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Corneal honeybee sting
Corneal honeybee sting Stephen C.B. Teoh, MMed (Ophth), MRCSEd (Ophth); Jong-Jian Lee, MMed (Ophth), FRCSEd (UK), FRCS (Ophth) (Glas); Han-Bor Fam, MMed (Ophth), FRCS (Ophth) ABSTRACT • RÉSUMÉ Background: We report the complications and management of a retained bee sting injury to the cornea. The case highlights the acute and chronic management of an uncommon injury and its pathogenesis. Methods: A 67-year-old man was attacked by a swarm of bees and was referred for severe chemosis on the right eye. A retained corneal bee stinger (ovipositor) was seen but removal was only partially successful. He subsequently developed a large corneal epithelial defect, anterior uveitis, intractable glaucoma, traumatic cataract, toxic optic neuropathy, and corneal scarring.We reviewed the literature on corneal bee sting injuries and their complications. Results: Inflammation was controlled with topical steroids and the patient underwent a combined phacoemulsification and trabeculectomy with mitomycin-C for uncontrolled glaucoma. However, optic neuropathy did not resolve. Interpretation: Corneal bee sting injuries are uncommon but can result in severe sight-threatening complications such as toxic optic neuropathy. Early recognition of the possible complications and appropriate treatment may help to prevent permanent loss of vision. Removal of a retained corneal bee stinger remains controversial. Contexte : Nous faisons état des complications et du traitement d’une blessure de la cornée où s’était logé le dard d’une abeille. Le cas souligne le traitement urgent et chronique d’une blessure rare ainsi que la pathogenèse de la blessure causée par le dard d’abeille. Méthodes : Un homme de 67 ans a été amené pour un chémosis grave à l’œil droit, après avoir été attaqué par un essaim d’abeilles. On a repéré le dard qui s’était logé dans la cornée, mais on n’a pu l’extraire que partiellement. L’homme a par la suite développé un important défaut épithélial cornéen, une uvéite antérieure, un glaucome réfractaire, une cataracte traumatique, une névropathie optique toxique et une cicatrisation de la cornée. Nous avons passé en revue la littérature sur les blessures de la cornée dues au dard d’abeille et leurs complications. Résultats : L’inflammation a été maîtrisée avec des stéroïdes topiques et le patient a subi une phacoémulsification combinée à une trabéculectomie avec mitomycine C pour le glaucome non maîtrisé.Toutefois, la névropathie optique n’a pu être résolue.
From The Eye Institute, Tan Tock Seng Hospital, Singapore
Seng Hospital, 11 Jalan Tan Tock Seng, Singapore 308433; fax (065) 6357 7718; [email protected]
Originally received Aug. 27, 2004 Accepted for publication Mar. 15, 2005
This article has been peer-reviewed.
Correspondence to: Dr Stephen C.B. Teoh, The Eye Institute, Tan Tock
Can J Ophthalmol 2005;40:469–471
Corneal honeybee sting—Teoh et al
469
Corneal honeybee sting—Teoh et al
Interprétation : Les blessures de la cornée dues à un dard d’abeille sont rares, mais elles peuvent entraîner des complications graves et dangereuses pour la vue, comme la névropathie optique toxique. La reconnaissance rapide des possibilités de complication et un traitement approprié peuvent aider à prévenir une perte de vision permanente. L’extraction du dard retenu dans la cornée demeure sujet à controverse.
O
cular injuries by bee sting are uncommon. When they occur, the cornea is the most common site, and ocular complications are widespread and unpredictable. Locally, damage occurs through toxic and immunologic reactions that may result in sight-threatening problems. We report the complications of a retained intracorneal bee stinger (ovipositor) and discuss the management of this uncommon injury and its pathogenesis. CASE
REPORT
A 67-year-old man was referred for painful right eye after being attacked by a swarm of bees 12 hours earlier. Vision was hand movement with good light projection. Ophthalmologic examination showed a sluggishly reactive mid-dilated pupil but no relative afferent pupillary defect (RAPD) was elicited. There was severe chemosis, conjunctival hyperaemia, and the cornea was edematous with a total epithelial defect. Eighty percent of the bee stinger was embedded in the paraxial cornea and was surrounded by infiltrates and associated with endotheliitis. It did not penetrate into the anterior chamber. The anterior chamber showed extensive flare with uveitis and no view of the fundus. There was no significant pathology in the left eye. Our attempt to remove the stinger under the slit lamp was unsuccessful. The proximal portion broke off leaving two-thirds of the stinger embedded in the posterior stroma. The patient was treated with cefazolin (50 mg/mL) and gentamicin (14 mg/mL) eye drops hourly together with 1% prednisolone acetate and olopatadine drops. A week later, a grade 3 RAPD and an intumescent secondary cataract were seen. Two weeks later, intractable glaucoma of 30 to 40 mm Hg developed despite use of 0.5% timolol maleate , 0.2% brimonidine , and 0.005% latanoprost eye drops. Combined phacoemulsification and trabeculectomy with mitomycin-C was performed. Intraocular pressure was controlled postoperatively without medication. However, vision remained at counting fingers with evidence
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of optic atrophy. The epithelial defect healed slowly after 3 months but the cornea had decompensated. COMMENTS
The majority of insect sting reactions are caused by members of the Hymenoptera. Anatomical study of the female honeybee (Apis mellifera) stinger reveals it to be a modified ovipositor connected to a poison sac.1,2 When it stings, the entire apparatus enters the wound, discharging venom in a reflex action.3 Research has shown that the injuries sustained as a result of the retained stinger are secondary to the retained venom and toxins. In the absence of venom or if the venom has been neutralized, the chitinous exoskeleton of the bee stinger is believed to be inert and can remain in situ without any adverse reactions.4 Bee venom consists of both basic and acidic components. The major groups of allergens and toxins are the nonenzymatic polypeptides, enzymes, and biological amines, which are responsible for immediate hypersensitivity reactions.5 Melittin (40%–60% of the venom) causes cellular membrane disruption and protein denaturation resulting in cataract formation and zonulysis with lens subluxation5. Apamin is highly antigenic and is thought to be a neurotoxin that disrupts the potassium ion channels.6,7 It is believed to play a role in toxic optic neuritis by causing focal demyelination. Phospholipase A2 and B are the major hydrolytic enzymes resulting in cytolysis and haemolysis.5 Hyaluronidase increases permeability and facilitates spread of toxins. These high-molecular-weight enzymes are also highly antigenic, causing immediate IgE (Immunoglobulin E) mediated type I hypersensitivity reactions.6,8 Retained stingers cause different complications due to different poison components.9 However, they invariably cause corneal edema with striate and toxic keratopathy.2,8 Sterile infiltration usually occurs within a few hours. Immunologic reactions also incite extensive inflammation and uveitis, occasionally with sterile hypopyon or hyphema.2,4 Glaucoma due to
Corneal honeybee sting—Teoh et al
toxic trabeculitis or severe uveitis usually occurs.2 In the subacute stage, lens subluxation and cataract may result.10 Iris atrophy, hypochromia, iridoplegia and internal ophthalmoplegia have also been reported.2 Neuro-ophthalmic complications especially optic neuritis and papilledema usually result in optic atrophy and severe loss of vision with dismal prognosis.9,11 Early detection is important, as treatment with intravenous pulsed methylprednisolone may enhance visual function recovery.9 In our case, it was felt that the neuropathy was the result of delayed toxic neuritis rather than inflammatory glaucoma. Removal of the retained barbed stinger is difficult and controversial. Attempts often result in retained segments within the cornea.2–4,10 Authors have postulated that manipulation of the retained apparatus causes envenomization resulting in greater inflammation, and they have advocated leaving the inert chitinous stinger in situ.2,4 Yuen et al showed that microscopic parts may be retained in the cornea without causing severe symptoms.12 However, Visscher suggested that it should be removed as soon as possible as the amount of venom injected correlates with the amount of time it remains within. He calculated that the amount of venom injected did not correlate with the method of removal, whether by teasing it out or by direct grasp and removal by pinching.3 Based on our experience, we recommend that the acute management of a corneal bee sting should be aimed at prevention of secondary infection with intensive broad-spectrum topical antibiotics, reduction of inflammation with aggressive hourly topical steroids (1% prednisolone acetate), treatment of anterior uveitis, early detection and treatment of inflammatory glaucoma, and pain relief. Recognition of
toxic optic neuritis is important, as early intervention with pulsed steroids may prevent permanent loss of vision. Surgical removal of the retained bee stinger, however, is still controversial. If performed, extreme care should be exercised to remove it in its entirety. REFERENCES 1. Snodgrass RE, Erickson EH. The anatomy of the honey bee. In: The Hive and the Honey Bee. Hamilton, Illinois: Dadant and Sons; 1992:150–7. 2. Arcieri ES, Franca ET, de Oliveria HB, De Abreu Ferreira L, Ferreira MA, Rocha FJ. Ocular lesions arising after stings by Hymenopteran insects. Cornea 2002;21:328–30. 3. Visscher PK, Better RS, Carmazine S. Removing bee stings. Lancet 1996;348:301–2. 4. Gilboa M, Gdal-On M, Zonis S. Bee and wasp stings of the eye. Retained intralenticular wasp sting: a case report. Br J Ophthalmol 1977;61:662–4. 5. King TP, Spangfort MD. Structure and biology of stinging insect venom allergens. Int Arch Allergy Immunol 2000;123: 99–106. 6. Smolin G, Wong I. Bee sting of the cornea: case report. Ann Ophthalmol 1982;14:342–3. 7. Chen CJ, Richardson CD. Bee sting-induced ocular changes. Ann Ophthalmol 1986;18:285–6. 8. Singh G. Bee sting of the cornea. Ann Ophthalmol 1984;16: 320–2. 9. Choi MY, Cho SH. Optic neuritis after bee sting. Korean J Ophthalmol 2000;14:49–52. 10. Smith DG, Roberge RJ. Corneal bee sting with retained stinger. J Emerg Med 2001;20:125–8. 11. Song HS, Wray SH. Bee sting optic neuritis: a case report with visual evoked potentials. J Clin Neuroophthalmol 1991; 11:45–9. 12. Yuen KSC, Lai JSM, Law RWM, Lam DS. Confocal microscopy in bee sting corneal injury. Eye 2003;17:845–7. Key words: bee sting, cornea, hymenoptera, complications
CAN J OPHTHALMOL—VOL. 40, NO. 4, 2005
471
From The Eye Institute, Tan Tock Seng Hospital, Singapore
Seng Hospital, 11 Jalan Tan Tock Seng, Singapore 308433; fax (065) 6357 7718; [email protected]
Originally received Aug. 27, 2004 Accepted for publication Mar. 15, 2005
This article has been peer-reviewed.
Correspondence to: Dr Stephen C.B. Teoh, The Eye Institute, Tan Tock
Can J Ophthalmol 2005;40:469–471
Corneal honeybee sting—Teoh et al
469
Corneal honeybee sting—Teoh et al
Interprétation : Les blessures de la cornée dues à un dard d’abeille sont rares, mais elles peuvent entraîner des complications graves et dangereuses pour la vue, comme la névropathie optique toxique. La reconnaissance rapide des possibilités de complication et un traitement approprié peuvent aider à prévenir une perte de vision permanente. L’extraction du dard retenu dans la cornée demeure sujet à controverse.
O
cular injuries by bee sting are uncommon. When they occur, the cornea is the most common site, and ocular complications are widespread and unpredictable. Locally, damage occurs through toxic and immunologic reactions that may result in sight-threatening problems. We report the complications of a retained intracorneal bee stinger (ovipositor) and discuss the management of this uncommon injury and its pathogenesis. CASE
REPORT
A 67-year-old man was referred for painful right eye after being attacked by a swarm of bees 12 hours earlier. Vision was hand movement with good light projection. Ophthalmologic examination showed a sluggishly reactive mid-dilated pupil but no relative afferent pupillary defect (RAPD) was elicited. There was severe chemosis, conjunctival hyperaemia, and the cornea was edematous with a total epithelial defect. Eighty percent of the bee stinger was embedded in the paraxial cornea and was surrounded by infiltrates and associated with endotheliitis. It did not penetrate into the anterior chamber. The anterior chamber showed extensive flare with uveitis and no view of the fundus. There was no significant pathology in the left eye. Our attempt to remove the stinger under the slit lamp was unsuccessful. The proximal portion broke off leaving two-thirds of the stinger embedded in the posterior stroma. The patient was treated with cefazolin (50 mg/mL) and gentamicin (14 mg/mL) eye drops hourly together with 1% prednisolone acetate and olopatadine drops. A week later, a grade 3 RAPD and an intumescent secondary cataract were seen. Two weeks later, intractable glaucoma of 30 to 40 mm Hg developed despite use of 0.5% timolol maleate , 0.2% brimonidine , and 0.005% latanoprost eye drops. Combined phacoemulsification and trabeculectomy with mitomycin-C was performed. Intraocular pressure was controlled postoperatively without medication. However, vision remained at counting fingers with evidence
470
CAN J OPHTHALMOL—VOL. 40, NO. 4, 2005
of optic atrophy. The epithelial defect healed slowly after 3 months but the cornea had decompensated. COMMENTS
The majority of insect sting reactions are caused by members of the Hymenoptera. Anatomical study of the female honeybee (Apis mellifera) stinger reveals it to be a modified ovipositor connected to a poison sac.1,2 When it stings, the entire apparatus enters the wound, discharging venom in a reflex action.3 Research has shown that the injuries sustained as a result of the retained stinger are secondary to the retained venom and toxins. In the absence of venom or if the venom has been neutralized, the chitinous exoskeleton of the bee stinger is believed to be inert and can remain in situ without any adverse reactions.4 Bee venom consists of both basic and acidic components. The major groups of allergens and toxins are the nonenzymatic polypeptides, enzymes, and biological amines, which are responsible for immediate hypersensitivity reactions.5 Melittin (40%–60% of the venom) causes cellular membrane disruption and protein denaturation resulting in cataract formation and zonulysis with lens subluxation5. Apamin is highly antigenic and is thought to be a neurotoxin that disrupts the potassium ion channels.6,7 It is believed to play a role in toxic optic neuritis by causing focal demyelination. Phospholipase A2 and B are the major hydrolytic enzymes resulting in cytolysis and haemolysis.5 Hyaluronidase increases permeability and facilitates spread of toxins. These high-molecular-weight enzymes are also highly antigenic, causing immediate IgE (Immunoglobulin E) mediated type I hypersensitivity reactions.6,8 Retained stingers cause different complications due to different poison components.9 However, they invariably cause corneal edema with striate and toxic keratopathy.2,8 Sterile infiltration usually occurs within a few hours. Immunologic reactions also incite extensive inflammation and uveitis, occasionally with sterile hypopyon or hyphema.2,4 Glaucoma due to
Corneal honeybee sting—Teoh et al
toxic trabeculitis or severe uveitis usually occurs.2 In the subacute stage, lens subluxation and cataract may result.10 Iris atrophy, hypochromia, iridoplegia and internal ophthalmoplegia have also been reported.2 Neuro-ophthalmic complications especially optic neuritis and papilledema usually result in optic atrophy and severe loss of vision with dismal prognosis.9,11 Early detection is important, as treatment with intravenous pulsed methylprednisolone may enhance visual function recovery.9 In our case, it was felt that the neuropathy was the result of delayed toxic neuritis rather than inflammatory glaucoma. Removal of the retained barbed stinger is difficult and controversial. Attempts often result in retained segments within the cornea.2–4,10 Authors have postulated that manipulation of the retained apparatus causes envenomization resulting in greater inflammation, and they have advocated leaving the inert chitinous stinger in situ.2,4 Yuen et al showed that microscopic parts may be retained in the cornea without causing severe symptoms.12 However, Visscher suggested that it should be removed as soon as possible as the amount of venom injected correlates with the amount of time it remains within. He calculated that the amount of venom injected did not correlate with the method of removal, whether by teasing it out or by direct grasp and removal by pinching.3 Based on our experience, we recommend that the acute management of a corneal bee sting should be aimed at prevention of secondary infection with intensive broad-spectrum topical antibiotics, reduction of inflammation with aggressive hourly topical steroids (1% prednisolone acetate), treatment of anterior uveitis, early detection and treatment of inflammatory glaucoma, and pain relief. Recognition of
toxic optic neuritis is important, as early intervention with pulsed steroids may prevent permanent loss of vision. Surgical removal of the retained bee stinger, however, is still controversial. If performed, extreme care should be exercised to remove it in its entirety. REFERENCES 1. Snodgrass RE, Erickson EH. The anatomy of the honey bee. In: The Hive and the Honey Bee. Hamilton, Illinois: Dadant and Sons; 1992:150–7. 2. Arcieri ES, Franca ET, de Oliveria HB, De Abreu Ferreira L, Ferreira MA, Rocha FJ. Ocular lesions arising after stings by Hymenopteran insects. Cornea 2002;21:328–30. 3. Visscher PK, Better RS, Carmazine S. Removing bee stings. Lancet 1996;348:301–2. 4. Gilboa M, Gdal-On M, Zonis S. Bee and wasp stings of the eye. Retained intralenticular wasp sting: a case report. Br J Ophthalmol 1977;61:662–4. 5. King TP, Spangfort MD. Structure and biology of stinging insect venom allergens. Int Arch Allergy Immunol 2000;123: 99–106. 6. Smolin G, Wong I. Bee sting of the cornea: case report. Ann Ophthalmol 1982;14:342–3. 7. Chen CJ, Richardson CD. Bee sting-induced ocular changes. Ann Ophthalmol 1986;18:285–6. 8. Singh G. Bee sting of the cornea. Ann Ophthalmol 1984;16: 320–2. 9. Choi MY, Cho SH. Optic neuritis after bee sting. Korean J Ophthalmol 2000;14:49–52. 10. Smith DG, Roberge RJ. Corneal bee sting with retained stinger. J Emerg Med 2001;20:125–8. 11. Song HS, Wray SH. Bee sting optic neuritis: a case report with visual evoked potentials. J Clin Neuroophthalmol 1991; 11:45–9. 12. Yuen KSC, Lai JSM, Law RWM, Lam DS. Confocal microscopy in bee sting corneal injury. Eye 2003;17:845–7. Key words: bee sting, cornea, hymenoptera, complications
CAN J OPHTHALMOL—VOL. 40, NO. 4, 2005
471