Asthenoteratozoospermia: Causes, Examination, and Treatment in Men

Asthenoteratozoospermia is a combination of two sperm disorders: decreased sperm motility (asthenozoospermia) and a pathological form (teratozoospermia). In practice, the diagnosis is made based on the results of a standard ejaculate analysis, when the proportion of progressively motile cells is reduced, and the proportion of normally formed sperm is below reference values. It is important to remember: this is a description of the laboratory picture, not a definitive fertility diagnosis; the prognosis depends heavily on the cause, associated factors, and the chosen strategy. [1]

In the 6th edition of its guidelines, the World Health Organization standardized methods for assessing motility (including rapid and slow progressive motility) and morphology using "strict" criteria. The guidelines emphasize that reference limits are not "normal/abnormal" for each man, but rather statistical boundaries for a population of fertile men; clinical decisions are based on a combination of factors for the couple. [2]

Classic causes of asthenoteratozoospermia include varicocele, genital tract infections and inflammation, oxidative stress, metabolic and endocrine disorders, exposure to toxins, and, in some patients, monogenic defects in the structure/function of the sperm flagellum or head. Identifying treatable causes and targeted correction is the main principle of modern strategy. [3]

Treatment always includes two layers: 1) etiotropic measures (e.g., surgery for varicocele, anti-inflammatory/antibacterial therapy for infection, correction of metabolic factors, smoking cessation); 2) reproductive technologies (intrauterine insemination, in vitro fertilization with intracytoplasmic sperm injection), if time is limited or the cause is irreparable. Plus - new methods of sperm selection (microfluidics, hypoosmotic test, MACS/PICSI) and personalization by DNA fragmentation. [4]

Code according to ICD-10 and ICD-11

There is no specific "separate" code for asthenoteratozoospermia; male infertility and/or abnormalities in ejaculate analysis are coded. In ICD-10, the basic section is N46 "Male infertility" (with clarifying subheadings, including N46.1 "Oligospermia," N46.11 "Organic oligozoospermia," etc.), and, if necessary, abnormal laboratory findings from block R86.* are reflected. In reporting practice, N46 is most often used ± accompanying cause codes (varicocele, infection, etc.). [5]

In ICD-11, male infertility is represented by the section GB04 "Male infertility" (including GB04.0 "Azoospermia," GB04.Y "Other specified male infertility," and GB04.Z "Unspecified"). Clinical laboratory records are used to record laboratory abnormalities, but the key remains the coding of the etiology (varicocele, infection, genetic defect) and the infertility itself GB04.* - this is important for routing and insurance statistics. [6]

Table 1. How asthenoteratozoospermia is coded (landmarks)

Clinical situation	ICD-10	ICD-11
Male infertility	N46 (± clarifying N46.0/1/8/9)	GB04 (± GB04.Y/GB04.Z)
Laboratory abnormality of ejaculate	R86.* (other/unspecified findings)	accompanying record, main code - GB04.*
Causal diagnosis (example: varicocele)	I86.1	BD82 (varicocele) / ICD-11 code

Epidemiology

Male factors are found in approximately half of infertile couples; "pure" male factors account for approximately 20%. Sperm abnormalities most commonly include decreased concentration and motility; abnormal morphology by strict criteria is a common finding even in fertile men, so the assessment is always linked to other parameters and the clinical context. [7]

The prevalence of asthenoteratozoospermia as a combination varies across publications due to different thresholds and methods; however, the combination of "low motility + poor morphology" is statistically more common in the presence of varicocele, obesity, smoking, chronic genital tract inflammation, and oxidative stress. Increasing metabolic disorders and age at fatherhood contribute to the prevalence. [8]

Guidelines emphasize that a single "bad" spermogram is insufficient—the analysis should be repeated at least twice, 2-6 weeks apart, with standard preparation (2-7 days of abstinence, avoidance of overheating, and avoidance of acute intoxications). This reduces the risk of diagnostic errors due to fluctuations in spermatogenesis. [9]

The influence of overall health is increasingly being discussed in association with male infertility: men with significant ejaculate abnormalities are more likely to have comorbidities (metabolic syndrome, hypogonadism, varicocele). Healthy lifestyle counseling is now standard. [10]

Reasons

Varicocele is the most common: venous congestion and scrotal overheating disrupt spermatogenesis, increase oxidative stress, and impair motility and morphology. Meta-analyses show improvements in semen parameters after varicocele correction in appropriately selected patients. [11]

Infections/inflammation (epididymitis, prostatitis, urethral infections) impair sperm quality through cytokines and reactive oxygen species. Adequate diagnosis and treatment can partially restore sperm parameters, especially motility. [12]

Oxidative stress and lifestyle: smoking, obesity, excess processed foods, overheating (saunas, hot baths), lack of sleep and chronic stress are factors that reduce progressive mobility and increase the proportion of atypical forms. [13]

Genetic and structural sperm defects range from primary flagellar dyskinesia and mitochondrial disorders to monogenic syndromes (e.g., DPY19L2-associated globozoospermia, AURKC-associated macrocephalic pathology). In these cases, natural correction is limited, and the route is to assisted reproductive technologies. [14]

Risk factors

Smoking and toxic exposures (solvents, pesticides, heavy metals) are proven factors in reduced motility and deterioration of morphology. The longer the period of smoking and the higher the dose, the more pronounced the effect. Smoking cessation is a mandatory part of the plan. [15]

Obesity and metabolic syndrome worsen hormonal balance, increase oxidative stress, and inflammation. Weight loss, physical activity, and correction of insulin resistance improve sperm quality and treatment prognosis. [16]

Overheating (working in hot weather, hot baths, tight thermal underwear) and varicocele can cause "heat stroke" in spermatogenesis. Avoiding overheating and promptly correcting varicocele reduces the risk of progression. [17]

Urogenital infections, previous orcho-epididymitis, and prolonged fever (including viral infections) temporarily impair spermatogenesis for 2-3 months - this should be taken into account when interpreting spermograms. [18]

Pathogenesis

Impaired motility (asthenozoospermia) is the result of a combination of factors: damage to the mitochondria and flagellar axoneme, energy deficiency, excess reactive oxygen species, and impaired calcium flux regulation. Morphology is affected by disruptions in spermatogenesis: abnormal head formation, acrosome defects, and neck/flagellum disproportion. [19]

Varicocele causes hypoxia and overheating of the testicle, activating oxidative stress and apoptosis in spermatogenic cells; this leads to an increased incidence of abnormal forms and decreased progression. Decompression of the venous plexus reduces these factors. [20]

During inflammation, a "cytokine storm" and leukocyte infiltration play a key role, increasing sperm DNA fragmentation and impairing sperm function. This explains why some patients with moderately altered sperm counts have problems with fertilization. [21]

Monogenic defects (e.g., DPY19L2 in globozoospermia) result in the absence of acrosomes and severe teratozoospermia; AURKC mutations result in the formation of macrocephalic spermatozoa with polyploidy. In these cases, special sperm selection protocols and ICSI are required. [22]

Symptoms

The patient himself often experiences no symptoms; asthenoteratozoospermia manifests itself as difficulty conceiving. Sometimes there are indirect signs of the cause: heaviness in the scrotum and "clusters" of veins with varicocele, pain during ejaculation/pelvic pain with inflammation, energy deficiency and weight gain with hypogonadism/metabolic syndrome. [23]

Indirect clues are provided by the patient's medical history: heat at work, excessive sauna use, smoking, toxic exposure, frequent genitourinary infections, and prolonged fever 2-3 months before the test. All of this is important to discuss during the appointment. [24]

A small proportion of patients have features of genetic syndromes (eg, respiratory problems and chronic sinusitis in primary ciliary dyskinesia), which require genetic counseling.[25]

The psycho-emotional aspect is underestimated: anxiety about sperm analysis, guilt, and stress in the couple directly worsen behavior and habits that affect spermatogenesis. Support and a realistic action plan are an important part of treatment. [26]

Forms and stages

A distinction is made between a predominantly asthenozoospermic variant (motility is more severely affected, morphology is moderate) and a predominantly teratozoospermic variant (morphology is significantly impaired with a moderate reduction in motility), as well as a mixed form. This helps in choosing a strategy—for example, in cases of severe morphology, ICSI is considered first. [27]

Based on the reversibility of the causes, they are conventionally divided into removable (varicocele, infection, overheating, lifestyle) and difficult to remove/genetic (primary flagellar dyskinesia, globozoospermia, macrocephalic forms, etc.). The proportion of reproductive technologies in the plan depends on this. [28]

The degree of influence on fertility is determined by a combination of factors: concentration, progressive motility, morphology according to strict criteria, volume, pH, leukocytospermia, as well as the partner's age and ovarian reserve. This influences the choice between "trying natural/insemination" and "going with IVF/ICSI." [29]

In some men, the indicators fluctuate over time - there are transient deteriorations (after fever/stress) and persistent disorders requiring more aggressive correction and/or ART. [30]

Complications and consequences

The main consequence is a reduced chance of natural conception, especially if asthenoteratozoospermia is accompanied by oligozoospermia. However, for many couples, the chance remains, especially after varicocele correction, inflammation elimination, and lifestyle changes. [31]

Chronic oxidative stress increases sperm DNA fragmentation, which is associated with lower pregnancy rates and an increased risk of early loss; in difficult cases, management changes (e.g., selecting sperm with less fragmentation, using testicular sperm). [32]

In genetic forms, specific risks for offspring (anomalies, transmission of the defect) are possible; in this case, consultation with a geneticist and discussion of preimplantation genetic diagnosis are mandatory. [33]

Psychological consequences include anxiety, depression, and conflict within the couple. Current recommendations explicitly emphasize the need for information about the relationship between male infertility and overall health and referral to psychological support if needed. [34]

When to see a doctor

If pregnancy does not occur within 12 months of regular sexual intercourse without contraception (or 6 months if the partner is ≥35 years old), if there have been previous injuries/operations on the scrotum, episodes of orchoepididymitis, “veins like grapes” on the scrotum (suspected varicocele), episodes of high fever in the last 3 months - these are reasons for early consultation. [35]

You should seek medical attention sooner if you have severe pain/heaviness in the scrotum, testicular asymmetry, signs of hypogonadism (decreased libido, energy), long-term smoking, obesity - all of these are risk factors for decreased sperm quality. [36]

In case of two or more pathological spermograms, an in-person consultation with a urologist-andrologist with a standard examination and correction plan is required. [37]

If a couple is already using or considering assisted reproduction, a visit to an andrologist is important to optimize the male component (increasing the chances of success, reducing costs and risks). [38]

Diagnostics

The base consists of two spermograms according to the WHO-6 standard (preparation, liquefaction time, assessment of volume, pH, concentration, progression, viability, and morphology according to strict criteria). In case of discrepancies, the analysis is repeated; the laboratory must implement quality control. [39]

Further expansion according to indications: culture/microscopy of ejaculate in case of leukocytospermia, hormones (follicle-stimulating hormone, luteinizing hormone, total testosterone ± prolactin, estradiol), ultrasound of the scrotum with Valsalva maneuver in case of suspected varicocele, Doppler. In case of recurrent sweating - assessment of sperm DNA fragmentation to stratify tactics. [40]

Genetics - based on clinical features: severe teratozoospermia (globozoospermia/macrogoloid forms), signs of ciliary dyskinesia, family history. Targeted sequencing may be required (e.g., DPY19L2, AURKC, CFTR, etc.). [41]

Oxidative stress and DNA damage are assessed by validated tests (SDF) where this will influence the decision (e.g. choice of sperm selection method, switch to testicular sperm in case of repeated failures). [42]

Table 2. What is mandatory and what is indicated

Step	Necessarily	According to the readings
Basis	2× spermogram according to WHO-6	Viability, MAR test
Infection/inflammation	General analysis/microscopy, culture	PCR for STIs
Reasons	Ultrasound of the scrotum (varicocele)	Hormones (FSH, LH, T), SDF
Genetics	-	NGS/targeted panels for phenotype

Differential diagnosis

It is important to distinguish transient deteriorations (after fever, intoxication, acute stress) from persistent disorders of spermatogenesis - in the first case, a repeat analysis after 6-8 weeks often normalizes. [43]

In case of a marked decrease in motility without morphological defects, one thinks of isolated asthenozoospermia (overheating, inflammation, varicocele, toxic factors); in case of extremely low morphology with a typical pattern, one thinks of genetic syndromes (globo/macroglobotomy). [44]

It is necessary to exclude retrograde ejaculation and obstructive processes of the vas deferens; if the volume of ejaculate is small, the pH is acidic, and there is no fructose, this is already a “different branch” of diagnostics. [45]

Finally, attention to the female factor: the age and ovarian reserve of the partner can outweigh the limits of “expectation”, shifting the choice in favor of more active reproductive technologies. [46]

Table 3. “Portraits” of conditions similar to asthenoteratozoospermia

State	Tips	What to do
Post-febrile deterioration	Recent temperature, general decline	Repeat the spermogram in 6-8 weeks
Isolated asthenozoospermia	Mobility ↓, morphology moderate	Possible causes: overheating, varicocele
Genetic forms	"typical" morphology (globo/macro)	Genetics, ICSI/special sperm selection
Obstruction/retrograde	Volume ↓, pH, fructose, clinical	Urological route (instrumental/ART)

Treatment

1) Lifestyle changes and reduction of oxidative stress. Essential measures: quitting smoking and vaping, normalizing body weight, aerobic exercise 150-300 minutes per week, sleeping 7-8 hours, avoiding scrotal overheating (hot baths, sauna marathons, tight thermal underwear), and reducing alcohol consumption. These are the "low-hanging fruits" with a proven effect on motility and morphology. [47]

2) Antioxidants - cautious optimism. A 2022 Cochrane review showed a possible increase in live birth and pregnancy rates in couples with male factor factors with antioxidants, but when excluding studies with a high risk of bias, the effect on live births loses statistical significance. Conclusion: supplements (coenzyme Q10, carnitine, vitamins C/E, zinc, etc.) can be considered as a complement to, rather than a replacement for, etiotropic therapy, with informed consent. [48]

3) Varicocele: When to operate. In symptomatic men with clinical varicocele and abnormal spermogram, EAU/AUA recommends considering varicocelectomy (microsurgical subinguinal/inguinal). Meta-analyses show improved motility and morphology after surgery and an increase in spontaneous fertility in properly selected patients. An alternative/addition is endovascular embolization. [49]

4) Anti-inflammatory/antibacterial therapy. In case of leukocytospermia and proven infection, treatment should be standard, followed by sperm analysis and, if necessary, antioxidant support. Avoid overuse of antibiotics "just in case." [50]

5) SDF-targeted therapy. In cases of high SDF, consideration should be given to an enhanced antioxidant strategy, elimination of the source of oxidative stress (varicocele, inflammation), and sperm selection using MACS/PICSI/microfluidics; in cases of repeated IVF/PGT failures, switching to testicular sperm (often with lower SDF) may be possible. Recent consensus guidelines systematize the indications for SDF testing and correction. [51]

6) Sperm selection: what's new. Microfluidic chips and related techniques show lower SDF and are encouraging in terms of embryological outcomes; there is a growing evidence base for improved pregnancy/live birth rates in certain groups, but this is an addition to ICSI/IVF, not a replacement. The choice of selection method (microfluidics, PICSI, IMSI, MACS) is being personalized. [52]

7) Reproductive technologies (ART). In cases of moderate asthenoteratozoospermia and favorable female factors, intrauterine insemination can be attempted (especially if there are progressive forms and a sufficient total motile count). In cases of severe disorders or after unsuccessful attempts, IVF/ICSI is recommended (ICSI overcomes low sperm motility and morphology, but does not correct genetic defects). The decision is a team effort, taking into account the partner's age and the timeframe. [53]

Table 4. What, to whom and why

Situation	First steps	Next steps
Clinical varicocele + poor sperm analysis	Lifestyle, antioxidants (optional)	Varicocelectomy/embolization
Leukocytospermia/infection	Etiotropic therapy	SDF/spermogram control
High SDF, IVF failures	Antioxidants, source elimination	Selection (microfluidics/PICSI/MACS) ± testicular sperm
Time is limited (female factor)	Parallel optimization	AI/IVF/ICSI according to indications

Table 5. Antioxidants: What the evidence says (summary)

Group	Possible benefits	Restrictions
Coenzyme Q10, carnitine, vit. S/E, zinc	+ to mobility; potentially ↑ pregnancy/live birth	Live birth effect is not consistent in rigorous analysis; dose/schedule heterogeneity

Table 6. WHO-6: Key Methodological Emphasis

Parameter	What is important
Repeatability	2-3 tests with an interval of 2-6 weeks
Preparation	Abstinence for 2-7 days, avoid overheating/alcohol
Morphology	Strict criteria; interpretation in context
Laboratory quality	Internal/external quality control

Table 7. Sperm selection in ICSI: an overview

Method	Idea	Potential benefits
PICSI (with hyaluronan)	Selection of mature spermatozoa	Lower SDF, better embryo outcomes for some couples
MACS (annexin V)	Removal of apoptotic cells	Reducing SDF, improving sample quality
Microfluidics	Gentle filtration by self-floating	Less SDF, promising clinical outcomes
IMSI	Optics ×6600 for morphology	More precisely, selection for severe teratozoospermia

Prevention

Quitting smoking and limiting alcohol are simple steps with high impact. Maintaining a healthy weight and engaging in regular aerobic and strength training activities reduce systemic inflammation and improve hormonal balance. [54]

Avoid scrotal overheating and toxic exposures at work; use protective equipment and observe safety precautions. Schedule semen analysis outside of periods of fever and severe stress. [55]

Diet: More whole foods, fish, nuts, vegetables and fruits, less trans fats, excess salt and sugar. Adequate sleep and stress management complement the program. [56]

Monitoring and treatment of varicocele/inflammatory diseases at early stages is a contribution to the prevention of deterioration of spermatogenesis. [57]

Forecast

For treatable causes (varicocele, inflammation, overheating, lifestyle), the prognosis is favorable: in a significant proportion of men, mobility and morphology improve within 3-6 months after correction. The effect of varicocelectomy is most noticeable in properly selected patients. [58]

In cases of genetic defects/severe teratozoospermia, the prognosis for natural conception is more modest, but ICSI with modern sperm selection methods provides a high chance of having a child. [59]

High DNA fragmentation worsens outcomes, but it can be reduced by eliminating sources of oxidative stress and by choosing the right sperm selection method or source (including testicular). [60]

The key to success is a team-based, step-by-step plan and reasonable deadlines: do not delay the correction of factors, evaluate the female component in parallel and, if necessary, move on to ART in a timely manner. [61]

FAQ

Is it possible to "cure" asthenoteratozoospermia with pills?
Sometimes yes (if there is inflammation/deficiencies), but more often a combination of lifestyle changes, varicocele/infection correction, and, if necessary, reproductive technologies are needed. Antioxidant supplements are only a supplement. [62]

How long does it take to see results after lifestyle changes or surgery?
Spermatogenesis lasts approximately 74 days; the first improvements are visible after 3 months, with more pronounced results by 6 months. The dynamics are similar after varicocelectomy. [63]

Is it worth taking a sperm DNA fragmentation test?
It is useful in cases of repeated IVF failures/miscarriages, high oxidative stress, varicocele, age, and when the results will influence the choice of tactics (sperm selection, testicular sperm). [64]

Is it possible to avoid ICSI?
If motility and morphology are moderately reduced, the female factors are favorable, and time is available, insemination can be used. In cases of severe disorders or limited time, ICSI is more often chosen. [65]