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CHAPTER 10 Urology
362
Benign prostatic hyperplasia
Key facts
Benign prostatic hyperplasia (BPH) is a non-malignant enlargement of
the prostate gland. There is an increase in both stromal and glandular components.
Incidence of BPH is about 25% in age 40–60y, 40% in over 60s.
Commonest cause of lower urinary tract symptoms (LUTS) in
middle-aged and elderly men.
Pathological features
Aetiology is largely unknown. Possible factors include:
Androgens. No BPH in those who have had early castration.
Oestrogens. Increased oestrogen:testosterone ratio with age.
Growth factors, e.g. high concentration of TGFA in BPH.
Clinical features
Symptoms
Storage symptoms, such as frequency, urgency, nocturia, and
incontinence.
Voiding symptoms, including hesitancy, poor stream, intermittency,
terminal dribble, and abdominal straining.
Superimposed infection may cause dysuria and haematuria.
Incomplete emptying and chronic or acute retention of urine.
Signs
Smooth enlargement of the prostate detected by digital rectal
examination.
Possible palpable bladder if chronic retention.
Always examine for neurological signs in those with LUTS.
Complications of BPH
Intractable LUTS.
Haematuria.
UTI.
Stone formation.
Acute retention of urine.
Chronic retention of urine.
Overfl ow incontinence.
Obstructive renal failure.
Diagnosis and investigations
Prostate symptom score to assess severity.
Digital rectal examination and serum PSA measurement to assess for
features of malignancy.
Basic investigations
Serum creatinine, urinalysis in all patients.
Urine fl owmetry and residual volume estimation in those considered
for intervention.
BENIGN PROSTATIC HYPERPLASIA
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Advanced investigations
Cystoscopy. To exclude bladder disease.
Transrectal ultrasound 9 guided biopsy. If concern over underlying
malignancy.
Renal ultrasound, invasive urodynamic studies.
Treatment
Recommended for those with LUTS that are impacting on quality of life or those with complications.
Medical treatment
Patients with mild symptoms and no complications may be observed
(watchful waiting).
A-adrenergic antagonists. Relax smooth muscle of prostatic urethra
to decrease outlet resistance; side effects include dizziness and hypotension (especially postural).
5A-reductase inhibitors. Block conversion of testosterone to
dihydrotestosterone (DHT) and shown to cause involution of BPH; side effects include loss of libido and erectile dysfunction.
Combination drug therapy with both the above agents. May reduce
the clinical progression and decrease the need for surgery.
Surgical treatment
Reserved for those with any of the complications or symptoms not
responding to medical therapy.
Surgical options include:
Transurethral resection of the prostate (TURP), the most • commonly performed procedure for BPH in the UK. Open retropubic prostatectomy.• Transurethral incision in the prostate (TUIP).• Bladder neck incision.• Laser ‘prostatectomy’.• Microwave thermotherapy ablation of the prostate.
363
Key revision points—anatomy of the prostate
Three glandular zones:
Peripheral (70%), most prone to carcinoma formation.• Central (25%), most prone to BPH.• Transitional (5%), most prone to BPH.
Blood supply:
Arterial supply is triple, mainly inferior vesical, some from inferior • rectal and internal pudendal. Venous drainage, extensive plexus beneath capsule.
Innervation:
Autonomic, extensive from inferior hypogastric plexus as a • capsular plexus supplying prostate, seminal vesicles, and urethra, which also supplies the penile structures (glands, corpora, and urethra). Somatic, from pudendal nerve (S2, 3, 4) to supply external • urethral sphincter.
CHAPTER 10 Urology
364
Stricture of the urethra
Key facts
Classifi ed according to site and aetiology, e.g. post-infl ammatory
bulbar stricture or traumatic membranous stricture.
Graded according to length and (in the anterior urethra) degree of
fi brosis of corpus spongiosum (spongiofi brosis).
Any part of the urethra may be involved.
The propensity for stricture recurrence parallels the severity (grade).
Aetiology
Trauma.
Pelvic fracture.• Falls astride, e.g. on bicycle crossbar.• Urinary tract instrumentation/surgery.
Infection.
Neisseria gonorrhoea • and Chlamydia trachomatis. Catheter-associated UTI.
Lichen sclerosis et atrophicus.
Pathological features
Annular narrowing by scar tissue composed of dense collagen and
fi broblasts, which may extend into corpus spongiosum.
Lichen sclerosus (balanitis xerotica obliterans (BXO)) consists of
dermal sclerosis with epidermal atrophy; urethral lesions are usually confi ned to the meatus and fossa navicularis.
Clinical features
History of urethritis, trauma, or urinary tract instrumentation.
LUTS, divergent or diminished stream, straining to void, urgency,
frequency.
Haematuria (‘initial’ or ‘terminal’, i.e. at the beginning or end of the
stream).
UTI (often recurrent).
Urinary retention, acute or chronic.
Overfl ow incontinence.
Complications
Urinary tract calculi formation.
Infection, including UTI, prostatitis, epididymitis, and (rarely) Fournier’s
necrotizing fasciitis.
Renal failure secondary to chronic obstruction.
Diagnosis and investigations
Urinalysis (microbiology, biochemistry, and cytology).
U&E.
Urofl owmetry and measurement of post-void residual bladder volume.
Voiding cystourethrogram with or without retrograde urethrogram.
Endoscopy.
STRICTURE OF THE URETHRA
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Ultrasound scan (transperineal or endoluminal) to assess extent of
spongiofi brosis.
Magnetic resonance tomography.
Treatment
Initial
Treat infection before surgical treatment.
For acute urinary retention, severe symptoms, or renal failure,
temporary suprapubic catheterization.
Defi nitive
All urethral reconstructive surgery has an ‘attrition rate’.
Initial internal urethrotomy may cure up to 30%, but repeat
procedures are rarely successful and may cause progression.
Urethroplasty may be used for some cases.
Short strictures are excised and the urethra primarily • re-anastomosed. For longer or complex strictures, pedicled fl ap reconstruction or • graft reconstruction is used; the graft or fl ap may be applied as an onlay (to augment the native urethra) or as a tube. For free grafts, buccal mucosa is currently favoured.• More complicated repairs are best managed with staged repairs.
Perineal urethrostomy may be required.
365
CHAPTER 10 Urology
366
Scrotal swellings
Major causes
Intratesticular lesions
Malignant testicular tumours.
Benign intratesticular lesions. Simple intratesticular cyst or epidermoid
cysts and benign teratoma (especially in the prepubertal testis).
Infl ammatory lesions
Acute epididymo-orchitis or viral orchitis.
Chronic tuberculous epididymo-orchitis, schistosomal epididymitis,
sperm granuloma.
Traumatic lesions
Scrotal haematoma.
Haematocele (haematoma within tunica vaginalis).
Testicular haematoma (within tunica albuginea testis).
Derangement of testicular, adnexal, or cord anatomy
Epididymal cysts or spermatocele of the epididymis.
Varicocele (varicosities of the pampiniform plexus).
Inguinal hernia (patent processus vaginalis in children).
Hydrocele (vagina = within tunica vaginalis or cordal).
Late (missed) or prenatal torsion of the spermatic cord.
Persistence of embryological vestigial structures.
Müllerian duct remnant (appendix testis).• Wolffi an duct remnants (appendix epididymis, vas aberrans of • Haller, paradidymis).
Miscellaneous
Acute idiopathic scrotal oedema.
Cutaneous lesions, e.g. sebaceous cysts.
Henoch–Schönlein purpura.
Clinical features/diagnosis
2 Testicular tumours:
Firm intratesticular or progressively enlarging lesions are tumours • until proven otherwise. Do not be misled by painful testicular swelling following relatively • trivial trauma; tumours may present this way.
Tuberculous epididymitis may occur with or without evidence of
pulmonary, systemic, or other genitourinary involvement.
Hydroceles, patent processus vaginalis, and large spermatoceles are
transilluminable, may be fl uctuant, and are usually confi ned to the scrotum.
Varicocele. Often associated with subfertility or dragging discomfort
that worsens on standing and settles when recumbent. More obvious as a fl uctuant swelling with the patient standing. A cough impulse may be felt. Ipsilateral testis may be atrophied. Examine the abdomen to exclude an associated renal tumour.
SCROTAL SWELLINGS
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Inguinal hernias tend to be intermittent, associated with groin
discomfort, and when ‘out’, the examining hand cannot ‘get above’ the swelling in the cord/inguinal canal. A history of longstanding enlargement is typical.
Investigations
Urinalysis for M,C,&S.
Blood tests. Consider tumour markers (AFP, β-HCG), infl ammatory
markers (CRP, WCC).
Ultrasound scanning of the scrotal contents has several important uses.
Distinguishes intratesticular from paratesticular swellings, solid from • cystic lesions, cellulitis from abscess, etc. Can examine impalpable testes, e.g. within large hydroceles.• Can identify rupture of the tunica albuginea testis.• Examination of the abdomen can identify renal mass associated with • varicocele or ascites with hydrocele/scrotal oedema, etc. Colour fl ow Doppler ultrasound can identify hyperaemia, • underperfusion, and varicocele.
Treatment
Testicular tumours, acute epididymo-orchitis (see b pp. 382, 388).
Suspected paratesticular tumours are approached surgically in the
same way as testis tumours. Surgery may be conservative with benign testicular and paratesticular tumours.
Sperm granuloma may be excised or epididymectomy may be
performed. Reassurance may be all that is required in many cases. Recurrence rates after surgery are high.
Epididymal cysts/spermatocele may be aspirated, but recurrence is
common. Excision risks loss of epididymal patency, is associated with risk of recurrence, and should probably be discouraged in men who have not completed their family.
Hydroceles. Treat if symptomatic. Procedures usually reconfi gure the
serosal remnant of tunica vaginalis so as to allow lymphatic drainage via scrotal lymphatics. Reduction, inversion (Jaboulay), or imbrication (Lord’s) of the tunica vaginalis is used.
Embryological remnants. No treatment if asymptomatic.
Varicocele. Treat if symptomatic, associated with infertility, or with
failure of testicular growth. Venous embolization and retroperitoneal ligation (laparoscopic or open) of the testicular vein have similar results. Minimally invasive treatments are preferable. Gubernacular veins and other collaterals may account for failures. Open surgical ligations via an inguinal incision can deal with these.
Acute idiopathic penoscrotal oedema of childhood usually settles with
conservative treatment. Antihistamines and antibiotics are frequently prescribed, but there is little evidence to support this.
367
CHAPTER 10 Urology
368
Disorders of the foreskin
Phimosis (see Fig. 10.2a)
Key facts
Narrowness of the preputial opening, preventing retraction and
exposure of the glans.
May be physiological in infants and young children and will resolve.
Pathological phimosis is secondary to scarring such as BXO or
following monilial balanoposthitis.
Pathological phimosis may be associated with discomfort, UTI,
balanoposthitis, and (perhaps) carcinogenesis.
Clinical features
In childhood, physiological phimosis may be identifi ed by absence of
scarring of the preputial tip and by pouting of the inner layer of the prepuce when a gentle attempt is made to retract it.
A whitish sclerotic preputial tip and no pouting characterize BXO.
Parents may complain of ballooning of their child’s foreskin or of
recurrent balanoposthitis. In adults, the diagnosis is obvious.
Treatment
Physiological phimosis needs no treatment.
Early BXO may be treated by application of topical steroid cream.
Surgical treatment of phimosis includes circumcision and dorsal slit.
Paraphimosis (see Fig. 10.2b)
Key facts/diagnosis
The retracted foreskin acts as a constricting ring, reducing lymphatic
and venous drainage of tissues distal to the ring (glans, inner layer of foreskin). Subsequent oedema makes reduction more diffi cult.
Involved tissues typically appear odematous and infl amed with
progression to infection, ulceration, and necrosis if left untreated. Can occur in normal penises.
3 Treatment
Early cases. Gentle manual compression of the oedematous tissues
within a saline-soaked swab will allow reduction of the foreskin after a few minutes without anaesthesia.
Established cases. LA penile block or anaesthesia may be necessary.
Hyaluronidase can be injected under the constriction.
Neglected/severe cases. A relaxing dorsal incision may be made through
the constriction and the tissues immediately proximal and distal to it. Subsequent circumcision is often offered.
DISORDERS OF THE FORESKIN
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(a)
Phimosis
Manual reduction of paraphimosis by counter pressure between thumbs and fingers
(b)
369
Paraphimosis
Fig. 10.2 (a) Phimosis. (b) Reduction of an acute paraphimosis.
CHAPTER 10 Urology
370
Common conditions of the penis
Peyronie’s disease
Key facts
Damage to tunica albuginea penis, forming inelastic penile plaques
mostly in the dorsal midline, causing local pain and deformity.
Associated with Dupuytren’s contractures, plantar fascial contractures,
and tympanosclerosis.
One-third of patients have erectile dysfunction.
Clinical features
History and examination
Gradual or sudden development of palpable penile plaques with
painful distortion of the erect penis in two-thirds of patients.
Occasional history of penile trauma, urethral instrumentation.
Erectile dysfunction may involve the whole or part of the penis.
Pain usually resolves, but deformity does not.
Penetrative sexual intercourse may be more diffi cult or impossible
because of pain, angulation, or buckling.
The plaque is palpable with the fl accid penis stretched.
Erection is induced pharmacologically and a photo record kept.
Investigations Plain fi lm soft tissue radiography or grey-scale ultrasound may demonstrate calcifi cation, an indicator of plaque maturity.
Treatment
Medical
Indicated for those able to engage in intercourse and whose disease is still evolving.
Oral treatment options. Colchicine, vitamin E, or Potaba
Intralesional injections. Verapamil or collagenase (investigational).
Treatment of associated erectile dysfunction.
Surgical
Indicated for those with stable lesions, severe deformity.
Plication techniques. Plication of the tunica opposite the deforming
plaque.
Grafting techniques. The plaque is excised and the defect grafted.
Prosthesis insertion within corpora cavernosa. Generally reserved for
patients with severe erectile dysfunction refractory to medical therapy.
Priapism
Key facts Abnormally sustained erection unrelated to sexual stimulation. It is classifi ed as high fl ow (arterial) or low fl ow (veno-occlusive).
Low fl ow priapism
Congestion secondarily reduces arterial blood fl ow, leading to local
hypoxia, acidosis, and hypercapnoea.
Causes include:
Drugs (intracavernosal prostaglandin and papaverine, psychotropics, e.g. trazodone, chlorpromazine).
®
.
COMMON CONDITIONS OF THE PENIS
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Abnormal blood viscosity (sickle cell, myeloma, leukaemia, • thalassaemia, total parenteral nutrition). Neurological disease, e.g. spinal or cerebrovascular disease.• Miscellaneous, e.g. infi ltration by solid tumour.
Characterized by painful persistent erection, not involving the glans
and corpus spongiosum.
High fl ow priapism
Most commonly follows blunt trauma to penis or perineum, but has
been caused by intracavernosal injection or revascularization.
The mechanism is arterio-cavernosal fi stula with unregulated arterial
infl ow and increased venous outfl ow.
Characterized by partial, painless swelling of the glans and corpus
spongiosum.
Investigation
Colour Doppler ultrasonography or cavernosal blood gases.
pH <7.25, pO
FBC and differentials; Hb electrophoresis.
<30mmHg, pCO2 >60mmHg suggest low fl ow.
2
Treatment—low fl ow
Correct underlying abnormalities, e.g. sickle cell (rehydration, O
transfusion), myeloma (plasmapheresis).
,
2
Oral B-agonists, e.g. terbutaline 5mg + further 5mg 15min later.
Intracavernosal phenylephrine.
Corpora cavernosa aspiration (up to 50mL) + manual pressure.
Surgical techniques augment venous drainage of the corpora
cavernosa.
Treatment—high fl ow
Selective pudendal arteriography and embolization.
371