Материал: Oxford American Handbook of Urology ( PDFDrive )

PRIAPISM 497

Table 12.4 Causes of lowand high-flow priapism

Table 12.5 Examples of drugs that may cause priapism

of <30 mmHg, PCO2 >60 mmHg, and pH <7.25. Nonischemic priapism commonly shows a PO2 of > 90 mmHg, PCO2 <40 mmHg, and pH 7.4. Normal flaccid penile cavernous blood gas levels are roughly equal to those of normal mixed venous blood (PO2 40 mmHg, PCO2 50 mmHg, pH 7.35).

•Color Doppler ultrasound scan of cavernosal artery and corpora cavernosa. Reduced blood flow in ischemic priapism; ruptured artery with pooling of blood around injured area in nonischemic priapism

Management

Low-flow priapism

Ischemic priapism of >4 hours implies a compartment syndrome and requires decompression of the corpora cavernosa. Aspiration of blood from corpora (50 mL portions using a 18–20 gauge butterfly needle) ± intracavernosal injection of A1-adrenergic selective agonist (phenylephrine 100–200 µg (0.5–1 mL of a 200 µg/mL solution to a maximum of 1 mg) are performed every 5–10 minutes until detumescence occurs.

498 CHAPTER 12 Erectile function and ejaculation

Monitor blood pressure and pulse during drug administration. Oral terbutaline may be effective for intracavernosal injection-related cases.

Sickle cell disease requires, in addition, aggressive rehydration, oxygenation, analgesia, and hematological input (consider exchange transfusion). Repeated aspirations or irrigations and sympathomimetic injections during several hours are often necessary and should be performed before initiation of surgical therapy.

High-flow priapism

Early stages may respond to a cool bath or icepack (causing vasospasm

± arterial thrombosis). Delayed presentations require arteriography and selective embolization of the internal pudendal artery.

Complications

These include fibrosis and impotence.

Neuropathic bladder

Innervation of the lower urinary tract (LUT) 500 Physiology of urine storage and micturition 504 Bladder and sphincter behavior in the patient with

neurological disease 506

The neuropathic lower urinary tract: clinical consequences of storage and emptying problems 508

Bladder management techniques for the neuropathic patient 510

Catheters and sheaths and the neuropathic patient 516 Management of incontinence in the neuropathic patient 518 Management of recurrent urinary tract infections (UTIs) in

the neuropathic patient 520

Management of hydronephrosis in the neuropathic patient 522

Management of autonomic dysreflexia in the neuropathic patient 523

Bladder dysfunction in multiple sclerosis, in Parkinson disease, after stroke, and in other neurological disease 524

Neuromodulation in lower urinary tract dysfunction 528

500 CHAPTER 13 Neuropathic bladder

Innervation of the lower urinary tract (LUT)

Motor innervation of the bladder

Parasympathetic motor innervation of the bladder

This neural pathway is primarily responsible for stimulating detrusor contractions, and to a lesser degree, relaxation of the bladder outflow region (bladder neck and urethra).

Preganglionic, parasympathetic nerve cell bodies are located in the intermediolateral column of spinal segments S2–4. These preganglionic, parasympathetic fibers pass out of the spinal cord through the anterior primary rami of S2, S3, and S4 and, contained within nerves called the nervi erigentes, they head toward the pelvic plexus. In the pelvic plexus (in front of the piriformis muscle) the preganglionic, parasympathetic fibers synapse, within ganglia, with the cell bodies of the postganglionic parasympathetic nerves, which then run to the bladder and urethra.

Half of the ganglia of the pelvic plexus lie in the adventitia of the bladder and bladder base (the connective tissue surrounding the bladder), and 50% are within the bladder wall. The postganglionic axons provide cholinergic excitatory input to stimulate contraction of the smooth muscle of the bladder.

Sympathetic motor innervation of the bladder

The primary role of the sympathetic innervation is to contract the bladder base and the urethra.

In the male, preganglionic sympathetic nerve fibers arise from the intermediolateral column of T10–12 and L1–2. These preganglionic neurons synapse in the sympathetic chain, and postganglionic sympathetic nerve fibers travel as the hypogastric nerves to innervate the trigone, blood vessels of the bladder and the smooth muscle of the prostate and preprostatic sphincter (i.e., the bladder neck).

In the female, there is sparse sympathetic innervation of the bladder neck and urethra, with the major continence mechanism being the external sphincter.

In both sexes, some postganglionic sympathetic nerves also terminate in parasympathetic ganglia (in the adventitia surrounding the bladder and within the bladder wall) and exert an inhibitory effect on bladder smooth muscle contraction.

Afferent innervation of the bladder

Afferent nerves from receptors throughout the bladder ascend with parasympathetic neurons back to the cord and from there up to the pontine storage and micturition centers or to the cerebral cortex. They sense bladder filling.

Other receptors are located in the trigone, and afferent neurons from these neurons ascend with sympathetic neurons up to the thoracolumbar cord and from there to the pons and cerebral cortex.

INNERVATION OF THE LOWER URINARY TRACT (LUT) 501

Additionally, afferent receptors are located in the urethra. The afferent neurons pass through the pudendal nerve and again ascend to the pons and cerebral cortex. All these neurons have local relays in the cord.

Somatic motor innervation of the urethral sphincter: the distal urethral sphincter mechanism

Anatomically, this is located slightly distal to the apex of the prostate in the male (between the verumontanum and proximal bulbar urethra) and in the mid-urethra in the female. It has three components:

•Extrinsic skeletal muscle. This is the outermost layer, the pubourethral sling (part of levator ani). It is composed of striated muscle and innervated by the pudendal nerve (spinal segments S2–4, somatic nerve fibers). It is activated under conditions of stress and augments urethral occlusion pressure.

•Smooth muscle within the wall of the urethra. Cholinergic innervation. This is tonically active and relaxed by nitric oxide.

•Intrinsic striated muscle (i.e., skeletal muscle within the wall of the urethra, hence known as the intrinsic rhabdosphincter). It forms a U shape around the urethra, around the anterior and lateral aspects of the membranous urethra, and is absent posteriorly (i.e., it does not completely encircle the membranous urethra). It may produce

urethral occlusion by kinking the urethra rather than by circumferential compression.

Preganglionic somatic nerve fibers (i.e., neurons that innervate striated muscle) are, along with parasympathetic nerve fibers (which innervate the bladder), derived from spinal segments S2–4, specifically from Onuf nucleus (also known as spinal nucleus X), which lies in the medial part of the anterior horn of the spinal cord.

Onuf nucleus is the location of the cell bodies of somatic motoneurons that provide motor input to the striated muscle of the pelvic floor—the external urethral and anal sphincters. These somatomotor nerves travel to the rhabdosphincter via the perineal branch of the pudendal nerve (documented by direct stimulation studies and horseradish peroxidase [HRP] tracing, which accumulates in Onuf nucleus following injection into either the pudendal or pelvic nerves).

There also seems to be some innervation to the rhabdosphincter from branches of the pelvic plexus (specifically the inferior hypogastric plexus) via pelvic nerves. In dogs, complete silence of the rhabdosphincter is seen only if both the pudendal and pelvic efferents are sectioned. Thus, pudendal nerve block or pudendal neurectomy does not cause incontinence.

The nerve fibers that pass distally to the distal sphincter mechanism are located in a dorsolateral position (5 and 7 o’clock). More distally, they move to a more lateral position.

Consequences of damage to the nerves innervating the LUT are provided in Box 13.1.