Obtain and interpret semen analysis correctly, confirm genuine abnormalities, identify endocrine, obstructive and genetic patterns, and direct evidence-based treatment without stigma or unsupported add-ons.
Male-factor infertility encompasses impaired sperm production, obstruction, ejaculatory failure, sexual dysfunction and sperm-delivery problems. It can occur alone or with a female factor. Use neutral language and assess the couple or intended parents in parallel; a semen abnormality is neither a judgment about masculinity nor proof that no spontaneous conception can occur.
Before interpreting the report, establish how the sample was produced, whether the entire ejaculate was collected, abstinence interval according to laboratory instructions, delay to analysis, fever or systemic illness in the preceding months and use of exogenous testosterone, anabolic steroids, recreational drugs or medicines. Collection problems can falsely lower volume or total count. A recent febrile illness may transiently impair spermatogenesis, so the context belongs on the request and in interpretation.
NICE NG257 adopted the WHO sixth-edition lower reference distribution: semen volume at least 1.4 mL, pH at least 7.2, concentration at least 16 million/mL, total sperm number at least 39 million per ejaculate, total motility at least 42%, progressive motility at least 30%, vitality at least 54% and normal morphology at least 4%. These are reference limits from a fertile population, not thresholds separating fertile from infertile people.
Sperm concentration below the WHO lower reference value is interpreted with total ejaculate count and confirmed because concentration varies between samples.
Reduced progressive or total motility may impair sperm transport; vitality distinguishes immotile viable sperm from a high proportion of dead sperm.
No sperm detected requires prompt repeat confirmation and differentiation between impaired production and obstruction using history, examination, hormones and targeted genetics.
Low testosterone with low or inappropriately normal gonadotrophins suggests deficient hypothalamic-pituitary stimulation and a potentially treatable mechanism.
Azoospermia with relatively preserved testicular volume, lower semen volume, absent vasa or epididymal findings suggests obstruction and may indicate CFTR-related disease.
Confirm the central diagnosis, exclude pituitary pathology where indicated and counsel that response takes months; this is not empirical treatment for idiopathic abnormal semen.
The WHO lower limits describe a distribution among fertile men; results on either side overlap and must be interpreted probabilistically.
Concentration alone can look reassuring in a small ejaculate, so volume and total sperm number are essential companions.
Exogenous androgen suppresses LH, FSH and intratesticular testosterone, potentially causing severe oligozoospermia or azoospermia despite improving serum testosterone symptoms.
NG257 uses below 1 million/mL for Y-microdeletion testing and below 5 million/mL to consider karyotype, with mandatory karyotype testing in idiopathic azoospermia.
Surgical sperm retrieval should not be offered with AZFa or AZFb microdeletion because the prognosis is effectively futile; counselling precedes assisted reproduction.
Declaring infertility from one borderline semen parameter or calling a report normal without considering the whole ejaculate.
Waiting three months to confirm azoospermia or severe oligozoospermia when NICE advises repeat testing as soon as possible.
Prescribing testosterone for low testosterone in a person actively seeking fertility without recognising suppression of spermatogenesis.
Ordering sperm DNA fragmentation, routine antisperm antibodies or antioxidant supplements despite the 2026 NICE recommendations.
Missing CFTR, karyotype or Y-microdeletion testing in the specific severe or obstructive phenotypes.
Focusing exclusively on semen while delaying assessment of the person trying to become pregnant and the couple's total prognosis.
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A 32-year-old has a semen analysis during parallel fertility assessment. Which value matches the current WHO lower reference used by NICE NG257 for progressive sperm motility?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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Interpret related measures together. A normal concentration with low volume can still yield a low total count. A low motility percentage has different implications when total count is very high or very low. Vitality helps distinguish immotile live sperm from necrozoospermia. Morphology is method dependent and a low percentage of normal forms should not be used in isolation to make irreversible conclusions.
Confirm any abnormal first analysis. About 3 months allows a cycle of sperm formation before repeating, but gross deficiency requires earlier confirmation so investigation is not delayed. Once two or more tests are abnormal, offer examination of the testes and scrotum and consider testosterone, FSH and LH. Testicular size, consistency, presence of the vasa and a palpable varicocele help distinguish impaired production, obstruction and potentially correctable disease.
An endocrine pattern can localise the problem. Low testosterone with low or inappropriately normal LH and FSH suggests hypogonadotrophic hypogonadism, which may respond to specialist gonadotrophin therapy. Low testosterone with high gonadotrophins suggests primary testicular failure. Exogenous testosterone suppresses intratesticular testosterone and gonadotrophins, often markedly reducing sperm production; simply adding more androgen is therefore not treatment for an abnormal semen analysis.
The 2026 genetic pathway is concentration and phenotype led. Test Y-chromosome microdeletions in idiopathic azoospermia or concentration below 1 million/mL. Test karyotype in idiopathic azoospermia and consider it when persistent concentration is below 5 million/mL. Suspected obstructive azoospermia or a vasal abnormality requires CFTR mutation testing. Offer genetic counselling for a defined fertility-associated defect, including implications for relatives and transmission through ICSI.
Avoid unsupported investigations and treatments. NICE advises against sperm DNA-fragmentation testing, routine antisperm antibodies, androgen treatment, empirical antibiotics for seminal leucocytes without infection, and supplements or antioxidants intended to improve DNA integrity. Management instead addresses smoking and gonadotoxins, endocrine deficiency, obstruction, ejaculatory failure and assisted conception. In someone trying to conceive spontaneously, treatment of a clinically detected varicocele with reduced semen parameters may be considered after accounting for the other partner's fertility factors. ICSI is considered for abnormal semen according to severity, surgically retrieved sperm or previous failed or very low fertilisation; it is not a general add-on when semen is normal.