Chapter 172 Ocular Disease in the Intensive Care Unit Steven R. Hollingsworth, DVM, DACVO, Bradford J. Holmberg, DVM, MS, PhD, DACVO KEY POINTS • Ocular disease is a common manifestation of systemic illness seen in critically ill patients. • Identification of ocular disease is completed by a thorough ophthalmic examination including indirect ophthalmoscopy, Schirmer tear testing, fluorescein staining, tonometry, and possibly cytologic studies, culture, or biopsy. INTRODUCTION Ophthalmic disease can be associated with or secondary to conditions that require a patient to be in a critical care facility. This chapter presents common ocular signs and discusses the appropriate interpretation of these signs and treatment of the ocular disease. BLEPHAROSPASM Blepharospasm is a nonspecific sign of ocular pain and may be associated with enophthalmos, elevation of the third eyelid, and spastic entropion. Both surface and intraocular disease can result in blepharospasm. The origin of ocular pain is determined by a thorough ophthalmic examination, including diagnostic tests such as fluorescein staining, Schirmer tear test evaluation, and tonometry. A topical anesthetic (e.g., 0.5% proparacaine) may facilitate examination by eliminating pain related to surface disease. RED EYE Veterinary clinicians will commonly encounter patients with a “red eye.” The redness represents new or congested blood vessels within the episclera, conjunctiva, or cornea. Episcleral vessels are stout, easily identifiable vessels that course perpendicular to the limbus and usually stop before reaching the limbus. Congestion of these vessels is associated most commonly with intraocular disease, specifically uveitis and glaucoma. However, with moderate to severe corneal disease these vessels may become engorged. Conjunctival blood vessels are extremely fine; without the aid of magnification individual vessels are difficult to identify. When vessels are engorged, a pink-red flush is observable. Mild conjunctival hyperemia may be apparent with intraocular disease, but moderate signs are consistent with surface disease (i.e., conjunctivitis or keratoconjunctivitis). Differential diagnostic considerations for conjunctivitis include infections (canine distemper virus, feline herpes virus, feline Chlamydophila, leishmaniasis, onchocerciasis), allergies, postradiotherapy conditions, keratoconjunctivitis sicca (KCS), and exposure. Diagnosis is based on history and Schirmer tear test, fluorescein staining, cytologic studies, and biopsy results. Conjunctival hyperemia can be easily confused with a conjunctival or subconjunctival infiltrate. This infiltrate may be fluid (chemosis) or cells. Mild chemosis is common with conjunctivitis. Severe chemosis may obstruct visualization of the cornea and intraocular structures. The most common cause of primary chemosis is topical toxicity (from neomycin, atropine, caustic agents). Removing the toxin and treating supportively will allow resolution of signs. Rarely, intravenous fluid overload at a rate of 2 to 3 times maintenance for a period of 2 days or longer can result in marked chemosis. Tapering the fluid rate will allow the chemosis to resolve. Subconjunctival infiltrates may cause the conjunctiva to appear thickened. They may be focal or diffuse. Carefully examining the color of the conjunctiva may help differentiate an infiltrate from common hyperemia. A diffuse yellow appearance of the conjunctiva in the absence of thickening is consistent with icterus. This may be the first clinical sign of icterus and should prompt the clinician to pursue further diagnostic tests concerning hepatobiliary status. Neoplastic cells within the subconjunctiva frequently result in thickening and a yellow to orange hue. Lymphoma is the most common neoplasia presenting in the subconjunctiva and may represent the primary tumor site. Other masses observed in the subconjunctiva include systemic histiocytosis (orange), hemangiosarcoma (red), melanoma (brown), and granulomatous scleritis (pink). A definitive diagnosis can usually be obtained by biopsy. Light sedation and topical anesthesia are typically all that is needed to obtain a diagnostic sample. Subconjunctival hemorrhage in a critically ill patient, observed as petechiae or ecchymoses, warrants investigation for an underlying coagulopathy. Hemorrhage may be isolated to the subconjunctiva or seen in the anterior chamber (hyphema). Causes of hemorrhage not associated with a coagulopathy include trauma, strangulation (choke collars), and rarely constipation. A blue-green discoloration of the sclera and/or conjunctiva may be observed. This has been observed in dogs receiving mitoxantrone chemotherapy. Signs are temporary and usually resolve within hours to days after cessation of treatment. TEAR FILM ABNORMALITIES The tear film is comprised of three layers: an outer lipid layer, middle aqueous layer, and an inner mucin layer. A deficiency in any of these components may result in decreased tear production or increased tear clearance (evaporation) and may be diagnosed with a Schirmer tear test. Clinical signs of a tear film abnormality depend on the severity, chronicity, and underlying cause of the tear deficiency. The most consistent and obvious finding is a thick mucoid discharge, commonly accumulated on and around the eyelids. Additional clinical signs include conjunctival hyperemia, a lackluster appearance to the corneal surface, and in chronic cases corneal vascularization and melanosis. Chronic tear film deficiencies lead to thickening of the corneal epithelium, and therefore ulceration is not common. However, the critically ill patient may develop acute KCS resulting in rapid, severe, and potentially globe-threatening corneal ulcers. There are numerous causes of decreased tear production (KCS) and increased tear clearance. Undoubtedly the most common cause of KCS is immune-mediated destruction of the lacrimal gland and gland of the third eyelid. This will likely be a preexisting disease in critically ill patients. Treatment with topical cyclosporine and artificial tear ointments should be continued. Other causes of decreased tear production include radiation therapy, drug toxicity (sulfonamides, atropine, etodolac), chronic blepharoconjunctivitis, general anesthesia, orbital trauma, neurogenic, and congenital (Yorkshire Terrier, Pug) and, rarely, secondary to an endocrine disorder (hypothyroidism, diabetes mellitus, hyperadrenocorticism). Megavoltage radiation near the orbit resulted in KCS in 24% of dogs within 1 to 6 months of therapy secondary to direct destruction of glandular tissue.1 Medical therapy is solely supportive, including the application of artificial tear ointments (petroleum, lanolin, mineral oil base) and gels as frequently as possible. Sulfa-containing drugs are well known to decrease aqueous tear production, with 65% of patients having decreased tear production, 15% with clinical signs of KCS.2 Sulfonamides should be used with caution in small breeds, brachycephalic breeds, and those breeds predisposed to KCS. Stopping therapy at the onset of KCS may allow lacrimal function to return in some patients. An idiosyncratic reaction resulting in irreversible, absolute xerophthalmia has been demonstrated in a small percentage (0.0003%) of dogs receiving etodolac. Patients should have a normal Schirmer tear test result before treatment and should be monitored closely during therapy. Any decrease in tear test results warrants cessation of oral therapy and initiation of topical therapy. General anesthesia, especially with atropine as a premedication, dramatically decreases aqueous tear production that may persist for 24 hours.3 Many patients receive a topical lubricant before anesthesia but rarely afterward. A topical lubricating ointment should be applied at least every 4 hours for 24 hours following anesthesia to decrease ocular surface drying that may lead to corneal ulceration. Neurogenic KCS results from disruption of the parasympathetic fibers coursing with the facial and trigeminal nerves to the lacrimal gland. Clinical signs are similar to those of immune-mediated KCS, except that in these cases dysfunction is usually unilateral. If the lesion is near the pterygopalatine ganglion, the caudal nasal nerve will also be affected and a dry, crusty nose ipsilateral to the dry eye will be noted. Treatment is aimed at stimulating the denervated gland to secrete aqueous tears. Oral 4% pilocarpine (1 drop/4.4 kg PO q12h and increased slowly to effect) may be effective, although there is a fine line between a therapeutic and a toxic dose. Signs of toxicity include vomiting, diarrhea, and ptyalism. Treatment with topical lubricants and cyclosporine is also warranted. Increased tear clearance secondary to evaporation accounts for most cases of dry eye in the intensive care patient. Increased evaporation may be secondary to a tear lipid deficiency, lagophthalmos, or decreased reflex tearing. Meibomianitis, blepharitis, and conjunctivitis damage the meibomian glands or conjunctival goblet cells, resulting in instability of the tear film. Treatment with mucinomimetic preparations such as 1% to 2% methylcellulose or sodium hyaluronate will help restore tear film stability. Lagophthalmos is the inability to completely close the eyelids and may be a conformational (brachycephalic breeds, cicatricial ectropion, eyelid agenesis) or neurologic (facial or trigeminal nerve dysfunction, obtundation) disorder. The lack of a consistently complete palpebral reflex is diagnostic. With lagophthalmos, the tear film is exposed and rapidly evaporates, especially in the interpalpebral fissure. Obtunded animals frequently have decreased or absent palpebral reflexes and decreased reflex tearing, which further complicates the tear deficiency. Regardless of the cause, hourly application of an artificial tear ointment or gel is necessary. Left untreated, progressive corneal ulceration will ensue. Chronic cases (e.g., ventilator patients) may require a lateral temporary tarsorrhaphy.4 Only gold members can continue reading. 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Chapter 172 Ocular Disease in the Intensive Care Unit Steven R. Hollingsworth, DVM, DACVO, Bradford J. Holmberg, DVM, MS, PhD, DACVO KEY POINTS • Ocular disease is a common manifestation of systemic illness seen in critically ill patients. • Identification of ocular disease is completed by a thorough ophthalmic examination including indirect ophthalmoscopy, Schirmer tear testing, fluorescein staining, tonometry, and possibly cytologic studies, culture, or biopsy. INTRODUCTION Ophthalmic disease can be associated with or secondary to conditions that require a patient to be in a critical care facility. This chapter presents common ocular signs and discusses the appropriate interpretation of these signs and treatment of the ocular disease. BLEPHAROSPASM Blepharospasm is a nonspecific sign of ocular pain and may be associated with enophthalmos, elevation of the third eyelid, and spastic entropion. Both surface and intraocular disease can result in blepharospasm. The origin of ocular pain is determined by a thorough ophthalmic examination, including diagnostic tests such as fluorescein staining, Schirmer tear test evaluation, and tonometry. A topical anesthetic (e.g., 0.5% proparacaine) may facilitate examination by eliminating pain related to surface disease. RED EYE Veterinary clinicians will commonly encounter patients with a “red eye.” The redness represents new or congested blood vessels within the episclera, conjunctiva, or cornea. Episcleral vessels are stout, easily identifiable vessels that course perpendicular to the limbus and usually stop before reaching the limbus. Congestion of these vessels is associated most commonly with intraocular disease, specifically uveitis and glaucoma. However, with moderate to severe corneal disease these vessels may become engorged. Conjunctival blood vessels are extremely fine; without the aid of magnification individual vessels are difficult to identify. When vessels are engorged, a pink-red flush is observable. Mild conjunctival hyperemia may be apparent with intraocular disease, but moderate signs are consistent with surface disease (i.e., conjunctivitis or keratoconjunctivitis). Differential diagnostic considerations for conjunctivitis include infections (canine distemper virus, feline herpes virus, feline Chlamydophila, leishmaniasis, onchocerciasis), allergies, postradiotherapy conditions, keratoconjunctivitis sicca (KCS), and exposure. Diagnosis is based on history and Schirmer tear test, fluorescein staining, cytologic studies, and biopsy results. Conjunctival hyperemia can be easily confused with a conjunctival or subconjunctival infiltrate. This infiltrate may be fluid (chemosis) or cells. Mild chemosis is common with conjunctivitis. Severe chemosis may obstruct visualization of the cornea and intraocular structures. The most common cause of primary chemosis is topical toxicity (from neomycin, atropine, caustic agents). Removing the toxin and treating supportively will allow resolution of signs. Rarely, intravenous fluid overload at a rate of 2 to 3 times maintenance for a period of 2 days or longer can result in marked chemosis. Tapering the fluid rate will allow the chemosis to resolve. Subconjunctival infiltrates may cause the conjunctiva to appear thickened. They may be focal or diffuse. Carefully examining the color of the conjunctiva may help differentiate an infiltrate from common hyperemia. A diffuse yellow appearance of the conjunctiva in the absence of thickening is consistent with icterus. This may be the first clinical sign of icterus and should prompt the clinician to pursue further diagnostic tests concerning hepatobiliary status. Neoplastic cells within the subconjunctiva frequently result in thickening and a yellow to orange hue. Lymphoma is the most common neoplasia presenting in the subconjunctiva and may represent the primary tumor site. Other masses observed in the subconjunctiva include systemic histiocytosis (orange), hemangiosarcoma (red), melanoma (brown), and granulomatous scleritis (pink). A definitive diagnosis can usually be obtained by biopsy. Light sedation and topical anesthesia are typically all that is needed to obtain a diagnostic sample. Subconjunctival hemorrhage in a critically ill patient, observed as petechiae or ecchymoses, warrants investigation for an underlying coagulopathy. Hemorrhage may be isolated to the subconjunctiva or seen in the anterior chamber (hyphema). Causes of hemorrhage not associated with a coagulopathy include trauma, strangulation (choke collars), and rarely constipation. A blue-green discoloration of the sclera and/or conjunctiva may be observed. This has been observed in dogs receiving mitoxantrone chemotherapy. Signs are temporary and usually resolve within hours to days after cessation of treatment. TEAR FILM ABNORMALITIES The tear film is comprised of three layers: an outer lipid layer, middle aqueous layer, and an inner mucin layer. A deficiency in any of these components may result in decreased tear production or increased tear clearance (evaporation) and may be diagnosed with a Schirmer tear test. Clinical signs of a tear film abnormality depend on the severity, chronicity, and underlying cause of the tear deficiency. The most consistent and obvious finding is a thick mucoid discharge, commonly accumulated on and around the eyelids. Additional clinical signs include conjunctival hyperemia, a lackluster appearance to the corneal surface, and in chronic cases corneal vascularization and melanosis. Chronic tear film deficiencies lead to thickening of the corneal epithelium, and therefore ulceration is not common. However, the critically ill patient may develop acute KCS resulting in rapid, severe, and potentially globe-threatening corneal ulcers. There are numerous causes of decreased tear production (KCS) and increased tear clearance. Undoubtedly the most common cause of KCS is immune-mediated destruction of the lacrimal gland and gland of the third eyelid. This will likely be a preexisting disease in critically ill patients. Treatment with topical cyclosporine and artificial tear ointments should be continued. Other causes of decreased tear production include radiation therapy, drug toxicity (sulfonamides, atropine, etodolac), chronic blepharoconjunctivitis, general anesthesia, orbital trauma, neurogenic, and congenital (Yorkshire Terrier, Pug) and, rarely, secondary to an endocrine disorder (hypothyroidism, diabetes mellitus, hyperadrenocorticism). Megavoltage radiation near the orbit resulted in KCS in 24% of dogs within 1 to 6 months of therapy secondary to direct destruction of glandular tissue.1 Medical therapy is solely supportive, including the application of artificial tear ointments (petroleum, lanolin, mineral oil base) and gels as frequently as possible. Sulfa-containing drugs are well known to decrease aqueous tear production, with 65% of patients having decreased tear production, 15% with clinical signs of KCS.2 Sulfonamides should be used with caution in small breeds, brachycephalic breeds, and those breeds predisposed to KCS. Stopping therapy at the onset of KCS may allow lacrimal function to return in some patients. An idiosyncratic reaction resulting in irreversible, absolute xerophthalmia has been demonstrated in a small percentage (0.0003%) of dogs receiving etodolac. Patients should have a normal Schirmer tear test result before treatment and should be monitored closely during therapy. Any decrease in tear test results warrants cessation of oral therapy and initiation of topical therapy. General anesthesia, especially with atropine as a premedication, dramatically decreases aqueous tear production that may persist for 24 hours.3 Many patients receive a topical lubricant before anesthesia but rarely afterward. A topical lubricating ointment should be applied at least every 4 hours for 24 hours following anesthesia to decrease ocular surface drying that may lead to corneal ulceration. Neurogenic KCS results from disruption of the parasympathetic fibers coursing with the facial and trigeminal nerves to the lacrimal gland. Clinical signs are similar to those of immune-mediated KCS, except that in these cases dysfunction is usually unilateral. If the lesion is near the pterygopalatine ganglion, the caudal nasal nerve will also be affected and a dry, crusty nose ipsilateral to the dry eye will be noted. Treatment is aimed at stimulating the denervated gland to secrete aqueous tears. Oral 4% pilocarpine (1 drop/4.4 kg PO q12h and increased slowly to effect) may be effective, although there is a fine line between a therapeutic and a toxic dose. Signs of toxicity include vomiting, diarrhea, and ptyalism. Treatment with topical lubricants and cyclosporine is also warranted. Increased tear clearance secondary to evaporation accounts for most cases of dry eye in the intensive care patient. Increased evaporation may be secondary to a tear lipid deficiency, lagophthalmos, or decreased reflex tearing. Meibomianitis, blepharitis, and conjunctivitis damage the meibomian glands or conjunctival goblet cells, resulting in instability of the tear film. Treatment with mucinomimetic preparations such as 1% to 2% methylcellulose or sodium hyaluronate will help restore tear film stability. Lagophthalmos is the inability to completely close the eyelids and may be a conformational (brachycephalic breeds, cicatricial ectropion, eyelid agenesis) or neurologic (facial or trigeminal nerve dysfunction, obtundation) disorder. The lack of a consistently complete palpebral reflex is diagnostic. With lagophthalmos, the tear film is exposed and rapidly evaporates, especially in the interpalpebral fissure. Obtunded animals frequently have decreased or absent palpebral reflexes and decreased reflex tearing, which further complicates the tear deficiency. Regardless of the cause, hourly application of an artificial tear ointment or gel is necessary. Left untreated, progressive corneal ulceration will ensue. Chronic cases (e.g., ventilator patients) may require a lateral temporary tarsorrhaphy.4 Only gold members can continue reading. 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