Ovarian torsion occurs when the ovary (and often the ipsilateral fallopian tube) rotates on its vascular pedicle -- the infundibulopelvic ligament (containing the ovarian artery and vein) and the utero-ovarian ligament -- partially or completely occluding its blood supply. The pathophysiology follows a predictable ischemic cascade. Initial rotation typically compresses the thin-walled, low-pressure ovarian vein and lymphatics first, while the higher-pressure ovarian artery continues to deliver blood. This creates massive venous and lymphatic congestion, causing the ovary to swell rapidly with edematous, hemorrhagic fluid. The enlarging, congested ovary becomes heavier, which can worsen the torsion degree. Eventually, arterial inflow is also compromised, leading to complete ischemia and if untreated, hemorrhagic infarction and necrosis. The dual blood supply to the ovary (from both the ovarian artery originating from the aorta and the ovarian branch of the uterine artery) explains a critical diagnostic limitation: Doppler ultrasound may demonstrate preserved arterial flow even with significant torsion, as collateral blood supply through the uterine artery branch can maintain some perfusion. This is why Doppler sensitivity for torsion is only 60-70%, and a normal Doppler...