Peritonitis

Overview:

Definition: Inflammation of the peritoneum and peritoneal cavity, often due to infection.
Primary Peritonitis: Arises from a bacterial, chlamydial, fungal, or mycobacterial infection without perforation or inflammation of the gastrointestinal (GI) or genitourinary (GU) tract.
Secondary Peritonitis: Results from GI or GU perforation or inflammation. Common causes include acute appendicitis, colonic diverticulitis, and pelvic inflammatory disease. runyon criteria = Proteine > 1gm/dl , glucose <50 , LDH >upper limit of normal in ascitic fluid implies secP

Spontaneous Bacterial Peritonitis (SBP)

Definition and Etiology:

Defined as bacterial infection of ascitic fluid without an intraabdominal source.
Commonly associated with cirrhosis, but can also occur with nephrotic syndrome and congestive heart failure.
High protein ascites rarely lead to SBP, e.g., peritoneal carcinomatosis.

Pathogens:

Adults: Mainly aerobic enteric flora like Escherichia coli and Klebsiella pneumoniae.
Children: Group A streptococcus, Staphylococcus aureus, and Streptococcus pneumoniae are common.
Anaerobic organisms are seldom involved due to oxygen presence in the intestinal wall.

Pathogenesis:

Bacterial translocation from the GI tract is key.
Cirrhosis can impair GI motility and alter gut microflora.
Impaired immune function hinders bacterial clearance from mesenteric lymphatics and bloodstream.

Diagnosis:

More than 250 neutrophils/mm³ in ascitic fluid.
Symptoms may include abdominal pain, fever, or leukocytosis in a patient with low-protein ascites.
Ascitic fluid culture typically monomicrobial.
Bedsides leukocyte esterase reagent strips can be used for rapid screening, though this is controversial.

Treatment:

Immediate start of broad-spectrum antibiotics, like third-generation cephalosporins.
No need for repeated paracentesis with typical rapid improvement post-antibiotic therapy.
Narrow antibiotic coverage once sensitivity tests results are available.

Prognosis and Complications:

Immediate mortality risk is low if treated quickly.
Development of hepatic failure complications, like GI hemorrhage and hepatorenal syndrome, can be fatal.
SBP marks a critical point in cirrhosis progression, with low 1- and 2-year survival rates.
Albumin plasma expansion can improve circulatory function and decrease mortality and hepatorenal syndrome risk in SBP patients.

Comprehensive Summary: Peritonitis, an inflammatory process of the peritoneal cavity, can be primary or secondary, with the latter being more common due to GI or GU tract issues. SBP, a subset of primary peritonitis, is a serious infection of the ascitic fluid often linked to liver cirrhosis, presenting significant diagnostic and therapeutic challenges. Rapid and accurate diagnosis followed by immediate antibiotic intervention is critical to patient outcomes. Despite low initial mortality, SBP is indicative of advanced liver disease and can precipitate severe complications. Management includes the use of broad-spectrum antibiotics and, in specific cases, adjunctive treatments like albumin plasma expansion to improve overall prognosis.

Tuberculous Peritonitis

Epidemiology:

Common in impoverished areas and among immunocompromised populations (e.g., HIV, chronic immunosuppression).
Associated with conditions like alcoholic cirrhosis and chronic renal failure.
Sixth most common form of extrapulmonary tuberculosis.

Pathogenesis:

Most cases from reactivation of latent disease, initially spread hematogenously from primary pulmonary infection.
Roughly 17% associated with active pulmonary tuberculosis.

Clinical Presentation:

Insidious onset with symptoms developing over weeks to months.
Abdominal swelling due to ascites in over 80% of cases.
Non-specific, vague abdominal pain.
Constitutional symptoms (low-grade fever, night sweats, weight loss, anorexia, malaise) in about 60%.
Concomitant chronic conditions can obscure symptoms.
Abdominal tenderness in about 50%.

Diagnostic Indicators:

Positive tuberculin skin test in most cases.
Abnormal chest radiograph in about 50%.
Ascitic fluid serum-ascites albumin gradient (SAAG) < 1.1 g/dL.
Ascitic fluid analysis shows high protein, erythrocytes, and lymphocyte predominance.
Ascitic fluid adenosine deaminase activity and PCR are rapid, noninvasive, sensitive, and specific tests.

Imaging:

Ultrasound: Echogenic ascitic fluid with mobile strands or particulate matter.
CT: Thickened, nodular mesentery; mesenteric lymphadenopathy; omental thickening.

Definitive Diagnosis:

Laparoscopy with directed biopsy of the peritoneum is preferred.
- Whitish nodules and caseating granulomas on histologic examination.
- Multiple intra-abdominal adhesions common.
Differential includes peritoneal carcinomatosis, sarcoidosis, and Crohn disease.
Low yield for acid-fast bacilli on ascitic fluid microscopy; cultures positive in less than 20% and take up to 8 weeks.

Treatment:

Standard antituberculous drugs (isoniazid and rifampin) for 9 months.
Monitor for hepatotoxicity, especially in patients with alcoholic cirrhosis.

Comprehensive Summary: Tuberculous peritonitis, often presenting with ascites and non-specific symptoms, is a significant diagnostic challenge, particularly in immunocompromised or chronic disease patients. It typically arises from the reactivation of latent peritoneal tuberculosis and requires careful interpretation of clinical and diagnostic tests, including a positive tuberculin skin test and specialized ascitic fluid analysis. Imaging studies provide supportive evidence, but the gold standard for diagnosis is laparoscopy with directed peritoneal biopsy, identifying characteristic caseating granulomas. Treatment parallels that for pulmonary tuberculosis but requires careful monitoring due to potential hepatotoxicity in patients with pre-existing liver conditions.

CAPD-Associated Peritonitis

Epidemiology:

In the U.S., 6% of chronic renal failure patients are on CAPD.
Incidence of peritonitis: Roughly one episode every 1 to 3 years.
In Scotland (1999-2002): One episode every 19.2 months of dialysis.
Leading cause of technical failure in CAPD (43% of cases).

Clinical Presentation:

Symptoms: Abdominal pain, fever, and cloudy dialysate.
Diagnosis criteria: >100 leukocytes/mm³ in dialysate, with >50% neutrophils.

Diagnostic Challenges:

Gram stain detects causative organisms in 10% to 40% of cases only.

Microbial Causes:

75% of infections are due to gram-positive organisms.
Staphylococcus epidermidis (30-50% of cases).
Other significant pathogens: S. aureus, gram-negative bacilli, and fungi.

Treatment:

Intraperitoneal antibiotics, often a first-generation cephalosporin.
Culture-directed antibiotic therapy cures 75% of infections.
Cure rates vary by organism:
- Coagulase-negative staphylococci: 90%.
- S. aureus: 66%.
- Gram-negative bacilli: 56%.
- Fungi: 0% (requiring catheter removal).

Management of Refractory Cases:

Recurrent or persistent peritonitis necessitates dialysis catheter removal.
Patients typically revert to hemodialysis.

Comprehensive Summary: Peritonitis is a significant complication for patients undergoing CAPD, marking a common endpoint for technical failure of the dialysis technique. Clinical indicators include abdominal discomfort, fever, and a characteristic change in the dialysate's clarity. While gram-positive bacteria predominate in etiology, with Staphylococcus epidermidis being the most common, gram-negative and fungal infections are notable for their difficulty in treatment and poor resolution rates. The primary treatment approach with intraperitoneal antibiotics is largely successful, but the persistence of infection often warrants catheter removal and transition back to hemodialysis. This information is crucial for healthcare providers managing CAPD patients and for ensuring prompt and effective treatment of peritonitis, thus prolonging the efficacy of CAPD and improving patient outcomes.