clinical study and Management of Secondary Peritonitis due to perforated hollow Viscous. Arch Med Sci 2007 March; 8: 62-68. 2) Shyamkumar, Gupta, Rajan, Gupta,Gurdev, Singh,Sunil Gupta. PerforationPeritonitis : A Two Year Experience.JK Science 2010 July-September ; 12( 3) :141-144 3) John T Langell,Sean J.Mulvihill. Gastrointestinal perforation and acute abdomen . Med Clin N Am 2008; 92: 599-625. 4) Rajender Singh Jhobta,Ashok kumar Attri, Robin Kaushik, Rajeev Sharma ,Anupam Jhobta. Spectrum of perforative peritonitis in India Review of 504 consecutive cases. World J Emerg Surg 2006; 1:26. 5) Sanjay Gupta , Robin Kausik . Peritonitis The Eastern Experience.World J 6) 7) 8) Emerg Surg 2006 April; 26.

Lewis practice of surgery : The Peritoneum vol 7 Inderbir Singh A. Human Embryology. 7th edition: 204-205 Susan Standring . Grays Anatomy . 40th edition; Elsevier churchill livingstone elsevier ltd: 2005

9)

Susan Standring Grays Anatomy for students ; Elsevier churchill livingstone elsevier ltd: 2007

10) Lee Mc gregger .Synopsis of surgical anatomy. LeemcGregor Varghese publishing

103

house 12th edition1999 ; 99-102 11) Seymour I Schwartz, Shires G Tom, Frank C Spencer, Wendy Cowles Husser. Principles of Surgery, 7th Edition. McGraw Hill: 2001, Vol. 2: 1515-1539 12) Micheal Joseph Hausmann,Boris Rogachev,Michal Weiler,Cidio Chaimovitz,Amos Douvdevani . Cell biology- Immunology- Pathology Kidney Int 2000;57: 476-4 13) Felix Broche JoseM.Tellado . Defense mechanisms of peritoneal cavity. Current opinion in Critical Care 2001; 7: 105-107

14) Yao V,Platell.C,Hall.J.C. Role of Peritoneal Mesothelial Cells in Peritontis. Br J Surg2003; 90:1187-1194.
.

15) Cristopher J Godshall,Meanie J.Scott,Phillip T. Burch,James C. Peyton, William G. Cheadle. Natural killer cells participate in bacterial clearance during septic peritonitis through Interaction with macrophages. Shock 2003 February; 19(2):144-149.

16) Heel.K.A,Hall.J.C. Peritoneal Defenses and Peritoneum Associated lymphoid Tissue. Br J Surg 1996 ;83: 1031-1036. 17) Masja Leendertse, Rob Willems J.L, Ida Giebelen A.J, Joris Reolofs J.T.H,Nicovan R, Marc J.M, Tom vander poll. Peritoneal Macrophages are imporatnat for the early containment Of Enterococcus feacium peritonitis in mice Innate Immun 2009;15:3 18) Rotstien Ori D,Timothy L.P,Richard L.S. Fibrin in Peritonitis. Ann Surg 1986 April; 203 (4): 413-419. 19) Binda.M.M, Molinas C.R, Koninckx.P.R. Reactive oxygen species and adhesion formationClinical implications in adhesion prevention . Human Reproduction ,
104

2003;18(12):25032507. 20) Cheong.Y.C,Liard.S.M,Shelton.J.B, Ledger.W.L, Cooke.I.D. Peritneal healing and adhesion formation / reformation Human reproduction update. 2001; 7( 6): 556-566 21) Sanjay munireddy,Sandra.L.K, Adrian. B, .Intra-abdominal healing Gastrointestinal tract and adhesions. Surg clin N Am 2010; 90:1227-1236. 22) John Mazuski.E, Joseph S.S. Intra Abdominal Infections .Surg clin N Am 2009; 89: 421-437 23) Massimo Sartelli . A Focus on intra- abdominal infections . World J Emerg surg 2010; 5(9) : 3-20 24) Nicole Lopez, Leslie Kobayashi, Raul Coimbra. A Comprehensive review of abdominal infections . World J Emerg surg 2011; 6(7): 5-10 25) van GOOR .H, Bom.V.J.J,Meer vander.J, Sluiter.W.J, Bleichrod.R.P. Coagulation and fibrinolytic responses of human peritoneal peritonitis . Br J Surg 1996; 83: 1133-1135 26) Mark A Malangoni . Contribution to the management of intra-abdominal infections. Am J Surg 2005;190; 255-259. 27) C.J .Miney . Peritonitis and intra- abdominal abscess. Principles of Surgical Patient care. Vol-2 28) Russell RCG, Williams NS, Bulstrode CJK. Bailey & Loves Short
105

fluid and Plasma to bacterial

Practice of Surgery. 25th Edition. Edward Arnold Ltd; 2008. 29) Ronald F Martin, Ricardo L Ross. Abdominal Emergencies: Has Anything Changed?.Surg clin N Am 1997 Dec; l77(6):1234-1236. 30) Michael J Zinner, Seymour I Schwartz, Harold Ellis, Stanley W Ashley, David W McFadden. Maingots Abdominal Operations. 10th Edition . McGraw Hill; 2001. 31) Onderdonk A.B, Moon.N.E, Kasper.D.L, Bartlett.J.G. Adherence of bacteria fragilis in vivo : Infection and Immunity 1978 March;19(3):1083-1087.

32)

John J.B,Henry Rogers.J,Paul Spalding.B, Gillon Ward.C . Natural resistance, iron and infection ; a challenge for clinical medicine J Med Microbiol 2006;55:251-258

33)

David .L. Dunn,Roderick .Barke.A,David .H.A,Edward.W.H,Richard.L.S. The Adjuvant Effect of Peritoneal Fluid in Experimental Peritonitis. Ann. Surg. 1984 January: 1999(1) :37-43.

34) Dunn . Antibiotic Treatment for Surgical Peritonitis. Ann Surg 1991 November; 214(5): 550-552. 35) Santosh Saini,Naveen Gupta, Aparna,Lokveer,Griwan.M.S. Surgical infection ; A Microbiological study . Braz J Infect Dis 2004;8(2) 118-125. 36) Pieracci.F.M,Barie.P.S. Management of severe sepsis of abdominal origin ; Scand J Surg 2007; 96: 184-196. 37) Lloyd M Nyhus, Robert J Baker, Josef E Fischer. Mastery of Surgery. 5th Edition. Little Brown and Company ;2007. 38) William Silen. Copes Early Diagnosis of Acute Abdomen . 7th edition 107-114
106

39)

Russell RCG, Norman NS Williams, Christopher JK, Bulstrode. Bailey & Loves Short Practice of surgery 25th edition Hodder Arnold; 2008.

40) Lloyd M Nyhus, Robert J Baker, Josef E Fischer. Mastery of Surgery. 3rd Edition. Little Brown and Company; 1997. . 41) Wittmann H Dietmar,Moshe Schein,Robert.E.C. Management of secondary Peritonitis. Ann Surg 1996 July ;22(1): 10-18. 42) John Marshall.C. Intra Abdominal infections. Microbes Infect 2004;6 :1015-25 43) William Cheadle.G,David Spain.A. The Continuing challenge of intraabdominal infection . Am J Surg 2003 Nov ; 186 (5A): 15S-22S. 44) Bosscha.K, Van Vroonhoven Th.J.M.V. Vander Werken.Ch. Surgical management of severe secondary peritonitis. Br J Surg1996;86:1371-1377. 45) Joseph Solomkin.S, John Mazuski. Intra abdominal sepsis ; Newer interventional and antimicrobial Therapies. Infect Dis Clin North Am 2009;23:593-608 46) Lamme.B,Boermeester.M.A,Belt .E.T.J,Van till .J.W.O, Gouma.D.J, Obertop.H. Mortality and morbidity of planned relaparotomy vs laparotomy on demand for Secondary peritonitis . British journal of surgery 2004;91; 1046-54 47) Lamme.B,Boermeester.M.A, Reitsma.J.B, Mahler.C, , Gouma.D.J, Obertop.H. Metalysis of relaporotomy for secondary peritonitis. Br J Surg 2002; 89:1516-1524 48) Boemeester.M.A. Surgical approaches to peritonitis . Br J Surg2007; 94: 1317-1318 49) Ferdinando Agresta,Ciardo.F.L, Mazzarolo.G, Ivan Mechelet,Guido Orsi,Guiseppe.T, Natalino Bedin et al .Peritonitis Laparoscopic approach. World J Emerg surgery 2009; 1:9
107

50) Daniel T. Dempsey. Schwartz Principles of Surgery .9th edition Chicago McGraw Hill; 2010. 51) Marietta J.O.E, Johan.F.L. Perforated peptic ulcer disease review of history and treatment Dig Surg 2010;27:160-169. 52) Richard Saad.J, James Scheinman.M .Diagnosis and management of peptic ulcer disease ; Clinics in family Practice 2004 Sept;6(3):569-587. 53) Ronald Martin.F. Surgical management of ulcer disease : Surg Clin N Am 2005;85: 907-929. 54) Paul Jordan H,Jack .T. Perforated Pyloroduodenal ulcer Long term results with omental patch closure and parietal cell vagotomy. Ann Surg 1995;225(5): 479-488 55) Michael J Zinner, Seymour I Schwartz, Harold Ellis, Stanley W Ashley, David W McFadden. Maingots Abdominal Operations. 10th Edition, McGraw Hill 2001; Vol. 1: 940-965. 56) Masao Matsuda,Motoharu N,Tsunekazu Hanai,Satomi.S,Toshiaki.W. Laparoscopic Omental patch reoair fot perforated peptic ulcer. Ann Surg 1995;221(3):236-240 57) Stanley W . Ashley. Schwartz Principles of Surgery .9th edition. Chicago McGraw Hill 2010; 1007-1009 58) Rauf A Wani,Fazl.Q.P, Nadeem Bhat.A, Mehamood wani .A, Tasaduk.H.B, Fowzia .F.Non traumatic ileal perforation ; World J Emerg Surg 2006;1: 7 59) Rajgopalan.A.E,Jack Pickleman. Free perforation of small intestine . Ann Surg 1982 Nov;196(5):576-578.
108

60)

Cesar Athie.G, Clemente.B.G,Avisai.V.A,Guillermo.H.A,Eduardo.J.M.Ttwenty five yr experience in surgical treatment of perforation of the ileum Caused by salmonella typhi at mexico Surgery 1998 Jun;632-636.

61)

Ameh E.A, Dogo.P.M,Attah.M.M, Nmadu.P.T. Comparison of three operations for typhoid perforation ; Br J Surg 1997;84:558-559.

62)

Chaw Suradam,Sombphulphipat.P, Keawaseadkorn.S. Non traumatic perforation of colon a5 yr retrospective study at Uthaithani hospital THAI J Surg 2009;30:52-57

63) Sebastiano Biondo,David pares,Juan Marti R, Javier De Oca,David Toral, Fransisco.G.B. Emergency operations for non diverticular perforation of left colon. Am J Surg 2002;183:256-260. 64) Vasilis A.C,Alexander H,Feza.R,Ara darzi, Asha senapathi, Victor .W. et al. Operative strategies for diverticular peritonitis.Ann Surg 2007 Jan;245(1):94-102 65) Neil Mandava, Surya kumar, Walter.F.P,Joseph Aprile, .Perforated colorectal Carcinomas . Am J Surg1996 Sept; l72:236-238. 66) Nitin Agarwal, Sudipta.S, Anurag.S, Sunil .C, Anitha. D, Sanket.G. Peritonitis : 10 years experience in single surgical unit. Trop Gastroenterol 2007;28:117-120. 67) Shahida Parveen Afridi , Faiza .M, Shafiq Ur- Rahman,Shahid.S, Khursheed. Spectrum of peritonitis in Pakistan : 300 cases Eastern Experience.World J Emerg Surg 2008 Nov;3:3-31. 68) Nuhu Ali, Bata Mtaku Gali. Causes and treated outcome of perforation peritonitis in north eastern Nigeria.Surgical Practice 2010;14:92-96. 69) Lalit.S, Sanjay .G,Soin.A.S, Sadiq.S, Vinay .K. Generalised Peritonitis in
109

India The Tropical Spectrum.Jpn J Surg 1991 ;21(3):272-277. 70) Raju singh ,Nishant kumar, Abhijit.B, Homay.V. Preoperative predictors of mortality in adult patients with perforation peritonitis. Indian J Crit Care Med 2011 July ; 15(3):157-163. 71) Punekar SV, Patel CV, Parlukar GB. Fatal perforative peritonitis .J Postgrad Med 1977;23(1):28-32.

110

PROFORMA

NAME: AGE : SEX : ADRESS:

DOA: DOS: DOD:

CHIEF COMPLAINTS: Pain abdomen Vomiting Distension of abdomen Fever

HISTORY OF PRESENTING ILLNESS: Pain ; Duration Site Vomiting Duration Frequency and contents

111

PERSONAL HISTORY: Bowel Bladder Habits PAST HISTORY: H/O Drugs H/O surgery H/O Pain abdomen FAMILY HISTORY: MENSTRUAL HISTORY:

GENERAL PHYSICAL EXAMINATION: Pallor PR BP Icterus lymphadenopathy

SYSTEMIC EXAMINATION: PER ABDOMEN: Inspection ; Distended/Flat/Scaphoid Movement with respiration

112

Palpation; Tenderness

Guarding

Rigidity

Percussion Liver dullness ; Obliterated/Not obliterated

Auscultation Bowel sounds Per Rectal

RESPIRATORY SYSTEM: CARDIOVASCULAR SYSTEM:

PROVISIONAL DIAGNOSIS:

113

INVESTIGATIONS: Hb Blood urea X ray erect abdomen RBS S.creatine

USG Abdomen

TREATMENT:

PRE-OP:

OPERATIVE NOTES:

POST OPERATIVE COURSE:

114

KEY TO MASTER CHART

A-Absent AL- Alcohol AP- Appendix ARF-Acute renal failure BS- Bowel sounds BP-Blood pressure D-Died DOS- Date of surgery DA- Distension of abdomen DU- Duodenal ulcer DVT- Deep vein thrombosis F - Fever Gr- Guarding GD- Gas under diaphragm HD- History of drugs HS Hospital stay LT- Light OBL- Obliteration of liver dullness OC-Out come P-Present PR-Pulse rate PF- Perforation
115

PC Primary closure PL- Peritoneal lavage Pn - Pain R- Recovered Rg- Rigidity RT- Right Res E-E Anast- Resection with end to end anastomoses Sm Smoking SC+OP- Simple closure with omental patch Tn- Tenderness Vm- Vomiting WL- Widal .

116

BIBLIOGRAPHY

1. Mathikere Lingaiah Ramachandra . Clinical study and Management of Secondary Peritonitis due to perforated hollow Viscous .Arch Med Sci 1 , March / 2007; 62-68. 2 Shyam kumar Gupta et al . Perforation Peritonitis : A Two Year Experience . JK SCIENCE . Vol 12 No. 3 July- September 2010 ; 141-144. 3 John T Langell et al : Gastrointestinal perforation and acute abdomen .The Medical . Clinics of North America 2008; 92: 599-625

4 Rajender Singh Jhobta et al . Spectrum of perforative peritonitis in India Review of

117

504 consecutive cases . World journal of emergency surgery. 2006 1:26doi:10 1186/1749-7922-1-26 5 Sanjay Gupta and Robin Kausik . Peritonitis The Eastern Experience.World journal of emergency surgery 2006 April 26.doi;10.1186/1749-7922-1-13 6 7 8 9 10 11 Lewis practice of surgery : The Peritoneum vol 7 Inderbir Singh A. Human Embryology. 7th edition: 204-205 Grays Anatomy . 40th edition: 1099 Grays Anatomy for students : 269 Lee Mc gregger .Synopsis of surgical anatomy. 12th edition; 99-102 Seymour I Schwartz, Shires G Tom, Frank C Spencer, Wendy Cowles Husser. Principles of Surgery, 7th Edition. McGraw Hill: 2001, Vol. 2: 1515-1539 12 Micheal Joseph Hausmann : Cell biology- Immunology- Pathology Kidney international 2000;57 476-4 13 Felix Broche et al . Defense mechanisms of peritoneal cavity . Current opinion in Critical 14 Care .2001; 7: 105-107

V . Yao ; Role of Peritoneal Mesothelial Cells in Peritontis :British journal of

surgery 2003; 90:1187-1194

118

15 Godshall cristopher et al. Natural killer cells participate in bacteria l clearance during septic peritonitis through Interaction with macrophages. Shock. February

2003; 19(2):144-149.

16 of

Peritoneal Defenses and Peritoneum Associated lymphoid Tisssue . British journal

Surgery 1996 : 83. 1031-1036 17 Masja Leendertse et al . Peritoneal Macrophages are imporatnat for the early containment Of Enterococcus feacium peritonitis in mice Innate Immunity. 2009: 15:3 18 419 Ori D Rotstien . Fibrin in Peritonitis . Annals of surgery .1986 april; 203 (4.) 413-

19 M.M . Binda.Reactive oxygen species and adhesion formation Clinical implications in adhesion prevention . Human Reproduction. Vol.18, No.12 25032507, 2003 . 20 Y. C . Cheong : Peritneal healing and adhesion formation / reformation Human reproduction update 2001 vol 7 no 6; 556-566 21 Sanjay munireddy et al .Intra-abdominal healing Gastrointestinal tract and adhesions . Surgical clinics of north America. 90(2010); 1227-1236
119

22

John E . Mazuski . Intra Abdominal Infections .Surgical clinics of north America 89(2009); 421-437

23

Massimo Sartelli . A Focus on intra- abdominal infections . World journal of. emergency Surgery 2010; 5:9 3-20

24

Nicole Lopez . A Comprehensive review of abdominal infections . World journal Of Emergency surgery 2011; 6:7 5-10

25

H van GOOR et al. Coagulation and fibrinolytic responses of human peritoneal fluid and Plasma to bacterial peritonitis . British journal of surgery. 1996; 83, 1133-1135

26

Mark A Malangoni . Contribution to the management of intra-abdominal infections. The American journal of surgery 190(2005); 255-259.

27

C.J .Miney . Principles of Surgical Patient care. Vol-2 Peritonitis and intraabdominal abscess.

28

Russell RCG, Williams NS, Bulstrode CJK. Bailey & Loves Short Practice of Surgery. 23rd Edition. Arnold: 2000: 1007-1020

. 29

Ronald F Martin MD Ricardo L Rossi MD .Abdominal Emergencies: Has Anything Changed?.Surgical clinics of north America . Dec 1997; Vo-l77 issue 6 1234-1236. Michael J Zinner, Seymour I Schwartz, Harold Ellis, Stanley W Ashley, David W McFadden. Maingots Abdominal Operations. 10th Edition, McGraw Hill 2001; Vol. 1: 633-650
120

30

31

Onderdont AB ; Adherence of bacteria fragilis in vivo : Infection and Immunity 1978,19, 1083

32

John J Bullen et al . Natural resistance, iron and infection ; a challenge for clinical medicine. Journal of Medical Microbiology 2006,55,251-258

33 DAVID L. DUNN,et al The Adjuvant Effect of Peritoneal Fluid in Experimental Peritonitis Ann. Surg. * January 1984 Vol. 199 * No. I 34 Dunn et al Surgical peritonitis ; Annals of surgery nov 19 34 DUNN. Antibiotic Treatment for Surgical Peritonitis. Ann. Surg. * November 1991 Vol. 214 * No. 5 550-552 35 Santosh Saini et al ; Surgical infection ; A Microbiological study ; The Brazilian journal 36 of Infectious Diseases 2004;8(2) 118-125

F .M.Pieracci ; Management of severe sepsis of abdominal origin ; Scandinavian journal of Surgery 96:184-196,2007

37 Samir s Awad . Multiple organ dysfunction syndrome pathogenesis management and Prevention . Mastery of Surgery vol -1 5th edition 110-111 38 William Silen et al . Copes Early Diagnosis of Acute Abdomen . 7th edition 107114 . 39 Russell RCG, Norman NS Williams, Christopher JK, Bulstrode. Bailey & Loves Short Practice of surgery 24th edition Hodder Arnold 2004 ; 1136

40

Lloyd M Nyhus, Robert J Baker, Josef E Fischer. Mastery of Surgery.

121

3rd Edition. Little Brown and Company. 1997; Vol. 1: 146-154 . 41 Wittmann H Dietmar ; Management of secondary peritonitis ; Annals of surgery Vol -22 No-1 10-18 42 John .C . Marshall ; Intra Abdominal infections ; Microbes and Infection 6(2004) 1015-25 43 William G. Cheadle et al ;The Continuing challenge of intraabdominal infection ; The American journal of Surgery 186/5A(NOV 28, 2003) 15S-22S

44 K . Bosscha : Surgical management of severe secondary peritonitis : British journal of Surgery 1996,86,1371-1377 45 608 46 B Lamme et al . Mortality and morbidity of planned relaparotomy vs laparotomy on demand for Secondary peritonitis ; British journal of surgery ,2004;91; 1046-54 Joseph S . Solomkin ; Intra abdominal sepsis ; Newer interventional and antimicrobial Therapies. Infectious disease clinics of north America 23(2009) 593-

47

B Lamme ; Meta analysis of relaporotomy for secondary peritonitis : British journal

of Surgery 2002,89,1516-1524. 48 M.A Boemeester ; Surgical approaches to peritonitis ; British journal of surgery 2007; 94: 1317-1318

49

Ferdinando Agresta et al ; Peritonitis ; Laparoscopic approach ; World journal of

122

Emergency surgery 2009, 1;9 50 51 Daniel T. Dempsey. Schwartz Principles of Surgery .9th edition 907-908.. Marietta J.O.E et al ; Perforated peptic ulcer disease review of history and treatment Digestive surgery 2010;27 160-169

52

Richard J . Saad ; Diagnosis and management of peptic ulcer disease ; Clinics in family Practice vol-6, no3 sept 2004.

53

Ronald F Martin: Surgical management of ulcer disease : Surg Clin N Am85(2005) 907-929

54

Paul H Jordan ; Perforated Pyloroduodenal ulcer ; Annals of surgery vol-221 no 5 1995; 479-488

55

Michael J Zinner, Seymour I Schwartz, Harold Ellis, Stanley W Ashley, David W McFadden. Maingots Abdominal Operations. 10th Edition, McGraw Hill 2001; Vol. 1: 940-965.

56

Masao Matsuda ; Laparoscopic Omental patch reoair fot perforated peptic ulcer ; Annals Of surgery vol-221 no 3 236-240 1995.

57

Stanley W . Ashley. Schwartz Principles of Surgery .9th edition. 1007-1009

58 Rauf A Wani ; Non traumatic ileal perforation ; World journal of emergency surgery 2006,1: 7

123

59 A .E . Rajgopalan . Free perforation of small intestine . Annals of surgery vol196;no 5. Nov 1982.

60

Cesar G Athie ; twenty five yr experience in surgical treatment of perforation of the ileum Caused by salmonella typhi at mexico ; Surgery june 1998

61

E .A .Ameh ; Comparison of three operatios for typhoid perforation ; British journal of Surgery 1997,84,558-559

62

Chaw Suradam et al ; Non traumatic perforation of colon a 5 yr retrospective study At Uthaithani hospital ; THAI journal of surgery 2009 ,30.52-57

63

Sebastiano Biondo ; Emergency operations for non diverticular perforation of left colon The American journal of surgery 183(2002) ;256-260.

64

Vasilis A et al ; Operative strategies for diverticular peritonitis ; Annals of surgery Vol-245.no 1 jan 2007.

65 Neil Mandava, MD, .et al .Perforated colorectal Carcinomas . Am J Surg. 199&l 72:236238.

124