Vaginal hematomas arise from disruption of blood vessels within the highly vascularized vaginal and paravaginal tissues, most commonly following vaginal delivery, episiotomy, or operative vaginal birth (forceps or vacuum-assisted). The rich arterial supply from branches of the internal iliac artery — specifically the vaginal artery, inferior vesical artery, and pudendal artery — creates a venous plexus that is vulnerable to shearing forces during delivery. Hematomas are classified by anatomical location: vulvar hematomas (below the pelvic diaphragm, most common), vaginal hematomas (within the paravaginal space extending into the ischiorectal fossa), and supralevator or retroperitoneal hematomas (above the levator ani, extending into the broad ligament — the most dangerous due to occult blood loss). The pathogenesis involves vascular injury with extravasation of blood into the loose connective tissue of the vaginal submucosa and paravaginal space. Tissue distensibility allows accumulation of significant blood volumes (500–1500 mL) before clinical detection, particularly in supralevator hematomas where the retroperitoneal space provides minimal tamponade effect. Hemostatic failure may result from obstetric coagulopathy (DIC from placental abruption, amniotic fluid embolism), pre-existing coagulation disorders (von Willebrand disease, factor deficiencies),...