Peritoneum Introduction, Disorders, Peritonitis

1. DISORDERS OF THE
PERITONIUM &
PERITONITIS
PRESENTED BY
MS. NAVANEETA KUSUM
MSC. NSG, 2ndYEAR

2. Anatomy and Physiology

3. Peritoneum
The word peritoneum is derived from the Greek terms peri (“around”) and
tonos (“stretching”). The peritoneum, which lines the inner most surface
of the abdominal wall and the majority of the abdominal organs.
In men, the peritoneum is completely enclosed, whereas in
women, it is open because of uterine tubes, the uterus, and the vagina.
It is a thin, serous, continuous glistening membrane lining the
abdominal & pelvic walls and clothing the abdominal and pelvic viscera.

4. PERITONEAL LAYER
• Parietal peritoneum is the outer
layer, attached to the abdominal
wall and the pelvic walls
• It is sensitive to pain, pressure,
temperature & touch.
• Parietal peritoneum is supplied by:
Lower thoracic nerves (T7-T12).
• Visceral peritoneum is the
inner layer wrapped around the
visceral organs, located inside the
intraperitoneal space for
protection. It is thinner than the
parietal peritoneum.
• Visceral peritoneum is sensitive to
stretch & tearing.
• I t is supplied by autonomic afferent
nerves which supply the viscera.

5. PERITONEAL LAYER

6. Retroperitoneum
The retroperitoneum is defined as the space between the posterior
parietal peritoneum and the posterior body wall.
Organs are classified as retroperitoneal in location such
as: duodenum, ascending colon, and descending colon.
Retroperitoneal surgeries is beneficial for a number of reasons:
It avoids entrance in to the peritoneum and thus, decreases the risk of
injury to intra-abdominal organs. Minimal manipulation of the small
intestine. Intra-abdominal adhesions are also minimized.

7. Retroperitoneal Organs

8. Peritoneal cavity
• The peritoneal cavity is a potential
space between the parietal peritoneum and
visceral peritoneum.
• It is the largest serosal sac, and the largest
fluid-filled cavity, in the body and secretes
approximately 50 mL of fluid per day.
• This fluid acts as a lubricant and has anti-
inflammatory properties.

9. Features of Peritoneal cavity
• It is a common injection site used in intraperitoneal injection.
• An increase in the capillary pressure in the abdominal viscera can
cause fluid to leave the interstitial space and enter the peritoneal
cavity called as Ascites.
• Body fluid sampling from the peritoneal cavity is “Peritoneocentesis”.
• The peritoneal cavity is involved in peritoneal dialysis.

10. Peritoneal cavity
It is divided into two main sacs:
1- Greater sac.
2- Lesser sac or omental bursa.
These two sacs are interconnected
by a single oval opening called the
epiploic foramen or opening into
lesser sac or foramen of Winslow

12. GREATER SAC
It is the part of peritoneal cavity
which lies behind the anterior
abdominal wall.
Peritoneum lines the anterior
abdominal wall then the under
surface of diaphragm, from
where it is reflected on to
superior surface of liver forming
the upper layer of coronary
ligament

13. LESSER SAC
The lesser sac, also known as
the omental bursa, is the cavity in
the abdomen that is formed by
the lesser and greater omentum.
It is connected with the greater
sac via the omental
foramen (previously known as
the Foramen of Winslow).

14. The lesser sac is divided into two "omenta":
1. The lesser omentum (or gastrohepatic) is attached to the lesser curvature of
the stomach and the liver.
2. The greater omentum (or gastrocolic) hangs from the greater curve of the
stomach and loops down in front of the intestines before curving back upwards
to attach to the transverse colon. In effect it is draped in front of the intestines
like an apron and may serve as an insulating or protective layer.
The mesentery is the part of the peritoneum through which
most abdominal organs are attached to the abdominal wall and supplied
with blood and lymph vessels and nerves.

15. Omentum & Mesentry

16. OMENTUM
• The omentum (greater and lesser omentum) is a well-vascularized double
fold of peritoneum with fat that contributes to the control of intra-
abdominal infection and inflammation.
• It aids in sealing off perforations (as in perforated ulcer or perforated
appendicitis) and controls inflammation (i.e., unruptured appendicitis).
• It delivers phagocytes that destroy bacteria, functions in the body’s
defense system against infection.

17. Peritoneal Fluid
The peritoneal cavity typically contains less than 100 mL of
sterile peritoneal fluid. This peritoneal fluid may act as both part of
the local defense system and a lubricant for intraperitoneal organs.
In certain disease such as nephrotic syndrome, congestive
heart failure, cirrhosis, or portal hypertension, the amount of
peritoneal fluid may increase from the normal less than 100ml
protective amount to several liters in volume.

18. Peritoneal ligaments
Peritoneal ligaments are folds of peritoneum that are
used to connect viscera to viscera or the abdominal wall.
There are multiple named ligaments that usually are
named in accordance with what they are.
 Gastrocolic ligament (stomach and colon)
 Splenocolic ligament, (spleen and colon)
 Round ligament
 Triangular ligament

20. Blood supply
The peritoneum has an extensive blood supply:
• Visceral peritoneum is supplied by the mesentric arteries that drains
into Portal circulation
• Parietal peritoneum is supplied by intercostal, lumbar, and epigastric
arteries that drains into IVC .
• Total Peritoneall blood flow is 50-100ml/min.

21. Nerve Supply
The innervation of the two components is divided:
The visceral peritoneum is supplied by non-somatic nerves.
The parietal peritoneum is supplied by somatic nerves.
This detail is important while evaluating for pain. Visceral pain is
poorly localized and vague and is generally caused by stretching,
distention, torsion, and twisting motion. Parietal pain is caused by direct
stimulation of nerve fibers and is described as sharp and well localized.

22. Function of peritoneum
• It suspend the organs within the peritoneal cavity. It fixes some organs
within the abdominal cavity.
• Storage of large amount of fat in the peritoneal ligaments (e.g. Greater
omentum)
• Peritoneal covering of intestine tends to stick together in infection. Greater
omentum is called the policeman of abdomen to prevent spread of
infection.
• It secretes the peritoneal fluid which helps in the gliding of the mobile
viscera over one another.

23. Disorder of the Peritoneum
1. ASCITES
2. PERITONEAL INFECTIONS: Intraperitoneal Abscesses
3. PERITONITIS:
• Primary (Bacterial) Peritonitis
• Secondary or Surgical Peritonitis
• Tuberculous Peritonitis

24. ASCITES
Ascites is the pathologic accumulation of fluid within the peritoneal
cavity.
The primary cause of non-malignant ascites accumulation is liver
disease (cirrhosis and portal hypertension). In cirrhotic patients, the
onset of ascites is an overall poor prognostic factor as patients are more
likely to develop spontaneous bacterial peritonitis (SBP), renal
(hepatorenal) failure, decreased quality of life, and decreased overall
survival.

25. PATHOPHYSIOLOGY:
Collagen deposition and fibrosis
SPLANCHNIC
VASODILATION
INCREASED
SPLANCHNIC PRESSURE
DECREASED ARTERIAL FILLING
Sodium Retention
PORTAL
HYPERTENSION
Lymphatic
Increased
Vasoconstrictons
Water retention
ASCITIS

26. CLINICAL MANIFESTATION
• Approximately 1.5 L of fluid must be present before dullness can be
detected by percussion.
• Because cirrhosis is the most common cause of ascites, evaluation of
any physical evidence of cirrhosis is important, such as palmar
erythema, dilated abdominal wall collateral veins (varicosities), and
multiple spider angiomas.
• Other systemic causes of ascites, such as congestive heart failure,
may also have signs on physical examination (i.e., jugular venous
distention).

27. MANAGEMENT
• Paracentesis is beneficial in both diagnosis and treatment.
• It allows for symptomatic relief of pressure or pain secondary to ascites.
• Paracentesis for ascitic fluid analysis is the most rapid and cost-effective method
of determining the etiology of ascites.
• It can be performed safely in most patients, including those with cirrhosis and
mild coagulopathy.
• Only clinically evident disseminated intravascular coagulation and fibrinolysis are
contraindications to paracentesis in patients with ascites.
• The SAAG is the most reliable method for quickly categorizing the various
causes of ascites.
• This gradient is the difference between serum albumin concentration and ascitic
fluid albumin concentration. SAAG values greater than 1.1 g/dl.

28. Intraperitoneal abscess
It is an infection within the abdominal cavity. The areas in which
abscesses commonly occur are defined by the configuration of the
peritoneal cavity as compartmentalized by the peritoneal ligaments,
small bowel mesentery and transverse and sigmoid mesocolons.

29. Etiology:
• Intraperitoneal abscess may be caused by gastrointestinal (GI)
perforations, post-operative complications, penetrating trauma,
and genitourinary (GU) infections.
• GI sources (diverticulitis, perforated peptic ulcer) and biliary
causes.
• Perforated appendicitis and gall-stone are frequent causes of
abscesses in this space.

30. Symptoms:
• Fever
• Tachycardia
• Pain may be mild or absent, especially in patients receiving
antibiotics.
• Prolonged ileus in a patient who has had recent abdominal
surgery or peritoneal sepsis,
• Worsening leukocytosis

31. Management:
• Immediate recognition
• Identification and control of the primary cause of the abscess (such
as GI perforation).
• Initiation of broad-spectrum antibiotics Aminoglycosides (except for
streptomycin), Ampicillin, Augmentin, Carbapenems, Tazact.
• Prompt drainage of the abscess, Percutaneous drainage is the
preferred route for localized intraperitoneal abscesses that are
approachable via image guidance.
• Operative drainage is reserved for intra-peritoneal abscesses for
which percutaneous drainage is inappropriate or unsuccessful.

32. Primary (Bacterial) Peritonitis
• SBP is defined as an infection of previously sterile ascitic fluid without an
apparent intra-abdominal source of infection, in particular, without obvious
GI perforation.
• It occurs in patients with cirrhosis or portal hypertension and results into
ascites.
• Patients with ascites unrelated to cirrhosis, such as nephrotic syndrome or
congestive heart failure, may also develop SBP.
• SBP results from bacterial, chlamydial, fungal, or mycobacterial infection in
the absence of a perforation of the GI

33. Primary Peritonitis cont....
SBP can occur in patients with asymptomatic ascites, therefore,
the diagnosis should be suspected in all hospitalized cirrhotic
patients with ascites exhibiting any symptoms of abdominal pain
or abdominal tenderness.
SBP should also be considered in patients with fever,
leukocytosis, signs of sepsis, renal insufficiency, or a history of
hepatic encephalopathy.

34. Diagnostic Evaluation:
• Paracentesis is established by an elevated neutrophil count of the ascitic
fluid greater than 250 cells/mL.
• Peritoneal fluid from the paracentesis should be sent for Gram stain and
cultures at the same time. If the neutrophil count is greater than 250
cells/mL.

35. •Broad-spectrum antibiotics including cover-age of gram-negative aerobes and
anaerobes (particularly Escherichia coli and Klebsiella) should be initiated
ceftriaxone, cefotaxime, ceftazidime, fluoroquinolones (ciprofloxacin,
levofloxacin), aminoglycosides (gentamicin, amikacin), imipenem.
•Antibiotic coverage, such as a third-generation cephalosporin should be
started and then tailored once peritoneal fluid culture results reveal the
specific organism causing SBP.
•Surgical intervention is rarely indicated.
Management:

36. Secondary or Surgical Peritonitis
• Secondary peritonitis is a result of an inflammatory process in the
peritoneal cavity due to inflammation, perforation, or gangrene of the GI
or GU tract.
• It is defined as the presence of pus in the peritoneal cavity.
• Diagnosis and early treatment of certain GI diseases, such as appendicitis
or gangrenous cholecystitis, prior to the development of secondary
peritonitis significantly decreases morbidity.
• Once peritonitis develops, surgical intervention is typically required
because in most cases, secondary peritonitis will lead to septic shock and
death if left untreated.

37. •Gram-negative and Enterococcus bacterial species.
•The large surface area of the peritoneal cavity can lead to massive fluid loss
as well as the sequestration or accumulation of peritoneal fluid secondary
to bacteremia.
•Furthermore, peritoneal circulation provides a route for rapid absorption of
bacteria, endotoxin (in the case of gram-negative bacteria) and
inflammatory cytokines into the systemic circulation.
Etiology:

38. Causes of Secondary Peritonitis
Estimated
Mortality Rate
Severity Causes (%)
Mild Appendicitis < 10
Perforated gastroduodenal ulcers
Acute salpingitis
Moderate Diverticulitis < 20
Small bowel perforation
Cholecystitis (gangrenous)
Severe Colonic perforations 20–50
Ischemic bowel
Necrotizing pancreatitis

39. Diagnostic Test:
• is based on the history, physical examination, and radiologic findings.
•Secondary peritonitis has a number of potential causes including perforated
peptic ulcer, perforated appendicitis, perforated diverticulitis, acute
cholecystitis or postsurgical complications.
•Therefore, sources that introduce blood into the peritoneal cavity, such as
gynecologic causes, including rupture of an ectopic pregnancy or ruptured
ovarian cyst, can also lead to peritoneal signs and should be included in the
differential diagnosis.

40. Radiologic Findings

41. Management:
•Broad-spectrum antibiotic therapy is required preoperatively, during
surgery, and postoperatively.
•In general, colonic perforations necessitate coverage for gram-negative
aerobic and anaerobic bacteria, whereas a peptic ulcer perforation
may require additional antifungal coverage.
•Operative intervention should occur as soon as possible after the
patient is stabilized and antibiotics have been initiated.
•Laparotomy remains the standard of care in the treatment of SBP.

42. TUBERCULOUS PERITONITIS
• Tuberculous peritonitis is seen in 0.5% of new cases of TB and is the sixth
most common site of extrapulmonary TB just after lymphatic, GU, bone and
joint, miliary, and meningeal TB.
• Tuberculous peritonitis presents as a primary infection without active
pulmonary, renal, or intestinal involvement.

43. Nonspecific chronic symptoms can be present for weeks to months prior
to recognition and can include:
•Low-Grade Fever
•Night Sweats
•Weight Loss
•Anorexia
•Malaise
•Abdominal tenderness is +nt in only half of patients with TB peritonitis.
•A positive tuberculin skin test is typically present
•Ascitic fluid will have an elevated WBC count.
Sign & Symptoms:

44. Diagnostic Evaluation
• Diagnosing this condition is difficult.
• Additionally, comorbid conditions (for example, cirrhosis) or age may show
the symptoms, most commonly, patients present with ascites (93%),
abdominal pain (73%), and fever (58%).
• Many patients present with distended, tender abdomens, but otherwise
physical examination signs are typically nonspecific.
• Ascitic fluid analysis with SAAG calculation, microbiological tests
(mycobacterial culture growth), peritoneal biopsy, laparoscopy.
• Chest x-ray may show old evidence of pulmonary tuberculosis but is
relative nonspecific (Srivastava et al, 2014).

45. Medical Management:
• TB Peritonitis is generally responsive to medical treatment alone, so early
diagnosis can prevent unnecessary surgical intervention
• The treatment of this is the same lines as for pulmonary tuberculosis.
• Conventional antitubercular therapy for at least 6 months including initial 2
months of HREZ (e.g. isoniazid, rifampicin, ethambutol and pyrazinamide)
followed by 4 month HR is recommended.
• Monitoring During Treatment of patients with tuberculosis requires careful
monitoring for adverse effects.
• Since hepatotoxicity may be caused by INH, RIF or PZA, patients receiving
antituberculous therapy with first-line drugs should undergo baseline
measurement of hepatic enzymes (transaminases, bilirubin and alkaline
phosphatase).

46. Surgical Management
• Surgery is usually adviced for those who developed complications,
including free perforation, confined perforation with abscess or fistula,
massive bleeding, complete obstruction, or obstruction not
responding to medical management.
• Surgical diagnostic methods: Laparoscopy, Laparotomy &
Colonoscopy

47. Nursing Management:
1. Deficient Fluid Volume related to Fluid shifts from extracellular,
intravascular, and interstitial compartments into peritoneal space.
2. Acute pain related to accumulation of fluid in peritoneal cavity
(abdominal distension) as evidenced by Muscle guarding, rebound
tenderness.
3. Risk for imbalanced nutrition less than body requirements as evidenced
by Nausea/vomiting and intestinal dysfunction.
4. Risk for Infection as evidenced by sign and symptoms.
5. Anxiety related to Physiological factors, hypermetabolic state as
evidenced by Apprehension and uncertainty.
6. Deficient Knowledge related to disease condition.

48. Deficient fluid volume related to fluid shifts from extracellular, intravascular, and
interstitial compartments into peritoneal space as evidenced by dry mucous membranes,
poor skin turgor, delayed capillary refill, weak peripheral pulses.
Nursing Interventions:
• Monitor vital signs for hypotension (including postural changes), tachycardia, tachypnea, fever.
• Measure CVP & Maintain accurate I&O and correlate with daily weights.
• Monitor body weight. Include measurements from gastric suction, drains, dressings,
diaphoresis, and abdominal girth for third spacing of fluid.
• Measure urine specific gravity.
• Observe skin or mucous membrane dryness, turgor.
• Notify peripheral and sacral edema.
• Change position frequently, provide frequent skin care, and maintain dry or wrinkle-free
bedding.
• Monitor laboratory studies: Hb/ Hct, electrolytes, protein, albumin, BUN, Cr.
• Administer plasma or blood, fluids, electrolytes, diuretics such as RL, DNS etc.

49. Acute pain related to accumulation of fluid in
peritoneal cavity (abdominal distension) as evidenced
by Muscle guarding, rebound tenderness.
Nursing Interventions
• Monitor pain: location, duration, intensity (0–10 scale) and
characteristics (dull, sharp, constant).
• Give semi-Fowler’s position.
• Provide comfort measures: massage, back rubs, deep breathing.
• Instruct in relaxation and visualization exercises.
• Administer Analgesics, Narcotics as prescribed by physician.

50. Risk for imbalanced nutrition less than body requirements as
evidenced by Nausea/vomiting and intestinal dysfunction
Nursing Interventions
• Measure abdominal girth.
• Monitor NG tube output. Note presence of vomiting, diarrhoea.
• Assess abdomen frequently for return to softness, reappearance of normal bowel sounds,
and passage of flatus.
• Auscultate bowel sounds, noting absent or hyperactive sounds.
• Monitor Weight regularly.
• Monitor BUN, protein, albumin, nitrogen balance as indicated.
• Advance diet as tolerated.
• Provide clear liquids to soft food.
• Administer TPN as indicated.

51. Risk for Infection as evidenced by sign and symptoms
Nursing Interventions:
• Note the risk factors such as: Abdominal trauma, acute appendicitis, peritoneal
dialysis are common risk factors.
• Monitor vital signs for hypotension, decreased pulse pressure, tachycardia, fever,
tachypnea.
• Notify the skin color, temperature, moisture.
• Maintain strict aseptic technique in care of abdominal drains, incisions or open
wounds, dressings, and invasive sites.
• Observe drainage from wounds or drains.
• Obtain specimens and monitor results of Blood, urine, wound cultures.
• Administer antimicrobials amikacin, clindamycin etc.
•

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