Veterinary Ophthalmology (2016) 19, 2, 149–160
DOI:10.1111/vop.12276
Ophthalmic abnormalities secondary to periocular or ocular snakebite (pit vipers) in dogs—11 cases (2012–2014) Bianca C. Martins, Caryn E. Plummer, Kirk N. Gelatt, Dennis E. Brooks, Sarah E. Czerwinski, Caroline Monk, Shari M. Greenberg, Brendan G. Mangan, Leonel Londo~ no, Luiz Bolfer, Carsten Bandt and Michael Schaer Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, 2015 SW 16th Ave, Gainesville, FL 32610, USA
Address communications to: C. E. Plummer Tel.: (352) 392-2235 Fax: (352) 392-6125 e-mail: [email protected]
Abstract Objective To describe ophthalmic abnormalities secondary to periocular and ocular snakebite in dogs. Animal Studied Retrospective review of medical records from dogs presenting to the Small Animal Hospital at University of Florida following snakebites to the face (2012– 2014). Two groups were identified: periocular bites (PB) and ocular bites (OB). Results Records from eleven dogs matched the search criteria and were included in the study (PB=9, 81.8%; OB=2, 18.2%). Both OB cases involved the cornea. Facial edema, blepharospasm, chemosis, and conjunctival hyperemia occurred in all cases (100%). Hemorrhage from the eyelids occurred in eight cases (72.7%; PB=7, OB=1). Subconjunctival hemorrhage occurred in seven cases (63.6%; PB=6, OB=1). Third eyelid laceration and nictitans gland prolapse occurred in 1 case each (9%; PB=1). Lagophthalmia was present in three cases (27.3%; PB=3), with secondary corneal ulcer in two cases (18.2%; PB=2). Corneal ulcer due to direct corneal bite occurred in two cases (18.2%—partial thickness with melting 1 and full thickness 1). Uveitis was present in 6 cases (54.5%; PB=4, OB=2), with flare and miosis in 4 cases (36.4%; PB=2, OB=2). Hyphema, fibrin in anterior chamber, and cataract occurred in one case (9%; OB=1). Vision loss occurred in two cases (18.2%; PB=2), secondary to retinal degeneration (PB=1) and amaurosis (PB=1). Mean follow-up time was 7 weeks (range: 3 days–11 months). Most clinical signs had resolved by last examination. Conclusions Periocular symptoms were more commonly observed than ocular alterations, regardless of bite location. Appropriate supportive therapy should be instituted according to clinical signs. Key Words: dog, envenomation, eye, ocular, pit viper, snakebite
INTRODUCTION
In humans, the American Association of Poison Control Centers recorded over 6500 snakebites in 2012, of which over 4000 were confirmed to be venomous bites.1 As reporting is not mandatory, many snakebites go unreported. It is speculated that snakebites in the pet population occur in similar, if not greater, incidence than in humans because of a high outdoor exposure rate and poor threat judgment by the animal victim. However, there is no precise data available to document the exact numbers.2–4 There are two families of venomous snakes indigenous to the United States: the Elapidae, represented in North America by the coral snakes (Micrurus fulvius), and © 2015 American College of Veterinary Ophthalmologists
Viperidae, subfamily Crotalidae (pit vipers). In North America, members of the subfamily Crotalidae belong to three genera: the rattlesnakes (Crotalus and Sistrurus spp.), the copperheads (Agkistrodon contortrix), and cottonmouths or water moccasins (Agkistrodon piscivorus).4,5 Approximately 99% of all venomous snakebites in the United States are inflicted by pit vipers, and the rattlesnakes account for most fatalities. Pit vipers can be identified by their characteristic retractable front fangs, bilateral heat sensing ‘pits’ between the nostrils and eyes, elliptical pupils, a single row of subcaudal scales distal to the anal plate, and triangular shaped heads.5 In humans, 98% of the bites are on extremities, most often on the hands and arms, often the result of deliberate
150 martins
ET AL.
attempts to handle, harm, or kill the snake.1 This incidence differs markedly from statistics in dogs, where the majority of the snakebites (77–81.2%) involve the face or neck, likely associated with the manner in which the dog confronts the snake.4,6 Most bites occur between April and October, when snakes are active, and humans and pets are outdoors.1,4 The primary purpose of the snake venom is not to kill but rather to immobilize the prey and predigest its tissues. Components of the venom affect almost every organ system, and the most deleterious effects are seen in the cardiovascular, hematologic, respiratory, and nervous system.1 Pit viper venom has been considered to be vasculotoxic and necrogenic, while North American and South American elapid snake venom has been considered to be neurotoxic and hemolytic.4 The nature of the venom is unique to each snake, but in general venoms are a chemically complex mixtures of proteins, many with enzymatic properties.7 In pit vipers, the enzymes include hyaluronidase and collagenase, which aid in the spread of the venom through interstitial spaces; proteases that cause tissue necrosis and coagulopathies; and phospholipases, which produce direct cytotoxic effects, including endothelial damage and inflammation. The nonenzymatic fraction of the venom has direct effects on the cardiovascular and respiratory systems, resulting in ventricular arrhythmias, hypotension, and pooling of blood, especially in the splanchnic vascular beds.1,7 Various factors influence the degree of envenomation. The severity of envenomation depends upon species of the victim, body mass, age, location of the bite, individual sensitivity to the venom, postbite excitability, medications, and the type of first aid treatment and subsequent medical care provided. Other factors affecting the severity of the envenomation include species, age, and size of the snake, motivation of the attack (defensive, offensive, or agonal strike), number and depth of strikes, and degree of venom regeneration since last use.5,7 Clinical signs caused by pit viper snakebite envenomation may occur within the first 30 min; however, monitoring for delayed effects over the first 24 h is recommended. A complete physical examination should be carried out immediately since clinical signs may worsen over ensuing hours.5 Local tissue reactions to most pit viper envenomation include puncture wounds, progressive hemorrhage, and lymphedema along with rapid onset of pain. Tissue necrosis may also occur. Systemic signs include mental depression, hypotension, tachypnea, tachycardia, thrombocytopenia, and evidence of coagulopathies, such as ecchymosis and melena.5,7 The mainstay of therapy for snakebite envenomation includes the use of antivenin and intravenous (i.v.) fluids. Other supportive treatment measures may include pain management, glucocorticoids, blood products, antihistamines, and antimicrobials.3–7 Although uncommon, there are a few reports of ophthalmic abnormalities secondary to snakebite envenoma-
tion in humans, regardless of the bite location. For example, ocular abnormalities have been reported following bites on the leg. Snake venom neurotoxins act mainly on the peripheral nervous system and may affect the extraocular muscles, resulting in exotropia, ptosis, diplopia, and ophthalmoplegia.8–11 Other complications may include optic neuritis, globe necrosis, and retinal degeneration.11–14 Reports of ophthalmic manifestations after viperine snakebites in humans include subconjunctival hemorrhage, hyphema, uveitis, endophthalmitis, glaucoma, vitreous hemorrhage, retinal hemorrhage, central retinal artery occlusion, macular infarction, and blindness secondary to cortical infarction.15–22 To the authors’ knowledge, despite several papers describing the systemic and local manifestation of snakebite envenomation in dogs, there have been no reports of ocular abnormalities in those cases. The purpose of this study was to describe the ophthalmic abnormalities that may occur secondary to periocular and ocular snakebite (pit vipers) in dogs. MATERIALS AND METHODS
Records of dogs examined and treated at the University of Florida Veterinary Medical Center (UFVMC) by the emergency and critical care service (ECC) for envenomation that received an examination by the ophthalmology service during the period of 2012 through 2014 were reviewed. Criteria for inclusion were witnessed contact of the snake with the dog by the owner, and/or clinical lesions compatible with envenomation by rattlesnake/pit viper. The lesions included sudden occurrence of puncture wounds (with or without overt bleeding), severe regional swelling, shock, and petechial/ecchymotic hemorrhages. All cases received a full ophthalmic evaluation by a faculty Diplomate of the American College of Veterinary Ophthalmologists and by a resident in Comparative Ophthalmology. The data reviewed included patient signalment, time of presentation to the emergency clinic (determined as time between the witnessed attack and observation of the initial development of clinical signs by the owner until presentation at the referring veterinarian or UFVMC), time until ocular examination (determined as time between presentation at UFVMC emergency service and consultation with the Ophthalmology Service at UFVMC), anatomic location of the bite (ocular or periocular bites), ocular clinical signs at initial ophthalmic evaluation, treatment, complications or additional clinical signs observed on follow-up examinations, follow-up time, and ocular clinical outcome. Ocular bites were determined by the visualization of puncture wounds on the cornea or sclera, while those with puncture wounds on the adnexa were considered periocular bites. RESULTS
Eleven cases fulfilled the selection criteria and were included in the study. Seven females (three intact and four
© 2015 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 19, 149–160
periocular and ocular snakebite in dogs 151
spayed) and four males (three intact and one neutered) were present, and nine different breeds were represented. Mean age in years was 3.9 2.2 (range 1–8 years old). Signalment, bite location, time elapsed until presentation at emergency clinic, time elapsed from initial presentation until ophthalmic consultation, initial ophthalmic findings, therapy, and outcome are described (Table 1). Five cases (45.5%) presented at the referring veterinarian or at UFVMC emergency service within 1 h of the attack or initial development of the clinical signs. Three dogs (27.3%) presented within 6 h, and the other remaining cases (3 dogs—27.3%) presented on the same day of the attack; however, the time of the attack was not available. Cases presented at the referring veterinarian received emergent initial therapy and then transferred to the UFVMC emergency service. Ophthalmology consultation was performed on the day of presentation in one case (9%). In seven cases (63.6%), ophthalmic consultation was performed the day after presentation, and in three cases (27.3%), the ocular examination was performed 2 days after initial presentation. The delay of ophthalmologic examination was due to marked periocular lymphedema that impaired a detailed evaluation or an unstable systemic condition. Clinical signs are described in this manuscript in order of the most commonly observed to the least frequent. In all cases, more than one clinical sign was present concomitantly. After initial evaluation by the UFVMC emergency and critical care service, all dogs received antivenin therapy (dosage dependent on the clinical signs) and i.v. fluids. Additional supportive therapy was instituted on a case-by-case basis. Nine dogs (81.8%) presented with PB, while two dogs (18.2%) had OB. Initial ophthalmic clinical signs were observed ipsilaterally in all cases, while progression to bilateral involvement was observed in three cases (27.3%). The ophthalmic manifestations on the contralateral side were less severe in all three cases and were limited to conjunctival hyperemia (3 cases), chemosis (2 cases), facial edema, and blepharedema (1 case). Severe ipsilateral facial edema (Fig. 1), blepharospasm, blepharedema (Fig. 2), severe chemosis, and severe conjunctival hyperemia (Fig. 3) were the most common clinical signs and were present in all cases (100%), regardless of bite location. All dogs were painful to touch of the face. Diffuse hemorrhage from the eyelids was observed in eight cases (72.7% of all cases; 7 PB and 1 OB). Subconjunctival hemorrhage was present in 7 cases (63.6%; 6 PB and 1 OB). Uveitis was diagnosed in six eyes (54.5%; 4 PB and 2 OB). Only one of those cases presented with bilateral ophthalmic signs. Uveitis manifested as aqueous flare in four cases (36.4%; 2 PB and both OB), miosis in four cases (36.4% of all cases; two eyes exhibiting PB and both cases of OB), and hyphema and fibrin in the anterior chamber in oen eye (9%; 1 OB).
Lagophthalmia secondary to severe chemosis and/or blepharedema was observed in three cases (27.3%; all PB). Corneal ulcers were observed in four cases (36.4%); two of those cases were secondary to lagophthalmia associated with PB. The other two dogs exhibited corneal ulcer secondary to direct bite to the cornea; of those, one case had a partial thickness bite with associated malacia of the cornea (Fig. 4) that resolved 3 days after initial examination (Fig. 5). Slit-lamp examination of the cornea of the second dog revealed a full thickness corneal bite, observed as an opaque track through the entire thickness of the cornea with hyphema and a fibrin clot in the anterior chamber adherent to the corneal endothelium at the site of the corneal wound (Fig. 6). Nevertheless, no active leakage was observed as a Seidel test was negative. The hyphema had resolved by the last examination (Fig. 7). Both dogs presenting with direct bite to the cornea also had corneal edema associated with the corneal wound. Necrosis of the periocular skin (Fig. 8) was observed in two dogs (18.2%, PB). Laceration of the third eyelid was present in one eye (9%, PB), third eyelid elevation was present in one dog (9%, PB), and third eyelid gland prolapse (Figs 10 and 11) was observed in one case (9%, PB). Topical therapy for the affected eyes was initiated after examination by the ophthalmology service. Ophthalmic solutions or ointments containing steroids (with or without antibiotics) were initiated in all cases, when corneal ulcers were not present (n = 7). Topical atropine (Falcon pharmaceuticals, Fort Worth, TX) was applied in all cases presenting with signs of uveitis or corneal ulcer (n = 7). Ophthalmic antibiotics and topical collagenolytics were instituted if corneal ulcers were present (n = 4). Temporary tarsorrhaphy was carried out in all cases exhibiting lagophthalmia or at risk of exposure keratitis (n = 3). Ocular clinical signs or complications observed on follow-up examinations included ipsilateral incomplete facial paralysis in one dog (9%, PB—case 5). This finding was observed 6 days after initial ophthalmic examination, and no muscle atrophy was identified. Focal anterior capsular and cortical cataract were observed in one dog (Fig. 7), observed 6 weeks after the initial evaluation (9%, OB). Vision loss of the affected eye was observed in two cases (18.2%, PB), and a flash electroretinogram (ERG) was performed in both cases. In one case (case 6), vision loss was noted 2 months after initial evaluation. The patient presented initially with severe pain to touch of the face, severe blepharedema, blepharospasm, severe chemosis, conjunctival hyperemia, subconjunctival hemorrhage, third eyelid elevation, third eyelid gland prolapse, lagophthalmia, and miosis. A fundic examination was not possible initially in this dog because of periocular swelling, miosis, and third eyelid gland prolapse (Fig. 9). The dog received topical atropine 1% ophthalmic ointment and a temporary tarsorrhaphy to protect the ocular surface structures. The tarsorrhaphy sutures were removed 1 week later, and most of the clinical signs had subsided, except for third eyelid
© 2015 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 19, 149–160
Breed
Bull Terrier
Mix breed
Jack Russell Terrier
West Highland White Terrier
Patient
5
6
7
8
Table 1. (Continued)
© 2015 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 19, 149–160
Male (intact)
Female (spayed)
Female (spayed)
Female (spayed)
Gender
7
6
2
5
Age (year)
Periocular
Periocular
Periocular
Periocular
Bite location
2 days
1 day
DOI:10.1111/vop.12276
Ophthalmic abnormalities secondary to periocular or ocular snakebite (pit vipers) in dogs—11 cases (2012–2014) Bianca C. Martins, Caryn E. Plummer, Kirk N. Gelatt, Dennis E. Brooks, Sarah E. Czerwinski, Caroline Monk, Shari M. Greenberg, Brendan G. Mangan, Leonel Londo~ no, Luiz Bolfer, Carsten Bandt and Michael Schaer Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, 2015 SW 16th Ave, Gainesville, FL 32610, USA
Address communications to: C. E. Plummer Tel.: (352) 392-2235 Fax: (352) 392-6125 e-mail: [email protected]
Abstract Objective To describe ophthalmic abnormalities secondary to periocular and ocular snakebite in dogs. Animal Studied Retrospective review of medical records from dogs presenting to the Small Animal Hospital at University of Florida following snakebites to the face (2012– 2014). Two groups were identified: periocular bites (PB) and ocular bites (OB). Results Records from eleven dogs matched the search criteria and were included in the study (PB=9, 81.8%; OB=2, 18.2%). Both OB cases involved the cornea. Facial edema, blepharospasm, chemosis, and conjunctival hyperemia occurred in all cases (100%). Hemorrhage from the eyelids occurred in eight cases (72.7%; PB=7, OB=1). Subconjunctival hemorrhage occurred in seven cases (63.6%; PB=6, OB=1). Third eyelid laceration and nictitans gland prolapse occurred in 1 case each (9%; PB=1). Lagophthalmia was present in three cases (27.3%; PB=3), with secondary corneal ulcer in two cases (18.2%; PB=2). Corneal ulcer due to direct corneal bite occurred in two cases (18.2%—partial thickness with melting 1 and full thickness 1). Uveitis was present in 6 cases (54.5%; PB=4, OB=2), with flare and miosis in 4 cases (36.4%; PB=2, OB=2). Hyphema, fibrin in anterior chamber, and cataract occurred in one case (9%; OB=1). Vision loss occurred in two cases (18.2%; PB=2), secondary to retinal degeneration (PB=1) and amaurosis (PB=1). Mean follow-up time was 7 weeks (range: 3 days–11 months). Most clinical signs had resolved by last examination. Conclusions Periocular symptoms were more commonly observed than ocular alterations, regardless of bite location. Appropriate supportive therapy should be instituted according to clinical signs. Key Words: dog, envenomation, eye, ocular, pit viper, snakebite
INTRODUCTION
In humans, the American Association of Poison Control Centers recorded over 6500 snakebites in 2012, of which over 4000 were confirmed to be venomous bites.1 As reporting is not mandatory, many snakebites go unreported. It is speculated that snakebites in the pet population occur in similar, if not greater, incidence than in humans because of a high outdoor exposure rate and poor threat judgment by the animal victim. However, there is no precise data available to document the exact numbers.2–4 There are two families of venomous snakes indigenous to the United States: the Elapidae, represented in North America by the coral snakes (Micrurus fulvius), and © 2015 American College of Veterinary Ophthalmologists
Viperidae, subfamily Crotalidae (pit vipers). In North America, members of the subfamily Crotalidae belong to three genera: the rattlesnakes (Crotalus and Sistrurus spp.), the copperheads (Agkistrodon contortrix), and cottonmouths or water moccasins (Agkistrodon piscivorus).4,5 Approximately 99% of all venomous snakebites in the United States are inflicted by pit vipers, and the rattlesnakes account for most fatalities. Pit vipers can be identified by their characteristic retractable front fangs, bilateral heat sensing ‘pits’ between the nostrils and eyes, elliptical pupils, a single row of subcaudal scales distal to the anal plate, and triangular shaped heads.5 In humans, 98% of the bites are on extremities, most often on the hands and arms, often the result of deliberate
150 martins
ET AL.
attempts to handle, harm, or kill the snake.1 This incidence differs markedly from statistics in dogs, where the majority of the snakebites (77–81.2%) involve the face or neck, likely associated with the manner in which the dog confronts the snake.4,6 Most bites occur between April and October, when snakes are active, and humans and pets are outdoors.1,4 The primary purpose of the snake venom is not to kill but rather to immobilize the prey and predigest its tissues. Components of the venom affect almost every organ system, and the most deleterious effects are seen in the cardiovascular, hematologic, respiratory, and nervous system.1 Pit viper venom has been considered to be vasculotoxic and necrogenic, while North American and South American elapid snake venom has been considered to be neurotoxic and hemolytic.4 The nature of the venom is unique to each snake, but in general venoms are a chemically complex mixtures of proteins, many with enzymatic properties.7 In pit vipers, the enzymes include hyaluronidase and collagenase, which aid in the spread of the venom through interstitial spaces; proteases that cause tissue necrosis and coagulopathies; and phospholipases, which produce direct cytotoxic effects, including endothelial damage and inflammation. The nonenzymatic fraction of the venom has direct effects on the cardiovascular and respiratory systems, resulting in ventricular arrhythmias, hypotension, and pooling of blood, especially in the splanchnic vascular beds.1,7 Various factors influence the degree of envenomation. The severity of envenomation depends upon species of the victim, body mass, age, location of the bite, individual sensitivity to the venom, postbite excitability, medications, and the type of first aid treatment and subsequent medical care provided. Other factors affecting the severity of the envenomation include species, age, and size of the snake, motivation of the attack (defensive, offensive, or agonal strike), number and depth of strikes, and degree of venom regeneration since last use.5,7 Clinical signs caused by pit viper snakebite envenomation may occur within the first 30 min; however, monitoring for delayed effects over the first 24 h is recommended. A complete physical examination should be carried out immediately since clinical signs may worsen over ensuing hours.5 Local tissue reactions to most pit viper envenomation include puncture wounds, progressive hemorrhage, and lymphedema along with rapid onset of pain. Tissue necrosis may also occur. Systemic signs include mental depression, hypotension, tachypnea, tachycardia, thrombocytopenia, and evidence of coagulopathies, such as ecchymosis and melena.5,7 The mainstay of therapy for snakebite envenomation includes the use of antivenin and intravenous (i.v.) fluids. Other supportive treatment measures may include pain management, glucocorticoids, blood products, antihistamines, and antimicrobials.3–7 Although uncommon, there are a few reports of ophthalmic abnormalities secondary to snakebite envenoma-
tion in humans, regardless of the bite location. For example, ocular abnormalities have been reported following bites on the leg. Snake venom neurotoxins act mainly on the peripheral nervous system and may affect the extraocular muscles, resulting in exotropia, ptosis, diplopia, and ophthalmoplegia.8–11 Other complications may include optic neuritis, globe necrosis, and retinal degeneration.11–14 Reports of ophthalmic manifestations after viperine snakebites in humans include subconjunctival hemorrhage, hyphema, uveitis, endophthalmitis, glaucoma, vitreous hemorrhage, retinal hemorrhage, central retinal artery occlusion, macular infarction, and blindness secondary to cortical infarction.15–22 To the authors’ knowledge, despite several papers describing the systemic and local manifestation of snakebite envenomation in dogs, there have been no reports of ocular abnormalities in those cases. The purpose of this study was to describe the ophthalmic abnormalities that may occur secondary to periocular and ocular snakebite (pit vipers) in dogs. MATERIALS AND METHODS
Records of dogs examined and treated at the University of Florida Veterinary Medical Center (UFVMC) by the emergency and critical care service (ECC) for envenomation that received an examination by the ophthalmology service during the period of 2012 through 2014 were reviewed. Criteria for inclusion were witnessed contact of the snake with the dog by the owner, and/or clinical lesions compatible with envenomation by rattlesnake/pit viper. The lesions included sudden occurrence of puncture wounds (with or without overt bleeding), severe regional swelling, shock, and petechial/ecchymotic hemorrhages. All cases received a full ophthalmic evaluation by a faculty Diplomate of the American College of Veterinary Ophthalmologists and by a resident in Comparative Ophthalmology. The data reviewed included patient signalment, time of presentation to the emergency clinic (determined as time between the witnessed attack and observation of the initial development of clinical signs by the owner until presentation at the referring veterinarian or UFVMC), time until ocular examination (determined as time between presentation at UFVMC emergency service and consultation with the Ophthalmology Service at UFVMC), anatomic location of the bite (ocular or periocular bites), ocular clinical signs at initial ophthalmic evaluation, treatment, complications or additional clinical signs observed on follow-up examinations, follow-up time, and ocular clinical outcome. Ocular bites were determined by the visualization of puncture wounds on the cornea or sclera, while those with puncture wounds on the adnexa were considered periocular bites. RESULTS
Eleven cases fulfilled the selection criteria and were included in the study. Seven females (three intact and four
© 2015 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 19, 149–160
periocular and ocular snakebite in dogs 151
spayed) and four males (three intact and one neutered) were present, and nine different breeds were represented. Mean age in years was 3.9 2.2 (range 1–8 years old). Signalment, bite location, time elapsed until presentation at emergency clinic, time elapsed from initial presentation until ophthalmic consultation, initial ophthalmic findings, therapy, and outcome are described (Table 1). Five cases (45.5%) presented at the referring veterinarian or at UFVMC emergency service within 1 h of the attack or initial development of the clinical signs. Three dogs (27.3%) presented within 6 h, and the other remaining cases (3 dogs—27.3%) presented on the same day of the attack; however, the time of the attack was not available. Cases presented at the referring veterinarian received emergent initial therapy and then transferred to the UFVMC emergency service. Ophthalmology consultation was performed on the day of presentation in one case (9%). In seven cases (63.6%), ophthalmic consultation was performed the day after presentation, and in three cases (27.3%), the ocular examination was performed 2 days after initial presentation. The delay of ophthalmologic examination was due to marked periocular lymphedema that impaired a detailed evaluation or an unstable systemic condition. Clinical signs are described in this manuscript in order of the most commonly observed to the least frequent. In all cases, more than one clinical sign was present concomitantly. After initial evaluation by the UFVMC emergency and critical care service, all dogs received antivenin therapy (dosage dependent on the clinical signs) and i.v. fluids. Additional supportive therapy was instituted on a case-by-case basis. Nine dogs (81.8%) presented with PB, while two dogs (18.2%) had OB. Initial ophthalmic clinical signs were observed ipsilaterally in all cases, while progression to bilateral involvement was observed in three cases (27.3%). The ophthalmic manifestations on the contralateral side were less severe in all three cases and were limited to conjunctival hyperemia (3 cases), chemosis (2 cases), facial edema, and blepharedema (1 case). Severe ipsilateral facial edema (Fig. 1), blepharospasm, blepharedema (Fig. 2), severe chemosis, and severe conjunctival hyperemia (Fig. 3) were the most common clinical signs and were present in all cases (100%), regardless of bite location. All dogs were painful to touch of the face. Diffuse hemorrhage from the eyelids was observed in eight cases (72.7% of all cases; 7 PB and 1 OB). Subconjunctival hemorrhage was present in 7 cases (63.6%; 6 PB and 1 OB). Uveitis was diagnosed in six eyes (54.5%; 4 PB and 2 OB). Only one of those cases presented with bilateral ophthalmic signs. Uveitis manifested as aqueous flare in four cases (36.4%; 2 PB and both OB), miosis in four cases (36.4% of all cases; two eyes exhibiting PB and both cases of OB), and hyphema and fibrin in the anterior chamber in oen eye (9%; 1 OB).
Lagophthalmia secondary to severe chemosis and/or blepharedema was observed in three cases (27.3%; all PB). Corneal ulcers were observed in four cases (36.4%); two of those cases were secondary to lagophthalmia associated with PB. The other two dogs exhibited corneal ulcer secondary to direct bite to the cornea; of those, one case had a partial thickness bite with associated malacia of the cornea (Fig. 4) that resolved 3 days after initial examination (Fig. 5). Slit-lamp examination of the cornea of the second dog revealed a full thickness corneal bite, observed as an opaque track through the entire thickness of the cornea with hyphema and a fibrin clot in the anterior chamber adherent to the corneal endothelium at the site of the corneal wound (Fig. 6). Nevertheless, no active leakage was observed as a Seidel test was negative. The hyphema had resolved by the last examination (Fig. 7). Both dogs presenting with direct bite to the cornea also had corneal edema associated with the corneal wound. Necrosis of the periocular skin (Fig. 8) was observed in two dogs (18.2%, PB). Laceration of the third eyelid was present in one eye (9%, PB), third eyelid elevation was present in one dog (9%, PB), and third eyelid gland prolapse (Figs 10 and 11) was observed in one case (9%, PB). Topical therapy for the affected eyes was initiated after examination by the ophthalmology service. Ophthalmic solutions or ointments containing steroids (with or without antibiotics) were initiated in all cases, when corneal ulcers were not present (n = 7). Topical atropine (Falcon pharmaceuticals, Fort Worth, TX) was applied in all cases presenting with signs of uveitis or corneal ulcer (n = 7). Ophthalmic antibiotics and topical collagenolytics were instituted if corneal ulcers were present (n = 4). Temporary tarsorrhaphy was carried out in all cases exhibiting lagophthalmia or at risk of exposure keratitis (n = 3). Ocular clinical signs or complications observed on follow-up examinations included ipsilateral incomplete facial paralysis in one dog (9%, PB—case 5). This finding was observed 6 days after initial ophthalmic examination, and no muscle atrophy was identified. Focal anterior capsular and cortical cataract were observed in one dog (Fig. 7), observed 6 weeks after the initial evaluation (9%, OB). Vision loss of the affected eye was observed in two cases (18.2%, PB), and a flash electroretinogram (ERG) was performed in both cases. In one case (case 6), vision loss was noted 2 months after initial evaluation. The patient presented initially with severe pain to touch of the face, severe blepharedema, blepharospasm, severe chemosis, conjunctival hyperemia, subconjunctival hemorrhage, third eyelid elevation, third eyelid gland prolapse, lagophthalmia, and miosis. A fundic examination was not possible initially in this dog because of periocular swelling, miosis, and third eyelid gland prolapse (Fig. 9). The dog received topical atropine 1% ophthalmic ointment and a temporary tarsorrhaphy to protect the ocular surface structures. The tarsorrhaphy sutures were removed 1 week later, and most of the clinical signs had subsided, except for third eyelid
© 2015 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 19, 149–160
Breed
Bull Terrier
Mix breed
Jack Russell Terrier
West Highland White Terrier
Patient
5
6
7
8
Table 1. (Continued)
© 2015 American College of Veterinary Ophthalmologists, Veterinary Ophthalmology, 19, 149–160
Male (intact)
Female (spayed)
Female (spayed)
Female (spayed)
Gender
7
6
2
5
Age (year)
Periocular
Periocular
Periocular
Periocular
Bite location
2 days
1 day
