Definition/General
Introduction:
Placental infarction is the ischemic necrosis of placental tissue due to compromised maternal blood flow
It results from occlusion of spiral arteries or their branches
Small infarcts (<3 cm) are common and insignificant
Large or multiple infarcts may cause fetal compromise
Infarction affects >10% of placental volume in pathological cases.
Origin:
Results from inadequate maternal perfusion to intervillous space
Spiral artery obstruction by thrombosis or atherosclerosis
Decidual necrosis with vascular compromise
Maternal vascular disease (hypertension, diabetes)
Immunological factors may contribute.
Classification:
Classified by age: Recent infarcts (red, soft)
Old infarcts (white, firm)
By size: Small (<3 cm)
Large (>3 cm)
By location: Central (more significant)
Peripheral (less significant)
By extent: Focal vs extensive.
Epidemiology:
Small infarcts in 25% of term placentas
Clinically significant in 3-5%
More common with maternal hypertension
Increases with advancing gestation
Associated with IUGR in 15-20% cases.
Clinical Features
Presentation:
Often asymptomatic
IUGR (intrauterine growth restriction)
Oligohydramnios
Decreased fetal movements
Abnormal fetal heart rate
Preterm labor
Stillbirth (extensive infarction).
Symptoms:
Maternal symptoms often absent
Reduced fetal movements
Abdominal pain (if associated with abruption)
Hypertensive symptoms
Proteinuria
Visual disturbances.
Risk Factors:
Maternal hypertension (chronic, gestational, preeclampsia)
Diabetes mellitus
Smoking
Advanced maternal age
Thrombophilia
Autoimmune disorders
Previous pregnancy complications
Multiple pregnancy.
Screening:
Ultrasound may show echogenic areas
Doppler studies (increased resistance)
Fetal growth monitoring
Biophysical profile
Amniotic fluid assessment
Maternal blood pressure monitoring.
Master Placental Infarcts Pathology with RxDx
Access 100+ pathology videos and expert guidance with the RxDx app
Gross Description
Appearance:
Well-demarcated areas of pale, firm tissue
Recent infarcts: red-purple, soft
Old infarcts: white-yellow, firm
Depressed surface
Sharp demarcation from normal tissue
Triangular shape common.
Characteristics:
Firm consistency (old infarcts)
Gritty texture (calcification)
Pale cut surface
Loss of normal spongy appearance
Sharply defined borders
May be multiple.
Size Location:
Size ranges from few mm to >10 cm
Peripheral location more common
Marginal infarcts often insignificant
Central infarcts more problematic
Multiple small infarcts common.
Multifocality:
Multiple infarcts in severe cases
Random distribution
Coalescent pattern possible
Progressive involvement over time
Associated with other placental pathology.
Microscopic Description
Histological Features:
Coagulative necrosis of villi
Loss of nuclei in affected areas
Collapsed chorionic villi
Intervillous fibrin deposition
Ghost outline of villous architecture
Sharp demarcation from viable tissue.
Cellular Characteristics:
Syncytiotrophoblast loss in infarcted areas
Cytotrophoblast degeneration
Stromal cell necrosis
Fetal capillary thrombosis
Nuclear pyknosis and karyolysis
Eosinophilic cytoplasm.
Architectural Patterns:
Collapsed villous architecture
Intervillous space obliteration
Fibrin mesh formation
Loss of normal branching pattern
Peripheral viable rim may persist.
Grading Criteria:
Fresh infarcts: Nuclear preservation, congestion
Recent infarcts: Nuclear loss, eosinophilia
Old infarcts: Complete necrosis, fibrosis
Calcified infarcts: Dystrophic calcification
Organized infarcts: Fibrous replacement.
Immunohistochemistry
Positive Markers:
Fibrin (extensive deposition)
Cytokeratin (ghost trophoblast outlines)
CD68 (macrophages at border)
Factor VIII (thrombosed vessels)
Smooth muscle actin (vessel walls).
Negative Markers:
Ki-67 (no proliferation in infarct)
Normal trophoblast markers lost
Endothelial markers absent in necrotic areas
Decidual markers if decidual necrosis.
Diagnostic Utility:
Limited diagnostic role
Fibrin stains highlight extent
Trophoblast markers show loss
Vascular markers identify thrombosis
Morphology sufficient for diagnosis.
Molecular Subtypes:
Recent infarction (active process)
Old infarction (organized)
Calcified infarction (chronic)
Hemorrhagic infarction (with bleeding).
Molecular/Genetic
Genetic Mutations:
Thrombophilia genes (Factor V Leiden, Prothrombin)
MTHFR polymorphisms
Antiphospholipid antibodies
Protein C/S deficiency
Antithrombin deficiency.
Molecular Markers:
Increased apoptosis markers
Hypoxia-inducible factors
Inflammatory cytokines
Coagulation cascade activation
Oxidative stress markers.
Prognostic Significance:
Size determines clinical significance
Location important (central worse)
Multiple infarcts increase risk
Associated IUGR
Recurrence risk in subsequent pregnancies.
Therapeutic Targets:
Anticoagulation (if thrombophilia)
Antihypertensive therapy
Low-dose aspirin
Fetal surveillance
Early delivery if indicated.
Differential Diagnosis
Similar Entities:
Intervillous fibrin deposition
Placental abruption
Septal fibrosis
Calcification
Maternal floor infarction
Massive perivillous fibrin.
Distinguishing Features:
Infarction: Coagulative necrosis
Loss of architecture
Sharp demarcation
Fibrin deposition: Preserved architecture
No necrosis
Abruption: Retroplacental hematoma
Acute hemorrhage.
Diagnostic Challenges:
Small infarcts vs normal aging
Fibrin deposition vs infarction
Recent vs old infarcts
Significance assessment
Correlation with clinical findings.
Rare Variants:
Hemorrhagic infarction
Septic infarction
Embolic infarction
Massive infarction (>50% placenta).
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 weighing [X] grams with areas of infarction
Diagnosis
Placental infarction, [extent and age]
Clinical Correlation
[IUGR/hypertension/other clinical findings]
Gross Findings
[Number] areas of [recent/old] infarction, largest measuring [X] cm
Microscopic Findings
Coagulative necrosis of villi, loss of nuclei, fibrin deposition
Infarct Characteristics
Age: [recent/old], Size: [small/large], Location: [central/peripheral]
Extent of Involvement
Approximately [X]% of placental parenchyma involved
Associated Findings
Maternal vascular malperfusion, [other findings]
Clinical Significance
[Clinically significant/insignificant] based on size and location
Final Diagnosis
Placental infarction, [X]% involvement