Case Report
Paralytic strabismus and papilloedema caused by dural sinus thrombosis after bee sting
Tropical Doctor 2015, Vol. 45(1) 44–45 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0049475514550062 tdo.sagepub.com
Leyla Niyaz1, Adem Gul1, Inci Gungor2 and Mustafa Duran3
Abstract A patient that developed paresis of the sixth cranial nerve and bilateral papilloedema after the bee sting to the periocular area is presented. Magnetic resonance venography showed a unilateral transverse and sigmoid sinus thrombosis. The patient was successfully treated with anticoagulation and intracranial pressure lowering treatment.
Keywords Bee sting, papilloedema, strabismus
Introduction Bee sting of the eye or periocular area can cause toxic and immunologic reactions causing anterior segment inflammation, conjunctivitis, corneal infiltrate and optic neuropathy. Vasculitis, peripheral neuritis, acute renal failure and anaphylactic reactions are other important systemic consequences of bee sting.1 Suggested treatment strategies comprise manual or surgical stinger removal if it is accessible, topical/systemic corticosteroids, antibiotics and cycloplegics.2 We describe a patient with a paralytic strabismus and bilateral papilledema secondary to increased intracranial pressure due to venous sinus thrombosis of the brain after a bee sting.
Case report A 4-year-old girl was referred to our clinic with a complaint of deviation in the eye after a bee sting to the forehead region between two eyebrows. The records of the physician revealed that the patient presented with headache, nausea, vomiting and deviation in the right eye 2 days after stinging. She received a mannitol 0.25 g/kg, dexamethasone 0.5 mg/kg as a bolus and 4 2 mg as maintenance therapy for 2 days but as the complaints persisted the patient was referred to our clinic for further research and therapy. On ophthalmologic examination she had intact direct and indirect pupillary reflexes. Visual acuity could not be measured because of the patient’s incompliance.
Ocular motility revealed right sixth nerve paresis with a resultant right esodeviation. On biomicroscopic evaluation, anterior segments were normal and fundus examination revealed bilateral swelling of optic discs. MRI venography showed a thrombus in the right distal cervical segment of jugular vein, right transverse and sigmoid sinuses obstructing normal blood flow (Figure 1). Lumbar puncture was not performed because of the risk of brain shift. The patient was hospitalised and systemic acetazolamide 110 mg t.i.d. and enoxaparin 14 mg b.i.d. was started. Thrombophilic panel screen was within normal limits except for PAI-1 (plasminogen activator inhibitor) heterozygosity. Nausea, vomiting and headache decreased significantly after a few days of therapy and the patient was discharged with enoxaparin and acetazolamide treatment. Best corrected visual acuity was 8/10 bilaterally on the first week and first month examination. Deviation in the right eye and bilateral papilloedema resolved completely in 1 month. Cerebral angiography performed 3 months later 1 Assistant Professor, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey 2 Associate Professor, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey 3 Resident, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey
Corresponding author: Leyla Niyaz, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey. Email: [email protected]
Downloaded from tdo.sagepub.com at UNIV TORONTO on November 15, 2015
Niyaz et al.
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Figure 1. MRI venography showing the obstruction of blood flow in the right transverse sinus.
appeared normal and enoxaparin and acetazolamide therapy was discontinued. The patient was free of symptoms for the following 6 months.
acuity decrease and delayed latency time on VEP examination after a bee sting to the left conjunctiva. The visual impairment and VEP latency returned to normal levels after treatment with systemic steroid therapy. It was proposed that time of treatment in patients with the optic nerve involvement is an important factor in determining visual prognosis and therapeutic action must be taken as soon as possible to offset the venom activity.6 In our patient vision was not affected significantly and pupillary reflexes were normal. Dural sinus thromboses strongly suggested that bilateral papilloedema and sixth cranial nerve paresis developed secondary to increased intracranial pressure. As the patient was PAI1 heterozygote, she had a susceptibility for thrombosis which might have been provoked by the bee venom. Yet the exact mechanism is unknown. Initial treatment with systemic steroids given before referral to our clinic did not improve the symptoms of this patient. Thrombus resolution and improvement of papilledema and strabismus was achieved with enoxaparin and acetazolamide therapy. We suggest that neurologic findings such as sixth cranial nerve and optic nerve involvement in a patient with bee sting can be caused by brain vascular thrombosis and increased intracranial pressure. Cautious evaluation of the patient and imaging should be performed to elicit the exact cause, so that the patient can be treated accordingly. Declaration of conflicting interests None declared.
Discussion
Funding
In this study we present a patient who developed paresis of the sixth cranial nerve and bilateral papilledema after the bee sting to the periocular area. Sigmoid and transverse sinus thrombosis was thought to cause these findings and the patient was treated with anticoagulation and intracranial pressure lowering treatment. Bee venom is a complex toxin which contains polypeptide toxins, enzymes and biogenic amines which cause toxic and allergic responses in humans.3 Bee stings to the eye can cause chemosis, corneal edema, iridocyclitis, cataract and optic neuritis.1 Anterior segment involvement is generally treated with stinger removal, topical steroids, antibiotics and cycloplegic medications.4 In patients with optic neuritis after bee stings, systemic steroid treatment was shown to have good results.5,6 Zambrano-Infantino et al. reported a 62-year-old woman who developed bilateral optic neuritis after a bee sting to the lower eyelid. She had a good clinical outcome after treatment with methylprednisolone.5 Choi et al. reported left optic neuritis with visual
This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
References 1. Reisman RE. Unusual reactions to insect stings. Curr Opin Allergy Clin Immunol 2005; 5: 355–358. 2. Razmjoo H, Abtahi MA, Roomizadeh P, Mohammadi Z and Abtahi SH. Management of corneal bee sting. Clin Ophthalmol 2011; 5: 1697–1700. 3. Gu¨rlu¨ VP and Erda N. Corneal bee sting-induced endothelial changes. Cornea 2006; 25: 981–983. 4. Chauhan D. Corneal honey bee sting: endoilluminator assisted removal of retained stinger. Int Ophthalmol 2012; 32: 285–288. 5. Zambrano-Infantino Rde C, Pin˜ierı´ ia-Gonsa´lvez JF, Montan˜o C and Rodrı´ guez C. Optic neuritis after a bee sting. Invest Clin 2013; 54: 180–185. 6. Choi MY and Cho SH. Optic neuritis after bee sting. Korean J Ophthalmol 2000; 14: 49–52.
Downloaded from tdo.sagepub.com at UNIV TORONTO on November 15, 2015
Paralytic strabismus and papilloedema caused by dural sinus thrombosis after bee sting
Tropical Doctor 2015, Vol. 45(1) 44–45 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0049475514550062 tdo.sagepub.com
Leyla Niyaz1, Adem Gul1, Inci Gungor2 and Mustafa Duran3
Abstract A patient that developed paresis of the sixth cranial nerve and bilateral papilloedema after the bee sting to the periocular area is presented. Magnetic resonance venography showed a unilateral transverse and sigmoid sinus thrombosis. The patient was successfully treated with anticoagulation and intracranial pressure lowering treatment.
Keywords Bee sting, papilloedema, strabismus
Introduction Bee sting of the eye or periocular area can cause toxic and immunologic reactions causing anterior segment inflammation, conjunctivitis, corneal infiltrate and optic neuropathy. Vasculitis, peripheral neuritis, acute renal failure and anaphylactic reactions are other important systemic consequences of bee sting.1 Suggested treatment strategies comprise manual or surgical stinger removal if it is accessible, topical/systemic corticosteroids, antibiotics and cycloplegics.2 We describe a patient with a paralytic strabismus and bilateral papilledema secondary to increased intracranial pressure due to venous sinus thrombosis of the brain after a bee sting.
Case report A 4-year-old girl was referred to our clinic with a complaint of deviation in the eye after a bee sting to the forehead region between two eyebrows. The records of the physician revealed that the patient presented with headache, nausea, vomiting and deviation in the right eye 2 days after stinging. She received a mannitol 0.25 g/kg, dexamethasone 0.5 mg/kg as a bolus and 4 2 mg as maintenance therapy for 2 days but as the complaints persisted the patient was referred to our clinic for further research and therapy. On ophthalmologic examination she had intact direct and indirect pupillary reflexes. Visual acuity could not be measured because of the patient’s incompliance.
Ocular motility revealed right sixth nerve paresis with a resultant right esodeviation. On biomicroscopic evaluation, anterior segments were normal and fundus examination revealed bilateral swelling of optic discs. MRI venography showed a thrombus in the right distal cervical segment of jugular vein, right transverse and sigmoid sinuses obstructing normal blood flow (Figure 1). Lumbar puncture was not performed because of the risk of brain shift. The patient was hospitalised and systemic acetazolamide 110 mg t.i.d. and enoxaparin 14 mg b.i.d. was started. Thrombophilic panel screen was within normal limits except for PAI-1 (plasminogen activator inhibitor) heterozygosity. Nausea, vomiting and headache decreased significantly after a few days of therapy and the patient was discharged with enoxaparin and acetazolamide treatment. Best corrected visual acuity was 8/10 bilaterally on the first week and first month examination. Deviation in the right eye and bilateral papilloedema resolved completely in 1 month. Cerebral angiography performed 3 months later 1 Assistant Professor, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey 2 Associate Professor, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey 3 Resident, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey
Corresponding author: Leyla Niyaz, Department of Ophthalmology, Ondokuz Mayis University Hospital, Samsun, Turkey. Email: [email protected]
Downloaded from tdo.sagepub.com at UNIV TORONTO on November 15, 2015
Niyaz et al.
45
Figure 1. MRI venography showing the obstruction of blood flow in the right transverse sinus.
appeared normal and enoxaparin and acetazolamide therapy was discontinued. The patient was free of symptoms for the following 6 months.
acuity decrease and delayed latency time on VEP examination after a bee sting to the left conjunctiva. The visual impairment and VEP latency returned to normal levels after treatment with systemic steroid therapy. It was proposed that time of treatment in patients with the optic nerve involvement is an important factor in determining visual prognosis and therapeutic action must be taken as soon as possible to offset the venom activity.6 In our patient vision was not affected significantly and pupillary reflexes were normal. Dural sinus thromboses strongly suggested that bilateral papilloedema and sixth cranial nerve paresis developed secondary to increased intracranial pressure. As the patient was PAI1 heterozygote, she had a susceptibility for thrombosis which might have been provoked by the bee venom. Yet the exact mechanism is unknown. Initial treatment with systemic steroids given before referral to our clinic did not improve the symptoms of this patient. Thrombus resolution and improvement of papilledema and strabismus was achieved with enoxaparin and acetazolamide therapy. We suggest that neurologic findings such as sixth cranial nerve and optic nerve involvement in a patient with bee sting can be caused by brain vascular thrombosis and increased intracranial pressure. Cautious evaluation of the patient and imaging should be performed to elicit the exact cause, so that the patient can be treated accordingly. Declaration of conflicting interests None declared.
Discussion
Funding
In this study we present a patient who developed paresis of the sixth cranial nerve and bilateral papilledema after the bee sting to the periocular area. Sigmoid and transverse sinus thrombosis was thought to cause these findings and the patient was treated with anticoagulation and intracranial pressure lowering treatment. Bee venom is a complex toxin which contains polypeptide toxins, enzymes and biogenic amines which cause toxic and allergic responses in humans.3 Bee stings to the eye can cause chemosis, corneal edema, iridocyclitis, cataract and optic neuritis.1 Anterior segment involvement is generally treated with stinger removal, topical steroids, antibiotics and cycloplegic medications.4 In patients with optic neuritis after bee stings, systemic steroid treatment was shown to have good results.5,6 Zambrano-Infantino et al. reported a 62-year-old woman who developed bilateral optic neuritis after a bee sting to the lower eyelid. She had a good clinical outcome after treatment with methylprednisolone.5 Choi et al. reported left optic neuritis with visual
This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
References 1. Reisman RE. Unusual reactions to insect stings. Curr Opin Allergy Clin Immunol 2005; 5: 355–358. 2. Razmjoo H, Abtahi MA, Roomizadeh P, Mohammadi Z and Abtahi SH. Management of corneal bee sting. Clin Ophthalmol 2011; 5: 1697–1700. 3. Gu¨rlu¨ VP and Erda N. Corneal bee sting-induced endothelial changes. Cornea 2006; 25: 981–983. 4. Chauhan D. Corneal honey bee sting: endoilluminator assisted removal of retained stinger. Int Ophthalmol 2012; 32: 285–288. 5. Zambrano-Infantino Rde C, Pin˜ierı´ ia-Gonsa´lvez JF, Montan˜o C and Rodrı´ guez C. Optic neuritis after a bee sting. Invest Clin 2013; 54: 180–185. 6. Choi MY and Cho SH. Optic neuritis after bee sting. Korean J Ophthalmol 2000; 14: 49–52.
Downloaded from tdo.sagepub.com at UNIV TORONTO on November 15, 2015
