PERITONITIS AND INTRAABDOMINAL INFECTION

PROFESSOR TURGUT IPEK

Peritonitis means inflamation of the

peritoneum or part of it.

Secondary peritonitis is defined as the

presence of purulent exudate in the
abdominal cavity derived from an enteric
source.
 The same terms are occasionally used to define different pathologic
conditions.
Perforation/Abcess/Fistula.
Following perforation of a hollow visceral organ bacteria leak into
surrounding tissue.
Host defense mechanisms confine this leakage to form an abscess.
This abscess may rupture into another hollow viscus or the skin and
thus form a fistula.
If the abscess perforates in the free peritoneal cavity, diffuse peritonitis
results.
Bacteremia.
The presence of bacteria in blood cultures without systemic signs of
infection.
 Septicemia.
The presence of bacteria in blood cultures originating from
an infectious focus with a systemic host response, in other
words, signs of systemic infection.
Sepsis.
Asystemic infection originating from a focus, with the
inability to obtain positive blood cultures.
Septic Shock.
Sepsis with either high cardiac output and low systemic
vascular resistance (hyperdynamic phase) or low cardiac
output (hypodynamic phase).
 Sepsis Syndrome.
The clinical signs and symptoms of sepsis without
a septic focus and without bacteria isolated from
the bloodstream. This term is synonymous with
tertiary peritonitis.
Organ Failure.
The sequential dysfunction of various organs,
usually starting with lung, kidney, heart, or
intestinal tract.
 ANATOMY OF THE PERITONEUM
The peritoneum is formed by a single layer of mesothelial
cells together with an underlying supporting layer of
highly vascularized loose connective tissue.
The total area of the peritoneum is approximately 1.8 m2,
which is almost equal to the body surface area of the skin.
Peritoneum covers all of the intestinal organs and the
abdominal wall, diaphragm, retroperitoneum, and pelvis.
Peritoneal fluid has the properties of lymph.
It is secreted everywhere by the peritoneal serosa and is
absorbed primarily through the diaphragm, 80 percent
reaching the central circulation via the thoracic lymphatics.
 Innervation.
The parietal peritoneum is innervated by both somatic and
visceral afferent nerves and is quite sensitive, responding
to various stimuli somewhat as does the skin.
In contrast to the parietal peritoneum, the visceral
peritoneum receives afferent innervation only from the
automatic nervous system and is relatively insensitive.
Visceral afferent nerves respond primarily to traction or
distention, but less well to pressure, and are not capable of
mediating pain and temperature sensation.
 PHYSIOLOGY OF THE PERITONEUM
General Response to Injury
Following injury, histamine and other permeability factors
are released from peritoneal mast cells, increasing vascular
permeability of the peritoneum with exudation of protien-
rich plasma containing fibrinogen into the peritoneal
cavity.
A myriad of inflammatory cells and cytokines, autocoids,
and other chemical moieties participate in this process.
Trapping of fluid within the peritoneum and peritoneal
cavity as well as within the bowel lumen considerably
increases intraabdominal pressure.
 Increased intraabdominal pressure not only
negatively influences pulmonary, cardiac, and
renal function, but also has deleterious effects on
hepatic and intestinal or splanhnic perfusion.
These secondary system impairments potentiate
the development of acute respiratory distress
syndrome (ARDS), multiple organ failure, and
death.
 Inflammation and Host Defenses
Any noxious stimulus, such as bacterial endo- or
exotoxins or trauma, might initiate the series of
events captured under the term host
inflammatory response.
It consists of soluble and cellular components.
The soluble components include
immunoglobulins, the complement system, the
contact activation system, leukotrienes,
inflammatort autacoids, and acute phase cytokines.
 Cellular components of inflammation include macrophages
and phagocytic cells, mast cells and basophils, platelets,
endothelial cells, lymphocytes, and leukocytes.
The terminal pathway of all events of inflammation
completes bacterial killing, eliminates foreign material,
and restores normal physiology and anatomy.
Bacterial killing, or cytotoxicity, may be achieved via such
factors as free oxygen radicals, nitric oxide, cytotoxic
lymphocytes, bactericcidal permeability-increasing (BPI)
proteins, cathepepsins, lactopherin, lysozymes, proteases,
lipidhydrolases, and nucleases. The clinical picture of
sepsis, ARDS, and multiple organ failure are intermediate
stages that clinically parallel sequential cell death.
 CLINICAL MANIFESTATIONS OF
PERITONITIS LEADING TO SEPTIC
SHOCK
Clinical findings include a disturbed sensorium,
tachypnea, tachycardia, hypotension, fever,
oliguria, and heart failure.
Two distinct phases of septic shock are
encountered clinically, an early hyperdynamic and
a late hypodynamic phase.
 CLINICAL PRESENTATION OF PERITONITIS
Signs and Symptoms
Abdominal pain is almost always the predominant
symptom.
A good example of the effects of the dual mechanism of
pain perception is the chain of events in the development
of acute appendicitis.
Initially, inflammation of the appendix is projected via
autonomic nerve fibers to the region of umblicus and
epigastrium with symptoms of diffuse epigastric pain,
nause, and, sometimes, vomiting.
The character of pain changes as the disease progresses.
 As the somatic pathways of paraappendiceal peritoneum
and adjacent structures become involved, the patient
experiences migration of pain from the epigastrium and
umblicus to the right lower abdomen, an increase in the
perceived intensity of pain, and then localization to
McBurneys point.
Anorexia is almost always present; nausea may be
accompanied later by vomiting.
Fever usually ranges between 38 and 41C.
Tachycardia and a diminished palpable peripheral pulse
volume indicate hypovolemia.
Abdominal distention is due to concomitant ileus.
 Tenderness is present over the entire extent of the
peritoneum involved in the inflammatory process.
Rigidity of the abdominal muscles is produced by
voluntary guarding initially and also by reflex muscle
spasm.
Laboratory and Other Tests
Leukocytosis is common in acute intraabdominal infection.
Slayt
A leukocyte count of more than 25000 or leukopenia of
fewer than 4000/mL3 are both associated with higher
mortality.
 The radiologic picture of intraabdominal infection mimics
that of paralytic ileus.
A lateral abdominal view might reveal superimposed
calcifications of the pancreas, indicating pancreatitis.
Free air may be visible on an upright abdominal or lateral
decubitus film if a ruptured hollow viscus is the cause of
peritonitis.
Computed tomography (CT) is not required in the initial
workup of acute peritonitis and may only delay needed
operative management.
CT and ultrasound, however, are very helpful in the
diagnosis of an intraabdominal abscess.
 PRIMARY BACTERIAL PERITONITIS
Spontaneous Peritonitis
Primary peritonitis refers to inflammation of the peritoneum from a
suspected extraperitoneal source, often via hematogenous spread.
It occurs in children and in adults, and can be a life-threatening illness,
particularly in patients with cirrhosis.
Spontaneous bacterial peritonitis is now more common in adults than
in children and shows no differential sex incidence.
Children with nephrosis, formerly the group most commonly affected,
have been replaced by adults with cirrhosis or systemic lupus.
E.coli is the most common isolated microorganism.
 In children, the bacteria responsible for primary peritonitis are
hemolytic streptococci and pneumococci.
The route by which bacteria are transmitted to the peritoneal cavity is
not known.
The mortality risk is of the order of 48 to 70 percent in cirrhotic adults
but is lower in nephrotic children.
Clinical Manifestations.
Most patients complain of some abdominal pain and distention;
vomiting, lethargy, and fever are more prominent in children.
Diarrhea is usual in neonates but seldom seen in adults.
Leukocytosis usually is present.
Free air usually is not seen on abdominal radiographs.
 Diagnosis
A peritoneal tap is the most useful diagnostic test.
A PMN cell count greater than 250/mm3 is considered
positive.
Treatment
Antibiotic therapy should be started and the patient
initially managed nonoperatively.
Usually, a cephalosporin or ampicillin-sulbactam is
appropriate since 90 percent of the organisms causing
spontaneous peritonitis are sensitive to these antibiotics.
 Peritonitis Related to Peritoneal Dialysis
Peritonitis is the dominant complication of continuous ambulatory
peritoneal dialysis (CAPD) in patients with end-stage renal disease.
Catheter-related infection is the most common mechanism.
Two-thirds of patients with positive cultures have a gram-positive
coccus as the causative organism, usually Staphylococcus aureus or S.
Epidermidis.
Anaerobes rarely are recovered.
The diagnosis is established when any of the following is present:
positive culture from the peritoneal fluid;
a cloudy dialysate effluent; and
clinical signs of peritonitis.
The initial treatment of dialysis-related peritonitis is administration of
antibiotics and heparin in the dialysate.
 Tuberculous Peritonitis
Tuberculous peritonitis, formerly frequently fatal as a manifestation of
uncontrolled generalized tuberculosis.
Clinical Manifestations
Clinically, tuberculous peritonitis is insidious, presenting with fever,
anorexia, weakness, and weight loss.In the past, the disease has been
classified into moist and dry phases.The moist phase refers to the
early, subacute stage with fever, ascites, abdominal pain, and
weakness.Ascites is progressive and may become massive.The dry
form presents later without ascites, following resolution during which
dense adhesions are formed.
Diagnosis
A peritoneal fluid tap will show mostly lymphocytes.
The laparoscopic appearance of tuberculous peritonitis is
characteristic.
Treatment
Treatment is administration of antituberculous drugs.
 SECONDARY BACTERIAL PERITONITIS
Perforation Peritonitis
Perforation peritonitis is the most common form of acute intraabdominal
infection.
Perforation of the Stomach and Duodenum.
nfection after peptic ulcer perforation presents acutely.
The proper management is simple closure of the perforation.
Small Bowel Perforation
Intraabdominal infection after small bowel erforation falls into two major
catogeries.
In the first, bowel obstruction is present.
In the second form, bowel wall necrosis due to inflammation or inadequate
vascular supply leads to perforation.
The mortality rate can be more than 50 percent.
 Typhoid Perforation
Typhoid perforation is usually seen in the third week of
infection with Salmonella typhi.
Typhoid bacilli are though to penetrate the Peyers patches
of the intestinal wall, mainly in the distal ileum.
These collections of lymphoid cells hypertrophy, leading
to hemorrhage and then perforation.
Trimethoprim-sulfamethoxazol is the treatment of choice
for uncomplicated typhoid, but in patients with peritonitis,
cefataxime plus metranidazole is a better treatment
regimen.
 Peritonitis Following Appendicitis
If the appendix has perforated, however, the
disease may become life-threatening, especially
when the omentum is not able to contain the
infection and diffuse suppurative peritonitis
results.
Treatment is more likely to be succesful once the
appendix is removed and the source of infection is
thus controlled.
 Colon Perforation
About 22 percent of cases of peritonitis have their
anatomic origin in the colon.
More than half of these are due to inflammatory disease
such as diverticulitis and colitis.
Colon perforation following diverticulitis is more common
but less serious since diverticulitis itself institutes local
host defenses.
Carcinoma of the colon, if the ileocecal valve is
component, may lead to diffuse fecal peritonitis as a result
of rupture of the cecum or ascending colon.
 Amebic Perforation
Entamoeba histolytica infection of the intestine usually
causes a dysentery-like illness, but sometimes liver abscess
or perforation of the large bowel occurs.
Liver abscess also can perforate secondarily and cause
diffuse peritonitis.
Peritonitis Following Pancreatitis
Translocation of bacteria is possibly the mechanism of
progress from the initial chemical inflammation of
pancreatitis to retro-and intraabdominal peripancreatic
infections.
 Peritonitis of Genitourinary Origin
A variety of conditions originating from the genitourinary tract can
cause peritonitis.
Ruptured perinephric abscess and ruptured chronic cystitis after
radiation therapy for female reproductive tract cancer are examples.
Pelvic peritonitis due to sexually transmitted infection is seen in young
women.
Postoperative Peritonitis
Postoperative peritonitis is usually due to a leak from a suture line and
is typically discovered only after some delay, as a rule between the
fifth and seventh postoperative day.
Delay contributes to a high mortality rate.
 Peritonitis after Trauma
Peritonitis may develop after blunt trauma in
patients who have unrecognized intraabdominal
injuries such as a ruptured mesentery with loss of
the vascular supply to the small or large bowel, or
a frank bowel perforation.
Patients suffering penetrating trauma, either
gunshot wound or stab wound, usually are
operated on and the wound repaired or controlled
immediately; these injuries lead to peritonitis only
when a leak occurs following the initial repair.
 OTHER FORMS OF PERITONITIS
Aseptic/Sterile Peritonitis
This form of peritonitis develops whenever irritant material
gains entry to the peritoneal cavity.
The soilage initially is sterile, or nearly so, which
distinguishes chemical peritonitis at onset from
suppurative peritonitis.
Foreign-Body Peritonitis
Foreign bodies may be deposited in the peritoneal cavity
during operations (sponge or instrument inadvertantly left
behind) or might result from penetrating injuries or
perforation of the intestines following ingestion.
 Periodic Peritonitis
Recurrent episodes of abdominal pain, fever, and
leukocytosis occur in certain population groups in and
around the Levant, notably in Armenians, Jews and Arabs.
The disease appears to be familial.
Colchicine is effective in preventing recurrent attacks.
Drug-Related Peritonitis
Administration of isoniazid and of erythromycin estolate
have been reported to cause acute abdominal symptoms
mimicking peritonitis but not development of true
peritonitis.
 Lead Peritonitis
Lead peritonitis has the same clinical picture as acute
intermittent porphyria.
It is associated with lead intoxication (occuring in painters,
smelter workers, pica in children) and a careful history will
lead to the correct diagnosis.
Hyperlipidemic Peritonitis
Abdominal pain mimicking peritonitis may be seen in
patients with type1 and type 5 hyperlipoproteinemia, a
group of heterogenous disorders resulting from increased
concentration of chylomicrons or very-low-density
lipoproteins in the blood.
 Porphyric Peritonitis
Porphyric peritonitis is a condition of perceived abdominal pain rather
than an inflammation of the peritoneum.
Intraabdominal infection can be ruled out by the demonstration of
porphobilinogen in the Watson-Schwartz test.
Talcum Peritonitis
Peritoneal inflammation, exudation and formation of pseudotumors
(chronic inflammatory omental tumors), and formation of dense
adhesions may follow contamination of the peritoneal cavity by glove
lubricants (talcum, lycopodium, mineral oil, cornstarch, rice starch) or
by cellulose fibers from disposible gauze pads, drapes, and gowns.
 TERTIARY PERITONITIS
This state has been called the nonbacterial sepsis
syndrome or the systemic inflammatory response
syndrome, or, following treatment of
intraabdominal infection, tertiary peritonitis.
The clinical picture is one mimicking occult
sepsis, as manifested by a hyperdynamic
cardiovascular state, low-grade fever, and general
hypermetabolism.
 INTRAABDOMINAL ABSCESS
Abscess Formation
In a developing abscess, bacteria continue to divide and to
produce toxins and enzymes that, together with the
proteolytic enzymes of dying phagocytes,liquify the
abscess contents and increase osmotic pressure.
Oxygen and nutrients diffuse poorly through the abscess
capsule, thus promoting anaerobic glycolysis, which
finally results in an anaerobic environment with high
pressure, low pH, low oxygen, and high carbon dioxide
levels.
 Clinical Features and Diagnosis
An intraabdominal abscess may be seen with either
primary and secondary peritonitis.
Left Subphrenic Abscess
Formerly uncommon, these are now the most common
variety of upper abdominal abscess residual after
peritonitis or leaking from a viscus.
Lesser Sac Abscess
Technically, this is a variety of left subhepatic-subphrenic
abscess, since the lesser peritoneal sac anatomically is a
portion of the left subhepatic space.
 Right Subphrenic Abscess
Abscess within this space are most frequently secondary to rupture of a
hepatic abscess or less frequently to operation on the stomach or
duodenum.
Right Subhepatic Abscess
The most posterior (deepest) part of this space is called Morisons
pouch.
A gastric procedure, especially an emergency operation for
complications of ulcer disease, is the most common antecedent event.
Interloop (Midabdominal) Abscess
These are often multiple abscess that arise as loculations between
loops of bowel, mesentery, abdominal wall, and omentum.
 Pelvic Abscess
This form of abscess most often follows a ruptured colonic
diverticulum, pelvic inflammatory disease, ruptured
appendix, or drainage into the pelvis during resolution of
generalized peritonitis.
Pancreatic Abscess
Acute necrotizing pancreatitis is the antecedent cause of
pancreatic abscess in the majority of cases.
Secondary infection of a pancreatic pseudocyst and
abdominal trauma with pancreatic injury are other
important causes.
 Retroperitoneal Abscess
Abscess within the retroperitoneal spaces are not
common.
An abscess located in the upper retroperitoneum is
usually secondary to infection of the pancreas.
Retroperitoneal abscess in other locations may be
caused by primary or secondary infections of the
kidneys, ureters, or colon, or osteomyelitis of the
spine or after trauma.
 Management
Percutaneous drainage
Percutaneous needle aspiration and closed catheter drainage, using CT
and ultrasound guidance, is preferred to operative drainage of most
intraabdominal abscess.
Percutaneous drainage of an intraabdominal abscess is usually
successful if the following criteria are met:
there is a well-established, unilocular fluid collection;
a safe percutaneous route of access is available; this often means
location of the abscess adjacent to the body wall;
joint evaluation by a surgeon and a radiologist is done so that correct
judgments and decisions are made; and
there is immediate operative backup available in case of failure or
complications.
 Open Surgical Drainage
The indications for open surgical drainage are failure of percutaneous
drainage, inability to safely drain percutaneously, the presence of a
pancreatic or carcinomatous abscess, an association with a bowel
fistula, the involvement of the lesser sac, or the presence of multiple,
isolated interloop abscesses.
Antibiotic Therapy in Conjunction with Abscess Management
Antibiotic therapy should be initiated before percutaneous or operative
abscess drainage, guided by the sensitivity studies obtained from
previous intraoperative specimens and antibiotics already used in
treatment of the antecedent abdominal infection.
 NONOPERATIVE MANAGEMENT OF
PERITONITIS
Preoperative Preparation
The essential features of preoperative treatment of
peritonitis involve fluid resuscitation, antibiotics,
oxygen and, if needed, ventilator support,
nasogastric intubation, urinary catheterization, and
possibly early hemofiltration, and monitoring of
vital signs and biochemical and hemodynamic
data.
 Fluid Resuscitation
Extensive inflammation of the peritoneal membrane causes fluid to
shift into the peritoneal cavity and the interstitial space.
Large volumes of fluid may be necessary to restore the intravascular
volume and to maintain a satisfactory urine output.
Oxygen and Ventilator Support
Oxygen is administred to overcome the mild hypoxemia commonly
present in peritonitis as a result of the increased metabolic demand of
infection, some degree of intrapulmonary shunting, and the mechanical
impairment of pulmonary ventilation by the distended, tender
abdomen.
 Intubation, Catheterization, and Hemodynamic
Monitoring
Vital signs (temperature, blood pressure, pulse,
respirations) are continuously recorded.
Preoperative biochemical evaluation should include
measurement of serum electrolytes, creatinine, glucose,
bilirubin, and alkaline phosphatase, and a urinalysis.
Epidural/Peridural Analgesia
Peridural analgesia is very helpful in patients with
peritonitis to reduce their requirement for parenteral
analgesics.
 Renal Support
Monitoring of renal function is essential and requires early corrective
measures.
Narcotics
Analgesic drugs should not be administered to patients with suspected
peritonitis, or any other acute abdominal process, until a firm diagnosis has
been made or, at least, a decision to operate has been made.
Vasoactive Drugs
Administration of drugs with predominant alpha-adrenergic effects is
sometimes of value in the treatment of the hyperdynamic phase of sepsis
secondary to peritonitis.
Steroids
Steroids are not currently recommended in the management of bacterial
peritonitis.
Fever
A temperature above 38.5C can be associated with difficulty in
administration of anesthesia.
Administration of salicylates often will be effective in reducing fever.
 OPERATIVE TREATMENT OF SUPPURATIVE PERITONITIS
Cleaning the Abdminal Cavity
Intraoperative High-Volume Lavage
This treatment involves extensive intraoperative lavage of the entire
abdominal cavity.
Initially, 1 to 5 L of physiologic saline or Ringers solution is placed
into the abdominal cavity, the viscera are manipulated so that the fluid
reaches all parts of the abdominal cavity to wash out pus, feces, and
necrotic material, and then the fluid is suctioned away.
This procedure is repeated until the suctioned fluid runs repetitively
clear.
Usually, a total of 8 to 12 L is used in adults.
 Radical Debridement
Radical debridement is a poorly defined technique because
it is almost impossible, witout causing too much bleeding,
to radically debride all necrotic tissue in intraabdominal
infections, including intraabdominal abscesses.
Continuous Postoperative Irrigation
In this method, four to six Tenckhoff catheters are placed
in the abdominal cavity and irrigation fluid is infused
through them for an hour.
The process is then reversed to drain the abdominal cavity,
and then the cycle is repeated.
 Open Abdomen and Staged Abdominal Repair
This concept of planned relaparotomies later fused with the
open-abdomen technique when the requirement for
tension-free abdominal wound closure became evident.
The new concept, termed stages abdominal repair, uses
new devices for closure such as a zipper with larger seams
(Ethizip), Marlex mesh with a zipper, or an artificial burr
device.
Relaparotomies are performed at 24-h intervals in the
operating room.
Once all problems are solved, the abdominal cavity is
closed definitively.
 Acute appendicitis
Incidence
Acute appendicitis is the most common acute surgical
condition of the abdomen. The disease occurs at all ages
but is most frequent in the second and third decades of life.
Etiology and Pathogenesis
Obstruction of the lumen is the domuniant factor in the
production of acute appendicitis. Fecaliths are usual cause
of appendiceal obstruction. Less common are hyperthropy
of lymhoid tissue;inspissated barium from previous X-ray
studies;vegetable and fruit ; seeds; and intestinal
worms;particularly ascarids.
 Bacteriology
A variety of anaerobs, aerobs, or facultative
bacteria have been cultured from peritoneal fluid,
abcess contents, and appendiceal tissue in patients
with gangrenaous or perforated appendicitis.
Bacteriodes fragilis and Escherichia coli were
isolated from almost all specimens. Other frequent
isolates were Peptostreptococcus (80 percent),
Pseudomanas (40 percent), B.splanchnicus (40
percent) and Lactobacillus (37 Percent).
 Clinical Manifestations
Symptoms:Abdominal pain is the prime symptom of cause
appendicitis.Classically the pain initially is diffusely centered in the
lower epigastrium or umblical area, is moderately severe and is steady-
sometimes with intermitent cramping superimposed. After a period
varying from 1 to 12 h, but usually within 4 to 6 h, the pain localizes in
the right lower quadrant.
Variations in the anatomic location of the appendix account for many
of the variatioms in the principal locus of the somatic phase of the
pain. For ezample a long appendix with the inflamed tip in the left
lower quadrant causes pain in that area;a retroceacal appendix may
cause principally flank or back pain ; a pelvic appendix may cause
testicular pain presumably from irritation of the spermatic artery and
ureter.
Anorexia naerly always accompanies appendicitis.Vomiting occurs in
about 75 percent of patients.
 Signs
Temparaature elevation is rarely more than 1 C.
Tenderness is often maximal at or near the point described by Mc Burney as
being `1located exactly between an inch and ahalf and two inches from the
anterior spinous process of the ileum on a straight line drawn from that process
to the umblicus``
Rovsing`s sign-pain in the right lower quadrant when palpatory pressure is
exerted in the left lower quadrant- aaaalso indicaates yhe site of the peritoneal
irritation.
As the examining finger exertspressure on the peritoneum of the cul-de-sac of
Douglas, pain is felt in the suprapubic areaas wel as locally.
The psoas sign indicates an irritative focus in proximity to that muscle. The
test is performed by having patients lie on their left side; the examiner then
slowly extends the right thigh, thus strecthing the iliopsoas muscle.
Similarly, a positive obturator sign of hypogastric pain on streching the
obturator internus indicates irritaion at the locus. The test is performed by
passive internal rotation of the flexed right thigh with the patient supine.
 Labarotory Findings
Moderate leukocytosis, from about 10.000 to
18.000/mm3.Pain films of the abdomen in acute
appenddicitis often reveal a distended loop or two
of small bowel in the right lower quadrant less
often a distended cecum.
Laparoscpoy
Laparoscopy can be used to distinguish
gynecologic disease and ileitis from appendicitis .
If the diagnosis of appendicitis is made
laparoscopic appendectomy can be performed.
 Differential Diagnosis.
Acute mesenteric adenitis
Acute gastroenteritis
Disease of the male
including torsions of the testis and acute epididymitis.
Meckel`s diverticulitis
Intussuception
Regional enteritis
Perforated peptic ulcer
Diverticulitis or Perforating Carcinoma Of the Cecum or of That Portion of the
Sigmoid That lies on the Right Side.
Epiploic appendagitis
Urinary tract infection
Uretral stone
Primary peritonitis
Henoch-Schonlein Purpura
Yersinosis
 Gynecologic Disorders; pelvic inflammaory
disease ,ruptured graafian follicul, twisted ovarian
cyst or tumor, endometriosis and ruptured ectopic
pregnacy.
Other diseases;: Closed loop intestinal
obstruction, mesenteric vascular occlusuion,
pleuritis of the right lower chest acute
cholecysstitis acute pancreatitis hamatoma of the
abdominal wall.
 Appendicitis in the Young
Diagnosis accuracy for acute appendicitis is
considerably lower than in adults.
The disease progresses more rapidly than in adults
gangrene and rupture occur earlier in the course
of acute appendicitis in children. The rupture rate
varies from 15 to 50 precent in reported series.
Rupture of gangrenous appendicitis is more
frequently followed by diffuse peritoinits and
distant intraabdominal abcesses than in adults.
 Appendicicitis in the Elderly.
Less than 10 percent of patients operated on
for acute appendiciis are over sixty years of
age but morethan 50 percent of all deaths
from appendicitis are in this age group. This
is attributable to delay of definitive
treatment greater frequency of progressive
uncontrolled infection and a high incidence
of concomitant disease.
 Appendicitis During Pregnancy
Diagnosis is difficult. Symptoms of appendicitis
such as abdominal pain and nausea are also
common in pregnancy. Displacement of the
appendix by the gravid uterus changes the location
of the somatic componentof abdominal pain and
the point of maximal tenderness to a higher and
more lateral position. Leukocytosis of pregnancy
,where white cell counts as high as 15.000/mm3
are normal,compromises the value of this
test.Laporoscopy can be used in atypical cases and
may laparotomy unnecessary.
 Appendicitis in Patients with AIDS/HIV Infection
Most immunodeficient patients have no WBC elevation
preoperatively. Diagnostic laporoscopy is helpful in
establishing or ruling out the diagnosis.
Treatment:
There is but one treatment for acute appendicitis and
complications. To attempt to treat appendicitis with
antibiotics is misguided because it ignores the obstructive
causaation of appendicitis and is to be condemned. Thus
the only question to be resolved is -when the timing of
surgical intervention.
 References
Wittmann DH, Walker AP, Condon RE
Peritonitis and Intraabdominal Infection.
Principles of Surgery ed. Schwartz SI McGraw
Hill 1994, 1449-1483.
Condon RE, Telford GL Appendicitis.
Textbook of Surgery, ed:Sabiston DC. W.B.
Saunders Philadelphia 1991,884-898.