It is seen protruding into the amniotic cavity near the insertion of the cord. Doppler examination shows anechoic cystic areas, with pulsatile flow in spectral analysis. Some chorioangiomas may be solid masses, and may not be identifiable in gray-scale imaging. Therefore, the investigation of choice is Colour Doppler, which also distinguishes it from placental hematoma.They can also be detected with MRI.Histologically, chorioangiomas consist of abundant vascular channels and may be cellular. Management
Expectant management is recommended for chorioangioma as majority of them are asymptomatic. Large tumors are monitored with ultrasonogram every 1–2 weeks. In case of maternal or foetal complications, possible interventions are serial foetal transfusions, fetoscopic laser coagulation of vessels supplying the tumor, endoscopic surgical devascularization and chemosclerosis using absolute alcohol. Prognosis
Large chorioangiomas with decreased echogenicity, decreased tumor volume and decreased blood flow in colour doppler images are may undergo spontaneous infarction. When chorioangiomas have deceased blood flow, fetal hemodynamics and clinical outcome are found to be improved. Epidemiology
It is the most common tumor of the placenta. Chorioangiomas over the size of 5 cm in diameter are rare, and occur at a rate of 1:3500 to 1:16,000 births. Smaller chorioangiomas are more frequent, with an incidence of 14‑139:10,000 births. However, many small chorioangiomas may not be sonologically visible and hence go unreported. In a clinical study, more than half of all tumors were discovered only by histological techniques. History
Chorioangioma was first described by Clarke in 1798. See also
Hemangioma
Chorangiosis

References
External links
Chorangioma (pathweb.uchc.edu)
Chorangioma (humpath.com)
Microvillus inclusion disease, previously known as Davidsons disease, congenital microvillus atrophy and, less specifically, microvillus atrophy (note: microvillus is often misspelled as microvillous), is a rare genetic disorder of the small intestine that is inherited in an autosomal recessive pattern. Presentation
It is characterized by chronic, intractable diarrhea in new-born infants, starting in the first few days of life. This results in metabolic acidosis and severe dehydration. Pregnancy and birth are usually normal. Pathophysiology
It is caused by a congenital villus atrophy, atrophy of apical microvilli and intracellular accumulation of apical enzymes and transporters in the epithelial cells of the small intestine. MVID is in ost cases caused by mutations in the MYO5B gene. A minority of cases involves mutations in the STX3 gene. Diagnosis
Prenatal screening in utero is currently offered by several medical centers since the gene(s) involved in the disease were recently discovered to be MYO5B; Diagnosis is typically made by biopsy of the small intestine. Biopsy
The appearance of microvillous inclusion disease on light microscopy is similar to celiac sprue; however, it usually lacks the intraepithelial lymphocytic infiltration characteristic of celiac sprue and stains positive for carcinoembryonic antigen (CEA). The definitive diagnosis is dependent on electron microscopy. Differential diagnosis
The differential diagnosis of chronic and intractable diarrhea is:
Intestinal epithelial dysplasia
Syndromatic diarrhea
Immunoinflammatory enteropathy

Prognosis
It is nearly always fatal unless, like short bowel syndrome patients, treated with parenteral nutrition or an intestinal transplant.