Definition/General

Introduction:
-Placental chorioamnionitis is the inflammatory infiltration of the fetal membranes and umbilical cord
-It represents the histological counterpart of clinical chorioamnionitis
-The condition involves ascending bacterial infection from the lower genital tract
-It occurs in 10-20% of term deliveries
-Higher incidence in preterm births (40-70%).
Origin:
-Results from ascending infection through the cervix
-Bacterial colonization of amniotic fluid
-Maternal inflammatory response in chorion and decidua
-Fetal inflammatory response in umbilical vessels
-Hematogenous seeding less common.
Classification:
-Staged by location and severity: Stage 1: subchorionitis/chorionitis
-Stage 2: chorioamnionitis
-Stage 3: necrotizing chorioamnionitis
-Maternal response vs fetal response
-Acute vs chronic inflammation.
Epidemiology:
-Incidence: 10-20% term pregnancies
-40-70% preterm births
-More common with prolonged rupture of membranes
-Associated with preterm labor
-Neonatal sepsis in 2-13% cases.

Clinical Features

Presentation:
-Maternal fever (>38°C)
-Maternal tachycardia (>100 bpm)
-Fetal tachycardia (>160 bpm)
-Uterine tenderness
-Malodorous amniotic fluid
-Maternal leukocytosis
-Preterm labor.
Symptoms:
-Fever and chills
-Abdominal pain
-Malodorous discharge
-Uterine contractions
-Nausea and vomiting
-General malaise.
Risk Factors:
-Prolonged rupture of membranes (>18 hours)
-Prolonged labor
-Multiple vaginal examinations
-Internal fetal monitoring
-Meconium-stained fluid
-Maternal GBS colonization
-Young maternal age
-Substance abuse.
Screening:
-Clinical criteria (fever, tachycardia, leukocytosis)
-Laboratory tests: CBC, CRP
-Amniotic fluid analysis (if indicated)
-Blood cultures
-Fetal monitoring.

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Gross Description

Appearance:
-Opaque, thickened membranes
-Yellow-green discoloration
-Purulent exudate on surfaces
-Friable, easily torn membranes
-Foul odor may be present
-Umbilical cord may appear inflamed.
Characteristics:
-Loss of membrane translucency
-Increased thickness
-Surface exudate
-Congested vessels
-Edematous cord.
Size Location:
-Diffuse involvement of membranes
-Placental surface changes
-Umbilical cord inflammation
-Maternal surface may show purulence.
Multifocality:
-Usually diffuse process
-May be focal initially
-Progressive extension
-Associated with funisitis.

Microscopic Description

Histological Features:
-Neutrophilic infiltration of membranes
-Maternal inflammatory response: chorion/decidua
-Fetal inflammatory response: umbilical vessels
-Stromal edema
-Vascular congestion
-Necrosis in severe cases.
Cellular Characteristics:
-Neutrophils predominant in acute phase
-Macrophages and lymphocytes
-Plasma cells in chronic cases
-Bacterial organisms may be visible
-Degenerative changes in amnion.
Architectural Patterns:
-Subchorionic space infiltration (stage 1)
-Chorioamniotic infiltration (stage 2)
-Necrotizing inflammation (stage 3)
-Umbilical vessel wall infiltration
-Concentric zones of inflammation.
Grading Criteria:
-Maternal response: Stage 1-3
-Fetal response: Grade 1-3
-Acute: neutrophilic
-Chronic: lymphoplasmacytic
-Severity assessment: mild, moderate, severe.

Immunohistochemistry

Positive Markers:
-CD68 (macrophages)
-CD45 (leukocytes)
-Myeloperoxidase (neutrophils)
-CD3 (T-lymphocytes)
-CD20 (B-lymphocytes)
-Cytokeratin (amnion epithelium).
Negative Markers:
-Specific pathogens require special stains
-Gram stain for bacteria
-PAS for fungi
-Silver stains for organisms.
Diagnostic Utility:
-Limited routine use
-Research applications
-Special stains for organisms
-Immunophenotyping inflammatory cells.
Molecular Subtypes:
-Bacterial chorioamnionitis
-Viral chorioamnionitis
-Fungal chorioamnionitis
-Sterile inflammation.

Molecular/Genetic

Genetic Mutations:
-Host genetic factors
-Cytokine gene polymorphisms
-Toll-like receptor variants
-Complement system genes
-Immunoglobulin variants.
Molecular Markers:
-Pro-inflammatory cytokines (IL-1β, TNF-α, IL-6)
-Chemokines (IL-8)
-Acute phase reactants (CRP)
-Matrix metalloproteinases
-Prostaglandins.
Prognostic Significance:
-Severity correlates with neonatal outcomes
-Fetal inflammatory response worse prognosis
-Funisitis increases morbidity
-Necrotizing inflammation severe complications.
Therapeutic Targets:
-Antibiotic therapy
-Early delivery
-Neonatal antibiotics
-Anti-inflammatory agents (experimental)
-Supportive care.

Differential Diagnosis

Similar Entities:
-Chronic villitis
-Decidual vasculopathy
-Meconium-associated changes
-Maternal floor infarction
-Subchorionic hematoma.
Distinguishing Features:
-Chorioamnionitis: Membrane inflammation
-Neutrophilic infiltrate
-Clinical correlation
-Villitis: Villous inflammation
-Lymphocytic infiltrate
-Meconium: Pigmented macrophages
-No neutrophils.
Diagnostic Challenges:
-Mild inflammation vs normal
-Chronic vs acute
-Sterile inflammation
-Post-mortem changes
-Sampling issues.
Rare Variants:
-Chronic chorioamnionitis
-Granulomatous inflammation
-Eosinophilic chorioamnionitis
-Candidal chorioamnionitis.

Sample Pathology Report

Template Format

Sample Pathology Report

Complete Report: This is an example of how the final pathology report should be structured for this condition.

Specimen Information

Placenta with membranes showing inflammatory changes

Diagnosis

Acute chorioamnionitis

Clinical Correlation

Maternal fever, prolonged rupture of membranes [X] hours

Membrane Examination

Opaque, thickened membranes with purulent exudate

Microscopic Findings

Neutrophilic infiltration of chorioamniotic membranes

Maternal Response

Stage [1/2/3] chorioamnionitis

Fetal Response

Funisitis: [present/absent], Grade [1-3] if present

Severity Assessment

[Mild/Moderate/Severe] acute inflammation

Microbiological Findings

Culture results: [organism/sterile/pending]

Final Diagnosis

Acute chorioamnionitis, Stage [X], with/without funisitis