1

EFFECTIVENESS OF MANNHEIM PERITONITIS INDEX IN

PREDICTING THE MORBIDITY AND MORTALITY OF

PATIENTS WITH HOLLOW VISCOUS PERFORATION

By

DR. NAGARAJ SHANKREPPA

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka

In partial fulfillment of the requirements for the degree of

MASTER OF SURGERY

In

GENERAL SURGERY

Under the guidance of

DR. BHANUPRAKASH K R

DEPARTMENT OF SURGERY

BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE

BANGALORE

YEAR-2017

8

ABSTRACT

BACKGROUND AND OBJECTIVES

This study attempts to evaluate the prognostic value of MPI scoring system in patients with

peritonitis due to hollow viscous perforation, to assess it as a clinical tool in stratifying these

patients according to individual surgical risk.

METHODS

100 patients with hollow viscous perforation admitted in the Dept. of Surgery Bangalore Medical

College and Research institute fromNovember 2014 to August 2016 were included in the study.

Necessary data was collected; MPI score was calculated for each patient and analysis done.

RESULTS AND INTERPRETATION

The number of post-operative complications, duration of ICU and hospital stay proportionately

increased with the MPI score. Out of the 8 variables used in this scoring system, duration of pain,

intra peritoneal fluid and organ failure on admission carried more significance in predicting the

morbidity in the post op period than the other variables.

CONCLUSION

MANNHEIM PERITONITIS INDEX is a simple and effective method in predicting the

morbidity of patients with hollow viscous perforation

KEY WORDS: Peritonitis, Scoring systems, Outcome predictors, morbidity

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TABLE OF CONTENTS

SL. NO.

CONTENTS

PAGE NO.

1. Introduction 13

2. Objectives 14

3. Review of Literature 15

4. Materials and methods 53

5. Results 57

6. Discussion 72

7. Conclusion 75

8. Bibliography 77

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LIST OF TABLES

SL. NO.

TABLES

PAGE NO.

1. Existing scoring systems 38

2. Various study results of ASA scoring 39

3. Boeys scoring system 40

4 Apache scoring system 43

5. MPI scoring system 45

6 Descriptive statistics of duration of pain 58

7 Descriptive statistics of origin of peritonitis 59

8 Descriptive statistics of Scoring system 62

9 Pulmonary complications & ARDS 64 & 65

10 Wound complications 65

11 ICU stay 66

12 Inotropes & mechanical ventilation statistics 67& 68

13 Site of perforation analyzed with no. of

complications

69

14 Final score analyzed with type of exudate 70

15 Duration of pain analyzed with number of

complications

70

11

CHARTS, BAR DIAGRAMS, PIE DIAGRAMS

SL. NO. TABLES PAGE NO.

1. Embryology 18

2. Classification of peritonitis 28

3. Origin of peritonitis 31

5. Descriptive statistics of duration of pain 58

6. Descriptive statistics of origin of peritonitis 59

7 Type of exudate 60

8 Number of complications 61

9 Peritonitis localized or diffuse 61

10 Descriptive statistics of Scoring system 62

11 Pulmonary complications 64

12 ICU stay 66

13 Need for Inotropes - statistics 67

14 Master chart

12

LIST OF FIGURES

SL. NO.

FIGURES

PAGE NO.

1. Compartments of peritoneum 20

2. Compartments of peritoneum –lat view 21

3. Drainage pattern in abdomen 22

4. Peritoneal response to infection 24

5 X ray with air under diaphragm 48

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INTRODUCTION:

Peritonitis due to hollow viscous perforation continues to be one of the most common surgical

emergencies to be attended by a surgeon. This may be due to persistence of the various risk

factors among the general population like H.pylori infection, NSAID‘s, enteric fever and several

others. This condition most of the times needs an emergency surgical intervention, a scoring

system should be able to assess the need, type, and quality of the care required for a particular

patient.

Realizing the need for a simple accurate scoring system in these conditions the present study was

undertaken to evaluate the performance of MPI scoring system in predicting the risk of morbidity

and mortality in patients with peritonitis due to hollow viscous perforation.

Several scoring systems are in place to stratify the patients with peritonitis due to hollow viscous

perforation like APS, SIS, APACHE and BOEYS. Utilization of scoring systems would be of

great help in salvaging a priceless life of a patient. Our study is aimed at testing the effectiveness

of MANNHEIMPERITONITIS INDEX .

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AIMS AND OBJECTIVES OF THE STUDY;

Aim is to predict the risk of mortality and morbidity in patients with peritonitis due to hollow

viscous perforation. Assessment of surgical risk in these patients is to help in choosing the

modality of post op management in a particular patient.

This study attempts to evaluate the prognostic value of MPI scoring system in patients with

peritonitis due to hollow viscous perforation, to assess it as a clinical tool in stratifying these

patients according to individual surgical risk.

15

REVIEW

of

LITERATURE

16

Peritonitis due to hollow viscous perforation has been documented by many historians.

Wacha and co-workers (1987) developed a separate peritonitis index,MANNHEIM

PERITONITIS INDEX (MPI) which incorporated information regarding age, gender, organ

failure, cancer, duration of perforation, involvement of colon, extent of spread within the

peritoneum and the characteristic of peritoneal fluid to define risk scores ranges from 00 to 471.

A Billing, D Frahlich, FW Behildberg considered patients of perforated or post-operative

peritonitis, peritonitis caused by pancreatitis, appendicitis and mesenteric ischemia for study.

Patients were divided into three categories of severity of MPI <21,21-29 and >29. MPI not only

reliable in predicting mortality but also be used for comparative study. Patients with scores of

< 21 has a mortality rate of 0-2.3% and those with MPI between 21-29 had a mortality rate of

approximately 65% and MPI score > 29 had highest mortality up to> 80% 2

Pacelli conducted study in1996 comparing MPI, APACHE, and Sepsis scores. They concluded

that MPI and APACHE correctly predicted death as outcome, but MPI was easier to calculate3

Notanh AY, Salini J, Rahimani H, Fesharaki MH, Abbasi A have shown important cut off point

to be 21 and 29, when using MPI, with mortality of 60% and upto 100% for scores more than 294

In 1980 Fry et al showed that mortality after major operative procedures increased as the number

of failed organs increases. Mortality was 3% with no organ failure, which increased to 30% with

one organ failure and to 100% with 4 major organ failure.5

Lohisiriwat et al studied patients with perforated peptic ulcer over 5 years from 2001 to 2006 and

concluded that average MPI score in patients with 30 days mortality was 25.92. The average

17

score among the patients with complications was 25.93 when compared to those without

complications average score was 19.51. They concluded that MPI scoring system was more

helpful in predicting the morbidity in patients.6

Kusumoto et al and others in their study published in 2004 included patients with hollow viscous

perforation used MPI score of 26 as cutoff value to predict the mortality. The sensitivity of the

cut off value for mortality was 77.7 and specificity was 97.7. The mortality for the group < 26

was 3.8% and for the group with score >26 it was 41%.7

AbrarMaqboolQuereshi and Afsheen Zafer et al in a study published in 2005 have come out with

following conclusions when MPI scoring was used to predict the mortality and morbidity in

patients with hollow viscous perforation. The mortality among the patients with MPI score < 20

was 1.9%. Mortality increased to 21.9% for score >30. The significance was higher for the

factors > 59 years of age, malignancy, pre-operative duration of > 24 hours and cloudy

intraperitonial exudates among the different variables used in this scoring system.8

Papyrus (Egypt) 1500 BC contains the first description of peritoneum. The anatomy of

peritoneum and various changes in pathological conditions has been described in detail by

various eminent personalities.

The first detailed description of the peritoneum was given by Douglas in 1730 following which

numerous personalities have given their contribution to the knowledge about its structure,

functions & pathological changes.

Morrison in 1894 described the right infrahepatic space (sub hepatic, hepatorenal space) and

vascular regenerative capacity of omentum.

18

Winslow in 1732 described greater and lesser omentum, lesser sac, and foramen (of Winslow)

It is an axiom that a surgeon must enter the peritoneal cavity

―Prepared for anything and everything9

Embryology;10

The peritoneal cavity is subdivided into interconnected compartments or spaces by 11

ligaments and mesenteries11

.

19

The peritoneal ligaments or mesenteries include the coronary, gastrohepatic, hepatoduodenal,

falciform, gastrocolic, duodenocolic, gastrosplenic, splenorenal, and phrenicocolic ligaments and

the transverse mesocolon and small bowel mesentery.

These structures partition the abdomen into nine potential spaces:

Right and left subphrenic,

Subhepatic,

Supramesenteric and inframesenteric,

Right and left paracolic gutters,

Pelvis and lesser space.

These ligaments, mesenteries, and peritoneal spaces direct the circulation of fluid in the

peritoneal cavity and thus may be useful in predicting the route of spread of infectious and

malignant diseases.

The left paracolic gutter is infracolic only, interrupted by phrenicocolic ligament whereas the

right paracolic gutter extends into supracolic space also.

Pelvic cavity is divided into right & left by sigmoid colon & rectum, further divided in females

into anterior & posterior by broad ligament, uterine tubes & uterus.

In males peritoneal cavity is a truly closed sac whereas in females the minute openings of uterine

tubes provide continuity with the environment external to the body.

Extra peritoneal spaces are

1. Bare area of liver &diaphragm.

2. Left extra peritoneal space

Formation of adhesions & pseudo membranes may contribute to the formation of collections of

abscesses in various parts of each space.

20

Parts of peritoneum;12

1. Omentum – greater & lesser

2. Mesentery – of small intestine, meso appendix , transverse mesocolon

3. Ligaments - of liver, bladder, uterus

4. Fossae – duodenal, ileal, intersigmoid

COMPARTMENTS OF PERITONEUM

21

.

COMPARTMENTS OF PERITONEUM – LATERAL VIEW

22

Spread of fluid in the peritoneal cavity depends upon :-

Location of source & rate of fluid production ,pressure difference in abdomen , mesenteric

partitions & peritoneal fossae and position of the body in relation to gravity

Most common site of fluid collection is pouch of Douglas – the most dependent part of

peritoneum the mesentery of small intestine & sigmoid mesocolon form barriers at which ascitic

fluid may accumulate before spilling to pelvis.

Posterior abdominal wall: Mesenteric attachments and chief sites of fluid collection in order of

frequency: 1, Pouch of Douglas; 2, Distal attachment of mesentery; 3, Attachment of sigmoid

mesocolon; 4, Right paracolic gutter; BA, Bare area; C, Attachment of colon; D, Attachment of

duodenum; PC, phrenocolic ligament; S, Attachment of stomach; SB, Attachment of mesentery

of small bowel13

23

HISTOLOGY & PHYSIOLOGY14

:

Both Parietal & visceral parts of the peritoneum have same histology – basement membrane

covered by single layer of mesothelial cells. Loss of these cells produces non physiological

adhesions between two parts. Parietal layer is very loosely attached to preperitoneal fat but

visceral layer is fixed firmly to subserosa of GI tract.Peritoneal cavity is a potential space with

about 50ml of isotonic fluid & less than 300 mononuclear cells.Peritoneal fluid has water,

proteins, electrolytes and diverse cellular types, provides lubrication to facilitate the movements

of viscera.

With an abnormal peritoneal collection of fluids, the phenomenon of absorption is limited in

lower abdomen. Absorption is more active in both subphrenic spaces, may be due to existence of

specialized subphrenic peritoneum with gaps/peritoneal stomata and slit like orifice.

Peritoneum can clear bacteria within minutes conversely it may rapidly transport bacteria into

systemic circulation via diaphragmatic lymphatics. Abscess formation is the final defense of this

remarkable membrane if cellular, humoral and clearance defense mechanisms are overwhelmed.

Bacteria can be seen in the thoracic duct in 6 min & blood in 30 min demonstrates the clearance

mechanisms of diaphragm.

Functions of peritoneum15

1. Pain perception.

2. Visceral lubrication.

3. Fluid and particulate absorption.

4. Inflammatory and particulate absorption.

5. Fibrinolytic activity.

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INNERVATION;

Parietal layer is innervated by somatic afferent nerves, contains many sensory fibers for sensation

of pain.Visceral layer is relatively insensitive to pain as there is no somatic afferents.

So a perforated viscous may produce anterior abdominal wall rigidity and intra peritoneal fluid

collection, produces sensation of traction or tension on the mesentery in the retroperitoneal space

but not localized pain.

HOST DEFENSES OF THE PERITONEUM:

Peritoneal response to infection16

25

1. DIAPHRAGMATIC LYMPHATICS17

Over the diaphragm the usual smooth flat layer of cells are interrupted by a large number of inter

cellular gaps calledStomata.(as named by VonReckling Hausen).These act as entrance to

diaphragmatic lymphatic channels called lacunae. These lacunae are oriented parallel to muscle

fibers of diaphragm and contain valves that prevent reflux of fluid back into abdomen, ultimately

draining into substernal lymph nodes & then to thoracic duct.

Factors influencing uptake

1. Mesothelial cell processes – usually in a contracted state, when relaxes - size of stomata

increases.

2. State of diaphragm contraction –

(a) Inspiration – diaphragm contracts – constriction of stomata

(b) Expiration – diaphragm relaxes – opening of stomata, fluid and particulate

matter gets sucked in.

3. Inflammation – increases stomata patency by inducing mesothelial cell retraction.

Normally up to 30% of total lymphatic drainage of the peritoneum is by diaphragm & rest

through parietal peritoneum.

Cellular defenses:

In a healthy individual the peritoneal cavity contains approximately 15 -50 mL of fluid with

about 6 x 105 cells/ml

18.

26

Macrophages:

Have two main functions in first-line defense:

(1) recognition, phagocytosis and killing and

(2) Participation in the immune response. –

Opsonized microorganisms are recognized by specific receptors on the phagocyte. The most

important receptors on macrophages are the Cl (CR1) and C3receptors (CR3; recognize particle -

associated C3b) and the Fc-receptors (recognize complexes between antigen and opsonizing

antibody, e.g., IgG). Other phagocyte receptors are fibronectin and lectin receptors.

A significant proportion of macrophages have also been located in the submesothelial

interstitium. 19

Peritoneum fibroblasts

1. Provide signals for the intraperitoneal recruitment of inflammatory bone marrow-derived

cells.

2. Acts as sentinel cells that combine structural and immunomodulatory function.20

The onset of peritonitis HPFBs (human peritoneal fibroblasts) may provide relatively more

signals triggering the intraperitoneal influx of neutrophils while subsequently the secretion of

HPFB-derived chemokines gradually shifts toward mononuclear cell chemo attractants.

The peritoneal membrane contributes to inflammation by generating prostaglandins (PGI2 and

PGE2) and cytokines (MCP-l, IL-I & beta;, IL-6, and IL-8) in response to cytokines released by

peritoneal macrophages (TNFa and IL-l) or directly to (parts of) bacteria.

27

PERITONEAL MESOTHELIAL CELLS:

Secrete plasminogen activator

Decrease in the fibrinolytic activity

Formation of fibrin adhesions

Initially helps in localizing the inflammation

EOSINOPHILS, BASOPHILS, MAST CELLS

Act by producing histamine which leads to endothelial cell contraction, thereby increasing the

vascular permeability &influx ofcomplement factors & leukotrienes.

In summary the peritoneum and peritoneal cavity respond to infection in five ways21

:

1. Bacteria are rapidly removed from the peritoneal cavity through the diaphragmatic

stomata and lymphatics, as described in the preceding paragraphs.

2. Peritoneal macrophages release proinflammatory mediators that promote the migration of

leukocytes into the peritoneal cavity from the surrounding microvasculature.

3. Degranulation of peritoneal mast cells releases histamine and other vasoactive products,

causing local vasodilatation and the extravasation of protein-rich fluid containing

complement and immunoglobulins into the peritoneal space.

4. Protein within the peritoneal fluid opsonizes bacteria, which, along with activation of the

complement cascade, promotes neutrophil- and macrophage-mediated bacterial

phagocytosis and destruction.

5. Bacteria become sequestered within fibrin matrices, thereby promoting abscess formation

and limiting the generalized spread of the infection.

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PERITONITIS: is an inflammatory or suppurative response of the peritoneal lining to direct irritation.

Table 10-7. Classification According to Etiology

I. Primary peritonitis C. Posttraumatic peritonitis

A. Spontaneous peritonitis in children 1. Peritonitis after blunt abdominal trauma

B. Spontaneous peritonitis in adults 2. Peritonitis after penetrating abdominal

trauma

C. Peritonitis in patients with CAPD 3. Other forms

D. Tuberculous peritonitis III. Tertiary peritonitis

E. Other forms A. Peritonitis without pathogens

II. Secondary peritonitis B. Peritonitis with fungi

A. Acute perforation peritonitis (acute suppurative

peritonitis)

C. Peritonitis with low-grade pathogenic

bacteria

1. GI tract perforation IV. Intra-abdominal abscess

2. Bowel wall necrosis (intestinal ischemia) A. Associated with primary peritonitis

3. Pelviperitonitis B. Associated with secondary peritonitis

4. Other forms C. Associated with tertiary peritonitis

B. Postoperative peritonitis

1. Leak of an anastomosis

2. Leak of a suture line

3. Stump insufficiency

4. Other iatrogenic leaks

29

Primary (spontaneous) peritonitis:

Peritonitis in the absence of gastrointestinal perforation is caused mainly by hematogenous

spread but occasionally by transluminal or direct bacterial invasion of the peritoneal cavity.

Impairment of the hepatic reticuloendothelial system and compromised peripheral destruction of

bacteria by neutrophils promotes bacteremia, which readily infects ascitic fluid that has reduced

bacterium-killing capacity.The pathogenesis of SBP remains unclear; however, several lines of

evidence suggest that bacterial translocation from the gastrointestinal tract plays an important

role in the development of this infection22

.

Primary peritonitis is most closely associated with cirrhosis and advanced liver disease with a

low ascitic fluid protein concentration. It is also seen in patients with the nephrotic syndrome or

systemic lupus erythematosus, or after splenectomy during childhood. Recurrence is common in

cirrhosis and often proves fatal.

The clinical presentation simulates secondary bacterial peritonitis, with abrupt onset of fever,

abdominal pain distention, and rebound tenderness. However, one-fourth of patients have

minimal or no peritoneal symptoms. Most patients will have clinical and biochemical

manifestations of advanced cirrhosis or nephrosis. Leukocytosis, hypoalbuminemia, and a

prolonged prothrombin time are characteristic findings. The diagnosis hinges upon examination

of the ascitic fluid, which reveals a white blood cell count greater than 500/µL and more than

25% polymorphonuclear leukocytes. A blood-ascitic fluid albumin gradient greater than 1.1

g/dL, a raised serum lactic acid level (> 33 mg/dL), or a reduced ascitic fluid pH (< 7.31)

supports the diagnosis. Bacteria are seen on Gram-stained smears in only 25% of cases. Culture

of ascitic fluid inoculated immediately into blood culture media at the bedside usually reveals a

single enteric organism, most commonly

30

E coli, Klebsiella, or Streptococci, but Listeria monocytogenes has been reported in

immunocompromised hosts.

Treatment23

Antibiotic prophylaxis is of no proven value. Systemic antibiotics with third-generation

cephalosporin (e.g., cefotaxime) or a beta-lactam-clavulanic acid combination along with

supportive treatment are begun once the diagnosis has been established.

Secondary peritonitis

Secondary peritonitis results from bacterial contamination originating from within viscera or

from external sources (e.g., penetrating injury). It most often follows disruption of a hollow

viscous.

BACTERIOLOGY OF PERITONITIS5

Systemic sepsis due to peritonitis occurs in varying degrees depending on the virulence of the

pathogens, the bacterial load, and the duration of bacterial proliferation and synergistic

interaction.

Except for spontaneous bacterial peritonitis, peritonitis is almost invariably polymicrobial;

cultures usually contain more than one aerobic and more than two anaerobic species. The

microbial picture reflects the bacterial flora of the involved organ.

As long as gastric acid secretion and gastric emptying are normal, perforations of the stomach are

generally sterile or associated with relatively small numbers of gram-positive organisms.

Normally there are <1000 bacteria per ml in stomach secretions. No obligate anaerobes but alpha

hemolytic streptococci, lactobacilli, yeasts & few oral bacteria.

Within the duodenum & jejunum there are 100 to 10000 bacteria per ml, primarily streptococci,

lactobacilli, transitory oral flora & rarely enterobacter species.

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Perforations or ischemic injuries of the distal small bowel (e.g., strangulated hernia) lead to

infection with aerobic bacteria in about 30% of cases and anaerobic organisms in about 10% of

cases. Bacterial count is 106

per ml to 107per ml. Streptococci, lactobacilli predominate,

bacteroids & enterobacter are found in equal proportions.

Fecal spillage, with a bacterial load of 1012

or more organisms per gram, is extremely toxic. 60%

of dry fecal matter is bacteria. Bacterial count is 3.8×1014

per mg dry stool. Streptococci, bacillus

species, enterococci, E.coli, bacteroids, clostridia & anaerobic cocci form the flora.

CAUSES OF SECONDARY PERITONITIS:24

Common causes of secondary peritonitis

1) Esophagus – Boerhaeve syndrome, iatrogenic instrumentation, trauma, malignancy.

2) Stomach & duodenum – APD, analgesic abuse, malignancy, trauma.

3) Small bowel – ischemic bowel, crohns disease, meckel`s diverticulitis, incarcerated hernia.

4) Large bowel - ischemic bowel, crohns disease, diverticulitis, ulcerative colitis, appendicitis

Origin of peritonitis25

32

H.PYLORI & PEPTIC ULCER:

Patients with H.pylori infection and antral gastritis are three and a half times more likely to

develop peptic ulcer disease than patients without H.pylori infection.

Up to 90% of patients with duodenal ulcers, and 70 to 90% of patients with gastric ulcers, have

H.pylori infection.

33

PATHOGENESIS OF PEPTIC ULCER DISEASE 26

Sex:The ratio is 2 men to 1 woman.

Age: The highest incidence is between 45 and 55 years.

Most often a peptic ulcer that perforates is situated on the anterior surface of the duodenum;

much less frequently it is situated on the anterior surface of the stomach, usually near the lesser

curvature or the pyloric antrum. Rarely an ulcer on the posterior wall of the stomach perforates

into the lesser sac. In 80 per cent of cases, there is a history — often a long history —of peptic

ulceration. In 20 per cent there is no such history; it is a silent chronic ulcer that perforates,

especially in those patients who are being treated with cortisone27.

NSAID induced GI damage:

Risk of significant serious adverse GI events in patients taking NSAIDs is more than three times

that of controls. This risk increases to five times in patients over age 60. In elderly patients taking

NSAIDs, the likelihood that they will require an operation related to a GI complication is 10

times that of the control group, and the risk that they will die from a GI cause is about four and a

half times higher28

.

>20% of patients with perforation of >60 years age group have had history of NSAID

consumption.

NSAIDs cause GI damage by

1. Topical biochemical reactions – inhibition of COX prevents mucosal repair because of

decreased prostaglandin synthesis leading to decreased mucosal blood flow.

34

2. Inflammatory tissue reaction because of increased permeability that allows luminal

aggressive factors access to mucosa – NSAIDs uncouple mitochondrial oxidative

phosphorylation with consequent decrease in intracellular ATPs loss of cytoskeletal control over

tight junctions.

Smoking, Stress, and Other Factors

Epidemiologic studies suggest that smokers are about twice as likely to develop peptic ulcer

disease as nonsmokers. Smoking increases gastric acid secretion and duodenogastric reflux.

Smoking decreases both gastro duodenal prostaglandin production and pancreatic duodenal

bicarbonate production.

Although difficult to measure, both physiologic and psychological stress undoubtedly play a role

in the development of peptic ulcer in some patients. In 1842, Curling described duodenal ulcer

and/or duodenitis in burn patients. Decades later, Cushing described the appearance of acute

peptic ulceration in patients with head trauma (Cushing ulcer). Patients still present with ulcer

complications (bleeding, perforation, and obstruction) that are seemingly exacerbated by

stressful life events.

Recently, the use of crack cocaine has been linked to juxtapyloric peptic ulcers with a propensity

to perforate. Alcohol is commonly mentioned as a risk factor for peptic ulcer disease, but

confirmatory data are lacking.

Perforation in enteric fever29

:

Enteric fever is caused by salmonella typhi . Most common in 21-30 age group.

Disease is common in lower socioeconomic status mainly due to contaminated water supply.

35

Majority of the perforations occur within 2 wks.of illness.

Mechanism – hyperplasia &necrosis of payers patches in terminal ileum leading to tissue

damage. Necrosis may end up with full thickness perforation.

Treatment:Closure of perforation & appropriate antibiotic.

Bile peritonitis27

;

Causes

1) Perforated cholecystitis

2) Post cholecystectomy

i. Cystic duct stump leakage

ii. Division of accessory duct

iii. Bile duct injuryiv. T -

tube drain dislodgement

3) Following other operations/ procedures

i. Leaking duodenal stump

post gastrectomy

ii. Leaking biliary enteric

anastomosis

iii. Leaking around

percutaneous placed biliary drains.

36

Unless the bile has extravasated slowly and the collection gets shut off from the general

peritoneal cavity usually the bile leak leads to diffuse peritonitis due to the high irritant nature of

the bile, the patient is often jaundiced due to absorption of peritoneal bile.

Treatment -Laparotomy or laparoscopy done to evacuate the bile, peritoneal lavage and

source of bile leakage identified and corrected.

Meconium peritonitis:

Meconium is a sterile mixture of epithelial cells, mucin, salts, fats and bile.

Meconium peritonitis is an aseptic peritonitis with meconium entering the peritoneal cavity

through an intestinal perforation which may be due to some form of neonatal intestinal

obstruction. It is considered when a baby is born with a tense abdomen, is vomiting and in whom

there is failure to pass meconium.

Radiography shows free air in the peritoneal cavity, fluid levels, fluid in the abdomen and

calcification most often on the surface of liver or spleen.

Treatment;

Laparotomy - closure of perforation and drainage of peritoneal cavity.

37

BACKGROUND FOR SCORING SYSTEMS

Many scoring systems have been created for assessing patient risks of death and morbidity

during an event of peritonitis. Reproducible scoring systems that allow a surgeon to determine

the severity of the intra-abdominal infection are essential to:

1) Ratify the effectiveness of different treatment regimens,

2) Scientifically utilize surgical intensive care units,

3) Help indicate individual risk to select patients who may require a more aggressive surgical

approach and

4) Be able to inform patient´s relatives with greater objectivity

Most surgical risk scores have been created from large operative databases, using statistical

analyses to determine which variables are most-strongly associated with outcome. When an

person presents to hospital requiring an emergency operation, it is the surgeon and anesthetist‘s

duty to assess the risks of anesthesia and surgery by establishing the patient's pre-morbid

condition, quality of life (QOL) and prognosis and to weigh this with the likelihood that a

surgical operation will be successful. Surgery may not be advised if the chance of success is

slight and the risk of causing a fatal outcome is considered greater by operating. In order to make

these difficult decisions more objective a number of scoring systems have been constructed.

38

Existing scoring systems; 42

Scores predicting mortality Scores predicting morbidity

Scores not requiring operative

information

ASA

APACHE-II

Sickness Assessment

Boeys Score

Hacetteppe Score

Physiological POSSUM

APACHE-II

Veltkamp Score

VA Pneumonia Prediction

Index

VA Respiratory Failure Score

Scores requiring operative

information

Mannheim Peritonitis Index

Reiss Index

Fitness Score

POSSUM, P-POSSUM

Cleveland Colorectal Model

Surgical Risk Scale

POSSUM, P-POSSUM

39

ASA scoring: 42

This is in spite of its subjective nature and the inter-observer variation in measuring has been

used for many years, and remains the score routinely used in most surgical emergency cases. It

was not designed to predict mortality but it has been shown to give a good estimate of mortality

risk with the great advantage of being simple to score. It is subjective and may be applied

inconsistently by different anesthetists. The fact that ASA scores vary between observers

suggests that it is really an expert clinical assessment of risk and not a score at all.

40

Boeys scoring system43

(a) Shock at admission (systolic blood pressure <90 mmHg),

(b) Severe medical illness (ASA III–V), and

(c) Delayed presentation (duration of symptoms >24 h).

Advantages

Simple, easy to remember and apply.

Disadvantages

1. Does not consider various other physiological factors which do have a significant role in

predicting the patient’s condition.

2. Less accurate.

41

Haceteppe score44

– used in peptic ulcer perforation

The four variables in the study

the presence of a serious coexisting medical illness,

acute renal failure,

white cell count of more than 20 × 109/l, and

Male sex.

There has been no study to revalidate this score or test its accuracy against others.

Sickness assessment45

Kennedy et al - first described this scoring system.

hypotension;

severe chronic disease and

Whether or not the patient was independent and self-caring.

These conditions were clearly defined. In the group of patients with a SA score of zero, there

were no deaths. Mortality in patients with one, two and three parameters present was 52%, 60%

and 100% respectively.

Not widely used.

Fitness score46

Playforthet al in 1987 introduced this scoring system .The 26 risk factors were chosen by the

authors and weighted arbitrarily from 1 – 4.

In addition to the difficulty of scoring 26 variables preoperatively, some, such as the presence of

perforation or obstruction and diagnosis of cancer, may not be available before surgery

42

Reiss index:47

Factors considered:

Age

Urgency of surgery

ASA

Presence of malignancy and

Diagnosis

An emergency laparotomy where the diagnosis was unknown could not be scored with this

system, which has been shown to be inferior to the ASA classification in predicting postoperative

morbidity and mortality. Scoring systems such as the Reiss Index or Fitness Score can be used

pre-operatively if there is time to gain enough data to complete the scoring.

Sepsis scores

As well as the APACHE score, several other scoring systems have been developed for

intraabdominal sepsis. These scores include the Simplified Acute Physiology Score (SAPS),

Sepsis Score, Multiple Organ Failure Score and Mannheim Peritonitis Index (MPI)

Scores predicting morbidity

1. Veltkampscore- 11 patient, disease and surgery-related variables are used .Minor

complications are less-successfully predicted hence less commonly used.

2. VA respiratory failure prediction index

The VA study was modelled on over 80, 000 men who developed respiratory failure (defined as

mechanical ventilation for 48 hours or more) after (non-cardiac) surgery. Weighted scores are

given for type of surgery, emergency surgery (less than 12 hours after admission), albumin,urea,

pre-morbid functional status, respiratory function history and age.

A score over 40 predicts a risk of respiratory failure of 31%.

43

APACHE II:

Presently, one of the most accepted scores is APACHE II, which integrates various physiologic

variables during the first 24 h within the intensive care unit (ICU) with age and chronic health

status of the patient.

The original APACHE was designed to predict mortality risk for stratification by assessing the

patient independent of effects of treatment (surgery).It was primarily designed to stratify ICU

admissions.

Drawbacks:

• The primary intra op findings are not considered in the data collected. These data have a

significant bearing on the outcome of the patient. These are especially important if the

APACHE was calculated after the primary surgery. The primary surgery would alter the

physiological variables used to calculate the APACHE score.

• Mortality prediction is less accurate

• It is difficult to use this scoring system for postoperative monitoring because of the need

to measure numerous laboratory parameters when deciding therapies for patients with

unsuccessful initial treatment

• The acquisition of so many physiological variables will always make it less readily

measured than other scoring systems.

• This initial stratification of risk factors and a predicative equation estimate patient

outcome. They are, however, both complex and time consuming.

44

POSSUM scoring–

Physiological and operative severity score for the enumeration of mortality based on Copeland,

Jones and Walters Br J Surg(1991) .Scores calculated taking into consideration 2 parameters

Physiological severity –

Age, cardiac signs, respiratory signs, systolic blood pressure, pulse, Glasgow coma scale,

hemoglobin, total count, urea, sodium, potassium and ECG

Operative severity –

Multiple procedures, total blood loss, peritoneal soiling, malignancy, operative severity and

mode of surgery.

Considered to be midway between too simple ASA scoring and too complex APACHEII scoring

system.

Uses 12 physiological variants and 6 operative variants

Drawbacks

- Tends to overestimate the mortality in low risk patients

- Tends to overestimate if used in other specialties.

P POSSUM –Portsmouth predictor equation for mortality –

Prytherch et al Br J Surg 1998 introduced the corrected version of the scoring system. This

scoring is more accurate than the original POSSUM scoring but it still overestimates the

mortality in low risk patients. Higher the risk more is the accuracy of the scoring system.

There have been new versions of this scoring system like V-POSSUM used specifically for

specialties. Predicted death rate=1/ (1+ e-R

)

Where R is (0.1692×physiological score) + (0.1550×oerative score) -9.065 in POSSSUM

R = (0.13×physiogical score) + (0.16 ×operative score)-7.04 in P-POSSUM

45

THE MANNHEIM PERITONITIS INDEX1 (MPI)

MPI was developed by Wacha and Linder in 1983.

Initially 20 possible risk factors were considered. Of these only 8 proved to be of prognostic

relevance and were entered into the MPI, classified according to predictive powers.

Since then MPI is used because of its accurateness and simplicity to predict the morbidity and

mortality in patients with hollow viscous perforation.

THE MANNHEIM PERITONITIS INDEX

RISK FACTOR SCORES

Age > 50 years 5

Female sex 5

Organ failure 7

Malignancy 4

Preoperative duration of peritonitis > 24 h 4

Origin of sepsis not colonic 4

Diffuse generalized peritonitis

Exudate

6

Clear 0

Cloudy, purulent 6

Fecal 12

Kidney failure = creatinine level > 177 umol/L or urea level> 167mmol/L or oliguria

<20ml/hour;

Pulmonary insufficiency = PO2 < 50 mmHg or PCO2 > 50 mmHg;

Intestinal obstruction/paralysis > 24hours or complete mechanical ileus.

Shock: systolic blood pressure<90mm of Hg, MAP<60mm of Hg.

46

CLINICAL FEATURES:

Localized peritonitis;

The clinical course is determined by the manner in which adhesions form around the affected

organ. Inflamed peritoneum loses its glistening surface and becomes reddened & velvety. Flakes

of fibrin appear and causes loops of intestines to become adherent to one another and to the

parietal wall.

There is an outpouring of serous inflammatory exudates rich in leukocytes and plasma proteins

that soon become turbid; if localization occurs, the turbid fluid becomes frank pus. The greater

omentum, by enveloping and becoming adherent to inflamed structures, often forms a substantial

barrier to the spread of infection.

Diffuse peritonitis27

;

A number of factors may favor the development of diffuse peritonitis

1) Speed of peritoneal contamination – is the prime factor. Any hollow viscous if perforates

before localization has taken place; there is a gush of contents into the peritoneal cavity

which may spread to a large area almost instantaneously.

2) Stimulation of peristalsis – hinders localization.

3) Virulence of the organism.

4) Young children have a small omentum which is less effective in localizing the infection.

5) Disruption of localized collections – due to injudicious and rough handling.

6) Deficient natural resistance.

47

Clinical features;

• Abdominal pain worse on movement

• Guarding/ rigidity of abdominal wall

• Pain/ tenderness on rectal/ vaginal examination

• Pyrexia

• Raised pulse rate

• Absent or reduced bowel sounds

• SIRS in later stages.

INVESTIGATIONS:

Raised white cell counts

Erect chest x ray or lateral decubitus - air under diaphragm or beneath the abdominal wall

A radiograph of the abdomen – may show dilated gas filled loops of bowel (consistent

with paralytic ileus).

USG and CT scanning – may be helpful in some patients by identifying the cause of

Peritonitis.

Peritoneal aspiration – usually done under USG guidance. Bile stained aspirate indicates

perforated peptic ulcer or gall bladder, purulent aspirate indicates bacterial peritonitis.

48

Treatment

Fluid and electrolyte replacement, operative control of sepsis, and systemic antibiotics are the

mainstays of treatment of peritonitis.

A. General Care:31

1) Intravenous fluids - The massive transfer of fluid into the peritoneal cavity must

be replaced by an appropriate amount of intravenous fluid. If systemic toxicity is

evident or if the patient is old or in fragile health, a central venous pressure (or

pulmonary artery wedge pressure) line and bladder catheter is inserted; a fluid

balance chart is kept;

49

2) Care for advanced septicemia -Cardiovascular agents and mechanical ventilation

in an intensive care unit are used in patients with advanced septicemia.

3) Antibiotics - Loading doses of intravenous antibiotics directed against the

anticipated bacterial pathogens is given after the samples have been obtained for

culture.

Initial antibiotics employed include third-generation cephalosporins, piperacilin

tazobactam, amikacin, aztreonam or imipenem-cilastatin for gram-negative

coliforms, metronidazole or clindamycin for anaerobic organisms

B. Operative Management:

Control of sepsis - The objectives of surgery for peritonitis are to remove all infected

material, correct the underlying cause, and prevent late complications.

• A midline incision offers the best surgical exposure. Materials for aerobic and anaerobic

cultures of fluid and infected tissue are obtained immediately after the peritoneal cavity is

entered.

• Occult pockets of infection are located by thorough exploration, and contaminated or

necrotic material is removed.

• The primary disease is then treated. This may require resection (e.g., ruptured appendix

or gallbladder), repair (e.g., perforated ulcer).

50

• Peritoneal lavage - In diffuse peritonitis, lavage with copious amounts (> 3 L) of warm

isotonic crystalloid solution removes gross particulate matter as well as blood and fibrin

clots and dilutes residual bacteria.

Bassett23

in his book on exploration of the abdomen and the maneuvers necessary to carry it out

suggested three sequences that may be used: regional, systemic, and circular. The following

sequence is drawn from Bassett's regional route:

1. Inspect the abdomen. Note any obvious pathology that (a) may need immediate treatment (i.e.,

a ruptured spleen) or (b) may contraindicate further exploration (i.e., a perforated colonic

diverticular abscess).

2. If the clinical status of the patient warrants further exploration,

o Examine the transverse colon. Pull the colon downward.

o Examine the supracolic region from right to left.

o Pull the transverse colon upward. Examine the infracolic region from

right to left.

o Examine the pelvic cavity.

Do not forget to examine the greater omentum. Torsion of the omentum may be the cause for

pain abdomen.24

Idiopathic infarction, especially at the right lower end, is obvious.25

if this or

any other system is used habitually, it will become automatic.

As Bassett23

said: "The goal is to achieve gentleness, accuracy, thoroughness, and speed."

51

C. Postoperative Care:

Intensive care monitoring, often with ventilatory support is needed if the patient is unstable and

frail. Achieving hemodynamic stability to perfuse major organs is the immediate objective, and

this may entail the use of cardiac inotropic agents besides fluid and blood product supportive

measures.

Antibiotics are given for 7-10 days, depending on the severity of peritonitis.

A favorable clinical response is evidenced by,

Well-sustained perfusion with good urine output,

Reduction in fever and leukocytosis,

Resolution of ileus, and

A returning sense of well-being.

The rate of recovery varies with the duration and degree of peritonitis.

The early removal of all nonessential catheters (arterial, central venous, urinary, and nasogastric)

is to be ensured. Drains are removed or advanced once drainage diminishes and becomes more

serous in nature.

COMPLICATIONS:

With modern treatment diffuse peritonitis carries a mortality of < 10%.

Systemic complications of peritonitis

Bacteremia / endotoxic shock

Bronchopneumonia / respiratory failure

Renal failure

Bone marrow suppression

Multi system failure

52

Abdominal complicationsof peritonitis

Adhesional small bowel obstruction

Paralytic ileus

Residual or recurrent abscess

Portal pyaemia/liver abscess.

Surgical site infections

Clinical features of an abdominal/ pelvic abscess:

Malaise

Sweats with or without rigors

Abdominal/ pelvic pain

Anorexia and weight loss

Swinging pyrexia

Symptoms from local irritation: hiccough (subphrenic), diarrhea & mucus (pelvic).

Localized abdominal tenderness.

The primary cause of prolonged hospital stay after the operation in patients with secondary

bacterial peritonitis is pulmonary and MODS & this is despite the technical success of the initial

operation. Peritonitis may induce a systemic inflammatory response in which the lungs succumb

more often and earlier than other remote organs.34

Although pulmonary failure alone did not

predispose to death, ARDS and MODS are both associated with increased mortality.

A primary mediator of remote organ injury after peritonitis is the neutrophil, although such injury

is multifactorial and complex in nature

53

.

MATERIALS

AND

METHODS

54

SOURCE OF DATA: Total of 100 patients with peritonitis due to hollow viscous perforation who

presented to BANGALORE MEDICAL COLLEGE AND RESEARCH INSTITUTE, BANGALORE from November

2014 to August 2016.

METHODS:

Diagnosis of peritonitis due to hollow viscous perforation made by

1. History and clinical examination

2. X-ray chest PA view with both domes of diaphragm which shows air under diaphragm.

3. Detailed history of presenting illness and history suggestive of chronic health disorders

such as cardiac, renal, hepatic conditions noted.

4. All biochemical investigations done on admission and relevant clinical details noted.

5. Standard operative procedures was followed for different causes of perforative peritonitis

Mortality defined as any death occurring during the hospital stay.

Morbidity assessed in terms of post-operative complications such as

Pneumonia or lung atelectasis,

Wound infection,

Acute myocardial infarction or heart failure,

Intra-abdominal collection,

Acute renal failure and urinary tract infection.

55

INCLUSION CRITERIA:

1. Patients with clinical suspicion and investigatory support for the diagnosis of peritonitis due to

hollow viscous perforation who are later confirmed by intra op findings.

2. Patients of either sex between 14 & 70 years of age.

Various etiologies causing such features include:

Acid peptic disease

Typhoid

Tuberculosis

Gangrenous cholecystitis

Appendicitis

Malignancy

EXCLUSION CRITERIA:

1. Patients with hollow viscous perforation due to trauma

2. Patients with any other significant illness which is likely to affect the outcome more than

the disease in study.

3. Pregnant mothers

4. Patients <14 years and > 70 years

Once diagnosis of peritonitis had been determined by operative findings, the patient was enrolled

into the study. Using history, clinical examination and lab values risk factors found in MPI were

classified according to values indicated and individual variable scores were added to establish

56

MPI score.The cases were first grouped into three, as described by Billing: those below 21 pts,

between 21-29 pts, and those above 29 pts.

In addition to personal data such as name, age, sex, etc., the following information was

registered: file number; dates of admission and discharge from the hospital; days hospitalized;

date of surgery and information related to illness (surgical findings, medical treatment and

evolution of illness).

Patient evolution was followed, occurrence of complications and discharge due to improvement

or death. Time elapsed from initial diagnosis to moment of event (death or discharge from

hospital) was determined.

Out-patient follow-up was continued for 30 days to establish perioperative morbidity and

mortality. The minimum possible score was zero, if no adverse factor were present, and

maximum was 47 if presence of all were confirmed. Analysis was done with each variable in the

scoring system as an independent predictor of morbidity or mortality and the scoring system as a

whole.

STATISTICAL ANALYSIS:

The data was analyzed using SPSS software version 16.3.Each variable in the MPI score along

with other patient variables was analyzed using chi square analysis with various outcomes that

were noted in the study. P value <0.05 was taken as significant in this study. The results were

averaged (mean + standard deviation) for each parameter for continuous data and numbers and

percentage for categorical data presented in table and figure. Proportions were compared using

Chi-square test of significance.

57

Results

58

DESCRIPTIVE STATISTICS

Males accounted for 70% of the patients in the present study whereas most of the other studies

show equal sex distribution.27, 28

. 70% of the patients were less than 50 years of age which is

similar to earlier studies.

Duration of pain

About 60% of the study group presented with pain abdomen of less than 24 hours duration. It

was seen in this study that longer the duration of pain higher was the morbidity in the post op

period

Duration of pain Frequency Percentage

< 24 hours 64 64

1 to 5 days 32 32

> 5 days 4 4

Total 100 100

frequency

<24 hrs 1-5 days >5 days

59

Site of perforation- statistics

Origin Frequency Percentage

Gastric 10 10

Duodenal 58 58

Ileal 18 18

Appendicular 14 14

Total 100 100

Site of perforation

The most common site of perforation was duodenum(58%),ileal perforation being the next

common.

10

58

18

14

60

Type of exudate - statistics

Frequency Percentage

Clear 60 60

Purulent 26 26

Feculent 14 14

Total 100 100

Only 13% had feculent collection noted intra op, majority (50%)had clear fluid exudate.

6026

14

0

percentage

clear purulent feculent

61

Number of complications -

58% of the study population had no post-operative complications, 20% had 2 or more

complications.

Peritonitis - statistics

66% of the study population presented with diffuse peritonitis. Only one case(2%) was

perforation due to malignancy.9

62

EVALUATION OF THE SCORING SYSTEM

MPI scores frequency Percentage

< 22 64 64

22 – 29 22 22

> 29 14 14

total 100 100

64% of the study population was in the low risk group (scores <22) and 14% were in high risk

(scores >29).Patients with organ failure on admission, longer duration of illness before the

surgery, diffuse peritonitis, feculent exudates were more likely to have higher scores and hence

fall into high risk group than their counterparts.

6422

14

0

percentage

<22 22-29 >29

63

Assessment of the individual outcomes in each group is as follows.

COMPLICATIONS IN RELATION TO SCORE

Post op complications

90% of the population which had no post procedure complications had a score of <22 (p<0.002)

whereas 70% of the patients with Mannheim peritonitis index of>29 had 2 or more complications

during the post op period.

64

Pulmonary complications

The pulmonary complications in the form of post op pneumonia, pleural effusion which required

continuous monitoring of oxygen saturation, nebulization and hence lead to longer post op

recovery were significantly higher as the score increased.

Pulmonary

complications

Score < 22 Score 22- 29 Score > 29 Total

NO 58 14 02 74

78.4 % 18.9 % 2.7 % 100%

YES 6 8 12 26

23.1% 30.8 % 46.2 % 100%

TOTAL 64 22 14 100

64% 22% 14% 100%

> 80% of patients with > 29 had some form of pulmonary complications , which was only about 10% in

patients with score < 22 ( p < 0.005)

65

Development of ARDS:

ARDS Score < 22 Score 22-29 Score > 29 Total

NO 64 18 10 92

69.6 % 19.6 % 10.9 % 100%

YES 00 04 04 08

00% 50% 50% 100%

TOTAL 64 22 14 100

64 % 22% 14% 100%

The development of ARDS in these pts was well predicted with scoring system. 50% of pts who developed

ARDS in their post op period had a score of > 29. 30% of pts with score > 29 eventually developed ARDS

in the post-operative period.

Development of wound complications:

SSI Score < 22 Score 22- 29 Score > 29 total

NO 56 12 06 74

75.7 % 16.2 % 8.1 % 100%

YES 08 10 08 26

30.8 % 38.5% 30.8 % 100%

TOTAL 64 22 14 100

64 % 22% 14 % 100%

Up to 60% of the patients with scores > 29 developed wound related complications in the post op

period which was about 40% in patients with score 22-29 and about 12% in patients with scores

<22(p <0.005) .The post op complications were significantly higher in the group with score>29.

This included the surgical site infections, pulmonary, renal complications and development of

multi organ failure. There was only one death in this study, analysis didn‘t reach significant

figures.

66

Effects on duration of illness:

ICU stay and ward stay is significantly prolonged in patients with higher scores .There is a

proportionate increase in the duration of stay with increase in scores. 90% of the patients who

were discharged within 10 days had a score of <22.

ICU STAY Score < 22 Score 22- 29 Score > 29 total

< than 5 days 64 14 08 86

74.4 % 16.3 % 9.3 % 100%

6 to 10 days 00 08 02 10

00% 80 % 20% 100%

> 10 days 00 00 04 04

00% 00% 100% 100%

67

Scoring system effect on severity of illness

INOTROPES Score < 22 Score 22 – 29 Score > 29 Total

NO 62 18 06 86

72.1 % 20.9% 07% 100%

YES 02 04 08 14

14.3% 28.6 % 57.2% 100%

TOTAL 64 22 14 100

64 % 22% 14% 100%

57% of the patients who required inotropic support in the post op period had a score of >29 and

only 1 patient (14%) required inotropes with a score <22.

68

Mechanical

ventilation

Score

< 22

Score

22 –29

Score >

29

Total

NO 62 18 08 88

70.5% 20.5% 9.1% 100%

YES 02 04 06 12

16.7% 33.3% 50% 100%

TOTAL 64 22 14 100

64% 22% 14% 100%

50% of the patients who required mechanical ventilation had score of >29. Score of >29 indicate

a higher risk of need for inotropes and mechanical ventilation and need for intensive care.

69

OTHER INDIVIDUAL PARAMETERS;

Site of perforation – duodenal perforations >80% cases had an uneventful recovery as

indicated by lesser post op complications, comparatively less requirement of inotropes and

mechanicalventilation and lesser hospital stay. Ileal and appendicular perforations had higher

rates of post op complications.

No of

complications

gastric duodenal Ileal appendicular Total

0 02 48 04 04 58

1 04 06 04 06 20

2 00 02 06 04 12

3 02 02 00 00 04

4 or more 02 00 04 00 06

Total 10 58 18 14 100

10% 58% 18% 14% 100%

70

Exudates–

Score Clear purulent Feculent Total;

< 22 52 10 02 64

81.25% 15.6% 3.125% 100%

22 -29 06 12 04 22

27.27% 54.5% 18.18% 100%

> 29 02 04 08 14

14.29% 28.6% 57.14% 100%

Total 60 (60%) 26 ( 26% ) 14 ( 14% ) 100 (100%)

Presence of feculent or purulent exudates was reflected in higher eventual scores. Feculent and purulent

exudates were associated with significantly increased post op complications requiring increased hospital

stay. Up to 80% of the patients with clear exudates had no post op complications which dropped to only

30% (p<0.005) with the other type. However there was no statistically significant difference between

feculent and purulent exudates, both having similar complication profiles

Duration of Pain:

Noof

complications

< 1

day

1 – 5

days

>5

days

Total

0 40 18 00 58

1 0 16 04 20

2 0 08 04 12

3 0 04 00 04

> than 4 0 02 04 06

Total 40 48 12 100

71

The study population which presented within 24 hrs.of the pain onset had significantly (p<0.05)

better outcome compared with their counterparts. This was reflected in lesser post op

complications shorter ICU and hospital stay. None of the patients in this group required post op

inotropes or mechanical ventilator. As the duration of pain increased morbidity associated also

proportionately increased.

Organ failure on admission – Patient presenting with any organ failure due to hollow

viscous perforation was significantly associated with (p<0.005) increased morbidity. 65% of the

patients with no organ failure on admission had uneventful recovery, 97% of the same population

had <2 post op complications. On the other hand 66% of the patients with organ failure on

admission had >2 complications in the post op. >90% of the patients with organ failure

neededpost op inotropes and mechanicalventilation whereas it was the same percentage of

patients whodid not require inotropes in the other group. >50% of the patients with organ failure

had pulmonary complications which was <3 % in the other group.

72

Discussion

73

There is no ideal scoring system for the pre-operative assessment of patients needing emergency

surgery. Some pre-operative scoring systems provide approximate estimates of mortality risk but

none have been shown to be sufficiently specific for use on individual patients. At present, the

Fitness Score has greatest specificity (80%) but would not be easy to use on all emergency

admissions due to significantly large number (26) of variables to be collected and few variables

like diagnosis of malignancy may not be available in the pre op settings. Post-operative scoring

systems such as P-POSSUM probably provide more accurate predictions, but are not useful in

pre-operative assessment. Unfortunately, there are very few studies that have revisited old

scoring systems or attempted to compare systems to assess which is best. Most articles in this

field have proposed another new system.

The timing of data collection to create risk scores is seldom mentioned in the literature. Not only

do physiological values vary during the acute admission, making the scores obtained by them

unreliable, but there is evidence that to include operative findings and post-operative parameters

on ICU improves the accuracy of the prediction Although a score at initial assessment would

help triage and plan treatment, comparative audit with postoperative scores remains the most

useful function of scoring systems at present.

Even if accurate pre-operative predictions of outcome were possible by estimation of a risk

score, an expert surgical opinion would be required to interpret these predictions at the bedside.

An experienced clinician can not only assess prognosis but also weigh up the local facilities

available, the patient's quality of life and ethical issues, as well as considering the patient or

relative's wishes. Scoring will never replace clinical judgment.

74

Scoring systems are generated and validated on specific populations that may be substantially

different from the patients being scored in a different hospital. One potential resolution would be

for each hospital to create a system specific to its own population, which is regularly revalidated.

This study done inBangalore medical college and research institute Bangalore, included 100

patients who presented to the surgery department and were diagnosed with hollow viscous

perforation. All the patients were appropriately assessed and managed according to standard

guidelines.

Few of the other studies confirmed age as a decisive factor related with mortality however this

study does not show any statistical significance38

.In other studies, patients with generalized

peritonitis range from 30–66%; in our study, generalized peritonitis was present in about 66% of

the patients38, 39

.

The influence of gender on prognosis has been shown of little importance in this study. Gender

composition cited in other publications showed percentages, varying from 43 to 52% females

and 48 to 57% male30,31

,72% were male in this study.

Mean MPI score reported in literature for localized peritonitis is 19 (range 0 to 35) and in

generalized peritonitis, 26 to 27 points (range 11 to 43)40, 41

which is similar to the values noted

in this study.

Duration of pain >24 hours, organ failure on admission & feculent exudate were found to be

independently significant factors in predicting the morbidity among the study population.

However presence of diffuse peritonitis wasn‘t a significant factor in contrast to various other

studies37

75

conclusion

76

There have been several attempts at creating a scoring system to predict mortality and

morbidity risk after emergency surgery.

Some scoring systems provide a prediction that approximates to the observed mortality

rate for a cohort, but none is sufficiently accurate to rely upon when considering an

individual patient.

This is a validation study of the MANNHEIM PERITONITIS INDEX scoring system for

predicting the morbidity and mortality in patients with peritonitis due to hollow viscous

perforation.

The results of this study proves that MPI scoring system is a simple and effective tool for

assessing this group of patients, and can be used as a guiding tool to decide on the

management of the patient after the definitive procedure is done.

Among the various variables of the scoring system duration of pain, organ failure on

presentation and presence of feculent exudates had a significant hand in predicting the

eventual outcome of the patient.

77

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20. Smith RS, Smith TJ, Blieden TM, and Phipps RP: Fibroblasts as sentinel cells: Synthesis of

chemokines and regulation of inflammation. Am J Pathol 1997, 151:317-322

21. Witmann DH: Intra-abdominal infections. New York: Marcel Dekker, 1991

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22. Doherty, Gerard M, Way, Lawrence W: Current Surgical Diagnosis & Treatment, 12th

Edition pg. no 495-497

23. Troidle L et al: Differing outcomes of gram-positive and gram-negative peritonitis. Am J

Kidney Dis 1998; 32:623

24. Mamud, Scott & Bjasmaron: .A unifying hypothesis for the mechanism of NSAID related GI

toxicity. Annals Of Rheumatic Disease 1996; 55:211-213

25. Origins of peritonitis. Wittmann DH. Intra-abdominal Infections. New York: Marcel Dekker,

1991;

26. Peek RM Jr, Blaster MJ: Pathophysiology of H pylori induced gastritis &peptic ulcer disease.

Ann J Med 02:200. 1997

27. Charles V. Mann, R.CG Russel and N.S. Williams: Bailey & Love's Short Practice of

Surgery, 22nd edition. (1995) Chapman &Hall,

28. F. Charles Brunicardi, MD, FACS (2010): Schwartz's Principles of Surgery, Ninth Edition

P.1766. The McGraw-Hill Companies, Inc.

29. Adesunkanni A R,Ajao G(1997):typhoid ileal perforation: a prospective study, journal of

royal college of surgeons, Edinburg,december25, issue4, page no 311-315

30. Clagett M: Greek Science in Antiquity. New York: Barnes & Noble, 1994, p. 40.

31. Bassett JW. Exploration of the Abdomen. Springfield IL: Charles Thomas, 1967.

32. Singhabhandhu B, Ritz C, Gray SW, Bohman MD, Skandalakis JE. Lesions of the omentum.

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33. Skandalakis JE. [Spontaneous idiopathic hemorrhagic infarction of the greater omentum].

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34. D J Wickel, W G Cheadle, M A Mercer-Jones, and R N Garrison: Poor outcome from

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Ann Surg. 1997 June; 225(6): 744–756.

35. Gotzinger P, Gebhard B, Wamser P, Sautner T, Huemer G, Fugger R. Revision of diffuse

peritonitis: planned versus on demand. Langenbecks Arch Chir 1996; 381(6):343-347.

36. Navez B, Tassetti V, Scohy JJ, Mutter D, Guiot P, Evrard S, et al. Laparoscopic management

of acute peritonitis. Br J Surg 1997; 85: 32-36.

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83

ANNEXURE I

CONSENT FORM FOR ANASTHESIA AND OPERATION

I ___________________ Hosp. No.___________ in my full senses hereby give my complete

consent for _________________________________ or any other procedure deemed fit

which is a / and diagnostic procedure/ biopsy/ operation to be performed on me/ my son /my

daughter/ my wife _______________ aged ______- under any anesthesia deemed fit. The

nature and risk involved in the procedure have been explained to me to my satisfaction.

Complications include hemorrhage, sepsis, seroma, MODS,ARDS, need of ICU

care,ventilator and including anesthetic complications. The staff, treating doctor / surgeon is

not held responsible for any untoward incidences during the course of the disease. For

academic and scientific purpose the operation / proceduremay be televised or photographed.

Date: signature / thumb impression

of patient

Name and signature of guardian

Relation and full address:

84

ANNEXURE II

MANNHEIM PERITONITIS INDEX

RISK FACTORS WEIGHTING ( IF PRESENT )

Age > 50 years 5

Female sex 5

Organ failure 7

Malignancy 4

Origin of sepsis not colonic 4

Diffuse generalized peritonitis 6

Pre operative duration of peritonitis > 24 hours 4

Exudate

Clear

Cloudy, purulent

Fecal

0

6

12

85

ANNEXURE III

ORGAN FAILURE CRITERIA

1 . Creatinine level > 177 micro mol per liter

2 . Urea level > 167 m mol per liter

3 .Oliguria < 20 ml / hour

4 . PaO2 < 50 mm of Hg

5 . Pa CO2 > 50 mm of Hg

6 .Shock: systolic blood pressure < 90 mm of Hg, MAP < 60 mm of Hg.

7 . Intestinal obstruction only if profound with paralytic ileus > 24 hours, complete mechanical

obstruction.

86

ANNEXURE IV

PROFORMA

Name : I P No:

Age : DOA :

Sex: DOD:

Marital status : Unit:

Occupation :hosp : B&LCH / VICTRORIA

Address :

A. Chief complaints

Pain abdomen:

Vomiting:

Fever:

Indigestion:

Abdominal distension:

Bowel disturbance:

Urinary disturbance:

Loss of weight:

Anyother:

B . History of presenting illness

1. Pain abdomen :

Site:

Duration:

Mode of onset: insidious / sudden

Severity:

Nature: aching / burning/ stabbing/constricting / throbbing / colicky /distending.

Progress: steady / gradually declining / gradually worsening /fluctuating / asso with appearance

of swelling.

Relieving factors:

Aggravating factors:

Radiation:

87

2 Vomiting :

Duration:

Frequency:

Spontaneous / induced:

Nature: food particles / digested food / clear acidic fluid / bilious /coffee ground /feculent.

3 Fever :

Duration:

Type: continuous / intermittent

Grade: high / moderate / low

4 Indigestion : discomfort after food / fullness

5 Loss of appetite : yes /no

6 Abdominal distension :

Onset

Progress

Associated factors

Pain

Relieving factors

7 Bowel disturbances :

Frequency:

Constipation / diarrhea

8 Loss of weight: yes / no

Percentage, duration

9 Any other:

C .Past history: similar illness, H/O surgery?, TB, DM, HTN.

D .Family history: TB , DM, HTN, malignancy, similar illness.

E Personal history: smoking, alcohol, type of diet, sleep, other habits, bowel and bladder habits.

F .Drug history: ATT, NSAID, steroids, insulin.

G . Menarche, menstrual history, menopause, any other disturbances.

H . Social history : Marital status, socio economic status.

I. General physical examination

Built: well / moderate / poor

Nourishment: well / moderate / poor

Pallor: mild / moderate / severe

Icterus: mild / deep

Pedal edema : pitting / non pitting

88

Febrile: yes / no

Dehydration: yes / no

Generalized lymphadenopathy: yes / no

Group involved

Tender / non tender

Consistency: soft/ firm/ rubbery/ hard/matted/discrete

Mobility: yes / no

Pulse:rate, rhythm, volume

Blood pressure

J .Local examination of abdomen

1 .Inspection

a) Shape: flat /scaphoid / distended

b) Any mass / fullness

Site, No., extent, shape, surface, border, movement with respiration, head raising test et

c) Umbilicus : shape, position

d) Visible veins: yes / no, site

e ) Visible peristalsis : yes / no , site

f) Flanks

g) Hernia orifices

h) All quadrants moving equally with respiration

i)Sinuses : site, No., surrounding skin, nature of discharge

j)Scars: site, No., nature of healing

k) Fistula

l) Any other

2. Palpation

a) Feel of abdomen: soft / doughy

Guarding :

Rigidity: localized /generalized

Tenderness: present / absent

89

b) Free fluid: fluid thrill, shifting dullness

c) Hepatomegaly /splenomegaly: yes / no

3 .Percussion

a) Dullness continuous with liver / spleen /extent

b) Free fluid: puddle sign. Shifting dullness

c) Bladder

d) Renal angle : normal / dull

4. Auscultation:bowel sounds: yes /no , frequency , character.

Examination of back and spine

a) Renal angle : fullness , tenderness -- yes / no

Percussion: resonant / dull

b) Spine : deformity, tenderness, Para spinal rigidity, fullness -- yes/no

Per rectal examination:wall, lumen, nature of finger stain

Per vaginal examination

Respiratory system examination

CVS examination

PROVISIONAL DIAGNOSIS

K .Investigations:

a) Blood : Hb, TLC, DLC, BL gp, RBS, B urea, S creatinine, SE

b) Urine : sugar, albumin, microscopy

c) Chest x-ray PA view

d) Erect x-ray abdomen

e) USG abdomen and pelvis.

L. CLINICAL DIAGNOSIS

M.Treatment: conservative / operative (simple / radical)

N. Post op period: complications if any

O. Follow up: good / fair / poor

P. Mortality: if any.

S N

O

I P N

O

NA

ME

AG

E

SEX

DA

TE O

F A

DM

DU

RA

TIO

N O

F P

AIN

AB

D

BP

(m

m h

g)

PU

LSE

(bp

m)

TYP

E O

F EX

UD

ATE

WO

UN

D C

OM

PLI

CA

TIO

NS

NEE

D O

F IO

NO

TRO

PES

NEE

D O

F V

ENTI

LATO

RS

PU

LMO

NA

RY

CO

MP

LIC

ATI

ON

S

AR

DS

FIN

AL

DIA

GN

OSI

S

MP

I SC

OR

E

TREA

TMEN

T G

IVEN

FIN

AL

OU

TCO

ME

1 75133 kishor 22 yrs M 2/11/2014 < 1 day 110/84 78 clear duodenal perforation 10 Grahms patch cured

2 76014 harilal 55 yrs M 3/11/2014 2 days 98/64 96 clear SSI LRTI duodenal perforation 26 Grahms patch cured

3 77011 manjunath 32 yrs M 3/11/2014 2 days 110/78 74 clear SSI appendicular perforation 14 appendectomy cured

4 77162 krishnamurthy 48 yrs M 5/11/2014 < 1 day 126/80 78 clear duodenal perforation 10 Grahms patch cured

5 77683 raju dev 26 yrs M 8/11/2014 < 1 day 112/70 86 clear LRTI duodenal perforation 10 Grahms patch cured

6 77557 raju E I 46 yrs M 8/11/2014 3 days 110/68 88 clear duodenal perforation 21 Grahms patch cured

7 77722 parveez 30 yrs M 11/11/2014 < 1 day 96/64 104 faecal appendicular perforation 22 appendectomy cured

8 77780 ramesh 36 yrs M 17/11/2014 < 1 day 102/80 86 clear duodenal perforation 10 Grahms patch cured

9 78085 veeman 54 yrs M 19/11/2014 2 days 90/60 128 purulant YES YES pulmonary aspiration YES duodenal perforation 25 Grahms patch DIED

10 78057 upendra 29 yrs M 25/11/2014 < 1 day110/90 84 clear duodenal perforation 10 Grahms patch cured

11 78804 muniswamy 45 yrs M 30/11/2014 4 days 100/66 78 purulant SSI LRTI duodenal perforation 20 Grahms patch cured

12 78885 parvatamma 47 yrs F 5/12/2014 < 1 day 104/70 92 purulant LRTI duodenal perforation 25 Grahms patch cured

13 80399 shamshad begum 35 yrs F 09/12/2014 < 1 day 90/58 130 faecal YES YES YES appendicular perforation 21 appendectomy DIED

14 80700 mintu kumar 21 yrs M 18/12/2014 < 1 day 110/80 80 clear duodenal perforation 10 Grahms patch cured

15 81417 abdul 51 yrs M 25/12/2014 2 days 98/70 86 purulant SSI duodenal perforation 25 Grahms patch cured

16 81450 nazir ahmed 20 yrs M 29/12/2014 < 1 day 114/84 76 clear duodenal perforation 10 Grahms patch cured

17 82185 narayan swamy 48 yrs M 31/12/2014 3 days 100/70 80 purulant SSI LRTI gastric perforation 20 Grahms patch cured

18 82436 rajesh 30 yrs M 5/1/2015 < 1 day 112/70 78 clear SSI duodenal perforation 10 Grahms patch cured

19 82652 francis joseph 18 yrs M 8/1/2015 < 1 day 110/74 92 clear duodenal perforation 10 Grahms patch cured

20 83092 balaram 38 yrs M 8/1/2015 < 1 day 88/60 128 faecal YES YES ileaL Perforation 22 primary closure DIED

21 83527 chandrashekhar 21 yrs M 11/1/2015 < 1 day 110/78 86 clear duodenal perforation 10 Grahms patch cured

22 83773 rangaswamy 68 yrs M 15/01/2015 3 days 100/68 104 purulant SSI YES duodenal perforation 32 Grahms patch cured

23 83974 rajiv 33 yrs M 20/01/2015 < 1 day 112/74 100 purulant duodenal perforation 16 Grahms patch cured

24 84529 shivanand 33 yrs M 22/01/2015 < 1 day 116/70 84 clear duodenal perforation 10 Grahms patch cured

25 84678 chinnakannamma 75 yrs F 29/01/2015 3 days 100/72 110 clear YES YES duodenal perforation 31 Grahms patch cured

26 85046 murugesh 26 yrs M 05/02/2015 < 1 day 116/80 76 clear duodenal perforation 10 Grahms patch cured

27 85349 krishna 36 yrs M 9/2/2015 < 1 day 116/70 86 clear duodenal perforation 10 Grahms patch cured

28 85388 reshma 28 yrs F 12/2/2015 2 days 84/58 138 faecal YES YES pulmonary aspiration YES ileaL Perforation 31 primary closure DIED

29 85492 siddappa 65 yrs M 25/2/2015 2 days 114/68 116 purulant SSI duodenal perforation 32 Grahms patch cured

30 85521 jani basha 50 yrs M 28/2/2015 6 days 90/64 110 faecal SSI YES LRTI ileaL Perforation 31 primary closure cured

31 85797 manjunath 40 yrs M 5/3/2015 < 1 day 114/68 94 clear duodenal perforation 10 Grahms patch cured

32 85886 somu 23 yrs M 08/03/2015 < 1 day 118/70 98 clear duodenal perforation 10 Grahms patch cured

33 87127 mathuraj 28 yrs M 15/03/2015 < 1 day 116/80 86 clear duodenal perforation 10 Grahms patch cured

34 86346 dheerendra 19 yrs M 22/03/2015 < 1 day110/86 94 clear duodenal perforation 10 Grahms patch cured

35 88805 sathiya babu 33 yrs M 05/04/2015 3 days 100/70 98 purulant SSI LRTI ileaL Perforation 20 primary closure cured

36 88728 ramachandra 45 yrs M 11/04/2015 2 days 102/74 100 purulant YES YES gastric perforation 27 Grahms patch cured

37 88466 jamina 18 yrs F 11/04/2015 2 days 100/70 98 purulant appendicular perforation 19 appendectomy cured

38 88834 md rafi 27 yrs MM 20/04/2015 < 1 day 100/80 78 clear duodenal perforation 10 Grahms patch cured

39 89819 susheela 20 yrs F 29/04/2015 3 days 84/60 140 faecal SSI YES YES pulmonary aspiration YES ileaL Perforation 25 primary closure DIED

40 89879 lakshamma 65 yrs F 05/05/2015 3 days 100/64 88 clear LRTI duodenal perforation 24 Grahms patch cured

41 90699 naushad 32 yrs M 11/05/2015 < 1 day 118/68 86 clear duodenal perforation 10 Grahms patch cured

42 91999 ravichandra 37 yrs M 15/05/2015 < 1 day 128/72 88 clear duodenal perforation 10 Grahms patch cured

43 92425 suresh 36 yrs M 25/05/2015 3 days 104/68 94 clear LRTI appendicular perforation 14 appendectomy cured

44 93540 mackar doch 39 yrs M 31/05/2015 < 1 day 118/80 96 clear gastric perforation 10 Grahms patch cured

45 93810 ramesh 28 yrs M 06/06/2015 2 days 102/68 90 clear appendicular perforation 10 appendectomy cured

46 94297 ali 27 yrs M 11/6/2015 2 days 104/70 90 purulant ileaL Perforation 20 primary closure cured

47 94331 zaibul 20 yrs M 11/6/2015 < 1 day 114/70 88 clear SSI appendicular perforation 10 appendectomy cured

48 50 babu bora 27 yrs M 20/06/2015 < 1 day 118/84 86 clear gastric perforation 10 Grahms patch cured

49 196 sridhar 27 yrs M 30/06/2015 3 days 106/68 104 faecal SSI YES YES ileaL Perforation 26 primary closure cured

50 291 subhakar 62 yrs M 10/7/2015 3 days 100/62 108 purulant LRTI duodenal perforation 25 Grahms patch cured

51 336 dungar singh 40 yrs M 15/07/2015 < 1 day 106/70 100 clear appendicular perforation 10 appendectomy cured

52 1095 babalu 24 yrs F 16/07/2015 < 1 day 116/68 98 clear duodenal perforation 10 Grahms patch cured

53 1154 stephen alexander 50 yrs M 30/07/2015 6 days 96/64 116 purulant SSI LRTI duodenal perforation 30 Grahms patch cured

54 1477 loganathan 30 yrs M 6/8/2015 < 1 day 112/80 100 clear duodenal perforation 10 Grahms patch cured

55 1815 anees 58 yrs M 14/08/2015 < 1 day 118/70 108 purulant ileaL Perforation 25 primary closure cured

56 1967 anand 26 yrs MM 16/8/2015 3 days 100/60 98 clear appendicular perforation 14 appendectomy cured

57 3001 syed fayaz 60 yrs M 25/08/2015 < 1 day 98/74 118 clear gastric perforation 26 Grahms patch cured

58 3425 lokesh 18 yrs M 31/08/2015 < 1 day 110/68 106 clear LRTI appendicular perforation 10 appendectomy cured

59 3585 venkatesh 52 yrs M 1/9/2015 < 1 day 116/76 120 faecal YES LRTI ileaL Perforation 31 primary closure cured

60 4851 asma 30 yrs F 9/9/2015 2 days 102/68 106 purulant appendicular perforation 25 appendectomy cured

61 51833 veeramma 42 yrs F 17/09/2015 3 days 110/62 104 purulant LRTI duodenal perforation 25 Grahms patch cured

62 5078 chandrakant 30 yrs M 28/09/2015 < 1 day 118/80 98 clear duodenal perforation 10 Grahms patch cured

63 6459 krishnappa 35 yrs M 7/10/2015 < 1 day 116/80 88 clear duodenal perforation 10 Grahms patch cured

64 6469 nagesh 43 yrs M 15/10/2015 3 days 102/76 108 faecal LRTI ileaL Perforation 26 primary closure cured

65 6604 venkatesh 40 yrs M 25/10/2015 < 1 day 118/70 88 clear duodenal perforation 10 Grahms patch cured

66 6744 akash gour 18 yrs M 26/10/2015 < 1 day 100/68 100 clear SSI ileaL Perforation 10 primary closure cured

67 7329 eramudappa 40 yrs M 30/10/2015 < 1 day 112/70 94 clear duodenal perforation 10 Grahms patch cured

68 7886 nagaraj 45 yrs M 12/11/2015 3 days 128/70 106 purulant SSI gastric perforation 27 Grahms patch cured

69 8190 swapna 22 yrs F 25/11/2015 < 1 day 120/72 98 clear duodenal perforation 15 Grahms patch cured

70 8317 charles 53 yrs M 04/12/2015 < 1 day 110/74 98 purulant SSI duodenal perforation 25 Grahms patch cured

71 8858 mehaboob basha 60 yrs M 10/12/2015 2 days 106/70 126 faecal SSI YES YES LRTI duodenal perforation 38 Grahms patch cured

72 9301 mubarak 20 yrs M 14/12/2015 3 days 102/62 114 faecal ileaL Perforation 26 primary closure cured

73 10105 mehaboob 42 yrs M 21/12/2015 < 1 day 118/80 98 clear duodenal perforation 10 Grahms patch cured

74 10152 surender kumar 40 yrs M 24/12/2015 < 1 day 124/76 96 clear duodenal perforation 10 Grahms patch cured

75 10658 shivakumar 25 yrs M 30/12/2015 < 1 day 118/68 84 clear duodenal perforation 10 Grahms patch cured

76 10769 ayesha banu 20 yrs F 2/1/2016 3 days 106/70 100 clear SSI appendicular perforation 26 appendectomy cured

77 11060 narasimha 20 yrs M 8/1/2016 < 1 day 130/72 90 clear duodenal perforation 10 Grahms patch cured

78 11312 subramani 32 yrs M 11/1/2016 < 1 day 110/70 94 clear ileaL Perforation 10 primary closure cured

79 11801 siddappa 50 yrs M 25/01/2016 < 1 day 100/60 102 purulant duodenal perforation 25 Grahms patch cured

80 11813 amravani 30 yrs F 5/2/2016 < 1 day 102/68 110 clear SSI duodenal perforation 26 Grahms patch cured

81 12004 raj 40 yrs M 16/02/2016 < 1 day 124/80 98 clear duodenal perforation 10 Grahms patch cured

82 12402 sagayaraj 42 yrs M 24/02/2016 < 1 day 114/68 96 clear duodenal perforation 21 Grahms patch cured

83 12538 dodda thayappa 60 yrs M 06/03/2016 < 1 day 114/70 118 purulant LRTI gastric perforation 32 Grahms patch cured

84 13162 babu bora 50 yrs M 18/03/2016 3 days 88/60 146 faecal SSI YES ileaL Perforation 31 primary closure DIED

85 13318 praranjith 21 yrs M 29/03/2016 < 1 day 114/68 84 clear duodenal perforation 10 Grahms patch cured

86 13980 ramadevi 43 yrs F 15/04/2016 < 1 day 128/70 110 purulant SSI LRTI ileaL Perforation 25 primary closure cured

87 14230 prasanna kumar 45 yrs M 19/4/2016 < 1 day 116/74 94 clear SSI duodenal perforation 10 Grahms patch cured

88 14418 abdul waheed 27 yrs M 30/4/2016 < 1 day 118/76 100 clear gastric perforation 10 Grahms patch cured

89 15857 sunil 28 yrs M 11/5/2016 < 1 day 128/80 98 clear duodenal perforation 10 Grahms patch cured

90 16254 syed aneef 31 yrs M 25/5/2016 < 1 day 112/68 92 clear appendicular perforation 10 appendectomy cured

91 171039 anand 35 yrs M 8/6/2016 6 days 100/76 120 faecal SSI YES LRTI ileaL Perforation 33 primary closure cured

92 171089 suresh 26 yrs M 18/6/2016 < 1 day 118/80 100 clear gastric perforation 10 Grahms patch cured

93 16848 ballappa 30 yrs M 25/6/2016 < 1 day 124/80 98 clear duodenal perforation 10 Grahms patch cured

94 16852 raju 26 yrs M 8/7/2016 < 1 day 118/70 118 purulant ileaL Perforation 16 primary closure cured

95 17534 ramu 26 yrs M 19/7/2016 < 1 day 112/70 84 clear duodenal perforation 10 Grahms patch cured

96 18020 das 54 yrs M 24/7/2016 2 days 100/70 110 faecal LRTI ileaL Perforation 31 primary closure cured

97 18102 selvi 45 yrs F 8/8/2016 < 1 day 130/76 108 purulant YES LRTI gastric perforation 30 Grahms patch cured

98 18798 sardar pasha 70 yrs M 12/8/2016 6 days 84/60 140 purulant SSI YES YES pulmonary aspiration YES duodenal perforation 32 Grahms patch DIED

99 19106 nirmala 40 yrs F 25/08/2016 3 days 102/70 110 purulant SSI LRTI appendicular perforation 25 appendectomy cured

100 19302 nithin 24 yrs M 29/08/2016 < 1 day 114/70 94 clear duodenal perforation 10 Grahms patch cured