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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
9
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
10
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
13
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 .
14
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.
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
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.
24
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.
28
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.
31
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
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.
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.
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
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.
78
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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
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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
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