Sudden Testicular Atrophy: Causes and Urgent Evaluation
Sudden testicular atrophy with hormonal imbalances requires immediate evaluation to distinguish between reversible causes (hormonal suppression, varicocele, infection) and irreversible testicular damage (torsion, genetic conditions, primary testicular failure), as the underlying cause determines both fertility preservation options and cancer risk. 1
Understanding What "Sudden" Atrophy Really Means
True sudden testicular atrophy developing over days to weeks suggests acute pathology requiring urgent evaluation, while gradual atrophy noticed suddenly may represent longstanding conditions only recently discovered. 1, 2
Acute Causes Requiring Immediate Action:
Testicular torsion with partial detorsion: Ischemia from torsion is the most frequent cause of primary testicular atrophy and represents a urological emergency even if pain has resolved. 3 Immediate scrotal ultrasound with Doppler is essential to assess testicular blood flow. 1
Severe infection (orchitis/epididymitis): Inflammatory processes can affect spermatogenesis and cause temporary testicular swelling followed by atrophy. 1 A trial of antibiotics may be appropriate if infection is suspected, but persistent abnormalities warrant further evaluation. 4
Exogenous testosterone or anabolic steroid use: This completely suppresses FSH and LH through negative feedback, causing rapid testicular atrophy and azoospermia that can take months to years to recover. 1 Immediate cessation is critical if fertility is desired.
Acute varicocele thrombosis: Grade 3 varicoceles can cause progressive testicular damage, and acute thrombosis may present as sudden size change. 1
Essential Immediate Workup
Physical Examination Priorities:
Measure testicular volume using Prader orchidometer: Volumes <12ml are definitively atrophic and associated with impaired spermatogenesis and increased cancer risk. 1, 2, 5 A 4cm testicular length corresponds to approximately 15-18ml volume, which is at the lower limit of normal. 5
Assess for varicocele on standing examination: Palpable varicoceles with testicular atrophy indicate progressive damage requiring surgical repair. 1
Check testicular consistency and symmetry: Size discrepancy >2ml or 20% between testes warrants ultrasound to exclude masses or structural pathology. 5
Palpate vas deferens and epididymis: Absence or abnormalities suggest congenital conditions or obstruction. 1
Hormonal Evaluation (Draw Today):
FSH level >7.6 IU/L with testicular atrophy strongly suggests non-obstructive azoospermia and primary testicular failure. 1 FSH levels of 10-12 IU/L indicate mild testicular dysfunction but do not preclude sperm production—up to 50% of men with non-obstructive azoospermia and elevated FSH have retrievable sperm. 1
Measure LH and total testosterone: Normal or elevated LH with low testosterone confirms primary testicular failure, while low LH with low testosterone suggests secondary hypogonadism from pituitary dysfunction requiring prolactin measurement. 1
Check thyroid function (TSH, free T4): Hyperthyroidism causes oligozoospermia, asthenozoospermia, and teratozoospermia that are reversible with treatment. 1 Hypothyroidism or inadequate thyroid replacement can elevate SHBG and impair spermatogenesis. 1
Imaging:
Scrotal ultrasound with high-frequency probe (>10 MHz): Confirms testicular volume using the Lambert formula (Length × Width × Height × 0.71), assesses for masses, varicoceles, and testicular microcalcifications. 5 Testicular microcalcifications increase cancer risk 18-fold in men with atrophy. 2
Doppler assessment of testicular blood flow: Essential to exclude torsion or vascular compromise. 1
Semen Analysis:
- Obtain at least two semen analyses separated by 2-3 months after centrifugation to confirm azoospermia or degree of oligospermia. 1 Single analyses are insufficient due to natural variability. 1
Genetic Testing Indications
If semen analysis confirms severe oligospermia (<5 million/ml) or azoospermia:
Karyotype analysis to exclude Klinefelter syndrome (47,XXY): Chromosomal abnormalities occur in 10% of men with severe oligospermia or azoospermia. 1, 2
Y-chromosome microdeletion testing (AZFa, AZFb, AZFc regions): Mandatory if sperm concentration <1 million/ml. 1 Complete AZFa and AZFb deletions predict near-zero sperm retrieval success and contraindicate testicular sperm extraction. 1
Most Common Causes by Clinical Pattern
Pattern 1: Elevated FSH (>7.6 IU/L) + Bilateral Atrophy + Azoospermia
Most likely: Primary testicular failure from:
- Klinefelter syndrome (47,XXY)—most common chromosomal cause 1, 2
- Y-chromosome microdeletions 1
- Prior cryptorchidism (undescended testicles)—single most important cancer risk factor 2
- Prior chemotherapy or testicular radiation 1
- Chronic medication use (opioids, corticosteroids) 1
Action: Proceed directly to genetic testing and consider microsurgical testicular sperm extraction (micro-TESE), which achieves 40-50% sperm retrieval rates even with elevated FSH. 1 Micro-TESE is 1.5 times more successful than conventional TESE. 1, 2
Pattern 2: Normal FSH + Unilateral or Asymmetric Atrophy + History of Hernia Repair
Most likely: Surgical trauma causing venous thrombosis of spermatic cord 6
Action: Ultrasound to assess contralateral testis and rule out compensatory hypertrophy. If contralateral testis is normal-sized with normal FSH, fertility prognosis remains good. 1
Pattern 3: Mildly Elevated FSH (8-12 IU/L) + Palpable Varicocele + Oligospermia
Most likely: Varicocele-induced progressive testicular damage 1
Action: Varicocelectomy is strongly indicated and can halt progression of atrophy, potentially reverse some damage, improve testosterone levels, reduce FSH, and stabilize testicular volume. 1 Varicocele repair improves semen parameters including sperm concentration, motility, and morphology. 1
Pattern 4: Low/Normal FSH + Low LH + Low Testosterone + Bilateral Small Testes
Most likely: Hypogonadotropic hypogonadism (secondary testicular failure) 1
Action: Measure prolactin to exclude prolactinoma. 1 Treatment with hCG followed by FSH analogues can successfully initiate spermatogenesis, with 75% of men achieving sperm in ejaculate. 1 One case report documented recovery from complete testicular absence (impalpable testes) to 10^5 mobile sperm after 12 months of rFSH/hCG treatment. 7
Pattern 5: Recent Testosterone/Steroid Use + Bilateral Atrophy
Most likely: Exogenous testosterone suppression 1
Action: Immediately discontinue testosterone/steroids. Recovery can take months to years. Consider hCG therapy to stimulate intratesticular testosterone production and restart spermatogenesis. 1 Never prescribe testosterone to men desiring fertility. 1
Fertility Preservation: Act Immediately
If any sperm are present on semen analysis, bank sperm NOW before further decline occurs. 1 Men with elevated FSH and small testicular volumes are at high risk for progressive spermatogenic failure. 1 Once azoospermia develops, even micro-TESE only achieves 40-50% retrieval rates. 1
Banking Protocol:
- Collect 2-3 separate ejaculates with 2-3 days abstinence between collections 1
- Split each collection into multiple vials for staged use 1
- Complete banking before any gonadotoxic exposures (chemotherapy, radiation) 1
- Mail-in kits available if access to andrology laboratories is limited 1
Cancer Risk Assessment
Men with testicular atrophy require monitoring for testicular cancer, as atrophic testes (<12ml) are a significant risk factor. 2, 5
High-Risk Features Requiring Urology Referral:
Age <30-40 years with volume <12ml: ≥34% risk of intratubular germ cell neoplasia (TIN) in contralateral testis if cancer develops. 2, 5 If untreated, invasive tumor develops in 70% of TIN-positive testes within 7 years. 2
History of cryptorchidism: Substantially increases cancer risk and mandates closer surveillance. 2
Testicular microcalcifications on ultrasound: 18-fold increased cancer risk—testicular biopsy should be offered. 2
Rapid testicular atrophy or palpable mass: Urgent urology evaluation required. 1
Teach testicular self-examination immediately given increased cancer risk. 2
Reversible Causes to Address Before Declaring Irreversible Damage
Correct hyperthyroidism: Semen quality improves after achieving euthyroid status. 1 Perform semen analysis only after 2-3 months of euthyroid state. 1
Optimize Type 1 diabetes control: Metabolic stress affects the hypothalamic-pituitary-gonadal axis. 1
Adjust thyroid replacement: Inadequate levothyroxine can elevate SHBG and impair spermatogenesis. 1 Bring TSH to lower portion of reference range if currently in upper half. 1
Weight loss if BMI >25: Obesity and metabolic syndrome impair male fertility. 1 Weight normalization can improve gonadotropins and testosterone. 1
Stop smoking and minimize heat exposure to testes: Modifiable factors affecting spermatogenesis. 1
Critical Pitfalls to Avoid
Do not start testosterone therapy if fertility is desired—it will cause complete azoospermia. 1
Do not rely on single semen analysis—natural variability requires 2-3 analyses separated by 2-3 months. 1
Do not use ellipsoid formula (0.52 coefficient) for testicular volume—it systematically underestimates volume by 20-30% and may lead to inappropriate classification of atrophy. 5 Always use Lambert formula (0.71 coefficient). 5
Do not treat subclinical varicoceles found only on ultrasound—only palpable varicoceles improve fertility outcomes after repair. 1
Do not assume elevated FSH means zero sperm—30% of men with azoospermia, testicular atrophy, and FSH >3 times normal have mature sperm on testicular biopsy. 8 Up to 50% of non-obstructive azoospermia patients have retrievable sperm with micro-TESE despite elevated FSH. 1