Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_959_Библиотеки_им_академика_М_И_Перельмана
.pdf
314 Challenging Concepts in Urological Surgery
https://t.me/med1917
Expert comment Martius fad pad
The Martius fat pad is the most suitable interposition pad to use for vaginal VVF repair. It receives its
blood supply through two pedicles, superior based on external pudendal and inferior based on the
internal pudendal artery. One pedicle is sacrificed, typically the superior one, and the labial fat pad is
then swung into the vaginal field after dissection of the space between the labia and the sidewall of
the vagina (Figure 32.2).
Figure 32.2 (a) Exposure of labial fat pad.1 (b) Martius fat pad swung into the vaginal surgical
field through a lateral vaginal wall tunnel. The graft is based on its inferior pedicle blood supply
in this case.
1
Discussion
The World Health Organization (WHO) has estimated that 2 million women from
sub- Saharan Africa and Asia have fistulae and approximately 50,000– 100,000 new
women are affected each year.2 Adler et al., in their systematic review and metaanalysis, were able to provide more robust estimates on prevalence, suggesting 1.60
Expert comment
Classification of VVF
Several classifications systems
exist and the commonest utilized
are those related to obstetric
VVF such as Waaldijk’s and Goh’s
classifications.
iatrogenic fistula, the International
Consultation on Incontinence
has suggested using the WHO
classification from 2006.
3,4
However, for
(95% confidence interval (CI) 1.16– 2.10) per 1000 women of reproductive age in
sub- Saharan Africa and 1.20 (95% CI 0.10– 3.54) per 1000 in South Asia regions.2 The
commonest cause in this population is obstructed labour. In the developing world,
there is a distinct lack of services, poor obstetric care, as well as a lack of healthseeking behaviour. However, in the industrialized world, gynaecological or pelvic
surgery are the main causes of VVF.
In general, there is a lack of high- quality studies in this field. According to the
European Association of Urology guidelines on the management of non- obstetric
urinary fistula, the majority of evidence is level 3 and recommendations are grade C,
suggesting a need for better quality studies.
5
315Case 32 Vesicovaginal fistula
https://t.me/med1917
Evidence base Systematic review: aetiology, treatment, and outcomes of urogenital fistulae
in low- and well- resourced countries
In a systematic review6 over a 35- year period, 49 articles were identified and suggested that in wellresourced countries, 83% of fistulae occurred following surgery, whereas in low- resourced countries,
95% were associated with childbirth. Conservative approaches, such as catheter drainage, are more
likely to be successful for non- radiotherapy fistulae. The median overall closure rate was 95% and
87%, in high- and low- resourced countries, respectively. Closure was significantly more likely using a
transvaginal rather than a transabdominal technique (91% vs 84% success).
Evidence base UK series of urogenital fistulae
Hilton reported on his own tertiary referral experience over 25 years from the UK.7 Hospital episode
statistics had suggested in the UK between 2000 and 2010 approximately 105 urogenital fistulae
cases were surgically treated per year in the UK, suggesting it is a relatively uncommon procedure.
Approximately three- quarters of the 348 women in his series were related to VVF. Of all urogenital
fistulae, the commonest cause was surgical (two- thirds of the entire cohort) and mostly due to
hysterectomy. Obstetrics aetiology was seen in 11% and radiotherapy cases were responsible for 10%.
Spontaneous closure occurred in 7% of women who were managed with no treatment, indwelling
catheter, or ureteric stenting. The anatomical closure rate at the first operation was 96%, although
2% reported residual urinary incontinence. Success was higher in patients who were undergoing
surgical repair for the first time. The author suggested the need for centralization of urogenital fistulae
as the volume was generally low in the UK and it was clear that previous failed repair had a negative
influence on the chance of subsequent successful repair.
Learning point WHO
classification of fistula (2006)
Simple fistula with good
prognosis
● Single fistula <4 cm.
● VVF.
● Bladder neck not involved.
● No circumferential defect.
● Minimal tissue loss.
● No ureteric involvement.
● First attempt at repair.
Complex fistula with uncertain
prognosis
● Fistula >4 cm.
● Multiple fistula.
● Mixed fistula (e.g. cervical, rectal).
● Bladder neck involvement.
● Scarring.
● Circumferential defect.
● Extensive tissue loss.
● Radiation.
● Intravaginal ureters.
● Previous failed repair.
Expert comment The 6th International Consultation on Incontinence
The management of VVF is summarized in the 6th International Consultation on Incontinence
document and is summarized in Figure 32.3.
8
HISTORY
CLINICAL
ASSESSMENT
PRESUMED
DIAGNOSIS
MANAGEMENT*
Figure 32.3 Algorithm for management of VVF.
316 Challenging Concepts in Urological Surgery
https://t.me/med1917
Future directions Minimally invasive VVF repair
Minimally invasive VVF repair has been performed using laparoscopic techniques,9 combined
vesicoscopic, laparoscopic, and vaginal approach,10 and with a robotic- assisted laparoscopic
approach.11 The robotic- assisted technique appears attractive as this approach has three- dimensional
vision and magnification, and suturing in the pelvis is technically easier compared to the laparoscopic
approach. In 2017, Bora et al. reported on 30 such cases, with a 93% successful outcome.12 At the
time of writing, this is the largest series to date. A four- port transperitoneal technique was employed
and the same principles of the open abdominal approach were adhered to. Packing of the vagina is
required with roller gauze to prevent leak of the pneumoperitoneum. Ninety per cent of the cases
were subsequent to hysterectomy. Mean fistula size was 10.4 mm (range 5– 30 mm). Eighteen patients
had an interposition flap consisting of omentum, peritoneum, or sigmoid colon epiploicae. Mean
duration of surgery was 133 minutes with a mean blood loss of 50 mL. Median duration of stay was
7.5 days. The authors comment that patients in general were ready for discharge on postoperative day
4 but due to the nature of their tertiary referral practice patients, they preferred to stay a little longer
for reassurance due to them living at very remote sites. Two early recurrences were seen, after 2 days
post catheter removal and at 3 months.
The outcomes of this approach are encouraging but it is clear that larger, comparator studies are
required before understanding if this approach is beneficial. Furthermore, this approach is more costly
and effectiveness in this regard will need to be studied carefully.
A final word from the expert
VVF is a devastating complication with considerable physical and psychosocial effects. Obstetric
trauma due to lack of obstetric healthcare resources is a major global health issue and the
majority of VVFs worldwide are preventable; in well- resourced countries VVF is a relatively rare
consequence of pelvic surgery or radiotherapy. Due to its considerable impact on quality of
life, as well as potential associated medicolegal consequences, it is important that patients are
referred early to specialist surgeons with expertise in VVF repair. The best chance for successful
VVF closure is the first chance, with any successive surgery converting a potentially ‘simple’
fistula into a challenging ‘complex’ fistula with lower rates of successful closure. Therefore,
detailed surgical planning is essential.
Evaluation of a patient with VVF fundamentally involves three key decisions:
1. When should the fistula be repaired?
2. How should it be repaired (abdominal or vaginal approach)?
3. Should an interposition graft be used (and if so, which)?
If recognized in the immediate postoperative period then early repair is recommended, even
up to 2 weeks following the initial surgery as long as the patient is clinically well (e.g. not
overtly septic or other factors that may compromise surgical repair). Otherwise, repair should
be delayed until 3 months to allow local tissue quality to improve, increasing the likelihood of
successful closure.
The decision of whether to perform a vaginal or abdominal approach depends upon patient
factors (body mass index, extent of previous pelvic surgery/ radiotherapy, vaginal access
and tissue quality, patient’s wishes), fistula factors (size, location, presence of any associated
ureteric injury), and expertise of the surgeon. These factors should be assessed with a thorough
evaluation consisting of cross- sectional imaging, cystoscopy, and examination under anaesthetic
in order to determine the optimal approach.
excision of avascular tissue, ensuring a tension- free, layered closure with non- overlapping suture
lines, and catheter drainage of the bladder for 2– 3 weeks (depending upon complexity of the
fistula and local tissue quality). The use of a pedicled interposition flap between the suture lines
https://t.me/med1917
can aid successful outcome, especially in complex fistula with poor local tissue vascularity (e.g.
following pelvic irradiation). Omental or labial fat pad flaps are most readily available depending
upon the surgical approach.
Finally, prevention is better than cure and improving obstetric care in low- resourced countries
will prevent most cases of VVF worldwide. Awareness of the surgical anatomy of the lower
urinary tract, and careful surgical technique, may prevent iatrogenic cases. The development
of specialist fistula centres in areas of high VVF prevalence would allow timely access and
treatment for patients with VVF, and in well- resourced countries early referral to a specialist VVF
surgeon is essential. Ultimately, abiding by the basic principles of reconstructive surgery will
ensure a successful outcome.
317Case 32 Vesicovaginal fistula
References
1. Malde S, Spilotros M, Wilson A, et al. The uses and outcomes of the Martius fat pad in female urology. World J Urol. 2017;35(3):473– 478.
2. Adler AJ, Ronsmans C, Calvert C, Filippi V. Estimating the prevalence of obstetric fistula: a
systematic review and meta- analysis. BMC Pregnancy Childbirth. 2013;13:246.
3. Goh JT. A new classification for female genital tract fistula. Aust N Z J Obstet Gynaecol.
2004;44(6):502– 504.
4. Waaldijk K. Surgical classification of obstetric fistulas. Int J Oynaecol Obstetr.
1995;49(2):161– 163.
5. Burkhard FC, Bosch JLHR, Cruz F, et al. EAU guidelines on urinary incontinence in adults.
European Association of Urology. 2018. https:// uroweb.org/ wp- content/ uploads/ EAUGuidelines- on- Urinary- Incontinence- 2018- large- text.pdf
6. Hillary CJ, Osman NI, Hilton P, Chapple CR. The aetiology, treatment, and outcome of
urogenital fistulae managed in well- and low- resourced countries: a systematic review. Eur
Urol. 2016;70(3):478– 492.
7. Hilton P. Urogenital fistula in the UK: a personal case series managed over 25 years. BJU
Int. 2012;110(1):102– 110.
8. De Ridder D, Browning A, Mourad S, et al. In: Abrams P, Cardozo L, Wagg A, Wein A, eds.
Incontinence, Vol. 2. 6th ed. Bristol: International Continence Society; 2016:2145– 2202.
9. Shah SJ. Laparoscopic transabdominal transvesical vesicovaginal fistula repair. J Endourol.
2009;23(7):1135– 1137.
10. Grange P, Giarenis I, Rouse P, Kouriefs C, Robinson D, Cardozo L. Combined vaginal and vesicoscopic collaborative repair of complex vesicovaginal fistulae. Urology.
2014;84(4):950– 954.
11. Sundaram BM, Kalidasan G, Hemal AK. Robotic repair of vesicovaginal fistula: case series
of five patients. Urology. 2006;67(5):970– 973.
12. Bora GS, Singh S, Mavuduru RS, et al. Robot- assisted vesicovaginal fistula repair: a safe and
feasible technique. Int Urogynecol J. 2017;28(6):957– 962.
https://t.me/med1917
https://t.me/med1917
SECTION 11
Male infertility and
sexual dysfunction
Case 33 Male factor infertility: management of the
azoospermic patient
Case 34 Erectile dysfunction
Case 35 Peyronie’s disease
Case 36 Ejaculatory orgasmic disorders
https://t.me/med1917
33
https://t.me/med1917
CASE
Male factor infertility:
management of the
azoospermic patient
Matthew Young
Expert commentary Oliver Kayes
Case history
A 31- year- old male is referred to the reproductive medicine clinic with an 18- month
history of failure to conceive. He is otherwise fit and well with no history of urogenital
infection, previous inguinoscrotal surgery, or cryptorchidism. He has no history of
erectile or ejaculatory dysfunction. He does not recall any significant family history.
His partner (age 32 years) has a child from a previous relationship for which she did
not require any fertility investigations or treatments. Clinical examination reveals a
phenotypical male with a body mass index (BMI) of 26 kg/ m2. There is no evidence
of gynaecomastia. Both testes are small (approximate volume 4 cc) but have a normal
consistency. No other abnormality is detected on regional examination.
Learning point Definition
of infertility
Expert comment Causes of male factor infertility
Approximately half of involuntarily childless couples involve male infertility- associated factors, usually
with abnormal semen parameters. For this reason, all male patients should undergo preliminary
testing and if diagnosed with subfertility then referred for further medical evaluation by a urologist
trained in male reproduction as part of a multidisciplinary assessment of infertility. Up to 30% of
cases may identify no identifiable cause which is historically termed idiopathic male infertility. Other
recognized causes of male infertility are highlighted in Table 33.1.
Table 33.1 Recognized cause of male factor infertility
Diagnosis Unselected patients with
male factor infertility (%)
All 100 11.2
Infertility of known (possible) cause 42.6 42.6
Undescended testes 8.4 17.2
Varicocele 14.8 10.9
Sperm autoantibodies 3.9 –
Testicular tumour 1.2 2.8
Other 5.0 1.2
Idiopathic infertility 30.0 13.3
Hypogonadism 10.1 16.4
Klinefelter syndrome (47,XXY) 2.6 13.7
XX male 0.1 0.6
Primary hypogonadism of unknown cause 2.3 0.8
Azoospermic
patients (%)
Infertility is defined as the inability
to achieve a spontaneous
pregnancy within 12 months
with regular (every 2– 3 days) and
unprotected sexual intercourse.
Primary infertility refers to couples
who have never had a child and
cannot achieve a pregnancy.
Secondary infertility refers to
individuals who have been able to
conceive at least once previously.
Ideally, all newly referred couples
who are struggling to conceive
should be assessed simultaneously
with a detailed clinical history and
examination.
322 Challenging Concepts in Urological Surgery
https://t.me/med1917
Table 33.1 Continued
Clinical tip Clinical
examination
Clinical examination should include
the following:
● Body composition— height/
weight/ BMI/ gynaecomastia.
● Evidence of inguinoscrotal
surgery.
● Regional lymphadenopathy.
● Penile abnormalities—
deformity/ hypospadias/ meatal
stenosis/ phimosis.
● Testes— volume/ consistency/
scrotal position/ mass or
swelling.
● Epididymis— dilatation/ defects/
induration/ cysts.
● Spermatic cord— varicocele/
Valsalva manoeuvre.
● Vas deferens abnormalities.
Diagnosis Unselected patients with
male factor infertility (%)
Secondary hypogonadism 1.6 1.9
Kallmann syndrome 0.3 0.5
Idiopathic hypogonadotropic hypogonadism 0.4 0.4
Residual after pituitary surgery <0.1 0.3
Late onset hypogonadism 2.2 –
Constitutional delay of puberty 1.4 –
Other 0.8 0.8
Systemic disease 2.2 0.5
Cryopreservation due to malignancy 7.8 12.5
Disturbance of erection/ ejaculation 2.4 –
Obstruction 2.2 10.3
Vasectomy 0.9 5.3
Cystic fibrosis 0.5 3.0
Others 0.8 1.9
Re- formatted from Nieschlag E, Behre HM and Nieschlag S (eds). Andrology: Male Reproductive Health and
Dysfunction. 2010, Springer Verlag: Berlin.
Clinical tip Clinical history
The following should be evaluated in the clinical history:
● Duration of failure to conceive (months).
● Primary (no history of children) or secondary (children from a previous relationship).
● History of cryptorchidism.
● History of infections— urogenital (e.g. mumps orchitis, tuberculosis) or sexually transmitted.
● Regional surgery (e.g. orchidopexy, hernia repair, vasectomy).
● History of trauma or testicular torsion.
● Previous malignancy.
● Age of puberty.
● Lifestyle— smoking/ alcohol/ anabolic steroid use/ recreational drugs (e.g. cannabis, cocaine).
● Family history (genetic abnormalities/ congenital abnormalities/ infertility history).
● Occupational exposure to radiation/ chemicals.
● Gonadotoxic treatments (e.g. chemotherapy, radiotherapy, immunotherapy).
● Sexual dysfunction— erectile dysfunction/ premature ejaculation.
Azoospermic
patients (%)
Mandatory first- line testing includes a semen fluid analysis in an accredited andrology laboratory and microbiological sampling, primarily to exclude any sexually
transmitted infections. If the semen fluid analysis is abnormal, then a repeat sample
is compulsory. Careful interpretation of the semen fluid analysis results should aim to
identify men with normal or abnormal parameters based on published WHO criteria
and establish (1) degree subfertility (mild, moderate, or severe); and (2) evidence
of obstruction, infection, or inflammation. Men with severe subfertility (total sperm
count <5 million) should go on to have further laboratory testing. Our patient’s results can be seen in Table 33.2.
Table 33.2 Semen analysis parameters for case study patient with WHO lower reference limits
https://t.me/med1917
323Case 33 Male factor infertility: management of the azoospermic patient
Parameter Case study
patient values
Semen volume (mL) 4.5 1.5 (1.4– 1.7)
Total sperm number (million/ ejaculate) 0 39 (33– 46)
Sperm concentration (million/ mL) 0 15 (12– 16)
Total motility (progressive, non- progressive, %) 0 40 (38– 42)
Progressive motility (PR, %) 0 32 (31– 34)
Vitality (live spermatozoa, %) 0 58 (55– 63)
Sperm morphology (normal form, %) 0 4 (3– 4)
pH 7.4 ≥7.2
Expert comment Semen analysis
Ejaculate analysis has been standardized (Table 33.3), with consensus that modern semen analysis
must follow these guidelines. However, it has become evident that more complex investigations
beyond simple semen analysis may be required. Such cases may include recurrent pregnancy loss (i.e.
miscarriage) following natural or assisted conception and men with unexplained male infertility. In
these patients there is evidence that the sperm DNA may be damaged, resulting in pregnancy failure.
Table 33.3 WHO standardized values for semen analysis
Parameter Lower reference limit (range)
Semen volume (mL) 1.5 (1.4– 1.7)
Total sperm number (106/ ejaculate) 39 (33– 46)
Sperm concentration (106/ mL) 15 (12– 16)
Total motility 40 (38– 42)
Progressive motility (PR, %) 32 (31– 34)
Vitality (live spermatozoa, %) 58 (55– 63)
Sperm morphology (normal forms, %) 4 (3– 4)
Other consensus threshold values
pH >7.2
Peroxidase- positive leukocytes (106/ mL) <1.0
Re- formatted from WHO, WHO Laboratory Manual for the Examination and Processing of
Human Semen, 5th edn. 2010.
Learning point Male urogenital infections
Male urogenital infections are a potentially reversible cause of male factor infertility. Men with
confirmed sexually transmitted infections have not been conclusively shown to be at increased risk
of infertility; however, such infections (e.g. Chlamydia) ae likely to pose a potential risk to the female
urogenital tract rather than a direct effect on male reproduction. The presence of bacteria in the
urogenital tract may lead to chronic inflammation of the prostate and epididymis which may cause
obstruction and lead to oligospermia and/ or reduced seminal volume. The role of the microbiome
and effects on sperm function requires further elucidation.
Lower reference limit
(WHO criteria)
Clinical tip Semen analysis
interpretation
It is important to distinguish
between the following conditions:
● Oligospermia: <15 million
spermatozoa/ mL.
● Asthenozoospermia: <32%
motile spermatozoa.
● Teratozoospermia: <4%
normal forms.
All three phenomenon occurring
simultaneously represent
oligoasthenoteratospermia (OAT)
syndrome.
Соседние файлы в папке Библиотека им академика М.И. Перельмана