1982, British Journal of Radiology, 55, 924-926

Case Reports

Priapism: successful management by arterial embolisation

By D. P. MacErlean, F.R.C.R., E. McDermott, F.R.C.S.I., and D. G. Kelly, F.R.C.S.I.
Departments of Radiology and Urology, St. Vincents Hospital, Elm Park, Dublin 4

(Received June 1982)

Priapism, a persistent painful penile erection, may be DISCUSSION

spontaneous in origin or secondary to a wide variety of Most patients with priapism belong to an idiopathic
haematological or infiltrative disorders. If left untreated or "primary group" (Ercole et al, 1981). Secondary
this condition invariably leads to cavernal fibrosis and priapism may be due to any haematological disorder
impotence and possibly to necrosis. (Nelson & Winter, producing an increased thrombotic tendency, to
1977). A wide range of therapeutic modalities exists, but neurological dysfunction, to trauma to the perineum or
in the most satisfactory of the series reported, 20% penis or to neoplasms or prostatitis. Increasingly the
remained impotent. (Wasmer et al, 1981). psychotropic antihypertensive and anticoagulant drugs
Recent case reports have attested to the effectiveness are found to cause priapism (Winter, 1981).
of transcatheter embolisation when other surgical Erectile tissue is supplied from the internal pudendal
modalities have failed, (Crummy et al, 1979; Wafula & arteries. Arteriolar dilatation leads to filling and
Davies, 1981; Wear et al, 1977). We report two patients turgidity of the corpora cavernosa. Return toflaccidityis
in whom trans-catheter embolisation was the initial and initiated by arteriolar constriction" and shunting into
definitive form of management. arteriovenous anastomoses. Priapism is considered to be
Trans-catheter embolisation was performed under
local anaesthesia using a French 7 end-hole catheter. The
catheter was advanced from the femoral artery into the
contra-lateral internal iliac artery and then advanced
selectively into the internal pudendal artery. Oxycel
(oxydised cellulose), cut into particles of 1 to 2 mm, was
used as the occluding agent. Embolisation was stopped
when obliteration of the terminal branches of the
internal pudendal artery was achieved. In both patients a
satisfactory outcome followed unilateral embolisation.

CASE REPORTS

Case 1
A 32-year-old married man presented with a ten-hour history
of persistent priapism of spontaneous origin. There were no
other relevant findings on history or physical examination.
Initial therapy of analgesia and local cold packs failed to resolve
the priapism. Selective left internal iliac and pudendal
angiography demonstrated persistent staining at the base of the
penis. (Figs. 1, 2). Following embolisation of the distal branches
of the left internal pudendal artery there was immediate
resolution of the priapism (Fig. 3).
At follow-up examination four weeks later full potency had
returned.

Case 2
A 64-year-old married man with extensive prostatic
malignancy presented with recurrent episodes of priapism and
pain. He had previously been treated with stilboestrol,
radiotherapy, decompression of a dural secondary, and bilateral
orchidectomy for advanced secondary malignant disease.
Physical examination revealed priapism and two neoplastic
nodules involving the base of the penis. Selective embolisation
of the right internal pudendal artery was performed, using
Oxycel particles. In view of our earlier experience, unilateral
embolisation only was attempted. Complete resolution of the FIG. 1.
priapism occured within 24 hours and there has been no Case I. Left internal iliac angiogram. Pudendal artery patent
recurrence. (arrows).
0O07-1285/82/5512-924S2.0O/0 924

Case reports
FIG. 2.
Case 1. Selective pudendal angiogram demonstrates contrast
staining at base of penis and in corpora cavernosa.
due to arterial inflow exceeding venous outflow. With a
relative obstruction to venous outflow there is increased
viscosity and sludging. Oedema results and reduces the
vascular lumen and further impedes outflow. Persistence
of this state for more than a few days leads to trabecular
fibrosis and subsequent impotence.
The range of therapeutic modalities for priapism
reflects their ineffectiveness. Conservative measures are
considered of little value. (Wasmer et al, 1981). Surgical
management, to be effective, must be instituted
preferably in the first 12 hours and even then carries a
high likelihood of impotence (Nelson & Winter, 1977).
As the pathophysiology of priapism involves a relative
increase in arterial flow in comparison to venous
drainage (Evans & Young, 1973), arterial embolisation,
in reducing arterial flow, would appear a logical form of
therapy (Wear et al, 1977). The use of an absorbable
occluding agent, such as Oxycel or Gelfoam, is
preferable because then re-canalisation will occur after
some weeks. The size of the embolic particles,
approximately 1 to 2 mm in diameter, determines that
925
DECEMBER 1982
FIG. 3.
Case 1. Left internal iliac angiogram immediately post
embolisation. Pudendal artery is occluded (arrows). Turgidity
has resolved.
they will lodge in proximal arterioles rather than more
distally and are therefore unlikely to result in tissue
necrosis. Relief of priapism has been achieved by
unilateral pudendal artery embolisation, in two post-
traumatic cases of priapism in which surgical methods
had failed (Crummy et al, 1979) and in one spontaneous
case in which bilateral corporosaphenous shunts had
failed (Wafula & Davies, 1981).
In both patients reported here arterial embolisation
was the initial and only form of interventional therapy.
Relief of priapism was achieved in both, with relief of
pain being achieved in one patient with advanced
neoplastic infiltration and potency being restored in the
other.
REFERENCES
CRUMMY, A. B., ISHIZUKA, J. & MADSEN, P. O., 1979., Post-
traumatic priapism: successful treatment with autologous
clot embolization. American Journal of Roentgenology, 133,
329-330.
1982, British Journal of Radiology, 55, 926-928
Case reports
ERCOLE, C. J. J., EDSON PONTES, J., & PIERCE, J. M., 1981.
Changing surgical concepts in the treatment of priapism.
Journal of Urology, 125, 210-211.
EVANS, L. I. & YOUNG, A. E., 1973. Internal pudendal
arteriography after priapism. British Journal of Surgery, 60,
329-330.
NELSON, J. H., & WINTER, C. C , 1977., Priapism: evolution of
management in 48 patients in a 22 year series. Journal of
Urology, 117, 455-458.
WAFULA, J. M. C , & DAVIES, P., 1981., Treatment of
Gas formation following hepatic tumour embolisation
By Elsebeth Siim and Peter Fleckenstein
Departments of Surgical Gastroenterology D and Radiology, University of Copenhagen, Herlev Hospital,
Denmark.
{Received May 1982)
Normal liver tissue receives its blood supply from both
the arterial and portal systems, whereas primary and
secondary hepatic neoplasms derive most of their blood
supply from the hepatic artery (Aune & Schistad, 1972;
Breedis & Young, 1954; Wheeler et al, 1979).
Dearterialisation of the liver by surgical ligation of the
hepatic artery or by injection of embolic material into
the artery has been used to induce necrosis in such
tumours for temporary relief of symptoms and reduction
of tumour bulk (Bernardino et al, 1981; Goldstein et al.
1975 a, b, 1976; Grace et al, 1976; Marks & Filly, 1979).
Only few major complications following hepatic
artery embolisation have been reported, the most serious
ones being displaced emboli (Grace et al, 1976; Wheeler
et al, 1979), abscess formation (Pueyo et al, 1979;
Trojanowski et al, 1980) and widespread liver necrosis
(Goldstein et al, 1975a; Trojanowski et al, 1980).
The present report describes a case in which gas was
detected within the liver tumour following arterial
embolisation.
CASE REPORT
The patient was a 70-year-old female who had had a sigmoid
resection performed five years previously for an
adenocarcinoma of Dukes' class C. At the time of operation no
secondaries in the liver were found. Physical examination now
revealed a large, irregular tender liver, and ultrasonography
indicated multiple hepatic metastases.
At percutaneous coeliac angiography a patent portal vein was
seen during the venous phase. After selective catherisation with
a 7 FR balloon-occlusion catheter the left and right hepatic
arteries were embolised with less than 1 mm fragments of
gelatin foam (Spongostan ®), suspended in contrast medium
(Urografin ®). The fragments were intermittently injected until
complete stagnation of the blood flow in the arteries was
Address for reprints: Elsebeth Siim, M.D., Department of
Surgical Gastroenterology D, University of Copenhagen,
Herlev Hospital, DK-2730 Herlev, Denmark.
0007-1285/82/5512-926S2.00/0
spontaneous priapism by embolisation of internal pudendal
artery. British Medical Journal, 282, 363-364.
WASMER, J. M., CARRION, H. M., MEKRAS, G. & POLITANO, V.
A., 1981. Evaluation and treatment of priapism. Journal of
Urology, 125, 204-207.
WEAR, J. B., CRUMMY, A. B. & MUNSON, B. O., 1977., A new
approach to the treatment of priapism. Journal of Urology,
117, 252-254.
WINTER, C. C , 1981. Priapism. (Guest Editorial) Journal of
Urology, 125, 212.
achieved. No intrahepatic air was seen during or immediately
after the procedure.
Following the procedure the patient had moderate epigastric
pain but no fever. A plain radiograph six days after
embolisation showed gas formation (estimated at about 100 cc)
in the liver, which was confirmed by ultrasonography, and was
still detectable after two months. There were initial rises in
serum bilirubin, serum alkaline phosphatases, serum
transaminases and erythrocyte sedimentation rate, but these
returned to normal within two months. Clinically the
embolisation reduced the size of the liver and relieved the pain.
The patient died eight months later. Autopsy revealed an
enlarged liver, about 25% of the tissue consisting of tumour
masses. No gas or liquid necrosis was then detectable.
DISCUSSION
Selective arterial embolisation of hepatic tumours is
used in inoperable cases and is generally felt to be
worthwhile as a palliative measure (Allison et al, 1977;
Almgard et al, 1973; Aune & Schistad, 1972; Goldstein
et al, 1976; Wheeler et al, 1979). Air collection in the
tumour after embolisation is probably a rare occurrence
as only five cases have been reported (Bernardino et al,
1981; Dubbins & Nunnerley, 1980). We have not noticed
it previously in our series of 19 liver embolisations in 13
patients. The phenomenon is readily distinguished from
air in the biliary system (Marks & Filly, 1979; Sherlock,
1975), in the portal venous system (Stewart, 1961) and in
hepatic abscesses (Pueyo et al, 1979; Trojanowski et al,
1980.
The gas has been found to consist mainly of carbon
dioxide and oxygen (Stewart, 1961). Several
explanations have been proposed:
(a) Parenchymal infection with gas-producing
organisms (Marks & Filly, 1979; Stewart, 1961).
This is unlikely in our case, as the patient had no
symptoms of infection prior to or after the
embolisation.
(b) In the necrotic tissue, carbon dioxide is produced
926