part1 and part 2

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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


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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.


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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.


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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


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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


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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


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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) Right anterior intraperitoneal compartment.

2) Right posterior intraperitoneal compartment.

3) Right extraperitoneal compartment.

4) Left anterior intraperitoneal compartment.

5) Left posterior intraperitoneal compartment.

6) 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


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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


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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


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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) Gravity

2) 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


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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


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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


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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


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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


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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.


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Biochemical and cellular cascade occurring after peritoneal injury21

Fig 1


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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


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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


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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) Inoculum size.

2) Virulence of contaminating organism.

3) The presence of adjuvants within peritoneal cavity.

4) Adequate local, regional and systemic host responses.

5) The adequacy of initial treatment.

Inflammation within the peritoneal cavity evokes a series of secondary changes

that produce clinical syndrome of peritonitis.26

Peritonitis produces profound

physiological alterations both locally within the abdominal cavity and also

systemically affecting the cardiovascular, respiratory, renal and neuro-endocrine

system.


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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 the vascular compartment.

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

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.


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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.


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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


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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 Host Defense Factors

Bacterial inoculums Dissemination of contaminant

Local adjuvant factors Clearance of peritoneal fluid

Hematoma Complement activation

Foreign body Fibrin deposition

Devitalized tissue Phagocytosis by macrophages and neutrophils

Systemic adjuvant factors Loculation of bacterial collections

Hypoxemia

Shock

Steroids

Malnutrition

Comorbid medical conditions


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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


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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


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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


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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 .


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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 90/ min

Respiratory rate >20/min or PaCO212x109cells / m

3

2) SEPSIS; SIRS + documented infection.

3) SEVERE SEPSIS; SIRS+ SEPSIS + Heamodynamic compromise.

4) MODS; This is a physiological derangements in which organ functions are not

capable of maintaining homeostasis.


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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


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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.


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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.


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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


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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


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MANAGEMENT OF PERITONITIS

Kirschner in 1926 formulated two surgical principles for management of

peritonitis which later have become the gold standard.

1) Plugging the source of infection.

2) 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 peritonitis:

1. 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.


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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


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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.


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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) Elimination of source of infection.

2) Reduction of bacterial contamination of peritoneal cavity.

3) Prevention of persistent or recurrent intra abdominal infection.


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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) Delay in initial intervention.

2) High severity of illness ( Acute physiology and chronic health evaluation)

3) Advanced age.

4) Comorbidity and degree of organ dysfunction.

5) Low albumin.

6) Poor nutritional status.

7) Degree of peritoneal involvement and diffuse peritonitis.

8) Inability to achieve adequate debridement or control of drainage.45


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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 .


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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


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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 closure of

abdominal fascia and skin. Abdominal cavity is left open like an 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.


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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 planned either before or during the

first operation called Index Star. 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.


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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.


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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


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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


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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 regardedas 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 hada significantly higher mortality

rate than similar patientswith comparable APACHE II scores in the ROD group. Hau et

al.(1995) found that postoperative MOF was morecommon in patients treated with PR

than in thosetreated 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 on-

demand strategy do not exist, the surgeon should be prepared to initiate frequent CT


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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

are expensive, not always conclusive and available in all settings . Laparoscopy is the

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.


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The high diagnostic yield of LAPS is important especially in patients with pelvic

diseasesuspected appendicitis, where LAPS allows for a better thorough exploration

of the abdominal cavity and identification of concomitant diseases than OP.(open

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

pneumoperitoneum49

.


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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 CAGA positive strain. The resulting increase in gastrin


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release and gastric acid secretion is key mechanism by which the H pylori infection

induces PUD.51

.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 the risk of PUD and ulcer


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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


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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


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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


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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 re-

evaluated.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


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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) Truncal vagotomy with gastrojejunostomy.

2) Antrectomy with vagotomy.

3) Pyloroplasty and vagotomy.

4) Partial gastrectomy with vagotomy.

5) Highly selective vagotomy with simple closure.


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Indications

1) When patient has had previous perforation treated by simple closure.

2) When perforation and bleeding occur together.

3) Presence of synchronous second ulcer complication.

4) Perforation of ulcer during medical treatment.

Contraindication

1) More than 24 hours of presentation.

2) Gross abdominal contamination.

3) Concurrent medical illness.

4) 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


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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


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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


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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


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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

part1 and part 2

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