Case Report
Recanalisation of the occluded brachiocephalic vein was an alternative therapeutic option but we chose not to do this because of the long-standing nature of the occlusion, and intimal hyperplasia caused by the shunt that would have increased the likelihood of stent occlusion. Upper limb dialysis fistulas can cause sight-threating intraocular pressure in the presence of central venous occlusion. Prompt treatment could save the patient’s vision. Contributors All authors contributed to care of the patient and writing of the report. Written consent to publication was obtained.
References 1 Barrow DL, Spector RH, Braun IF, Landman JA, Tindall SC, Tindall GT. Classification and treatment of spontaneous carotid-cavernous sinus fistulas. J Neurosurg 1985; 62: 248–56. 2 Hummer MG, Carlow TJ. Iatrogenic carotid cavernous sinus syndrome. Stroke 1981; 12: 689–91. 3 Watson RR, Russo C. Upper extremity arteriovenous dialysis fistula resulting in cavernous sinus arterialized blood flow. AJNR Am J Neuroradiol 2007; 28: 1155–56. 4 Gonsalves CF, Eschelman DJ, Sullivan KL, DuBois N, Bonn J. Incidence of central vein stenosis and occlusion following upper extremity PICC and port placement. Cardiovasc Intervent Radiol 2003; 26: 123–37. 5 Otten TR, Stein PD, Patel KC, Mustafa S, Silbergleit A. Thromboembolic disease involving the superior vena cava and brachiocephalic veins. Chest 2003; 123: 809–12.
Case Report Comment Putting raised intraocular pressure in context Fion D Bremner Correspondence to: Mr Fion D Bremner, National Hospital for Neurology & Neurosurgery, Queen Square, London WC1N 3BG, UK fi[email protected]
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In The Lancet, Miles Kiernan and colleagues1 report an unusual case of a patient who developed sight-threatening ophthalmic problems after upper arm surgery. The ipsilateral symptoms and signs in this case (red eye, proptosis, limited eye movements, raised intraocular pressure, and retinal haemorrhages) are all classic presenting features of orbital venous hypertension. The most common cause is an arteriovenous fistula in the cavernous sinus and ophthalmologists are well aware of the need to investigate this possibility in any patient presenting with a unilateral red eye and raised intraocular pressure. However, two valuable clues suggested that a different mechanism might be at play in this case. First, there was a close temporal relation between the surgical procedure and development of the ophthalmic symptoms; doctors are sometimes reluctant to accept responsibility for any new problems arising at a remote location from the site of their procedure, but Occam’s razor demands that we first investigate the possibility of a causal link before concluding that two events are unrelated. Second, the patient had reduced colour vision and a swollen optic disc in the contralateral eye, features that are not usually associated with cavernous arteriovenous fistulae. These contralateral signs are likely to be associated with papilloedema caused by intracranial venous hypertension. In other words, the clinical signs indicated venous hypertension simultaneously in two different anatomical compartments (intraorbital and intracranial) and followed shortly after formation of an extracranial arteriovenous fistula. Venous drainage from the head has a critical role in determining both intracranial pressure and intraocular pressure. In the eye, aqueous drains into the episcleral veins—so if the venous pressure in the orbit rises the aqueous cannot leave the eye and the intraocular
pressure rises quickly. If left untreated, a prolonged state of substantial intraocular hypertension will damage the sight by causing either secondary glaucoma or ocular ischaemia. The length of time that an eye can sustain such a rise in intraocular pressure before developing irreversible damage depends on several factors, such as the level of intraocular pressure, patient’s age, and other ocular and systemic disorders, but it might be only a matter of days. Similar principles apply to the intracranial compartment, in which cerebrospinal fluid (CSF) leaves the subarachnoid space via the dural venous sinuses, and intracranial pressure will rise as a consequence of any cause of intracranial venous hypertension. If left untreated, a prolonged period of intracranial hypertension will threaten sight by causing papilloedema. In most cases, the cause of orbital or intracranial venous hypertension lies within the head—for example, arteriovenous fistulae, dural sinus thrombosis or stenosis—and so under normal circumstances imaging studies limited to the intracranial venous system (magnetic resonance venography, CT venography) are sufficient. However, this unusual case reminds clinicians that any downstream venous pathology can cause venous hypertension, and in the right context it might be necessary to extend investigations to include the jugular and brachiocephalic venous systems. It is interesting to note that even buttoning your collar too tightly is sufficient to raise the intraocular pressure.2 References 1 Kiernan M, Bhogal M, Wong K, et al. Sight-threatening intraocular pressure due to an upper arm dialysis fistula. Lancet 2015; 386: 101–02. 2 Teng C, Gurses-Ozden R, Liebmann JM, Tello C, Ritch R. Effect of a tight necktie on intraocular pressure. Br J Ophthalmol 2003; 87: 946–48.
www.thelancet.com Vol 386 July 4, 2015
Recanalisation of the occluded brachiocephalic vein was an alternative therapeutic option but we chose not to do this because of the long-standing nature of the occlusion, and intimal hyperplasia caused by the shunt that would have increased the likelihood of stent occlusion. Upper limb dialysis fistulas can cause sight-threating intraocular pressure in the presence of central venous occlusion. Prompt treatment could save the patient’s vision. Contributors All authors contributed to care of the patient and writing of the report. Written consent to publication was obtained.
References 1 Barrow DL, Spector RH, Braun IF, Landman JA, Tindall SC, Tindall GT. Classification and treatment of spontaneous carotid-cavernous sinus fistulas. J Neurosurg 1985; 62: 248–56. 2 Hummer MG, Carlow TJ. Iatrogenic carotid cavernous sinus syndrome. Stroke 1981; 12: 689–91. 3 Watson RR, Russo C. Upper extremity arteriovenous dialysis fistula resulting in cavernous sinus arterialized blood flow. AJNR Am J Neuroradiol 2007; 28: 1155–56. 4 Gonsalves CF, Eschelman DJ, Sullivan KL, DuBois N, Bonn J. Incidence of central vein stenosis and occlusion following upper extremity PICC and port placement. Cardiovasc Intervent Radiol 2003; 26: 123–37. 5 Otten TR, Stein PD, Patel KC, Mustafa S, Silbergleit A. Thromboembolic disease involving the superior vena cava and brachiocephalic veins. Chest 2003; 123: 809–12.
Case Report Comment Putting raised intraocular pressure in context Fion D Bremner Correspondence to: Mr Fion D Bremner, National Hospital for Neurology & Neurosurgery, Queen Square, London WC1N 3BG, UK fi[email protected]
102
In The Lancet, Miles Kiernan and colleagues1 report an unusual case of a patient who developed sight-threatening ophthalmic problems after upper arm surgery. The ipsilateral symptoms and signs in this case (red eye, proptosis, limited eye movements, raised intraocular pressure, and retinal haemorrhages) are all classic presenting features of orbital venous hypertension. The most common cause is an arteriovenous fistula in the cavernous sinus and ophthalmologists are well aware of the need to investigate this possibility in any patient presenting with a unilateral red eye and raised intraocular pressure. However, two valuable clues suggested that a different mechanism might be at play in this case. First, there was a close temporal relation between the surgical procedure and development of the ophthalmic symptoms; doctors are sometimes reluctant to accept responsibility for any new problems arising at a remote location from the site of their procedure, but Occam’s razor demands that we first investigate the possibility of a causal link before concluding that two events are unrelated. Second, the patient had reduced colour vision and a swollen optic disc in the contralateral eye, features that are not usually associated with cavernous arteriovenous fistulae. These contralateral signs are likely to be associated with papilloedema caused by intracranial venous hypertension. In other words, the clinical signs indicated venous hypertension simultaneously in two different anatomical compartments (intraorbital and intracranial) and followed shortly after formation of an extracranial arteriovenous fistula. Venous drainage from the head has a critical role in determining both intracranial pressure and intraocular pressure. In the eye, aqueous drains into the episcleral veins—so if the venous pressure in the orbit rises the aqueous cannot leave the eye and the intraocular
pressure rises quickly. If left untreated, a prolonged state of substantial intraocular hypertension will damage the sight by causing either secondary glaucoma or ocular ischaemia. The length of time that an eye can sustain such a rise in intraocular pressure before developing irreversible damage depends on several factors, such as the level of intraocular pressure, patient’s age, and other ocular and systemic disorders, but it might be only a matter of days. Similar principles apply to the intracranial compartment, in which cerebrospinal fluid (CSF) leaves the subarachnoid space via the dural venous sinuses, and intracranial pressure will rise as a consequence of any cause of intracranial venous hypertension. If left untreated, a prolonged period of intracranial hypertension will threaten sight by causing papilloedema. In most cases, the cause of orbital or intracranial venous hypertension lies within the head—for example, arteriovenous fistulae, dural sinus thrombosis or stenosis—and so under normal circumstances imaging studies limited to the intracranial venous system (magnetic resonance venography, CT venography) are sufficient. However, this unusual case reminds clinicians that any downstream venous pathology can cause venous hypertension, and in the right context it might be necessary to extend investigations to include the jugular and brachiocephalic venous systems. It is interesting to note that even buttoning your collar too tightly is sufficient to raise the intraocular pressure.2 References 1 Kiernan M, Bhogal M, Wong K, et al. Sight-threatening intraocular pressure due to an upper arm dialysis fistula. Lancet 2015; 386: 101–02. 2 Teng C, Gurses-Ozden R, Liebmann JM, Tello C, Ritch R. Effect of a tight necktie on intraocular pressure. Br J Ophthalmol 2003; 87: 946–48.
www.thelancet.com Vol 386 July 4, 2015
