November 30, 2018 Conference
AM - Iatrogenic Complications - Neuro-ophthalmology and Oculoplastics
Retrobulbar and periocular hemorrhage is the most common complication of periocular anesthesia. Its incidence in the literature is reported between 0.03% and 3%, trending toward the lower aspect of this range (<1%) in the most recent large case series. Hemorrhage results from direct injury to vessels and although it is most commonly associated with retrobulbar and peribulbar blocks, it is also reported more rarely in blunt cannula sub-tenons blocks. Most hemorrhages are venous in nature, mild, amenable to conservative treatment and not vision threatening. Arterial hemorrhages are rare but have more serious potential for vision loss if not treated appropriately. Rapid onset of proptosis, ecchymosis and dramatic elevation of intraocular pressure should raise suspicion for arterial hemorrhage and prompt immediate evaluation and treatment. Lateral canthotomy remains an important treatment intervention to relieve orbital compartment syndrome; its steps are reviewed. Newer, simplified releases are also discussed.
Optic nerve penetration is a rare but well-recognized complication of periocular anesthesia. Mechanisms of vision loss associated with the infiltration of anesthetic agents through the optic nerve sheath include traumatic optic neuropathy, ischemic optic neuropathy, and retinal vascular occlusion. There is also a risk of cardiovascular, respiratory, and mental status depression with diffusion of anesthetic agents into the subarachnoid space surrounding the brainstem. The aim of this talk is to demonstrate the imaging findings associated with iatrogenic optic nerve penetration, review data on treatment for vision loss and supportive care in cases of central nervous system depression, and discuss injection techniques to minimize the risk of optic nerve injury.
Diplopia after ophthalmic surgery, especially in cataract surgery, is an unexpected outcome for both patients and their surgeons. Many mechanisms causing diplopia have been explored, including periocular anesthesia. Extensive literature can be found on diplopia secondary to myotoxicity from the anesthetics themselves. Direct trauma to the extraocular muscles and cranial nerves from the needle injecting the anesthetic can also result in diplopia. Because of trajectory of the needle, a majority of diplopia, regardless of the mechanism, is vertical. A mixture of hypertropias and hypotropias are seen depending if the extraocular muscles or cranial nerves are involved. While the length of the needle has not been found to make a significant difference in reducing the outcome of diplopia, efforts to reduce the toxicity of the anesthetics and alternatives to periocular anesthesia can reduce this unwanted outcome.
"Doc, thanks for fixing my problem, but now I see double!"
The post-operative complaint of binocular diplopia is enough to ruin your day, and significantly alter you patient's perspective on the value of surgery just performed. This complication has probably been experienced by everyone attending this meeting.
We will cover some common causes of post- procedure diplopia seen after ophthalmic surgery with an emphasis on orbital plastic surgery. We will cover risks and causes, and interventions available to resolve these problems.
Through a series of referred cases, topics covered will be diplopia related to repair of orbital fracture, after removal of a mass in the superior orbit, after excision of an orbital dermoid, and post decompression in TED. The impact of poor monocular vision and monovision on the development of diplopia will be noted as well.
We will discuss strabismus management and addressing patient expectations.
The causes of new onset proptosis are wide-ranging, including infection, neoplasm, trauma, vasculitis, vascular abnormalities, idiopathic inflammation, and, most commonly, thyroid eye disease. New onset proptosis in the post-operative setting is less common and has a narrower differential diagnosis but can be an indication of a vision threatening or, in rare cases, even a life-threatening complication. During this talk we will briefly review causes of new onset proptosis, and more specifically discuss potential iatrogenic etiologies of new onset proptosis as well as strategies for avoiding and evaluating these scenarios.
Bony changes seen with chronic intracranial hypotension will be discussed. Alteration is the pressure gradient between the intracranial and orbital compartments results in bony remodeling with upward bowing of the orbital roof. Clinical consequences of these bony changes range from barely perceptible to sight threatening. Enophthalmos progresses as orbital volume increased. In extreme cases loss of contract between the eyelids and the cornea develops. Other abnormalities seen include abnormal ocular motility and optic atrophy. Recognition of such changes is important to allow for diagnosis and treatment prior to advanced clinical deterioration. Routine radiographic assessment of bony changes may allow for identification of patients with abnormal ICP prior to the development of clinically significant disease.
Blepharoptosis, or a drooping eyelid, has been long recognized as one of many unplanned consequences of therapeutic ophthalmic procedures. Case reports of iatrogenic blepharoptosis also exist as a result of non-ophthalmic procedures, as well as medications and contact lenses. The incidence varies with each procedure, but even as of 2018 the pathophysiology that leads to this ptosis is poorly understood. Based on a thorough search of the medical literature , this presentation will review the most common procedures that can result in iatrogenic blepharoptosis, as well as the theories of causation, such that the audience can be prepared to convey this information to their patients as part of the informed consent process and differentiate it from other causes of eyelid ptosis.
Ischemic optic neuropathies are traditionally categorized in several groups, with non-arteritic anterior ischemic optic neuropathy (NAION) representing anterior ischemic optic neuropathy of any variety so long as it is not related to giant cell arteritis (AAION). There are a number of recognized risk factors for NAION. Many intraocular procedures have been reported to trigger NAION; most focus has been on cataract extraction. Although the precise mechanism is debated, assessment of the temporal association has strongly supported a causal relationship. NAION following intraocular surgery is divided into two categories: immediate and delayed. The immediate type occurs within hours of surgery and is almost invariably associated with marked elevation in intraocular pressure (IOP). The delayed type occurs days to weeks following surgery with a less well understood pathophysiology. Delayed occurrences likely relate to inflammation with posterior pole edema, possibly with mechanical compression of tenuous optic disc vasculature. It has been estimated that upwards of 50% of patients, with a history of NAION, may develop NAION in the fellow eye following cataract extraction. With evolving surgical technique, and the progression from large scleral incision to smaller corneal incision, the inherent surgical trauma and in turn inflammation presumably is diminishing. In line with this, the incidence of intraocular surgery associated NAION may be in decline. However, with the potential devastating consequence of bilateral NAION, proceeding with caution when considering cataract extraction in patients with a history of NAION seems prudent and appropriate.
Eye removal surgery including enucleation and evisceration can provide tumor or infection control and relief from a blind painful eye. However, there are complications to be aware of when caring for patients with an anophthalmic socket. Placing an alloplastic or autogenous orbital implant is the primary method of ensuring adequate orbital volume, improving motility, and obtaining a natural appearance with an ocular prosthesis. Many materials have been used for orbital implants including silicone, porous polyethylene, hydroxyapatite, and autogenous dermis and fat. Implants can also be pegged and thereby directly connected to the prosthesis. Complications related to the implant are implant exposure or extrusion, infection, and migration. Lid malpositions including ptosis, entropion, and ectropion may also occur. Complications related to the conjunctivalized socket include dry socket, giant papillary conjunctivitis, conjunctival cysts, contracted socket, and neoplasia. Postenucleation socket syndrome refers to a constellation of findings in a socket with insufficient volume: deep superior sulcus, shallow inferior sulcus, ptosis, lower lid laxity, and enophthalmos of the ocular prosthesis.
The facial nerve is subject to injury that can be complete or partial, temporary or permanent, in a variety of surgical procedures ranging from something as banal as temporal artery biopsy, to a brow-lift, facial cancer resection, or up to the complexity of a craniotomy, etc. When branches affecting the closure of the eyelids are affected, the ocular surface is at risk of severe dessication with the potential for corneal ulceration and possible perforation. If additional cranial nerves are dysfunctional, such as trigeminal or oculomotor, the risks to the eye may be compounded by either a neurogenic cornea and / or a lack of a protective Bells phenomenon, respectively. Initial interventions are aimed at protecting the ocular surface in the short term; subsequently, in relation to the prognosis for motor recovery, additional interventions, including surgery, may be appropriate to improve function and cosmesis as much as possible. This presentation will review the current status of management of periocular facial nerve paresis.