Optic neuropathy from Pseudomonas osteomyelitis of the skull base
Mon statut pour la session
Quoi:
Paper Presentation | Présentation d'article
Partie de:
Quand:
2:08 PM, Vendredi 1 Juin 2018
(6 minutes)
Où:
Metro Toronto Convention Centre (Édifice Sud)
- Salle 714 A
Authors: Amrit S. Rai, Yelin Yang, Victoria Leung, Imran Jivraj, Harmeet Gill
Author Disclosure Block: A.S. Rai: None. Y. Yang: None. V. Leung: None. I. Jivraj: None. H. Gill: None.
Abstract Body:
Purpose: Skull-base osteomyelitis (SBO) is a potentially life-threatening entity, most commonly caused by Pseudomonas aeruginosa in patients with immune compromise. While SBO may be associated with multiple cranial neuropathies, optic neuropathy is a rare complication. We describe the presentation and management of optic neuropathy from Pseudomonas SBO in the context of chronic lymphocytic leukemia (CLL).
Study Design: Case report
Methods: Case report and literature review
Results: A 53-year-old diabetic woman on Ibrutinib for relapsed CLL presented with left-sided headache, left periorbital pain and decreased visual acuity. Her oncology team started oral antibiotics for presumed sinusitis, and held chemotherapy. When ophthalmology was consulted one week later, she was noted to have limited supraduction, ptosis, and proptosis of the left eye. Visual acuity was 20/60 and colour vision was reduced. There was a relative afferent pupillary defect and a temporal field deficit suggestive of an optic neuropathy. Examination of the contralateral eye was normal. Gadolinium enhanced MRI of the brain demonstrated bony dehiscence and inflammation within the maxillary, sphenoid and cavernous sinuses diagnostic of a SBO. There was also soft tissue enhancement of the left superomedial orbit, involving the superior oblique, superior rectus, medial rectus and optic nerve. Urgent endoscopic sinus biopsy and debridement was performed and cultures revealed Pseudomonas aeruginosa with no fungal elements. The patient was treated with a six week course of intravenous Ceftazidime and her Ibrutinib was subsequently restarted. While her repeat MRI showed interval improvement, there remained an ill-defined infiltration within the orbital apex and cavernous sinus. On follow-up, her ptosis, proptosis and extraocular motility had improved, and there was no further worsening of her optic neuropathy.
Conclusions: The differential diagnosis of painful vision loss is broad, including arteritic, demyelinating, inflammatory, and infiltrative optic neuropathies. Among immunocompromised patients, the clinician must maintain a heightened suspicion for infectious optic neuropathy, particularly when there is evidence of orbital disease. Previous reports of optic neuropathy from SBO describe an aggressive clinical course resulting in severe vision loss. Presumptive treatment with corticosteroids for arteritic ischemic optic neuropathy, as well as unrevealing surgical cultures, may create diagnostic confusion and delay appropriate management. Our patient’s preserved visual function resulted from early neuro-imaging, successful surgical biopsy of accessible tissue with culture and sensitivity data, and targeted antibiotic therapy.
Author Disclosure Block: A.S. Rai: None. Y. Yang: None. V. Leung: None. I. Jivraj: None. H. Gill: None.
Abstract Body:
Purpose: Skull-base osteomyelitis (SBO) is a potentially life-threatening entity, most commonly caused by Pseudomonas aeruginosa in patients with immune compromise. While SBO may be associated with multiple cranial neuropathies, optic neuropathy is a rare complication. We describe the presentation and management of optic neuropathy from Pseudomonas SBO in the context of chronic lymphocytic leukemia (CLL).
Study Design: Case report
Methods: Case report and literature review
Results: A 53-year-old diabetic woman on Ibrutinib for relapsed CLL presented with left-sided headache, left periorbital pain and decreased visual acuity. Her oncology team started oral antibiotics for presumed sinusitis, and held chemotherapy. When ophthalmology was consulted one week later, she was noted to have limited supraduction, ptosis, and proptosis of the left eye. Visual acuity was 20/60 and colour vision was reduced. There was a relative afferent pupillary defect and a temporal field deficit suggestive of an optic neuropathy. Examination of the contralateral eye was normal. Gadolinium enhanced MRI of the brain demonstrated bony dehiscence and inflammation within the maxillary, sphenoid and cavernous sinuses diagnostic of a SBO. There was also soft tissue enhancement of the left superomedial orbit, involving the superior oblique, superior rectus, medial rectus and optic nerve. Urgent endoscopic sinus biopsy and debridement was performed and cultures revealed Pseudomonas aeruginosa with no fungal elements. The patient was treated with a six week course of intravenous Ceftazidime and her Ibrutinib was subsequently restarted. While her repeat MRI showed interval improvement, there remained an ill-defined infiltration within the orbital apex and cavernous sinus. On follow-up, her ptosis, proptosis and extraocular motility had improved, and there was no further worsening of her optic neuropathy.
Conclusions: The differential diagnosis of painful vision loss is broad, including arteritic, demyelinating, inflammatory, and infiltrative optic neuropathies. Among immunocompromised patients, the clinician must maintain a heightened suspicion for infectious optic neuropathy, particularly when there is evidence of orbital disease. Previous reports of optic neuropathy from SBO describe an aggressive clinical course resulting in severe vision loss. Presumptive treatment with corticosteroids for arteritic ischemic optic neuropathy, as well as unrevealing surgical cultures, may create diagnostic confusion and delay appropriate management. Our patient’s preserved visual function resulted from early neuro-imaging, successful surgical biopsy of accessible tissue with culture and sensitivity data, and targeted antibiotic therapy.
