PERITONITIS AND ASCITES

DR. ANIL.K.JHAJHRIA

• 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.

The etiology of disease depends on the type, as well as location, of peritonitis, as follows:

• Primary peritonitis• Secondary peritonitis• Tertiary peritonitis• Chemical peritonitis

ASCITIC FLUID INFECTION• A)SBP.• B)Monomicrobial non neutrocytic

bacterascites.• C)Culture negative neutrocytic ascites.• D)Secondary bacterial peritonitis.• E)Polymicrobial bacterascites (needle

perforation of the bowel).

PRIMARY PERITONITIS• Also called as spontaneous bacterial

peritonitis.• SBP is an inflammation of the peritoneum in a

patient with pre-existing ascites. It is commonly caused by bacterial infection and can present as a localized or generalized peritonitis.

• SBP occurs in both children and adults and is a well-known complication in patients with cirrhosis.

• Of patients with cirrhosis who have SBP, 70% are Child-Pugh class C.

• Once thought to occur only in those individuals with alcoholic cirrhosis, SBP is now known to affect patients with cirrhosis from any cause.

• In addition, SBP can occur as a complication of any disease state that produces ascites, such as heart failure and Budd-Chiari syndrome.

• Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing spontaneous bacterial peritonitis.

PATHOPHYSIOLOGY

• A key predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to delayed intestinal transit time.

• Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the RE 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.

• Some studies 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.

• Others suggest bacterial inoculation of ascites is hematogenous transmission in combination with an impaired immune system. Nonetheless, the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains controversial.

• Interestingly, adults with SBP typically have ascites, but most children with spontaneous bacterial peritonitis do not have ascites. The reason for and mechanism behind this is the source of ongoing investigation.

• Common organisms include E.coli(50%), Klebsiella pneumoniae, S.pneumoniae and other streptococcal species.

• Other pathogens implicated in SBP include M. tuberculosis, N. gonorrhoeae, C. trachomatis, and Coccidioides immitis.

• Primary tubercular peritonitis is becoming more common in HIV/AIDS patients, though it can occur separately also as an independent entitiy.

• However, some data suggest that the percentage of gram-positive infections may be increasing. One study cites a 34.2% incidence of streptococci, ranking in second position after Enterobacteriaceae. Viridans group streptococci (VBS) accounted for 73.8% of these streptococcal isolates.

• Anaerobic organisms are rare because of the high oxygen tension of ascitic fluid.

• A single organism is noted in 92% of cases, and 8% of cases are polymicrobial.

Signs and Symptoms may include the following:• Fever and chills• Abdominal pain or discomfort• Worsening or unexplained encephalopathy• Diarrhea• Ascites that does not improve following

administration of diuretic medication• Worsening or new-onset renal failure• Ileus• Abdominal tenderness-Findings can range from

mild tenderness to overt rebound and guarding.

• Physical examination may also disclose hypotension (5-14% of patients) or signs of hepatic failure such as jaundice and angiomata.

SECONDARY PERITONITIS

• Secondary peritonitis is an inflammation or mechanical break in the G.I tract, genitourinary tract, or a solid organ that causes the peritoneal cavity to be exposed to the resident flora of the gastrointestinal tract.

• The peritonitis may be localized (eg, walled-off perforated appendicitis) or generalized (eg, perforated diverticulitis with extensive contamination of the entire peritoneal cavity).

Bacterial infection due to a perforated viscus-• such as a perforated appendix or duodenal ulcer• severe pancreatitis (with more than three

Ranson criteria) with necrosis and infection of pancreatic and peri-pancreatic tissue

• ruptured ectopic pregnancy ,• inflammatory bowel disease ( Crohn disease and

ulcerative colitis),• acute cholecystitis , diverticulitis , bowel

obstruction, pelvic inflammatory disease , abdominal trauma, and complications following abdominal surgery.

• Anaerobes are uncommon if the perforation is high in the gut but common in colonic perforations where obligate anaerobes greatly outnumber aerobic bacteria (1,000:1).

• Common pathogens include E.coli, Bacteroides fragilis, enterococci, Fusobacterium, Clostridium species etc.

• If the perforation is from the upper G.I tract, the typical organisms include Lactobacillus , Candida, and Streptococcus species.

• Infection with multiple organisms is typical.

Features include –• abdominal pain• fever• tachycardia• hypotension • absent bowel sounds• peritoneal signs (tenderness upon light

percussion, rebound tenderness, guarding, and rigidity)

• Assess patient rapidly for presence of a surgical abdomen, which requires an emergent operative procedure.

• Initiate aggressive fluid and electrolyte resuscitation.

• Start appropriate antibiotic therapy immediately.

• Failure to treat or a delay in treatment may quickly lead to sepsis, multiorgan system failure, and death.

DIAGNOSIS AND MANAGEMENT

RUNYON’S CRITERIA

• Diagnosis of SecBP (according to Runyon's criteria) is based on-

• increased total protein in ascitic fluid > 10 g/l • elevated lactate dehydrogenase in ascites

(LDH is > 240 U/l) and • glucose < 50mg/dl

Laboratory Tests in SBP-• Ascitic fluid analysis reveals the following:• Cell count with an absolute

polymorphonuclear cell count >250/mm 3.

• Presence of bacteria on Gram stain.• pH <7.31.• Lactic acid >32 mg/dl.• Protein <1 g/dl.• Glucose >50 mg/dl.• Lactate dehydrogenase <225 mU/mL.• Positive culture of peritoneal fluid.

Measurement of the serum/ascites/albumingradient:• The serum/ascites/albumin gradient indirectly

measures portal pressure.• The albumin concentration of ascitic fluid and

serum must be obtained on the same day.• The ascitic fluid value is subtracted from the

serum value to obtain the gradient.• If the difference (not a ratio) is >1.1 g/dl, the

patient has portal hypertension, with 97% accuracy.

• If the difference is <1.1 g/dl, portal hypertension is not present. The majority of patients with SBP have portal hypertension as a result of cirrhosis.

Imaging Studies• Abdominal ultrasound: if there is clinical

difficulty in performing paracentesis.• CT scan: to rule out secondary peritonitis (if

indicated) and to exclude abscess, mass.

Treatment of SBP-• Cefotaxime (2 g IV q8h) or ceftriaxone (2 g IV q24h) or

ticarcillin-clavulanate or piperacillin-tazobactam. Continue therapy for 7 days. Repeat diagnostic paracentesis can be done at day 2. Repeat paracentesis at 48 hr will demonstrate a significant decrease in polymorphonuclear count in patients with SBP. If ascites PMN count decreases by at least 25% at day 2, IV therapy can be switched to PO (levofloxacin 250 mg PO bid) to complete 7 days of therapy.

• IV albumin (1.5 g/kg of body weight upon initial diagnosis and 1 g/kg of albumin on day 3) if BUN >30 mg/dL, serum creatinine >1 mg/dl, bilirubin >4 mg/dL.

• cirrhosis: frusemide, spirinolactone, Na+ restriction, TIPS procedure.

TREATMENT OF SEC PERITONITISTreatment-Nonpharmacologic Therapy-• IV hydration to correct dehydration,

hypovolemia.• Blood transfusion to correct anemia from

hemorrhage.• Nasogastric decompression, especially if

obstruction is present.• Oxygen: intubation if necessary.• Bed rest.

• Surgery to correct underlying pathology, such as controlling hemorrhage, correcting perforation, draining abscess.

• Broad-spectrum antibiotics to cover both gram-negative aerobic and gram-negative anaerobic bacteria:– 1. Mild-moderate disease: piperacillin-tazobactam 3.375 g IV

q6h or 4.5 g IV q8h or ticarcillin-clavulanate 3.1 g IV q6h. Alternative agents are ciprofloxacin 400 mg IV q12h or levofloxacin 750 mg IV q24h plus metronidazole 1 g IV q12h.

– 2. Severe life-threatening disease: imipenem 500 mg IV q6h or meropenem 1 g IV q8h. Alternative agents are ampicillin plus metronidazole plus ciprofloxacin.

• Pain control: morphine or meperidine as needed (hold until diagnosis confirmed)

TERTIARY PERITONITIS

• TP may be defined as a severe recurrent or persistent intra-abdominal infection after apparently successful and adequate surgical source control of secondary peritonitis.

• Various definitions have emphasized on failed surgical source control or inadequate antibiotic therapy of secondary peritonitis or even impaired host response to peritoneal infection.

• The latest ICU consensus conference guideline provides a precise definition of TP as intra-abdominal infection that persists or recur ≥48 h following successful and adequate surgical source control.

• Several other conditions can cause a primary or nonsurgical peritonitis:

• Infectious causes include-• tuberculosis , HIV , chlamydial infection, and

gonorrhea.• Noninfectious causes include polyarteritis

nodosa , systemic lupus erythematosus , scleroderma , and familial Mediterranean fever.

TUBERCULAR PERITONITIS• Peritoneal tuberculosis is an uncommon site of

extrapulmonary infection caused by Mycobacterium tuberculosis. Infection typically occurs with re- activation of latent tuberculosis in patients with the following risk factors: cirrhosis , HIV infection , diabetes mellitus , underlying malignancy, treatment with antitumor necrosis factor agents, and in peritoneal dialysis

• The most common features are ascites, abdominal pain and fever

• Only 33% of patients will have evidence of latent tuberculosis on chest radiograph

• A positive tuberculin skin test is seen in only 70% of patients

• The serum to ascites albumin gradient will be less than 1.1 g/dL

• The total protein concentration of the ascitic fluid is typically greater than 3.0 g/dL

• Neutrocytic ascites—and an initial ascitic fluid analysis—may meet criteria for secondary bacterial peritonitis; however, sometimes may present with features of mixed ascites.

• Examination of an acid-fast–stained smear of ascitic fluid will show a sensitivity of 0% to 6%. The frequency of a positive ascites culture is greater than 20%.

• Peritoneal biopsy is usually needed to diagnose tuberculous peritonitis.

• Treatment is anti-TB drugs for 6 months [2H3R3Z3E3+4H3R3]

CHEMICAL PEROITONITIS• Chemical (sterile) peritonitis may be caused by

irritants such as bile, blood, barium, or other substances or by transmural inflammation of visceral organs (eg, Crohn disease) without bacterial inoculation of the peritoneal cavity.

• Clinical signs and symptoms are indistinguishable from those of SP or peritoneal abscess, and the diagnostic and therapeutic approach should be the same.

ASCITES

MIXED ASCITES• When the as cites is due to more than one

cause, resulting in both transudative picture superimposed by exudative features.

• For example, liver cirrhosis and tubercular peritonitis or liver cirrhosis and malignancy.

• In malignancy protein content of ascitic fluid will be high while in TB markers of tb like ADA will be high.

• In these cases confirmation of diagnosis requires further investigation like AFB culture, looking for primary in case of malignancy.

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