2. Anatomy and Physiology
The peritoneum is a thick, double
layer of serous membrane in the
abdominal cavity
The area of the peritoneum is around
2 square meters
3.
4. Anatomy and Physiology
All organs are divided on 3 groups:
1) Intraperitoneal
2) Mesoperitoneal
3) Extraperitoneal
5. Anatomy and Physiology
Peritoneum tissue
is a typical connective tissue;
is covered by polygonal mesothelium;
has a very good blood supply.
6. Anatomy and Physiology
The parietal peritoneum is innervated
by the sensitive somatic nerves
The pain as a result of the parietal
peritoneum irritation is localized
(somatic pain)
The pelvic peritoneum has no somatic
innervations
7. Anatomy and Physiology
The visceral peritoneum has vegetative
(parasympathic and sympathic)
innervations
The pain as a result of the visceral
peritoneum irritation is not localized
9. Aetiology
o Vary according to age, gender and ge
ography.
o 3 most common causes of generalize
d peritonitis in low-income countries a
re probably
1. appendicitis,
2. perforated duodenal ulcer
3. and typhoid perforations, in no par
ticular order.
10. Aetiology
o In a study of Nigerian children 50% o
f patients had typhoid perforation.
o In women, the complications of pelvic
inflammatory disease predominate.
o Abdominal trauma resulting in intesti
nal injury is also a significant cause of
peritonitis, particularly in low-income
countries.
11. Aetiology
o In the West appendicitis remains the
most common cause of peritonitis, foll
owed by colonic perforation, usually a
s a result of diverticulitis.
12. Aetiology
o Iatrogenic causes, resulting from failu
re of intestinal anastomosis and inadv
ertent bowel injuries, need to kept in
mind.
o Certain clinical conditions, primary pe
ritonitis and appendicitis, are more co
mmon in children. Intra-abdominal inf
ection has its own features in the elde
rly.
13. Classification
Peritonitis is traditionally classified as:
o primary
o secondary
o tertiary.
o The form most commonly encountered by surg
eons is secondary peritonitis resulting from per
foration of a hollow viscus or other abdominal
pathology. Primary peritonitis results from spon
taneous bacterial infection of the peritoneum, a
lone or in association with peritoneal dialysis
14. Classification
o Tertiary peritonitis is characterized by
a class of very ill patients in whom se
condary peritonitis fails to resolve
despite what appear to be appropr
iate measures and is associated wi
th multi-organ failure.
15. Secondary peritonitis
o Commonest for surgeon
o Source control, reduction in bacterial
contamination and prevention of its r
ecurrence are the hallmarks of surgic
al treatment.
16. Primary peritonitis
o occur in children, patients with hepat
ic cirrhosis (usually alcohol) or the ne
phritic syndrome and ascites, in patie
nts on peritoneal dialysis and in HIV/
AIDS.
o Operation is unnecessary for SBP.
o Gram-negative aerobes were the mo
st common infecting agent, followed b
y streptococcus.
17. Primary peritonitis
o In patients with cirrhosis and ascites,
SBP may be prevalent in as many as
7-30% of patients.
o The pathophysiology appears to be ba
cterial translocation outside the bowel
lumen into extra-intestinal sites.
o E.coli and other gram-negative ba
cilli predominate..
18. Primary peritonitis
o The mortality varies in these patients
from 10-40% and over 50% of survivi
ng patients will have a recurrence.
o Therefore prophylactic antibiotics, Se
ptra or norfloxacin, should be prescrib
ed to all survivors to achieve selective
gut decontamination
19. Primary peritonitis
o Patients present with fever, abdomina
l pain, tenderness and often signs of
hepatic decompensation. Diagnosis is
confirmed by the presence of PMNL>2
50/mm³. The condition is a reflection
of serious hepatic failure and initial su
rvivors have a 2 year mortality rate of
50% in the absence of liver transplant
ation.
20. Primary peritonitis
o In patients undergoing peritoneal dial
ysis peritonitis remains one of the ma
jor complications.
o Gram positive organisms predominate
.
o Treatment consists of instilling antibio
tics into the dialysate.
21. Tuberculus peritonitis
o tuberculosis, which might be consider
ed a special case of primary peritoniti
s, represents a common extra-pulmo
nary manifestation of tuberculosis.
o It is associated with HIV infection.
o The disease has an insidious onset a
nd should be suspected in any case of
unexplained ascites.
22. T/peritonitis
o Abdominal pain, fever, weight loss an
d tenderness are the common present
ing features.
o The indolent nature of the process sh
ould assist in distinguishing it from ot
her forms of primary and secondary p
eritonitis.
o Analysis of ascitic fluid shows predom
inance of lymphocytes on gram stain.
23. T/peritonitis
o The highest sensitivity and specificity
is found with adenosine deaminase
ADA measurement.
o Laparoscopy is recommended as the
diagnostic procedure of choice in that
it allows inspection and biopsy of the
peritoneum.
o Treatment is pharmacologic.
24. Acute abd in HIV
o Presentation with acute abdominal pain occurs
in 12-48% of HIV patients.
o In the absence of anti-retroviral therapy over 5
0% of these have HIV-related pathology.
o These are, most commonly, cytomegalovirus
(CMV) gastroenteritis, followed by lympho
mas, Kaposi sarcoma and TB peritonitis.
25. Acute abd in HIV
o Specific HIV-related conditions include: primary
peritonitis, spontaneous bowel perforation, mes
enteric thrombosis, colitis (in adults), necrotizi
ng enterocolitis (in infants), acalculous cholecy
stitis and intra-peritoneal rupture of splenic or
hepatic abscess.
o Operation in HIV patients, particularly in the a
bsence of anti-retroviral therapy, is associated
with elevated morbidity and mortality rates.
o This mandates careful evaluation and avoidanc
e of unnecessary operation. Where diagnosis is
obscure, laparoscopy has been advised.
26. Classification
I Bacterial peritonitis
a) staphylococcus
b) streptococcus
c) proteus
d) enterococcus
II Sterile peritonitis
a) caused by bile
b) caused by pancreatic enzymes
30. Clinical features
o Abdominal pain
o Tenderness to palpation
o Rebound tenderness
o Increased abdominal wall rigidity
o Anorexia and nausea
o Vomiting
o Fever
o Tachycardia
31. Pathophysiology
o Injury results in an influx of protein ri
ch fluid, activation of the complement
cascade, up-regulation of peritoneal
mesothelial cell activity and invasion
of the peritoneum with polymorphonu
clear neutrophils and macrophages.
o There is stimulation of cytokine and c
hemokine production. Bacteria are op
sonized and killed by white blood cells
and cleared through the lymphatics
33. Pathophy
o The pathogenesis of intra-abdominal infections
is determined by bacterial factors which influen
ce the transition from contamination to infectio
n.
o Bacterial stimuli, especially endotoxin, lead to
an almost uniform activation response which is
triggered by reaction of mesothelial cells and in
terspersed peritoneal macrophages and which
also involves plasmatic systems, endothelial cel
ls and extra- and intravascular leukocytes.
34. pathophy
o The local consequences of this activat
ion are the transmigration of granuloc
ytes from peritoneal capillaries to the
mesothelial surface and a dilatation of
peritoneal blood vessels resulting in e
nhanced permeability, peritoneal ede
ma and lastly the formation of protein
-rich peritoneal exudate.
36. pathphy
o The first line of defense is clearance o
f noxious agents via the lymphatics of
the parietal peritoneum, diaphragm a
nd omentum. The formation of fibrin
acts to wall off the infection and is as
sociated with abscess formation.
37. pathophy
The response to intra-abdominal
infection depends on 5 key factors:
o inoculum size
o virulence of the contaminating organi
sms
o the presences of adjuvants within the
peritoneal cavity
o adequacy of local, regional, and syste
mic host defenses
o the adequacy of initial treatment.
38. Pathophy
o The specific microbial characteristics of
different regions of the gut determine th
e types of infecting organisms found wit
h specific diseases.
o Secondary peritonitis typically results in
polymicrobial infections with gram-negat
ive aerobes and anaerobes.
o Inflammation within the peritoneal cavit
y evokes a series of secondary changes
that produce the clinical syndrome of pe
ritonitis
39. pathophy
o The acute inflammatory process withi
n the abdomen results in sympathetic
activation, and suppression of intestin
al peristalsis, or ileus. Fluid absorptio
n through the wall of the bowel is imp
aired, and significant amounts of tissu
e fluid may be sequestered within the
lumen of the gut, resulting in systemi
c hypovolemia.
40. Diagnosis
o History and physical examination is of
paramount importance.
o Hx usually associated with abrupt ons
et of abd pain often localized at first t
hen generalized
o Some cases like perforated diverticulit
is,pain remains in the one quandrant.
41. Diagnosis cont
o A careful history often suggests the s
ource of the problem.
o Subsequently confirmed on physical e
xamination and investigations.
o Physical exam findings depend on aeti
ology, duration and whether localsed
or generalized.
42. Imaging Inx
o Depends on the differential diagnosis
from the hx and examination.
o X rays
o Abdominal ultrasound
o CT scan
43. Lab Analyses
o Leukocytosis or leukocytopenia
o Dehydration and acidosis
o Peritoneal fluid analysis
o Serum electrolytes
o Hb gping & xmatching
44. Treatment
o Antibiotic therapy
o Correction of existing serum
electrolytes disturbances
o Correction of coagulation abnormalities
o Surgery
45. Surgery
o To eliminate the source of
contamination
o To reduce the bacterial contamination
o To prevent further complications and
sepsis
