A 60-year-old male with no relevant past medical history was referred from the Urology Department of our centre with a diagnosis of stage IV prostate adenocarcinoma due to multiple metastatic bone involvement in phase.
In February 2004 and due to proband syndrome (mllaquiuria and voiding urgency), a PSA determination was performed by the Primary Care Physician (PCP), which yielded a value of 12 ng.
Transrectal ultrasound and ultrasound guided prostatic biopsy were performed and reported as: bilobular adenocarcinoma, Gleason 7 (4+3).
In the extension study (analytical, MRI and bone scintigraphy), retroperitoneal lymph node metastases and multiple foci of pathological uptake (vertebral spine, neck and femoral diaphysis) were evidenced.
A complete androgen deprivation was established with antiandrogen and A-LHRH agonist.
With this treatment, PSA level returned to normal within 4 months (June 04).
The patient was receiving analgesic treatment for osseous pain with NSAIDs and NSAIDs.
He was also treated with vertebral dorsolumbar irradiation with 30 Gy administered in 10 sessions.
In April 2006, with the asymptomatic patient, progressive PSA rises to 7.3, 13.1, 21 ng/ml, maintaining testosterone at castration levels.
It was decided at this time to suspend the antiandrogen.
The biochemical response was good, with normalization occurring in August 06.
Unfortunately, in November 06 she came to the emergency department complaining of intense generalized and disabling bone pain despite the rise in doses of analgesics (SVAS=8 with Nuclear Medicine) and received treatment with Nuclear Medicine (SEM=8-9),
In addition, the clinical picture is accompanied by PSA levels of 850 ng/ml.
The patient was treated conservatively with chemotherapy and prednisone.
We also started therapy with bone resorption inhibitors (zoledronic acid).
The clinical response was satisfactory with analgesic control (VAS=2-3) and PSA reduction to 150 ng/ml.
On February 15, 2007, the patient came to the emergency department complaining about the protrusion of the left eyeball and difficulty in completely separating the eyelids for about 15 days.
neurological findings
Proptosis, peptic malignant disease, low reactive mydriasis secondary to involvement of the third pair.
Not orbital murmurs.
Orbital MRI
Metastatic position of the entire central segment of the cranial base, bone marrow of the vertebrae included in the study and part of the cranial diploe.
Affectation of the roof and lateral wall of the left orbit, which are expanded and cause proptosis of the eyeball.
The left main wing is suspicious and thickened and there is a clear extension to the left nostril wall and cleft palate.
Similar changes are observed in the bones forming the contralateral orbit, but less advanced.
Left orbital roof injury is accompanied by a soft tissue injury that causes inferior displacement of the orbital muscles.
In contrast-enhanced sequences, heterogeneous uptake was identified in all the lesions described.
1.
He received irradiation of the affected areas with palliative character and presented a clear and rapid deterioration, dying on 21-03-07.
