ISSN 2398-2977      

Penis: paralysis / priapism

pequis

Introduction

  • Priapism is an erection unassociated with sexual desire.
  • Cause: failure of detumescence, due either to increased arterial blood flow into, or decreased venous outflow from, the corpus cavernosum penis (CCP). Often follows administration of phenothiazine tranquilizers.
  • Signs: partial erection of penis lasting several days.
  • Diagnosis: history; clinical signs.
  • Treatment: conservative, flushing, penile shunts, retraction, phallectomy.
  • Prognosis: fair, decreasing the longer the condition persists.

Pathogenesis

Etiology

  • Priapism most commonly results from administration of phenothiazine tranquillizers, eg propriopromazine or acepromazine Cyclosporine, during sedation or anesthesia for castration Anesthesia: premedication - overview.
  • Priapism has also been reported in association with a pelvic tumor; migration of a nematode in the spinal canal and general anesthesia.
  • Penile paralysis which may or may not be associated with priapism has been recorded in:
  • May also occur in geldings, especially if receiving exogenous testosterone therapy.

Predisposing factors

Specific

  • Use of phenothiazine tranquillizers, eg propriopromazine or acepromazine.

Pathophysiology

  • Prolonged erection unassociated with sexual desire and caused by failure of the detumescence mechanism due to neuromuscular and/or vascular mechanism disturbances.
  • Administration of phenothiazine tranquilizers → sludging of blood in cavernous spaces → partial erection.
  • Engorged CCP fails to detumesce due to (increased) arterial inflow or (decreased) venous outflow disturbances.
  • Speculated that phenothiazines cause priapism by blocking alpha sympathetic impulses that mediate detumescence.
  • Vascular stenosis in the CCP associated with prolonged erection leads to increased CO2 tension in the stagnant blood causing sickling of the erythrocytes.
  • This causes the blood to sludge.
  • Venous occlusion occurs where the sinusoidal spaces of the CCP join the collecting veins.
  • Trabecular edema further decreases venous outflow and irreversible occlusion occurs.
  • Early on the arterial supply is still patent but occlusion by clots, edema and fibrosis eventually becomes irreversible.
  • Fibrosis of the trabeculae further decreases the expansile capacity.
  • Injury to the pudendal nerves either from nerve tension or compression further exacerbates the vascular problems.

Timecourse

  • Acute onset; can last for weeks.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Feary D J et al (2005) Chemical ejaculation and cryopreservation of semen from a breeding stallion with paraphimosis secondary to priapism and haemorrhagic colitis. Equine Vet Educ 17 (6), 299-304 VetMedResource.
  • Boller M et al (2005) Complete recovery from long-standing priapism in a stallion after propionylpromazine/xylazine sedation. Equine Vet Educ 17 (6), 305-309 VetMedResource.
  • McDonnell S M (2005) Managing the paralysed penis, priapism or paraphimosis in the horse. Equine Vet Educ 17 (6), 310-311 VetMedResource.
  • Schumacher J, Varner D D, Crabill M R & Blanchard T L (1999) The effect of a surgically created shunt between the corpus cavernosum penis and corpus spongiosum penis of stallions on erectile and ejaculatory function. Vet Surg 28 (1), 21-24 PubMed.
  • Nie G J & Pope K C (1997) Persistent penile prolapse associated with acute blood loss and acepromazine maleate administration in a horse. JAVMA 211 (5), 587 PubMed.
  • Perkins N R & Frazer G S (1994) Reproductive emergencies in the stallion. Vet Clin North Am Equine Pract 10 (3), 571-638 PubMed.
  • Wilson D V, Nickels F A & Williams M A (1991) Pharmacologic treatment of priapism in two horses. JAVMA 199 (9), 1183-1184 PubMed.
  • Schumacher J & Vaughan J T (1988) Surgery of the penis and prepuce. Vet Clin North Am Equine Pract 4 (3), 473-491 PubMed.

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