LECTURE 20

Acute peritonitis. Primary peritonitis (primitive)

Peritonitis is inflammation of the peritoneum and represents an important cause of surgical
morbidity and mortality.
It may be localized or generalized, and is thought to pass through three phases:
firstly, a phase of rapid removal of contaminants from the peritoneal cavity into the
systemic circulation;
secondly, a phase of synergistic interactions between aerobes and anaerobes; and
thirdly, an attempt by host defences to localize infection.
Peritonitis is commonly caused by bacteria, but can be chemical (aseptic), biliary,
tuberculous, chlamydial, druginduced or induced by other, rarer causes.
!acterial peritonitis is subclassified into primary or secondary on the basis of whether or not
the integrity of the gastrointestinal tract has been compromised. "ypically, the patient with
peritonitis complains of severe abdominal pain and may e#hibit the characteristic $ippocratic
facies.
%bdominal palpation demonstrates tenderness, guarding and rebound tenderness.
Initial laboratory investigations should include urea and electrolytes, full blood count and
blood gases.
%n erect radiograph of the chest demonstrates pneumoperitoneum in about &'()'* of
visceral perforations.
+" often plays a role in confirming specific diagnoses (e.g. subphrenic abscess).
Immediate management should include fluid resuscitation, highflow o#ygen, appropriate
antibiotics (i.v.) and analgesia.
,efinitive management is surgical e#cept for a small group of patients in whom conservative
management with fluids (i.v.) and antibiotics (i.v.) is indicated.
-urgical management can be via a laparotomy or, in some conditions, laparoscopy control of
the primary site of sepsis is the main determinant of outcome.
I. ANATO!
"he peritoneal cavity is the abdominal space bounded by:
the diaphragm superiorly,
the pelvic floor inferiorly, the retroperitoneum posteriorly,
and the anterior abdominal wall anteriorly.
It contains all the abdominal viscera e#cept those that lie in the retroperitoneum, which
include the:
second, third, and fourth portion of the duodenum,
the distal rectum,
the pancreas,
the .idneys and
ureters,
the adrenal glands, and
/
the aorta and inferior vena cava.
"he peritoneal cavity is lined with the parietal peritoneum, made of mesothelium. "he
peritoneal lining reflects to cover partially or completely the intraabdominal viscera, thus
creating the visceral peritoneum.
"he parietal peritoneum is supplied by segmental nerves that also supply the abdominal wall
directly in contact.
"he nerve supply of the visceral peritoneum, however, is the nerve supply of the viscus it
covers.
"he entire small intestine, the appendi#, ascending and right colon, and the visceral
peritoneum covering these structures are supplied by thoracic +/', which also supplies the
s.in in the preumbilical region.
$ence, pain due to distension, ischemia, or inflammation in these structures is first referred to
the periumbilical region. 0nly when the parietal peritoneum overlying the diseased bowel is
involved does the pain localize to the region where the diseased bowel is actually located.
% number of potential spaces in the peritoneal cavity can be the site of intraabdominal
abscesses.
"he colon divides the abdomen into the supra and infracolic spaces and into the right and left
paracolic gutters.
T"e supraco#ic space contains the left and right subphrenic spaces and the subhepatic space,
which is continuous with the hepatorenal space.1hen a patient is lying supine, the
hepatorenal space is the most dependent part of the peritoneal cavity. "he supracolic space
also contains the lesser sac behind the lesser omentum.
T"e in$raco#ic space is divided by the mesentery of the small intestine, whose obli2ue
attachment to the retroperitoneum e#tends from the right side of 34 to the left side of 3/,
into a right and left infracolic space. "he pelvic cavity begins at the
promontory of the sacrum.
"he rectum divides the pelvic cavity into a prerectal space anteriorly5rectovesical in
men and rectovaginal (pouch of ,ouglas) in women5and posteriorly into a retrorectal or
presacral space.
%ll of these spaces are potential sites of intraabdominal abscesses.
%bdominal abscesses may also develop between loops of small intestine, where they are
referred to as interloop abscesses.
II. P%!&IOLO'!
"he peritoneum and omentum play several roles of physiologic significance:
/. Provision o$ a sur$ace t"at a##o(s smoot" )#i*in) o$ t"e sma## intestine (it"in t"e
peritonea# cavity. "his function is aided by the presence of free fluid (6'm3 of transudate)
within the peritoneal cavity.
7. +#ui* e,c"an)e. %ppro#imately 6''m3 of fluid or more per hour may be e#changed
between the peritoneal cavity and the circulation across the peritoneum. "his remar.able
property is e#ploited in the performance of peritoneal dialysis in renal failure. In infants,
circulating blood volume may be replenished by the administration of fluid intraperitoneally.
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8. Response to tissue *ama)e or in$ection. "he mesothelial and mast cells secrete histamine
and other vasodilators in response to in9ury or infection. "his leads to vascular permeability
and the e#udation of fibrinogenrich plasma, complement, and opsonins. "ogether with the
arrival of neutrophils and macrophages, this process contributes to bacterial destruction.
4. Omenta# mi)ration. "he omentum migrates to areas of inflammation, perforation, or
ischemia. "his wellvascularized tissue attempts to isolate the pathology and also e#erts
bacteriophagic function.
6. E#imination o$ -acteria an* to,ic pro*ucts. !acteria that are not destroyed and other
to#ic products of infection are circulated to the subdiaphragmatic surfaces, particularly on the
right, and absorbed into lymphatic channels and delivered into the right thoracic duct.
:ndoubtedly, the circulation of fluid from the lower abdomen to the subdiaphragmatic space
is due to negative pressure generated in the subdiaphragmatic space with respiration.
III. PAT%OP%!&IOLO'!
"he peritoneum mounts rapid response to infection, in9ury, and lea.age into the peritoneal
cavity of digestive fluid, bile, pancreatic 9uice, urine, or blood.
"he result is vascular permeability, fluid e#udation, and both neutrophil and cyto.ine
response. Pain fibers within both the visceral and parietal peritoneum are activated. "hese
fibers are believed to be +fibers containing substance P and calcitonin generelated peptide
(+;<P).
<efle# pathways cause muscular contraction in the abdominal wall to limit movement
(guarding and rigidity). -imilarly, peristaltic movement of the intestine is arrested (hypoactive
or absent bowel sounds).
=arlier, it was indicated that vascular permeability, as a result of tissue damage or infection,
causes fibrinrich plasma to flow into the peritoneal cavity. "his leads to the formation of
fibrin, which later organizes into collagen and causes adhesion formation.
:ntreated, generalized peritonitis most commonly cause death secondary to gramnegative
septicemia, septic shoc., and disseminated intravascular coagulation. 0n other occasions,
generalized peritonitis leads to intraabdominal abscesses, which tend to be multiple.
III. CLA&&I+ICATION
>any attempts have been made to classify peritonitis in general, and secondary peritonitis in
particular, which include a large variety of different pathologic conditions ranging in severity
from a local problem such as gangrenous appendicitis to a devastating disease such as diffuse
postoperative peritonitis due to a dehiscence of a gastroduodenal anastomosis.
It differentiates between the relatively rare forms of primary peritonitis, which usually
respond to medical treatment, and tertiary peritonitis, which does not respond to any
treatment, from the commonly occurring secondary peritonitis that mandates surgical
intervention.
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4
C#assi$ication o$ t"e various spaces (it"in t"e peritonea# cavity in ("ic" a-scesses can
$orm or $#ui* can accumu#ate.
Primary Peritonitis
.e$inition an* inci*ence
Primary peritonitis is an infection of the peritoneal cavity not directly related to other
intraabdominal abnormalities. "his term describes a peritoneal infection without an evident
source. -ince the vast ma9ority of cases are due to bacterial infection, this condition is also
commonly .nown as spontaneous -acteria# peritonitis.
In primary peritonitis bacteria invade the peritoneal cavity from a suspected e#traperitoneal
source via a hematogeneous, lymphogeneous or luminal route.
In cirrhotic patients the hematogenous route is most li.ely: microorganisms removed from
circulation by the liver may contaminate hepatic lymph and pass through the permeable
lymphatic walls into the ascitic fluid. In addition, portosystemic shunting greatly diminishes
hepatic clearance of bacteremia, which would tend to perpetuate peritonitis bacteria invade
the peritoneal cavity from a suspected e#traperitoneal source via a hematogeneous,
lymphogeneous or luminal route.
%lthough a rare condition, in adults primary peritonitis develops in up to 76* of patients with
alcoholic cirrhosis. %lso, it has been reported to occur in patients with postnecrotic cirrhosis,
chronic active hepatitis, acute viral hepatitis, congestive heart failure, metastatic malignant
(especially liver) disease, systemic lupus erythematosus, lymphedema and rarely in adults
with no underlying disease.
"he presence of ascites appears to be a common lin. among these various conditions.
"oday, spontaneous peritonitis in adults due to liver cirrhosis is considered to be an episode of
liver failure indicating the necessity of liver transplantation.
Primary bacterial peritonitis is also the most common complication in patients with chronic
renal failure undergoing continuous ambulatory peritoneal dialysis (+%P,) and is considered
to be a distinct entity.
0verall, the average incidence of this infection is /,8/,4 episodes per +%P, patient per year.
>ore than half of these episodes are e#perienced by only 76* of patients.
In children, in the preantibiotic era primary peritonitis accounted for about /'* of all
pediatric abdominal emergencies. It now accounts for less than /7*. "he decline has been
attributed to widespread use of antibiotics for minor upper respiratory tract illness.
%lthough primary peritonitis may occur in children without predisposing disease, it is
especially associated with postnecrotic cirrhosis and nephrotic syndrome.
Pat"o)enesis
%lthough the route of infection in primary peritonitis is usually not apparent it is thought to be
hematogenous, lymphogenous, via transmural migration through an intact gut wall from the
intestinal lumen or, in women, from the vagina via the fallopian tubes
In cirrhotic patients the hematogenous route is most li.ely: microorganisms removed from
circulation by the liver may contaminate hepatic lymph and pass through the permeable
lymphatic walls into the ascitic fluid.
In addition, portosystemic shunting greatly diminishes hepatic clearance of bacteremia, which
would tend to perpetuate bacteremia and increase the opportunity to cause metastatic infection
at susceptible sites, such as the ascitic collection.
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"he infre2uency of primary peritonitis in forms of ascites other than that due to liver disease
emphasizes the importance of intrahepatic shunting in the pathogenesis of this disease.
"he hepatic reticuloendothelial system is .nown to be a ma9or site for removal of bacteria
from blood and destruction of bloodborne bacteria by the reticuloendothelial system is
impaired in animal e#perimental cirrhosis and in alcoholic liver disease.
"he decrease in phagocytic activity seen in alcoholic cirrhosis is proportional to the severity
of the liver disease.
=nteric bacteria may also gain access to the peritoneal cavity by directly traversing the intact
intestinal wall. "he infre2uent occurrence of bacteremia and the multiplicity of species in
peritoneal fluid when anaerobic bacteria are involved suggest that transmural migration of
bacteria is the probable route of infection of ascitic fluid in most of these patients.
In prepubertal girls, the pathogenesis of primary peritonitis is li.ely related to an ascending
infection of genital origin, as suggested by the simultaneous presence of pneumococci in
vaginal secretions and peritoneal fluid.
%l.aline vaginal secretions that occur in this age group may be less inhibitory to bacterial
growth than the acidic secretions of postpubertal females. "ransfallopian spread is also
suggested by the development of primary peritonitis in women with intrauterine devices.
"he route of spread in women with gonococcal or chlamydial perihepatitis (?itz$ugh +urtis
syndrome) is presumably via the fallopian tubes and paracolic gutters to the subphrenic space,
but it may also be hematogenous.
"uberculous patients are considered to be a distinct category of patients e#posed to the ris. of
primary peritonitis development. %lthough tuberculous peritonitis may result from direct entry
into the peritoneal cavity of tubercle bacilli (from the lymph nodes, intestine or genital tract in
patient with active disease of these organs), it is more li.ely to be disseminated
hematogenously from remote foci of tuberculosis, most commonly in the lung.
"uberculous peritonitis may become clinically evident after the initial focus has completely
healed.
Pathophysiology of peritonitis includes comple# interactions between various triggers of the
mediator cascade, endogenous mediators and host responses.
icro-io#o)y
Primary peritonitis represent an infection that is microbiologically distinct from other
peritoneal infections because it is usually mono microbial.
In nephrotic children the most fre2uent primary peritonitis are due to gramnegative enteric
bacilli and staphylococci, while streptococcal peritonitis has declined.
In cirrhotic patients microorganisms of enteric origin account for appro#imately &'* of the
causative pathogens.
=.coli is the most fre2uently discovered pathogen, followed by @lebsiella pneumoniae,
-.pneumoniae and other streptococcal species, including enterococci. -taphylococcus aureus
is an unusual cause of primary peritonitis, accounting for only 74* of cases, but has been
noted especially in patients with erosion of an umbilical hernia. %naerobes and
microaerophilic organisms are infre2uently reported.
Possible e#planations include the intrinsic bacteriostatic activity of ascites against !acteroides
species, the relatively high p07 of ascitic fluid and the lac. of optimal anaerobic bacteriologic
techni2ues used to study patients in the past.
"he presence of anaerobes correlates strongly with polymicrobial infection. 0ccasionally,
primary peritonitis may also be caused by Aeisseria gonorrhoeae, +hlamydia trachomatis,
>ycobacterium tuberculosis or +occidioides immitis.
B
Patients who have positive cultures of ascitic fluid with few leu.ocytes and no clinical signs
of peritonitis are considered to have.
"his may represent early colonization of ascites before a host response. >ortality among
patients with a low leu.ocyte response is the same as among those with a greater response.
!loodcultures are positive in /C8 of these patients.
C#inica# presentation an* *ia)nosis
In children, primary peritonitis is an acute febrile illness often confused with acute
appendicitis. ?ever, abdominal pain, nausea, vomiting and diarrhea usually occur, with
palpatory diffuse abdominal tenderness, rebound tenderness and hypoactive or absent bowel
sounds.
In cirrhotic patients the clinical manifestation of primary peritonitis may be atypical. 0nset
may be insidious, without findings of peritoneal irritation.
?ever (D8),6*) is the most common presenting sign, occuring in 6')'* of cases and even in
the absence of abdominal signs or symptoms.
Primary peritonitis should always be considered in the differential diagnosis of
decompensation of previously stable chronic liver disease, especially hepatic encephalopathy.
Primary tuberculous peritonitis is usually gradual in onset, with fever, weight loss, malaise,
night sweats and abdominal distension.
"he abdomen may not be rigid and is often characterized as being EdoughyF on palpation.
"he findings at diagnostic surgery or laparoscopy consist of multiple nodules scattered over
the peritoneal surface and omentum. %dhesiones and a variable amount of peritoneal fluid are
usually present.
-imilarly, +occidioides immitis can cause a granulomatous peritonitis with variable clinical
manifestations.
%lthough the diagnosis of primary peritonitis can be established with certainty only after
thorough laparotomy to e#clude a primary intraabdominal site of infection, it can usually be
surmised from e#amination of the peritoneal fluid.
?luid obtained at paracentesis should be analyzed for cell count, differential count and protein
concentration and a gramstaining and culture should be performed.
!acteremia occurs in up to &6* of patients with primary peritonitis due to aerobic bacteria,
but it is rare in those with peritonitis due to anaerobes.
:sually the same organisms isolated from the peritoneal fluid are discovered in the blood.
"he ascitic fluid protein concentration may be low ( 8,6gC3) because of hypoalbuminemia and
dilution with transudate from the portal system.
"he leu.ocyte count in peritoneal fluid usually is 8''Cmm D/'''Cmm in )6*), with
granulocytes predominating in D)'* of cases. $owever, the total leu.ocyte count of some
patients with ascites uncomplicated by infection may be similarly elevated.
Indeed, an increase in ascitic leu.ocyte counts has been noted during diuresis in patients with
chronic liver disease.
0ther parameters of ascitic fluid that may help in diagnosing primary bacterial peritonitis are
p$ and lactate concentration.
%n ascitic fluid p$ of G& 86 and a lactate concentration of D76mgCd3 are more specific but
less sensitive than a leu.ocyte count of 6''Cmm8 for diagnostic purposes. -till, using all three
parameters together increases the diagnostic accuracy.
In patients with negative ascitic fluid cultures, laparoscopic peritoneal e#amination and
biopsy may be necessary.
&
Peritonitis secondary to other intraabdominal causes should be e#cluded and specimens for
fungal and mycobacteriologic cultures should be obtained.
In children, if gramnegative organisms, a mi#ed flora or no organisms are obtained from
peritoneal fluid, full e#ploratory laparotomy is generally indicate to rule out possible
intraabdominal sources of continuing peritoneal contamination.
$owever, in endstage cirrhotic patients e#ploratory laparotomy may be lifethreatening and
the li.elihood of finding a primary intraabdominal focus may be small.
-urgery for these patients can be deferred while the response to antimicrobial therapy is
awaited.
Patients with primary peritonitis usually respond within 4) hours to appropriate antimicrobial
therapy. "he rapid decrease of the number of ascitic fluid leu.ocytes that can be observed
after initiation of antimicrobial therapy for primary peritonitis has been found to help
differentiate primary from secondary bacterial peritonitis.
In patients with a subacute or chronic course of primary peritonitis, other pathogens must be
considered, including >.tuberculosis or +.immitis.
"he diagnosis of tuberculous peritonitis can usually be made at operation or laparoscopy and
confirmed by the histologic characteristics and bacteriologic e#amination of the peritoneal
biopsy specimen and fluid.
"he diagnosis of +.immitis peritonitis can be made with a wet mount of ascitic fluid, by
finding the organism in culture or on histologic e#amination.
ana)ement an* prevention
!ecause the gram stain is fre2uently negative in primary bacterial peritonitis, the initial choice
of antimicrobial drug is often empirical, based on the most li.ely pathogens.
-ome of the thirdgeneration cephalosporin antibiotics have been demonstrated to be as
efficacious as the combination of ampicillin plus an aminoglycoside in primary bacterial
peritonitis.
"hey also eliminate the ris. of nephroto#icity, which is sufficiently fre2uent in this group of
patients to warrant avoidance of aminoglycosides if an e2ually effective alternative
antimicrobial regimen can be used. 0ther antimicrobial agents such as the broadspectrum
penicillins (e.g., mezlocillin, ticarcillin, and piperacillin), carbapenems (e.g., imipenem) and
Hlactam antibioticCHlactamase inhibitor combinations (e.g., ticarcillinclavulanate and
ampicillinsulbactam) are potential alternatives.
If peritonitis develops during hospitalization, the therapeutic regimen such as administration
of an aminoglycoside antibiotic and an antipseudomonal penicillin or cephalosporin in
combination, should also be active against Pseudomonas aeruginosa.
?or those situations in which the gram stain is suggestive of a !acteroides species or
polymicrobial peritonitis is evident, antimicrobials with activity against the !acteroides
fragilis group and other anaerobic organisms should be added (e.g., metronidazole,
clindamycin).
"he antimicrobial regimen can be mo dified once the results of the culture and susceptibility
tests are available.
In cases where there is a strong clinical suspicion of primary bacterial peritonitis, but all
cultures are sterile, antimicrobial therapy should be continued. +linical improvement, together
with a significant decline in the ascitic fluid leu.ocyte count, should occur after 744) hours
of antimicrobial therapy if the diagnosis is correct.
?ailure to respond should prompt an e#amination for additional pathological conditions.
%ntimicrobial therapy is usually continued for /'/4 days if improvement is noted, but short
)
course therapy for 6 days has been shown to be as efficacious as the longer course in some
patients. %dministration of intraperitoneal antimicrobials is not necessary.
"reatment of primary peritonitis is successful in more than onehalf of cirrhotic patients, but
because of the underlying liver condition the overall mortality has been reported as high as
I6* in some series.
"hose patients with the poorest prognosis were found to have renal insufficiency,
hypothermia, hyperbilirubinemia and hypoalbuminemia.
"reatment of peritonitis caused by grampositive organisms, as well as of early infections, has
been more fre2uently successful than treatment of gramnegative or late infections. In
nephrotic patients with grampositive infections or in patients who do not have a preterminal
underlying illness, the survival rate is I'*.
+onsidering the common occurrence and high mortality of primary peritonitis in the setting of
cirrhosis with ascites, prevention is a desirable strategy. "his is particularly true for patients
who are awaiting liver transplantation.
-elective decontamination of the gut with oral norflo#acin (4''mg daily) has been shown to
reduce the incidence of spontaneous bacterial peritonitis. Aorflo#acin has the disadvantage of
selecting for grampositive organisms, including -.aureus and 2uinoloneresistant
gramnegative organisms.
>ore recently, trimethoprimsulfametho#azole (dublestrenght, given once daily for 6 days
each wee.) has been shown to be welltolerated and reduce the incidence of peritonitis.
Ris/ $actors $or ascitic $#ui* in$ection
Pat"o)enesis o$ primary peritonitis
I
In*ications $or *ia)nostic paracent"esis
Ana#ysis o$ ascitic $#ui*
Tra*itiona# t"erapy $or peritonitis
/'
&ur)ica# In$ection &ociety )ui*e#ines
$or anti-iotic treatment o$ esta-#is"e* peritonitis
Essentia#s. Primary (&pontaneous) Peritonitis
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