Ministry of Health of the Republic of Moldova [601736]

Ministry of Health of the Republic of Moldova
state Medical and Pharmaceutical University
“nicolae Testemitanu”
Faculty Of Medicine Nr.2
The Department of pediatric surgery
DIPLOMA THESIS
Secondry periotonitis in Children
Name and surname of the student: [anonimizat]
6th year ,group 1637

conductor:
Dr.Grosu lidia

Table of content:
INTRODUCTION
Actuality of the theme………………..……………….………………………………………4
Goal of research …………………………………………………………..…………………5
CHAPTER I: LITERATURE REVIEW
1.1 Etiology………………………………..………………………………………….…………….6
1.2 Physiopathology………………………………..………………………………………………7
1.3 classification………………………………..……………………….………………………..11
1.5 Anatomy………………………………..………………………….………………………….12
1.6 Signs\symptoms:……………………………….…………………..…………………..……17
1.6.1 physical examination………….………………………….………………………….17
1.7 Risk factors …………………………………..…………………….………………………..18
1.8 Management………………………………..……………………….………………….……19
1.9 Differential diagnosis…………………………………………………….………..………….20
1.10Test\Diagnosis………………………………..…………………….……………………….21
1.11 Complications………………………………..…………………….……………………….22
1.12 Treatment of secondary peritonitis………………………….………………………23
1.12.1 Antibiotic therapy …………………………..………………….……………………23
1.12.2 Surgical treatment:…………………………………………….……………………24
1.12.2.1 preoperative preparation…………………………………….…………………..24
1.12.2.2 postoperative care…………………………………………….………………….25
1.12.3 nutrition and dietary supplements…………………………………………………25
CHAPTER II: Materials and research methods
●Materials and research methods………………………………………………………………….. ..26
●Result……………………………………………………………………………………………..28
CHAPTER III: clinical case
●clinical case……………………………………………………………………………..29

Chapter IV Own results and discussion
●General Conclusion……………………………………………………………….,…..35
●Summary…………………………………………………………………………………36
●BIBLIOGRAPHY………………………………………………………………………..,37

&secondary peritonitis in children&

Introduction:
Actuality of the theme:
Peritonitis is defined as an inflammation of the serosal membrane that lines the
abdominal cavity and the organs contained therein. The peritoneum, which is an
otherwise sterile environment, reacts to various pathologic stimuli with a fairly uniform
inflammatory response. Depending on the underlying pathology, the resultant peritonitis
may be infectious or sterile (ie, chemica l or mechanical). Intra-abdominal sepsis is an
inflammation of the peritoneum caused by pathogenic microorganisms and their
products.[1] The inflammatory process may be localized (abscess) or diffuse in
nature.Intraperitoneal infection known as peritonitis is a major killer in the practice of
clinical surgery and it is also one of the most frequent diagnoses in a surgical intensive
care unit (ICU) leading to severe sepsis.
The more common type of peritonitis, called secondary peritonitis, happens when the
infection comes into the peritoneum through a perforation in the abdominal wall.
Secondary peritonitis is usually due to spillage of gastrointestinal or genitourinary
microorganisms into the peritoneal cavity as a result of loss of integrity of the mucosal
barrier. It is the most frequent form of peritonitis, and is the consequence of a local
infectious process within the abdominal cavity, with hollow viscous perforation, and can
lead to diffuse peritonitis. It requires timely surgical treatment with appropriate
antimicrobial therapy.
Secondary peritonitis is the most common entity in critical surgical patients and is
defined as an infection of the peritoneal cavity resulting from hollow viscus
perforation, anastomotic leak, ischemic necrosis, or other injuries of the
gastrointestinal tract. An exploratory laparotomy may be warranted to achieve
surgical control of the source of infectious focus and reduction of the bacterial load.

Goals and Objectives :
(1)To find out the etiology of secondary peritonitis .
(2) To find out a prophylactic way from secondary peritonitis .
(3) To distinguish some modern methods of treatment of secondary peritonitis .
Etiology:
●secondary to appendicitis
●perforation of meckel's diverticulum
●gastric ulcer perforation
●pancreatitis
●Traumatic perforation of the intestine
●Intussusception
●neutropenic colitis (typhlitis)
●Crohn disease with fistula and abscess formation
●Toxic megacolon
●Tuberculosis
●salpingitis
●staph aureus
●coag neg staph (s.Epidermidis)
●E.coli
●Pseudomonas
●Stenotrophomonas
●candida
●Atypical

Pathophysiology:
In peritonitis caused by bacteria, the physiologic response is determined by several
factors,
including the virulence of the contaminant, the size of the inoculum, the immune status
and overall health of the host (eg, as indicated by the Acute Physiology and Chronic
Health Evaluation II APACHE II] score), and elements of the local environment, such as
necrotic tissue, blood, or bile.[2]
Intra-abdominal seps is from a perforated viscus (ie, secondary peritonitis or suppurative
peritonitis) results from direct spillage of luminal contents into the peritoneum (eg,
perforated peptic ulcer, diverticulitis, appendicitis, iatrogenic perforation). With the
spillage of the contents, gram-negative and anaerobic bacteria, including common gut
flora, such as Escherichia coli and Klebsiella pneumoniae , enter the peritoneal cavity.
Endotoxins produced by gram-negative bacteria lead to the release of cytokines that
induce cellular and humoral cascades, resulting in cellular damage, septic shock, and
multiple organ dysfunction syndrome (MODS).
The mechanism for bacterial inoculation of ascites has been the subject of much debate
since Harold Conn first recognized it in the 1960s. Enteric organisms have traditionally
been isolated from more than 90% of infected ascites fluid in spontaneous bacterial
peritonitis (SBP), suggesting that the GI tract is the source of bacterial contamination.
The preponderance of enteric organisms, in combination with the presence of endotoxin
in ascitic fluid and blood, once favored the argument that SBP was due to direct
transmural migration of bacteria from an intestinal or hollow organ lumen, a
phenomenon called bacterial translocation. However, experimental evidence suggests
that direct transmural migration of microorganisms might not be the cause of SBP.
An alternative proposed mechanism for bacterial inoculation of ascites suggests a
hematogenous source of the infecting organism in combination with an impaired
immune defense system.
Nonetheless, the exact mechanism of bacterial displacement from the GI tract into
ascites fluid remains the source of much debate.
A host of factors contributes to the formation of peritoneal inflammation and bacterial
growth in the ascitic fluid.
A key predisposing factor may be the intestinal bacterial overgrowth found in people

with cirrhosis, mainly attributed to decreased intestinal transit time. Intestinal bacterial
overgrowth, along with impaired phagocytic function, low serum and ascites
complement levels, and decreased activity of the reticuloendothelial system, contributes
to an increased number of microorganisms and decreased capacity to clear them from
the bloodstream, resulting in their migration into and eventual proliferation within ascites
fluid.
Interestingly, adults with SBP typically have ascites, but most children with SBP do not
have ascites. The reason for and mechanism behind this is the source of ongoing
investigation.
Fibrinolysis
Alterations in fibrinolysis (through increased plasminogen activator inhibitor activity) and
the production of fibrin exudates have an important role in peritonitis. The production of
fibrin exudates is an important part of the host defense, but large numbers of bacteria
may be sequestered within the fibrin matrix. This may retard systemic dissemination of
intraperitoneal infection and may decrease early mortality rates from sepsis, but it also
is integral to the development of residual infection and abscess formation. As the fibrin
matrix matures, the bacteria within are protected from host clearance mechanisms.
Whether fibrin ultimately results in containment or persistent infection may depend on
the degree of peritoneal bacterial contamination. In animal studies of mixed bacterial
peritonitis that examined the effects of systemic defibrinogenation and those of
abdominal fibrin therapy, heavy peritoneal contamination uniformly led to severe
peritonitis with early death (< 48 h) because of overwhelming sepsis.
Bacterial load
Bacterial load and the nature of the pathogen also play important roles. Some studies
suggest that the number of bacteria present at the onset of abdominal infections is
much higher than originally believed (approximately 2 × 108 CFU/mL, much high er than
the 5 × 105 CFU/mL inocula routinely used for in vitro susceptibility testing). This
bacterial load may overwhelm the local host defense.
Bacterial virulence
Bacterial virulence factors [3] that interfere with phagocytosis and with neutrophil-
mediated bacterial killing mediate the persistence of infections and abscess formation.
Among these virulence factors
are capsule formation, facultative anaerobic growth, adhesion capabilities, and succinic
acid production. Synergy between cert ain bacterial and fungal organisms may also play

an important role in impairing the host's defense. One such synergy may exist between
Bacteroides fragilis and gram-negative bacteria, particularly E coli (see the image
below) ,where co-inoculation signific antly
increases bacterial proliferation and abscess formation.
Gram-negative Escherichia coli.
Enterococci
Enterococci may be important in enhancing the severity and persistence of peritoneal
infections. In animal models of peritonitis with E coli and B fragilis, the systemic
manifestations of the peritoneal infection and bacteremia rates were increased, as were
bacterial concentrations in the peritoneal fluid and rate of abscess formation.
Nevertheless, the role of Enterococcus organisms in uncomp licated intra-abdominal
infections remains unclear. Antibiotics that lack specific activity against Enterococcus
are often used successfully in the therapy of peritonitis, and the organism is not often
recovered as a blood-borne pathogen in intra-abdominal sepsis.
Fungi
The role of fungi in the formation of intra-abdominal abscesses is not fully understood.
Some authors suggest that bacteria and fungi exist as nonsynergistic parallel infections
with incomplete competition, allowing the survival of all organisms. In this setting,
treatment of the bacterial infection alone may lead to an overgrowth of fungi, which may
contribute to increased morbidity.
Abscess formation
Abscess formation occurs when the host defense is unable to eliminate the infecting
agent and attempts to control the spread of this agent by compartmentalization. This
process is aided by a combination of factors that share a common feature, ie,
impairment of phagocytotic killing. Most animal and human studies suggest that
abscess formation occurs only in the presence of abscess-potentiating agents. Although

the nature and spectrum of these factors have not been studied exhaustively, certain
fiber analogues (eg, bran) and the contents of autoclaved stool have been identified as
abscess-potentiating agents. In animal models, these factors inhibit opsonization and
phagocytotic killing by interference with complement activation.
Cytokines
The role of cytokines in the mediation of the body's immune response and their role in
the development of the systemic inflammatory response syndrome (SIRS) and multiple
organ failure (MOF) have been a major focus of research over the past decade.
Comparatively few data exist about the magnitude of the intraperitoneal/abscess
cytokine response and implications for the host.
Existing data suggest that bacterial peritonitis is associated with an immense
intraperitoneal compartmentalized cytokine response. Higher levels of certain cytokines
(ie, tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]-6) have been associated
with worse outcomes, as well as secondary (uncontrolled) activation of the systemic
inflammatory cascade.
Classification:
(1) Early or diffuse
(2) Late or localized
(3) Acute
(4) subacute
(5) chronic

Anatomy:
The peritoneum is the largest and most complex serous membrane in the body. It forms
a closed sac (ie, coelom) by lining the interior surfaces of the abdominal wall (anterior
and lateral), by forming the boundary to the retroperitoneum (posterior), by covering the
extraperitoneal structures in the pelvis (inferior), and by covering the undersurface of
the diaphragm (superior). This parietal layer of the peritoneum reflects onto the
abdominal visceral organs to form the visceral peritoneum. It thereby creates a potential
space between the 2 layers (ie, the peritoneal cavity).
The peritoneum consists of a single layer of flattened mesothelial cells over loose
areolar tissue. The loose connective tissue layer contains a rich network of vascular and
lymphatic capillaries, nerve endings, and immune-competent cells, particularly
lymphocytes and macrophages. The peritoneal surface cells are joined by junctional
complexes, thus forming a dialyzing membrane that allows passage of fluid and certain
small solutes. Pinocytotic activity of the mesothelial cells and phagocytosis by
macrophages allow for the clearance of macromolecules.
Normally, the amount of peritoneal fluid present is less than 50 mL, and only small
volumes are transferred across the considerable surface area in a steady state each
day. The peritoneal fluid represents a plasma ultrafiltrate, with electrolyte and solute
concentrations similar to that of neighboring interstitial spaces and a protein content of
less than 30 g/L, mainly albumin. In addition, peritoneal fluid contains small numbers of
desquamated mesothelial cells and various numbers and morphologies of migrating
immune cells (reference range is < 300 cells/μ L, predominantly of mononuclear
morphology).
The peritoneal cavity is divided incompletely into compartments by the mesenteric
attachments and secondary retroperitonealization of certain visceral organs. A large
peritoneal fold, the greater omentum, extends from the greater curvature of the stomach
and the inferior aspect of the proximal duodenum downward over a variable distance to
fold upon itself (with fusion of the adjacent layers) and ascends back to the taenia
omentalis of the transverse colon. This peritoneal fold demonstrates a slightly different
microscopic anatomy, with fenestrated surface epithelium and a large number of
adipocytes, lymphocytes, and macrophages, and it functions as a fat storage location
and a mobile immune organ.
The compartmentalization of the peritoneal cavity, in conjunction with the greater
omentum, influences the localization and spread of peritoneal inflammation and
infections.

*fig 1:Anatomy of the abdomin organs

*fig 2:The peritoneum is the membrane lining the abdominal cavity.

*fig 3: Peritonitis is an infection resulting i n inflammation of the peritoneum, which is a
thin membrane that lines the inside of the abdominal wall and the organs within the
abdominal cavity.

*fig 4: Inflammation of the peritoneum is usually due to perforation of a viscus contents into the abdominal
cavity (eg, stomach, intestines, gallbladder, appendix), with discharge of its contents into the peritoneal cavity.

Signs and Symptoms:
●Dependent on stage, age, and etiology
●Fever, chills, vomiting
●Generalized abdominal pain with rebound tenderness
●Decreased bowel sounds
●In SBP, ~10% of cases are entirely asymptomatic.
●Other less common findings include:
○Hypothermia
○Hypotension
○Diarrhea
○Increased ascites despite diuretics
○Worsening encephalopathy
○Unexplained decrease in renal function
(I)Physical Exam:
●Swollen rigid and painful abdomen

●Decreased bowel sounds
●Evidence of chronic liver disease
●Evidence of ascites
.
Risk Factors:
●Appendicitis (inflammation of the appendix)
●Stomach ulcers
●Torn or twisted intestine
●Pancreatitis
●Inflammatory bowel disease, such as Crohn's disease or ulcerative colitis
●Injury caused by an operation
●Peritoneal dialysis
●Trauma

Peritonitis Management:
Broad spectrum coverage Vancomycin (2.5g if more than 60kg / 2 g if 60kg or less)
Gentamicin (200mg if more than 60kg / 140mg if 60kg or less) IP is better than IV
Await culture.
If gram positive, then repeat the vanc dose in 1 week. If gram negative then usually
ceftriaxone 1g intraperitoneally daily for 14 days Things to note; if pseudomonas tube is
very often lost. May need to consider adding a second antibiotic such as daily
ciprofloxacin Initial symptoms may include; diarrhoea, vomiting, nausea, abdominal
pain, mental confusion or feeling unwell PERITONITIS MANAGEMENT

Differntial diagnosis:

●Appendicitis
●Constipation
●Diabetic ketoacidosis
●Familial Mediterranean fever
●Fecal impactions (constipation)
●Herpe s zoster (shingles)
●Lead poisoning
●Perforated ulcer
●Porphyria
●Sickle cell anemia
●Systemic lupus erythematosus (SLE)
●Tabes dorsalis
●Uremia

Tests\Diagnosis:
Diagnostic Procedures/Surgery
●Leucocytosis, increased C-reactive protein (CRP), leucopenia, and
thrombocytopenia are also possible.
●Diagnosis may be confirmed with paracentesis. To improve culture yield,
culture bottles should be inoculated immediately at the bedside in large-
volume blood culture bottles.
●Elevated PMN count in ascitic fluid is important in the early diagnosis of
SBP and is considered the most important laboratory indicator of SBP:
○Diagnostic criteria for SBP include PMN leukocyte counts of
>250/mm3 in ascitic fluid culture usually positive for a single
organism.
○Diagnostic criteria for secondary bacterial peritonitis include
ascitic fluid culture positive for polymicrobial infection, total
protein >1 g/dL, glucose <50 mg/dL, and lactate
dehydrogenase (LDH) level >225 mU/mL.
○Ultrasound, abdominal radiography, and CT scan may reveal
fluid, thickening of bowel wall, abscesses, and a
pneumoperitoneum.
●LFTs, amylase and lipase – particularly if pancreatitis is suspected.
●Blood cultures – aerobic and anaerobic to exclude blood sepsis.
●Peritoneal fluid – for culture and amylase level.
●Urinalysis – to exclude renal tract pathology.
●Imaging – this may include straight abdominal X-ray, upright CXR, MRI and contrast
studies.

Complications:
●Hypovolemia results from extravasation of fluid from the inflamed peritoneal
membrane. Intravascular volume must be supported with crystalloids and
blood products.
●Respiration may be impaired via mechanical mechanisms through
diaphragmatic spasm and reflex abdominal rigidity and through increased
permeability of the pulmonary vasculature in response to systemic
inflammation.
●Long term complications include adhesions.
● an abscess (a collection of pus).
● gangrenous bowel (dead bowel tissue)

Treatment:
(1) Antibiotic therapy:
Antibiotics most commonly used for treatment of sepsis have insufficient activity to
eliminate pathogens that commonly cause surgical sepsis. Regimens with little or no
activity against facultative gram-negative rods or anaerobic gram-negative rods are not
considered acceptable. Acceptable antimicrobial regimens are carbapenems and newer
chinolones (e.g., Imipenem-cilastin) or combinations, e.g., antianaerobes plus
aminoglycoside, antianaerobes plus third generation cephalosporins or chinolones, or
clindamycin plus monobactam. Community-acquired infections of mild to moderate
severity can be treated with Cefoxitin, Cefotetan, Cefmetazole, Ticarcillin-clavulanic
acid. Routine culture of the sites of infection seems worthwhile and empirical therapy
should be as comprehensive as possible and should cover all potential pathogens.
Conditions that do not require prolonged antibiotic therapy are early acute appendicitis,
acute suppurative appendicitis, simple acute cholecystitis, simple dead bowel,
gastroduodenal ulcer perforation, traumatic enteric perforations. Antibiotics are routinely
given for 5–7 days for generalized peritonitis. Antimicrobial agents should be continued
until temperature and white blood cell count are within normal limits. Duration of
antimicrobial therapy in postoperative peritonitis should not be longer than 7 days.

Persistent clinical signs of fever or leukocytosis should prompt a search for a drainable
focus of infection in the abdomen or treatable site elsewhere. (Grade A, B and C)
(2) Surgical Treatment:
The decision on the recommended procedure depends on the grading of the intra-
abdominal infection: contamination, infection or sepsis.In cases of contamination
(example: nonperforated appendicitis without pus in the abdominal cavity seen early),
treatment consists of appendectomy and lavage. Antibiotic therapy may not be
necessary. In the case of infection (example: acute perforation of appendicitis with local
pus and inflammation), treatment consists of the resection of the bowel plus intra-
abdominal lavage and closure of the abdomen. In case of sepsis (example: perforated
diverticulitis of the sigma accompanied by local and systemic infection) treatment
includes source control, lavage and a short course of antibiotics (< 5 days).
In most cases of intra-abdominal infections the basic operative procedure is the
Relaparotomy on demand which encompasses control of the infectious focus and
intra-abdominal lavage. Close postoperative monitoring of the patient and laparoto it
organ dysfunction or signs of sepsis indicate persistent abdominal infection follows
immediate Closure of the abdomen During the operation the infectious source is closed
(sutured), or resected, or exteriorized and irrigation or mechanical cleansing clear
remaining bacteria and adjuvants, e.g., blood. demonstrates the surgical management
of source control in laparotomy on demand.
(I)Preoperative preparation:

A nasogastric tube is inserted to deflate the stomach and bowels and to prevent
vomiting during induction of anesthesia.Intravenous fluids as saline or ringer solution
are administered to correct the hypovolemia.
Antibiotics: a combination of ampicillin, an aminoglycoside and metroniazol can cover
all aerobic and anaerobic organisms.
Analgesics are given for pain relieve.Foley catheter is inserted to check the urine
output and the adequacy of fluid replacement.
(II)Post operative care:
Continuous antibiotic treatment. Drains are inserted during the surgical procedure, and
the nurse must observe and record the character of the drainage postoperatively.
Care must be taken when moving and turning the patient to prevent the drains
from being dislodged.Prepare the patient and family for discharge by teaching him to
care for the incision and drains if he will be sent home with the drains.
(3) Nutrition and Dietary Supplements
These good nutrition habits may help you recover from any serious illness:
●Eat antioxidant foods, including fruits (such as blueberries, cherries, and tomatoes)
and vegetables (such as squash and bell peppers).
●Eat foods high in B-vitamins and calcium, such as almonds, beans, whole grains (if
no allergy), dark leafy greens (such as spinach and kale), and sea vegetables.

●Avoid refined foods, such as white breads, pastas, and especially sugar.
●Eat fewer red meats and more lean meats, cold-water fish, tofu, or beans for
protein.
●Use healthy oils in foods, such as olive oil or vegetable oil.
●Avoid caffeine, alcohol, and tobacco.
●Drink 6 – 8 glasses of filtered water daily.
●Ask your doctor about taking a multivitamin daily, containing the antioxidant
vitamins A, C, E, the B-complex vitamins, and trace minerals such as
magnesium, calcium, zinc, and selenium.
●Probiotic supplement (containing Lactobacillus acidophilus among other
species), 5 – 10 billion CFUs (colony forming units) a day, for gastrointestinal and
immune health. Probiotics can help when you are taking antibiotics, because
they can help restore the balance of "good" bacteria in the intestines. People with
autoimmune diseases, such as lupus or rheumatoid arthritis, or people with weakened
immune systems should ask their doctor before taking probiotics.
Material and methods:
This is a randomized, controlled clinical study., Fifty cases of secondary peritonitis
were studied, which were treated in various surgical units, between January 2013 and
November 2014. Typically the patient was admitted to the emergency room because
of abdominal pain and a systemic infl ammatory response. Initially, the diagnosis of
intra-abdominal infection was based on the symptoms and clinical findings on
presentation. Then all cases were subjected to detailed clinical examination and
laboratory and radiological investigations as descr ibed below. After the patient was
admitted to the hospital, a detailed history of the patient was taken and the signs and

symptoms were recorded along with a variety of information such as: pain – time of
onset of pain, mode of onset of pain, site of pain, character of pain; vomiting –
vomiting in relation to pain, frequency of vomiting, amount, colour and content; bowels
– last evacuation, constipated/normal, dysentery; distention – duration, location,
relation to pain; whether accompanied by Borborygmi. I n addition, previous personal
and family history of the patient was also recorded. A thorough physical examination
was done with special emphasis on the abdomen. A local examination including
contour of the abdomen, movement with respiration, visible peris talsis, umbilicus, and
hernial orifices was recorded. In addition, palpation (temperature, tenderness,
muscular rigidity, mass, abdominal girth), percussion (obliteration of liver dullness,
shifting dullness) and auscultation (bowel sounds: frequency, char acter) were also
recorded. Laboratory investigations including blood, urine and stool were also done for
each patient. Total count and differential counts were performed. Radiological
examination was conducted in all cases to detect pneumoperitoneum. A pla in X-ray of
the abdomen in the erect posture was taken to detect the presence of gas under the
dome of the diaphragm. Ulcer edge biopsy was taken from cases of peptic and non-
specific ileal perforations and then subjected to histopathological examination. In
operated cases, culture and sensitivity test was carried out with peritoneal exudate to
identify the presence of various microbial organisms and detect their sensitivity to the
antibiotics. The pre-operative preparation essentially consisted of correcti on of
dehydration, overcoming shock if it was present, gastric aspiration, parental broad-
spectrum antibiotic coverage and tetanus prophylaxis. The treatment to be adopted in
each case was decided based on the status, necessity and health condition of the
patient. In 76% of cases, surgery was undertaken within 3 to 6 hours after their
admission to the hospital. Depending upon the cases, right upper paramedian, upper
midline or right lower paramedian incisions were made. For the cases of suspected
small bowel perforations, right mid paramedian incisions were made and later they
were extended either upwards or downwards depending upon the need. Postoperative
fluid and electrolyte balance was maintained by input and output charts and adequacy
of replacement was judged mainly on the basis of clinical features. In most cases,
antibiotics started pre-operatively were continued and changed to suitable antibiotics

after the sensitivity of the organisms was known. In the majority of cases,
postoperative management inc luded injection of I.V. fluids, oral fluids, blood
transfusion and the removal of drains. The drainage tubes were removed on the 3rd
and 4th postoperative day and gastric aspiration was discontinued as soon as the
patient passed flatus. Postoperative compl ications were studied in the immediate
follow-up period. Late follow-up of these patients was only considered fair, as the
majority of them did not return for the check-up. The data collected in this study were
analyzed either using descriptive statistics or by chi-squared test/Student’s t-test,
whichever was appropriate.
Results:
Among 50 surgically proven perforative peritonitis patients, 90% (45) of them were
males and 10% (5) of them were females. Males were significantly (p<0.001) affected
with a male to female ratio of 9:1. The mean age of patients was with a range
between 16-18 years. 64% (32 patients) of patients had peptic ulcer perforations, 12%
(6) had non-specific ileal perforations, 12% (6) had enteric ileal perforation and the
remaining 12% (6) had appendicular perforations. The incidence of secondary
peritonitis was statistically different across different age groups (p<0.001). The highest
incidence of secondary peritonitis (32%) was observed in the age group 5 to 11 years,
followed by 12 to 18 years (26%) . Table I depicts the previous history of peritonitis
patients. Of the 32 cases of perforated peptic ulcer, 19 had a previous history of pain
in the abdomen lasting from 6 months to 15 years, 1 patient had a history of fever and

12 of them had no history of pain. In the case of appendicular perforations, 2 patients
had a previous history of pain in the abdomen, 2 had a history of fever and 2 of them
had no history. History of fever was present in all 6 cases of enteric ileal perforations.
Previous history of fever was present in 5 cases of non-specific ileal perforations.
describes the analysis of symptoms and signs. Table II gives elaborate information on
the patients’ characteristics, in terms of specific symptoms and signs exhibited, among
four commonly occurring perforations. All patients exhibited symptoms of pain,
distension of abdomen, tenderness and rigidity (p<0.001). The majority of subjects had
diminished bowel sounds (80%) and vomiting (64%), and liver dullness was obliterated
in 72% of subjects. Fever and shifting dullness were observed in half of the cases and
diarrhoea (4%) was rarely recorded. A plain X-ray of the abdomen in the erect posture
indicated that 72% of cases had gas under the diaphragm. 81% of the cases who
were diagnosed with peptic ulcer perforations had gas under the diaphragm, while
only 16% of the cases who were diagnosed with appendicular perforations had gas
under the diaphragm.
CASE REPORT:
{Secondary Peritonitis Caused by Streptomyces viridis}
A 16-year-old male presented to the medical emergency room with complaints of fever,
abdominal distension, and pain in the abdomen for 7 days.. There was no history of
melaena or hematemesis. There was also no history of any headache, rhinorrhea, sore
throat, cough, dysuria, or bowel complaints. The patient gave a history of multiple
paracenteses, done outside our hospital, for management of abdominal distension.

On examination, the patient was febrile (38°C) and was in mild distress due to dyspnea
and abdominal pain. His sclerae of both sides were icteric. On palpation, his abdomen
was firm, distended, and diffusely tender. The rest of the systemic examination was
within normal limits.
On admission, the peripheral leukocyte count was 17,000/mm3, with 84% neutrophils
and 12% lymphocytes. The platelet count was adequate. The serum creatinine level
was 1.5 mg/dl, and the sodium level was 135 mmol/liter. The total bilirubin level was
elevated, at 4.4 mg/dl, as were the alanine aminotransferase and aspartate
transaminase levels (93 and 105 U/liter, respectively) and the international normalized
ratio (1.1). The test for HIV was nonreactive. Upper gastrointestinal (GI) endoscopy
revealed grade II esophageal varices, and ultrasonography of the abdomen showed
signs of chronic liver disease with gross ascites. To rule out any infectious cause,
specimens of blood and ascitic fluid were submitted for culture before the patient was
started on ceftriaxone.
Ascitic fluid collected was pale yellow and turbid in appearance. It showed a white blood

cell count of 5,600/mm3, with a differential count of 80% neutrophils and 20%
lymphocytes. Gram staining showed the presence of pus cells with long, filamentous,
extensively branched, Gram-positive structures. Aerobic culture on blood agar showed
a significant number of large, folded, glabrous colonies with an earthy odor. Gram
staining from blood agar showed Gram-positive, branching, filamentous bacilli. Partial
acid-fast staining was negative. Based on culture characteristics, Gram staining, and
acid-fast staining, the isolate was presumptively identified as belonging to a
Streptomyces species and was sent to the Department of Medical Microbiology and
Infectious Diseases, for sequencing and final identification. 16S rRNA gene PCR
amplification was performed using the primers EUB-L
(5′-CTTTACGCCCATTTAATCCG-3′) and EUB-R (5′-AGAGTTTGATCCTGGTTCAG-3′)
(17). This amplified only about 600 bp of the 16S rRNA gene, not the whole gene. A
total of 480 bp of this product was analyzed, and the isolate was identified as
Streptomyces viridis . The sequence homology was 99%; only 1 bp differed from the
reference sequence in GenBank (accession number AB184361.2).

Based on the CLSI microdilution and breakpoint guidelines for nocardiae and other
aerobic actinomycetes, the isolate was susceptible to trimethoprim-sulfamethoxazole,
ceftriaxone, imipenem, erythromycin, tetracycline, amikacin, and clarithromycin but was
resistant to penicillin ( 3). All anaerobic, fungal, and mycobacterial cultures of as citic fluid
were negative. The blood culture was also found to be negative.
The patient was started on intravenous ceftriaxone at 1 g every 12 hours. A proton
pump inhibitor, diuretics, and lactulose were also given to alleviate the symptoms. After
4 weeks of treatment with ceftriaxone, the patient became afebrile, and a repeat culture
was negative. The patient was discharged and was advised to take oral
trimethoprim-sulfamethoxazole (double strength three times a day [TID]) for 5 months.
The patient's clinical condition improved, and treatment for his liver disease was
continued.
The aerobic actinomycetes consist of a large, diverse group of obligate aerobic and
relatively slow-growing Gram-positive bacilli with a tendency to form chains or filaments.
They are found as saprophytes in soil and other natural habitats. These organisms are

categorized on the basis of their acid fastness: Nocardia andRhodococcus species are
weakly acid fast, while Streptomyces and Actinomaduraspecies are non-acid fast (11).
Mycetoma, the most common manifestation of Streptomyces infection, usually involves
the subcutaneous tissue of legs and feet and occurs due to the direct inoculation of the
microorganism through an injury caused by a thorn ( 5). InvasiveStreptomyces
infections, defined as infections other than mycetoma or superficial skin infections, are
extremely rare. These infections occur most often in immunocompromised patients such
as those with HIV infection and those on immunosuppressive drugs such as
corticosteroids and anticancer drugs ( 11).
The clinical significance of recovering these organisms is often unclear, as there have
been many reports of isolation of Streptomyces species without definitive proof of their
pathogenic role. Therefore, the role of Streptomyces species in visceral infections has
been controversial, particularly in a polymicrobial setting ( 4). Diagnosis of invasive
Streptomyces infection is made by clinical (i.e., immune status of the patient and

infection other than superficial skin infection) and microbiological correlation. Isolation of
the organism in pure culture and from a sterile site, direct examination of infected tissue
(by Gram staining or biopsy), and exclusion of any other pathogen will confirm true
cases caused by Streptomycesspecies. Earlier identification to the species level was
based on morphological features and rapid enzyme tests of fluorophores .Currently,
16S rRNA gene sequencing is considered the best method for species identification .
To identify all cases of invasive infection due to Streptomyces, we performed a
search and also reviewed the references from previous publications on Streptomyces
infection. Only those cases which represented true invasive infections were included
(using the criteria given above). A total of 23 reports of Streptomyces species causing
infection other than mycetoma have been documented to date.
The majority of invasive Streptomyces infections were bacteremia and lung infections
(pneumonia, abscess, and pneumonitis) All of the species identified have been
different, showing the opportunistic potential of this pathogen. Most of the patients had
some underlying immunosuppressive condition, such as HIV infection, cancer, systemic

lupus erythematosus (SLE), Cr ohn's disease, etc. S. pelletieri, S. griseus, S. lanatus,
and S. albus have been isolated from various patients with lung pathology
The present case was unusual, as only one case of Streptomyces peritonitis, caused by
S. somaliensis and with no underl ying condition reported, has been described
previously . The patient we describe here represents the first reported case of
secondary peritonitis caused by S. viridis in a patient with gross ascites. The
Streptomyces isolate was considered the primary pathogen because it was seen on the
direct smear and isolated in pure form on culture media. Also unique to this case is the
likely mechanism by which this infection occurred. Most cases of secondary peritonitis
are caused by bacteria which arrive in the peritoneal cavity from a gut source, most
often due to rupture of abdominal viscera. In contrast, for our patient the likely source of
peritoneal infection was direct inoculation into the peritoneal cavity during paracentesis.
Streptomyces species rarely cause atypical visceral infections. Mossad et al. reported

an atypical case of Streptomyces endocarditis in a patient with a prosthetic heart valve
. S. griseus was isolated from a patient with a brain abscess by Clarke et al. .
Rose et al. also discussed a case of brain abscess caused by Streptomyces infection
following penetration trauma .
Based on various in vitro results, the best treatment options for visc eralStreptomyces
infection include macrolides, minocycline, doxycycline, ceftriaxone, amikacin, and
imipenem. Cotrimoxazole is not the drug of choice for treating invasive Streptomyces
infection, in contrast to the treatment of nocardiosis . A variety of antimicrobial regimens
were used in the previously reported cases, and in most cases the outcome was good,
with resolution of infection. However, the optimal choice of antimicrobial agent and
duration of therapy for treating Streptomyces visceral infections remain to be determined

Conclusions:
The present case was unusual, as only one case of Streptomyces peritonitis, caused by
S. somaliensis and with no underlying condition reported, has been described

previously . The patient we describe here represents the first reported case of
secondary peritonitis caused by S. viridis in a patient with gross ascites. The
Streptomyces isolate was considered the primary pathogen because it was seen on the
direct smear and isolated in pure form on culture media. Also unique to this case is the
likely mechanism by which this infection occurred. Most cases of secondary peritonitis
are caused by bacteria which arrive in the peritoneal cavity from a gut source, most
often due to rupture of abdominal viscera. In contrast, for our patient the likely source of
peritoneal infection was direct inoculation into the peritoneal cavity during paracentesis.
-Though Streptomyces species are not commonly recovered from clinical
specimens,these organisms can cause invasive infections.
The present case illustrates the potential of Streptomyces spp. to cause invasive
infection.

SUMMARY:
Despite improved diagnostic modalities, potent antibiotics, modern intensive care, and
aggressive surgical treatment, up to one third of patients still die of severe secondary
peritonitis. Against the background of current understanding of the local and systemic
inflammatory response associated with peritonitis, there is growing controversy
concerning the optimal antibiotic and operative therapy, intensified by lack of properly
conducted randomized studies. In this overview the authors attempt to outline
controversies, suggest a practical clinical approach, and highlight issues necessitating
further research.

References:
1.G. Soriano, J. Castellote, C. Alvarez, et al., “Secondary bacterial peritonitis in
cirrhosis: a retrospective study of clinical and analytical characteristics,
diagnosis and management,” Journal of Hepatology, vol. 52, no. 1, pp. 39–
44, 2010. View at Publisher · View at Google Scholar · View at PubMed
2.J. Such and B. A. Runyon, “Spontaneous bacterial peritonitis,” Clinical
Infectious Diseases, vol. 27, no. 4, pp. 669–676, 1999.
3.S. R. Targan, A. W. Chow, and L. B. Guze, “Role of anaerobic bacteria in
spontaneous peritonitis of cirrhosis: report of two cases and review of the
literature,” American Journal of Medicine, vol. 62, no. 3, pp. 397–403, 1977.
View at Scopus
4.G. F. Woelfel and J. F. Hansbrough, “Spontaneous bacterial peritonitis and
pneumoperitoneum: a false surgical emergency,” Journal of the American
Medical Association, vol. 249, no. 7, pp. 921 –922, 1983.View at Publisher ·
View at Google Scholar · View at Scopus
5.X. Xiol, J. Castellote, C. Baliellas et al., “Spontaneous bacterial empyema in
cirrhotic patients: analysis of eleven cases,” Hepatology, vol. 11, no. 3, pp.
365–370, 1990. View at Scopus
6.T. Harris, J. Lambert, and S. Broughton, “Clostridium perfringens
spontaneous bacterial peritonitis,”Australian and New Zealand Journal of
Medicine, vol. 25, no. 4, p. 366, 1995. View at Scopus
7.P. E. Young, R. R. Dobhan, and T. W. Schafer, “Clostridium perfringens
spontaneous bacterial peritonitis: report of a case and implications for

management,” Digestive D iseases and Sciences, vol. 50, no. 6, pp. 1124–
1126, 2005. View at Publisher · View at Google Scho lar · View at Scopus
8.B. A. Runyon, H. N. Canawati, and E. A. Akriviadis, “Optimization of ascitic
fluid culture technique,”Gastroenterology, vol. 95, no. 5, pp. 1351–1355,
1988. View at Scopus
9.E. A. Akriviadis and B. A. Runyon, “Utility of an algorithm in differentiating
spontaneous from secondary bacterial peritonitis,” Gastroenterology, vol.
98, no. 1, pp. 127–133, 1990. View at Scopus
10.B. A. Runyon, “Patients with deficient ascitic fluid opsonic activity are
predisposed to spontaneous bacterial peritonitis,” Hepatology, vol. 8, no. 3,
pp. 632–635, 1988. View at Scopus
11.Jhobta RS, Attri AK, Kaushik R, Sharma R, Jhobta A: Spectrum of
perforation peritonitis in India-review of 504 consecutive cases.
12.World J Emerg Surg 2006, 1:26. PubMed Abstract | BioMed Central Full Text
|PubMed Central Full Text
13.Wani RA, Parray FQ, Bhat NA, Wani MA, Bhat TH, Farzana F: Nontraumatic
terminal ileal perforation.
14.World J Emerg Surg 2006, 1:7. PubMed Abstract | BioMed Central Full Text |
Pu bMed Central Full Text
15.Kaur N, Gupta MK, Minocha VR: Early enteral feeding by nasoenteric tubes
in patients with perforation peritonitis.
16.World J Surg 2005, 29(8):1023-1027.

17.discussion 7-8
18.PubMed Abstr act | Publisher Full Text
19.Conroy JV: Acute ileitis with ulceration and perforation due to paratyphoid
fever; report of eighty-five cases.
20.Mil Med 1957, 120(2):79-92. PubMed Abstract
21.Qureshi AM, Zafar A, Saeed K, Quddus A: Predictive power of Mannheim
Peritonitis Index.
22.J Coll Physicians Surg Pak 2005, 15(11):693-696. PubMed Abstract
23.Chatterjee H, Jagdish S, Pai D, Satish N, Jayadev D, Reddy PS: Changing
trends in outcome of typhoid ileal perforations over three decades in
Pondicherry.
24.Trop Gastroenterol 2001, 22(3):155-158. PubMed Abstract
25.Chatterjee H, Pai D, Jagdish S, Satish N, Jayadev D, Srikanthreddy P:
Pattern of nontyphoid ileal perforation over three decades in Pondicherry.
26.Trop Gastroenterol 2003, 24(3):144-147. PubMed Abstract

27.Adesunkanmi AR, Ajao OG: The prognostic factors in typhoid ileal
perforation: a prospective study of 50 patients.
28.J R Coll Surg Edinb 1997, 42(6):395-399. PubMed Abstract