We present the case of a 59 year old female with history of severe neurologic dysfunction from advanced multiple sclerosis who presented with lethargy and oliguria several hours after urethral Foley catheterization. A contrast-enhanced CT scan of the abdomen/pelvis showed an aberrantly placed Foley catheter with its balloon inflated in the proximal left ureter, a rare complication of Foley catheterization with only 5 other cases reported. Incomplete ureteral rupture was demonstrated and confirmed by a followup CT scan in the urographic phase. One of our institution's Interventional Radiologists then placed a nephroureteral stent across the injured ureter to facilitate healing. The patient expired 9 days after the procedure from unrelated sepsis from a chronic stage IV decubitus ulcer, so long term monitoring could not be performed. Following description of our case, we conduct a literature review of presentations, imaging characteristics, and treatment of ureteral Foley catheter placement.

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We present the clinical, imaging and pathological findings of a case of primary sellar lymphoma of Tcell type with aggressive bony destruction. While reports of primary sellar lymphoma have been exceedingly rare, most of these are cases of B-cell lymphoma [1 -4]. Only two cases of sellar lymphoma of T-cell have been described in the literature [5,6]. While evaluating an invasive sellar mass with extensive bone destruction, this diagnosis should be considered particularly in elderly or immunocompromized patients.A 60-year-old female presented with progressively increasing history of headache which was initially localized and later became generalized. Associated symptoms were vomiting, facial weakness on the left side and ptosis of the right eye. There was no history of fever. Past medical history was significant only for hypertension. The patient was immunocompetent with no history of HIV.The patient was afebrile with normal respiratory and heart rate. Physical examination revealed a drowsy but arousable patient with no significant neck stiffness. There was no lymphadenopathy, hepatomegaly or splenomegaly. Motor function examination revealed upper motor neuron deficits in the form of increased deep tendon reflexes on the left side and pronator drift towards the left side and left facial weakness. Sensory examination revealed increased pain sensation on the left side. Cranial nerve deficits included bitemporal hemianopsia, ptosis of the right eyelid and a fixed and dilated right pupil.Laboratory values revealed partial hypopituitarism with decreased TSH (50.13), decreased T4 (0.59), decreased free T4 (0.59), decreased FSH (3.55), decreased LH (0.1), increased prolactin (46.7) and decreased cortisol levels (50.6). Estrodiol levels were not obtained. There was no evidence of diabetes insipidus at presentation (ADH 51). CD4/CD8 was increased (3.5).CT scan of the head demonstrated a hyperdense mass at the ventral skull base, extending into the suprasellar cistern with destructive changes in the clivus and erosive changes at the petrous apices, the sphenoid bone and medial margin of the left orbit (Figure 1(a)).CT scan of the sinuses showed further extension of the mass into the left pterygopalatine and infratemporal fossa, anterior extension into the nasal cavity and into the left osteomeatal complex.MRI using multi-planar T1 and T2 weighted images and post-gadolinium sequences showed a large sellar-suprasellar mass involving and expanding the clivus, extending into and expanding the ethmoidal cells anteriorly and into the cavernous sinus bilaterally and compressing the optic chiasm. The anterior and posterior pituitary was not seen separate from the mass. The center of this mass contained a cystic non-enhancing area and the remainder of this mass enhanced uniformly and showed dark signal on T2 weighted images (Figure 1(b) and (c)).PET scan demonstrated a focus of increased activity in the region of the mass (SUV 2.9), without any other area of abnormal uptake.

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