Ovarian Torsion

• Venous and lymphatic occlusion (initial phase): The ovarian vascular pedicle contains thin-walled veins that are more compressible than arteries. When torsion occurs, venous and lymphatic drainage becomes obstructed first, while arterial inflow continues transiently. This creates a compartment syndrome-like state within the ovary, leading to increased interstitial pressure, tissue edema, and progressive vascular engorgement. The resulting venous congestion triggers the release of inflammatory mediators, including cytokines (IL-1, IL-6, TNF-α) and reactive oxygen species (ROS), which further propagate endothelial damage and increase vascular permeability. This phase typically lasts 4-8 hours and is theoretically reversible with prompt detorsion.

• Arterial insufficiency and ischemia (intermediate-late phase): As edema accumulates and intravascular pressure increases, arterial perfusion becomes compromised. The combination of mechanical compression from venous engorgement and the pro-inflammatory milieu creates severe tissue hypoxia. Cellular metabolism shifts from aerobic oxidative phosphorylation to anaerobic glycolysis, generating lactate and other metabolic byproducts that further acidify the tissue microenvironment. Hypoxia-inducible factor 1α (HIF-1α) activation triggers both adaptive and maladaptive responses; while HIF-1α upregulates angiogenic factors (VEGF, FGF), prolonged ischemia instead drives apoptotic pathways and necrosis. If ischemia persists beyond 6-8 hours, irreversible cellular damage and follicle atresia occur, with permanent loss of ovarian function.

• Reperfusion injury (if torsion is partial or intermittent): Intermittent or spontaneously resolving torsion can activate repeated cycles of ischemia and reperfusion. During reperfusion, xanthine oxidase converts hypoxanthine and xanthine to uric acid while generating superoxide radicals. These ROS initiate lipid peroxidation of cell membranes, damage mitochondrial function, and activate caspase-dependent apoptosis. Neutrophil infiltration amplifies this injury through degranulation and further ROS production. This mechanism explains why some ovaries may recover function after apparent complete torsion—the extent of reperfusion injury depends on the degree and duration of ischemia, as well as the timing and completeness of detorsion.

• Mechanical derangement and anatomical factors: Torsion typically occurs when an enlarged ovary (due to cyst, tumor, or polycystic morphology) creates a change in the center of gravity and inertial forces that overcome the normal anchoring provided by the ovarian ligament and mesovarium. The elongation of the ovarian ligament (increased length increases mechanical advantage for rotation) and increased ovarian volume (>5 cm diameter significantly raises risk) are critical anatomical determinants. Rotation typically occurs along the long axis of the vascular pedicle; complete 360° torsion is most common, though partial torsion (180-270°) can also cause significant compromise.

• Enlarged or cystic ovary (most common predisposing factor): Approximately 50-60% of ovarian torsion cases occur in the setting of an ovarian cyst or mass. Functional cysts (corpus luteum cysts, follicular cysts) are the most frequent pathology in reproductive-age women; these occur naturally with ovulation but are more prone to torsion when they reach 5-8 cm diameter. Mature cystic teratomas (dermoid cysts) and other benign tumors have increased torsion risk because they are typically large and eccentric within the ovary. Ovarian hyperstimulation syndrome (OHSS), occurring after fertility treatment with gonadotropins or hCG administration, dramatically enlarges both ovaries through multiple developing follicles (>5 cm per ovary), making bilateral torsion risk significant in this population. Ovarian torsion can rarely be the presenting manifestation of an ovarian malignancy.

• Polycystic ovary morphology: Women with polycystic ovary syndrome (PCOS) have a 2-3 fold increased risk due to persistently enlarged ovaries (often >10 cm³ volume) with multiple small follicles, creating altered mass distribution and increased rotational forces. The degree of hyperandrogenism and insulin resistance does not directly correlate with torsion risk; rather, the physical morphology of the enlarged ovary is the critical factor.

• Age and reproductive stage: While ovarian torsion peaks in women aged 20-40 years, it can occur across all age groups. Prepubertal girls (mean age 9-11 years) represent 5-15% of cases and often present with larger ovarian masses (teratomas, simple cysts). Postmenopausal women account for fewer cases but have increased malignancy risk when torsion occurs, as any new ovarian enlargement in this population warrants investigation for malignancy. Torsion during pregnancy (0.5-5 cases per 10,000 pregnancies) typically occurs in the first or early second trimester; pregnant women have higher anesthetic and surgical risks.

• Adhesions and anatomical variations: Prior pelvic surgery, endometriosis, or pelvic inflammatory disease creating adhesions can mechanically predispose to torsion by creating fixed or mobile adhesion points. Long or lax ovarian ligaments (anatomical variation) increase the lever arm for rotational forces. Ovarian hypermobility secondary to elongated infundibulopelvic ligaments is a constitutional risk factor.

• Rapid ovarian growth: Any condition causing rapid change in ovary size increases torsion risk. Emergency contraceptive use (particularly high-dose estrogen-progestin regimens, though modern formulations carry lower risk) may promote cyst formation. Pregnancy itself (increased hCG and corpus luteum size) rarely precipitates torsion but can unmask pre-existing ovarian enlargement.

• Acute unilateral lower abdominal or pelvic pain (cardinal symptom): Pain is sudden in onset in most cases, occurring "like a thunderclap" or "worst pain I've ever felt," and is localized to the lower quadrant ipsilateral to the torsed ovary. The severity reflects both the mechanical torsion and the acute inflammatory cascade. Pain intensity typically does not correlate with whether torsion is complete or partial; partial torsion can cause severe intermittent pain due to repeated ischemia-reperfusion cycles. Pain may be described as sharp, stabbing, or colicky. Duration from onset to presentation is typically <24 hours in acute presentation, though some patients have had pain for several days if torsion is intermittent with spontaneous detorsion.

• Nausea and vomiting: Occurs in 70-80% of cases due to visceral innervation of the ovary via afferent T10 nerves with shared central processing with GI symptoms. Vomiting can be severe enough to cause dehydration and electrolyte abnormalities, particularly in patients with delayed presentation.

• Abdominal distension and peritoneal signs: Physical examination may reveal localized tenderness in the lower abdomen or pelvic region, often with guarding on the side of torsion. Rebound tenderness and rigidity suggest peritoneal inflammation from ischemic tissue damage and possible infarction. In cases of hemorrhagic infarction or rupture, generalized peritonitis develops. Abdominal distension may occur with associated ileus or if significant hemorrhage is present.

• Pelvic and adnexal findings on examination: Unilateral adnexal mass or fullness may be palpable on pelvic examination, particularly if the cyst is large (>8 cm). Acute cervical motion tenderness and adnexal tenderness are present in nearly all cases. Fever is absent in uncomplicated torsion (distinguishing it from salpingitis or tubo-ovarian abscess), though may develop if necrotic tissue becomes infected or abscess forms.

• Important clinical variants: Intermittent or recurrent torsion presents with episodes of severe pain separated by pain-free intervals; the ovary partially detorts spontaneously between episodes. This creates a diagnostic trap because imaging may appear normal if performed during a pain-free interval, and recurrent episodes may be dismissed as functional pain. Pediatric and adolescent presentation often occurs in girls with no prior gynecologic history and minimal risk factors for cyst formation, causing significant diagnostic delay as providers may not consider gynecologic emergency in this population. Torsion during pregnancy may be confused with threatened abortion, preterm labor, or placental abruption, necessitating high clinical suspicion.

• Clinical suspicion and history: The diagnosis begins with clinical suspicion in any woman of reproductive age presenting with acute unilateral pelvic pain of sudden onset. Critical historical features include: acute onset (distinguishes from chronic conditions), severity (typically described as worst pain ever), lack of fever (argues against infection), recent fertility treatment (increased OHSS risk), and prior similar episodes (suggests intermittent torsion). Absence of recent sexual contact, new contraceptive use, or urinary/GI symptoms helps narrow the differential. Pregnancy status should always be confirmed with serum β-hCG, as torsion can occur during pregnancy and influences imaging modality and management decisions.

• Pelvic ultrasound (imaging study of choice): Transvaginal ultrasound is the first-line imaging modality with sensitivity of 90-95% and specificity of 95-98% for torsion in non-pregnant patients. Gray-scale findings include: (1) Enlarged ovary (mean 12 cm in torsion vs 4-8 cm in functional cysts; volume >20 mL significantly raises torsion probability); (2) Peripheral follicles arranged in a "string of pearls" pattern, seen in polycystic-appearing ovaries with stroma edema from ischemia; (3) Stromal edema manifesting as increased echogenicity and heterogeneity of the ovarian stroma; (4) Massive stromal edema can create a "wheel spoke" appearance with follicles arranged radially around edematous stroma. Color and spectral Doppler findings are crucial: (1) Decreased or absent arterial flow (reduced or absent diastolic flow, increased resistive index >0.8) in the affected ovary compared to the contralateral ovary; (2) Venous flow loss is often the first Doppler abnormality, preceding arterial flow loss; (3) Preserved central arterial flow with peripheral flow loss (creating a "halo" sign) suggests partial torsion or early complete torsion. Critical point: The presence of flow does NOT exclude torsion, as dual ovarian blood supply (ovarian artery and artery of ovarian ligament) means partial torsion or early torsion may maintain some perfusion. Absent flow, when present, is highly specific but not maximally sensitive.

• Serum markers (limited utility): β-hCG confirms pregnancy and influences management. Leukocytosis (WBC >10,000) occurs in 50-60% of cases due to acute inflammatory response but is non-specific. Elevated C-reactive protein or erythrocyte sedimentation rate indicates inflammation but lack sensitivity and specificity for torsion specifically.

• Diagnostic criteria and probability assessment: There is no single validated scoring system for ovarian torsion diagnosis, but several ultrasound-based prediction models exist. A combination of clinical presentation (acute onset, severity) and ultrasound findings (ovarian enlargement >10-12 cm, stromal edema, absent or decreased Doppler flow) yields high diagnostic accuracy. The ovarian torsion scoring (OTS) system incorporates ultrasound variables: an OTS score >8 suggests high probability of torsion, though this has not been universally adopted. Clinical judgment integrating presentation + ultrasound remains the gold standard.

• Differential diagnosis and diagnostic considerations: Acute appendicitis presents with RLQ pain, fever, and leukocytosis; right adnexal ultrasound can differentiate. Pyelonephritis presents with costovertebral angle tenderness, fever, and pyuria; urinalysis clarifies. Ruptured ovarian cyst causes sudden pelvic pain but ultrasound shows free fluid in pelvis without an enlarged ovary; pain typically resolves within 24-48 hours. Ectopic pregnancy (confirmed with β-hCG + ultrasound showing IUP absence) presents with unilateral pain and vaginal bleeding. Salpingitis/pelvic inflammatory disease presents with fever, purulent discharge, cervical motion tenderness, and no discrete adnexal mass; fever and pelvic examination findings distinguish this. Kidney stone (CT imaging shows stone) presents with flank pain and hematuria. MRI is reserved for indeterminate ultrasound cases in non-pregnant patients or when concerned about malignancy given ovarian enlargement.

• Urgent surgical intervention (definitive treatment): Laparoscopic ovarian detorsion and cyst aspiration/drainage (if applicable) is the definitive treatment and should be performed emergently within 6-8 hours of symptom onset to maximize ovarian salvage. Mechanism: Detorsion physically restores vascular supply, halting further ischemic damage and permitting reperfusion and recovery of viable follicles. Surgical approach: Most cases are managed laparoscopically (preferred over laparotomy for reduced morbidity, faster recovery, and ability to assess bilateral ovaries). The procedure involves: (1) Inspection for hemorrhage, necrosis, or rupture; (2) Gentle detorsion by rotating the ovary back to normal anatomical position (counterclockwise if twisted clockwise, typically); (3) Visual assessment of color change (from dark purple/black back toward normal pink if viable); (4) Cyst aspiration or cystectomy if a cyst is present (aspiration alone preferred to preserve ovarian tissue in young women); (5) Ovarian preservation is attempted in nearly all cases, even if the ovary appears dark/ischemic, because non-viable appearing ovaries can recover function if detorsed promptly. Oophorectomy is reserved for cases with evident necrosis, rupture with contamination, or in older postmenopausal women where ovarian conservation has limited value.

• Timing and emergency status: The 6-8 hour window from torsion onset to detorsion is critical; torsion presenting beyond 12-24 hours may still benefit from detorsion and oophorectomy if necrosis is confirmed, but ovarian salvage rates decrease significantly. Intermittent torsion can be managed more conservatively if detorsion is confirmed on imaging and the ovary remains viable, though recurrence risk is 5-15% and elective ipsilateral oophoropexy (suturing the ovary to prevent future rotation) or cyst aspiration/marsupialization may be performed in the same setting.

• Medical management (limited role, not primary therapy): No pharmacologic agent prevents torsion or salvages an ischemic ovary, so medical management is not a substitute for surgery. However, analgesics (opioids for severe pain prior to surgery; NSAIDs like ibuprofen 400-800 mg IV/PO for postoperative pain and inflammation) are used symptomatically. Broad-spectrum antibiotics are initiated perioperatively if torsion is complicated by rupture, peritonitis, or sepsis, though are not routinely required for uncomplicated torsion. Prophylactic antibiotics (e.g., cefazolin 1-2 g IV at induction, redosed per protocol) are standard surgical prophylaxis.

• Special populations and considerations: Pregnant patients with ovarian torsion require **emergent laparosc

Disease-related (untreated or delayed torsion)

• Hemorrhagic infarction and ovarian necrosis (emergency): persistent arterial occlusion after venous outflow is lost converts congestion to infarction; signaled by worsening peritoneal signs, an enlarged ovary with free pelvic fluid on ultrasound, and a blue-black necrotic ovary at laparoscopy.
• Rupture with hemoperitoneum (emergency): capsular tension from massive stromal edema exceeds tensile strength; suspect with hypotension, tachycardia, falling hematocrit, and large-volume echogenic free fluid.
• Peritonitis, adnexal abscess, and sepsis (emergency): necrotic tissue seeds infection or provokes chemical peritonitis; fever and leukocytosis appearing after an initially afebrile presentation are the tip-off (recall that fever is absent in uncomplicated early torsion).
• Loss of ovarian reserve / need for oophorectomy: follicle atresia from prolonged ischemia; usually clinically silent because a normal contralateral ovary preserves fertility and cyclicity. Bilateral loss (as after bilateral torsion in ovarian hyperstimulation syndrome) causes surgical menopause.
• Recurrent torsion: the anatomic substrate — long ovarian ligament, persistent cyst, polycystic morphology — is unchanged by detorsion alone; recurrent episodic ipsilateral pain after treatment is the signal.

Treatment-related

• Standard laparoscopic risks: trocar or Veress injury to bowel, bladder, or iliac vessels; postoperative ileus; adhesion formation that itself predisposes to future torsion.
• Intraoperative cyst spillage: rupture of a mature cystic teratoma spills sebum causing chemical peritonitis; spillage of an unsuspected malignancy upstages disease — a reason postmenopausal torsion with suspicious features favors intact removal.
• Obstetric complications when torsion occurs in pregnancy (emergency): pain, prostaglandin release, and anesthesia contribute to miscarriage or preterm contractions; ACOG supports proceeding with indicated surgery regardless of trimester rather than delaying.
• Feared but not observed — thromboembolism from detorsion: the historical concern that untwisting dislodges ovarian vein thrombus is not supported by evidence, and ACOG explicitly endorses detorsion with ovarian conservation rather than prophylactic oophorectomy.

• The stem to recognize: reproductive-age woman, sudden severe unilateral pelvic pain, nausea and vomiting, no fever, and a tender adnexal mass. Fever or purulent discharge should push you toward pelvic inflammatory disease or tubo-ovarian abscess instead.
• Single best next step: pelvic ultrasound with color Doppler (transvaginal preferred), the first-line study endorsed by the ACR Appropriateness Criteria for acute pelvic pain in reproductive-age women — but obtain a β-hCG first, since pregnancy reframes the entire differential.
• The trap examiners love: normal or present Doppler flow does not exclude torsion. Dual arterial supply (ovarian artery plus the adnexal branch of the uterine artery) and the fact that venous flow is lost before arterial flow mean a perfused-appearing ovary can still be torsed. If clinical suspicion is high, the next step is diagnostic laparoscopy, not observation or repeat imaging.
• Definitive diagnosis and treatment are the same act: laparoscopy with detorsion. Do not choose CT, MRI, or laparotomy as the default answer in a stable non-pregnant patient.
• The one association tested: an ovarian mass, most often a benign mature cystic teratoma or a functional cyst, is the usual lead point; a normal-sized ovary rarely torses in an adult. Right-sided torsion is more common than left, attributed to the sigmoid colon limiting left adnexal mobility.
• Conserve the ovary, even if it looks black: ACOG advises detorsion with ovarian preservation in children, adolescents, and reproductive-age women; a dusky ovary frequently recovers function. Oophorectomy is the classic wrong answer unless there is frank necrosis with rupture or genuine malignancy concern.
• Do not withhold surgery for pregnancy: ACOG supports indicated non-obstetric surgery in any trimester; laparoscopy is acceptable. Fetal monitoring decisions follow gestational age.
• Prepubertal girls torse too — often with normal or minimally enlarged ovaries and no risk factors, which is precisely why torsion is missed in this group.