Dr Leonid Skorin Jr
OD DO MS FAAO FAOCO
Chronic ocular pain can arise as a result of a variety of aetiologies. Pathology such as neovascular glaucoma, end stage glaucoma, intraocular tumour, corneal ulcer and trauma are all possible causes of chronic ocular pain. To alleviate the patient’s pain, one must first determine its cause. The patient’s description of the discomfort can help determine the cause or causes.
Patients who describe their pain as superficial are typically suffering from pathology of the cornea or conjunctiva.1 Superficial pain is often described as sharp or shooting. Those who describe their pain as deeper in nature are often suffering from pain that may also originate from the cornea, but more likely stems from pathology of deeper structures such as the sclera, iris, ciliary body, orbital muscles or the sinuses.1 Deeper pain is usually described by the patient with adjectives like ‘dull’,’ constant’ and ‘aching’.
If after a thorough ophthalmic examination—including intraocular pressure assessment, and anterior and posterior segment evaluation—the cause of ocular pain is not clear, imaging may be required to elucidate the cause.
OCT scans of the orbit may be used to investigate possible orbital wall fracture or foreign body. Magnetic resonance imaging may be used to look for soft tissue causes such as retrobulbar swelling or orbital tumour.
The sensation of pain from the orbit is carried through branches of the trigeminal nerve, specifically those of the ophthalmic division. With the trigeminal nerve’s broad coverage throughout the facial region, it is possible that pain experienced in the orbit is of a referred origin. The ophthalmic division of the trigeminal nerve contains three of its own major branches: the frontal, lacrimal and nasociliary.
These branches decussate posterior to the extraocular muscle cone and anterior to the trigeminal ganglion. The frontal branch provides innervation to the upper eyelids, superior orbital rim and scalp areas. The lacrimal branch provides innervation to the lacrimal gland, as well as to the conjunctiva and the lateral aspect of the upper eyelid. The nasociliary nerve innervates the cornea, the lower eyelids and portions of the skin of the nose.2 The latter distribution is the anatomy behind Hutchinson’s sign in herpes zoster ophthalmicus.
A 94-year-old female presented to our clinic complaining of extreme ocular pain in her right eye that had awoken her two nights prior to her visit. She had been self-medicating with ice packs and extra strength acetaminophen, but said that these were no longer effective.
Her ocular history was positive for wet age-related macular degeneration in her right eye including a prominent disciform scar resulting in severe vision loss. She was pseudophakic in both eyes, and had been followed as a glaucoma suspect. Her medical history was unremarkable aside from an allergy to sulfa medications.
Her entering visual acuities were finger counting at three meters in her right eye and 6/6 in her left eye. Initial intraocular pressure in her right eye was 60 mmHg as measured with Goldmann applanation tonometry. Slitlamp examination of the right eye revealed normal lids and lashes, diffuse injection of the bulbar conjunctiva, diffuse corneal oedema, deep and quiet anterior chamber, a stable posterior intraocular lens, neovascularisation of the iris and ectropion uveae. Examination of the left eye yielded normal findings of all structures. Gonioscopy could not be performed at this time as the corneal oedema would not allow for visualisation of the angle structures.
Dilated fundus examination revealed evidence of widespread blot haemorrhages in all quadrants of the right eye. Detailed examination was difficult due to corneal oedema, and as such, no information of the optic nerve health could be attained at this time.
It was suspected that our patient had recently suffered an ischaemic central retinal vein occlusion in the right eye, which the patient had not noticed due to her previously noted profound acuity reduction in this eye. The ischaemic central retinal vein occlusion then resulted in neovascular glaucoma with significantly increased intraocular pressure.
Pharmacologic attempts to reduce pressure using brimonidine 0.1% were unsuccessful. Due to the patient’s sulfa allergy, oral acetazolamide tablets could not be administered. The patient was referred to the emergency room to receive an intravenous mannitol solution at a dose of one gram per kilogram of body weight, given over the course of 45 minutes. Mannitol and topical pharmacologic attempts to lower the patient’s intraocular pressure were unable to yield safe and comfortable pressure levels.
Panretinal photocoagulation laser therapy was performed, but extensive haemorrhaging blocked much of the retinal tissue, limiting the effectiveness of the procedure. After multiple return visits, the patient’s ocular pain had not subsided and her intraocular pressure continued to be in the 50 mmHg range. At this point cryotherapy, enucleation, and retrobulbar alcohol injection were presented as further treatment options. Our patient decided to undergo retrobulbar alcohol injection.
Retrobulbar alcohol injection
A retrobulbar needle was used to administer a 1% lidocaine solution with 1:100,000 epinephrine into the muscle cone. The injection was done into the lateral third of the lower lid just superior to the inferior orbital rim. To ensure correct application, the needle was directed as close to the back of the globe as possible. A total of 2 ml of the anaesthetic was initially injected into the retrobulbar space. Anaesthetic is injected first to prevent the severe burning sensation that a patient would otherwise experience from the injection of absolute alcohol.
After the anaesthetic injection, a pause of five minutes was observed to allow full anaesthetic effect. During this time, the syringe containing the anaesthetic was detached, but the needle position was not altered (Figure 1). After the five minute period, a separate syringe containing 2 ml of absolute alcohol was attached to the previously placed needle, and the alcohol was injected (Figure 2). Gentle pressure was then applied over the globe for two minutes, to help distribute the medication.
Figure 1. Retrobulbar needle in place after anaesthetic injection, prior to absolute alcohol administration
Figure 2. Delivery of absolute alcohol to the retrobulbar space
On the day of this procedure the patient had reported that her pain level was ‘nine out of 10’. The following day, the patient noted that her pain level was ‘five out of 10’. Two days after the injection the pain had subsided to a reported ‘two out of 10’. At a follow-up appointment nine weeks after the injection, the patient reported that she was happy with the results of the retrobulbar injection She reported that about once every week she would have a flare-up of ocular pain and would need a dose of acetaminophen, but that on a day-to-day basis she had been almost pain free, with a reported pain level of one out of 10.
A variety of treatment approaches for chronic severe ocular pain secondary to elevated intraocular pressure exist (Table 1). The most drastic of these treatment approaches is enucleation, which is reserved as a final measure; however, even this does not ensure resolution because pain persists in as many as seven per cent of patients after enucleation.3
|Table 1. Treatment options for severe chronic ocular pain secondary to neovascular glaucoma
Less invasive techniques come by way of retrobulbar injections. The main pharmacologic agents used in these situations are absolute alcohol 97% and chlorpromazine at a dose of 25 mg/mL.4,5
Oral pain medications are often not effective. Even when they are effective, these medications often lose their efficacy as the chronicity of the condition drags on.
Panretinal photocoagulation is a first line therapy for neovascular glaucoma. The process works by destroying retinal tissue with argon or diode laser. Destruction of tissue decreases the oxygen requirement of the retina, thereby decreasing the release of vascular endothelial growth factor, which decreases the amount of neovascularisation in the anterior chamber angle. Cyclocryotherapy is effective at decreasing ocular pressure by destroying the ciliary processes, which are responsible for aqueous humour production.
Retrobulbar alcohol injections have been used in the management of pain in blind eyes since the early 1900s.4,5 Alcohol achieves analgesia, through nerve cell destruction via phospholipid and cholesterol extraction as well as precipitation of mucoprotein and lipoprotein.1
Alcohol does not work by diffusion, which can both help and hinder the outcome. This helps the outcome in that it reduces unwanted destruction of neighbouring structures. The lack of diffusion creates a challenge in that it requires the injection to be given in close proximity to the targeted nerves for full destruction.1 If the nerves are not sufficiently destroyed, they will regenerate earlier and bring back the symptoms of pain.3-5 Successful injections have been shown to provide pain relief for up to two years, with 20-87 per cent lasting for at least three months.3-5
Retrobulbar injection of chlorpromazine
Another medication that can be administered via retrobulbar injection is the phenothiazine anti-psychotic mediation chlorpromazine. Chlorpromazine is thought to cause anaesthesia by cell lysis and/or membrane stabilisation.1,4,5 Chlorpromazine injection has been proposed to have a efficacy of 80 per cent to 90 per cent and to possess a longer duration of relief than alcohol injection.6 The most notable advantage of chlorpromazine over other treatment methods is in the treatment of seeing eyes. Chlorpromazine has become the treatment of choice for treating pain in eyes that have useful vision. One study showed that 50 per cent of patients with seeing eyes that underwent chlorpromazine injection retained vision after injection.6
Alcohol and chlorpromazine injections have similar potential side-effects. Both medications carry the risk of eyelid oedema, conjunctival chemosis, external ophthalmoplegia, cellulitis and blepharoptosis.1,4,5 Retrobulbar alcohol injections also carry the risk of neurotrophic keratopathy. Chlorpromazine injections carry additional risk of nausea, vomiting, brief loss of consciousness and fat necrosis.1 It is also possible for patients receiving chlorpromazine injection to experience transient loss of vision due to membrane stabilising effects on the optic nerve.1,4,5
Retrobulbar injections have made the management of both seeing and non-seeing painful eyes less devastating. When a patient presents with this magnitude of misfortune, the idea of having an eye removed may be perceived as not a treatment, but as more misfortune. By having these retrobulbar injection options available for patients, we can set their minds at ease, and improve their quality of life.
- Kumar C, Dowd T, Hawthorne M. Retrobulbar alcohol injection for orbital pain relief under difficult circumstances: a case report. Annals Academy of Medicine 2006; 35: 260-265.
- Remington LA. Clinical Anatomy and Physiology of the Visual System, 3rd Ed. St. Louis, Missouri: Elsevier Butterworth Heinemann, 2012: 218-224.
- Custer PL, Reistad CE. Enucleation of blind, painful eyes. Ophthalmic Plastic and Reconstructive Surgery 2000; 16: 5: 326-329.
- Skorin L. Treatment for blind and seeing painful eyes. Optometry Today 2004; 44: 1: 34-36.
- Skorin L. Treatment for blind and seeing painful eyes. Audio-Digest Ophthalmology 2005; 43: 3.
- Chen TC, Ahn Yuen SJ, Sangalang MA, Fernando RE, Leuenberger EU. Retrobulbar chlorpromazine injections for the management of blind and seeing painful eyes. J Glaucoma 2002; 11: 209-213.