Part1 and Part 2
-
Upload
shankarrao3 -
Category
Documents
-
view
219 -
download
0
Transcript of Part1 and Part 2
-
7/28/2019 Part1 and Part 2
1/124
1
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
-
7/28/2019 Part1 and Part 2
2/124
2
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.
-
7/28/2019 Part1 and Part 2
3/124
3
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.
-
7/28/2019 Part1 and Part 2
4/124
4
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
-
7/28/2019 Part1 and Part 2
5/124
5
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
-
7/28/2019 Part1 and Part 2
6/124
6
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
-
7/28/2019 Part1 and Part 2
7/124
7
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
-
7/28/2019 Part1 and Part 2
8/124
8
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
-
7/28/2019 Part1 and Part 2
9/124
9
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
-
7/28/2019 Part1 and Part 2
10/124
10
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
-
7/28/2019 Part1 and Part 2
11/124
11
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
-
7/28/2019 Part1 and Part 2
12/124
12
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
-
7/28/2019 Part1 and Part 2
13/124
13
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
-
7/28/2019 Part1 and Part 2
14/124
14
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
-
7/28/2019 Part1 and Part 2
15/124
15
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.
-
7/28/2019 Part1 and Part 2
16/124
16
Biochemical and cellular cascade occurring after peritoneal injury21
Fig 1
-
7/28/2019 Part1 and Part 2
17/124
17
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
-
7/28/2019 Part1 and Part 2
18/124
18
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
-
7/28/2019 Part1 and Part 2
19/124
19
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.
-
7/28/2019 Part1 and Part 2
20/124
20
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.
-
7/28/2019 Part1 and Part 2
21/124
21
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.
-
7/28/2019 Part1 and Part 2
22/124
22
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
-
7/28/2019 Part1 and Part 2
23/124
23
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
-
7/28/2019 Part1 and Part 2
24/124
24
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
-
7/28/2019 Part1 and Part 2
25/124
25
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
-
7/28/2019 Part1 and Part 2
26/124
26
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
-
7/28/2019 Part1 and Part 2
27/124
27
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 .
-
7/28/2019 Part1 and Part 2
28/124
28
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.
-
7/28/2019 Part1 and Part 2
29/124
29
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
-
7/28/2019 Part1 and Part 2
30/124
30
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.
-
7/28/2019 Part1 and Part 2
31/124
31
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.
-
7/28/2019 Part1 and Part 2
32/124
32
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
-
7/28/2019 Part1 and Part 2
33/124
33
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
-
7/28/2019 Part1 and Part 2
34/124
34
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.
-
7/28/2019 Part1 and Part 2
35/124
35
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
-
7/28/2019 Part1 and Part 2
36/124
36
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.
-
7/28/2019 Part1 and Part 2
37/124
37
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.
-
7/28/2019 Part1 and Part 2
38/124
38
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
-
7/28/2019 Part1 and Part 2
39/124
39
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 .
-
7/28/2019 Part1 and Part 2
40/124
40
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
-
7/28/2019 Part1 and Part 2
41/124
41
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.
-
7/28/2019 Part1 and Part 2
42/124
42
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.
-
7/28/2019 Part1 and Part 2
43/124
43
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.
-
7/28/2019 Part1 and Part 2
44/124
44
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
-
7/28/2019 Part1 and Part 2
45/124
45
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
-
7/28/2019 Part1 and Part 2
46/124
46
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
-
7/28/2019 Part1 and Part 2
47/124
47
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.
-
7/28/2019 Part1 and Part 2
48/124
48
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
.
-
7/28/2019 Part1 and Part 2
49/124
49
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
-
7/28/2019 Part1 and Part 2
50/124
50
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
-
7/28/2019 Part1 and Part 2
51/124
51
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
-
7/28/2019 Part1 and Part 2
52/124
52
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
-
7/28/2019 Part1 and Part 2
53/124
53
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
-
7/28/2019 Part1 and Part 2
54/124
54
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
-
7/28/2019 Part1 and Part 2
55/124
55
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.
-
7/28/2019 Part1 and Part 2
56/124
56
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
-
7/28/2019 Part1 and Part 2
57/124
57
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
-
7/28/2019 Part1 and Part 2
58/124
58
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
-
7/28/2019 Part1 and Part 2
59/124
59
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
-
7/28/2019 Part1 and Part 2
60/124
60
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