Corneal abrasion.
Corneal abrasion management: Although prevention is preferable to treatment, most corneal abrasions heal spontaneously within 48 hours without sequela. Ophthalmological treatment may consist of antibiotic drops (to prevent bacterial infection), topical analgesics, lubricants, or patching of the affected eye. Deeper abrasions or abrasions that become frank corneal ulcerations may cause scarring and permanent visual impairment and require consultation.
Blurry vision: Blurry vision after surgery is common. This may be caused by the purposeful installation of lubricants onto the surface of the eye to retard drying or from the pharmacological effects of perioperative medications upon focus and ocular accommodation. A scopolamine patch applied prior to surgery for prophylaxis against postoperative nausea and vomiting may be causative, but many perioperative medications may affect vision. Blurred vision occurring in a patient with a history of diabetes mellitus or pancreatic surgery warrants exclusion of acute hyperglycemia.
Blurry vision lasting more than 3 days occurs at approximately 1 in 20,000 patients when measured retrospectively,[1] but many patients may not report visual changes so retrospective databases may underestimate the incidence. When followed prospectively, 28 of 671 patients (4.2%) had blurred vision lasting at least 3 days after various surgical procedures, with most of the affected patients having resolution at 1 to 2 months.[4] For the patients in this study with blurred vision at 3 days, 25% still had changes at 18 months and required either new or different corrective lenses. The etiology of persistent visual changes after non-ophthalmological surgery is poorly understood. Treatment is supportive care with particular focus on preventing a sedated patient from causing ocular injury by eye rubbing. Persistent blurry vision lasting more than a few days may require consultation.
Anisocoria: Unequal pupil size (if not present prior to surgery) and eye pain may be acute glaucoma, a true ophthalmological emergency. Medications with anticholinergic effects may precipitate closed angle glaucoma. The pupil in the affected eye is typically mid-range size and poorly or non-reactive to light. In addition to pain and blurry vision, the patient may experience severe headache, nausea and vomiting, or loss of peripheral vision, or may see a halo around light sources. Treatment requires urgent ophthalmological consultation.
Inflammation: Inflammation of the cornea (keratitis) or cornea and conjunctiva (keratoconjunctivitis) has a variety of etiologies, but when it occurs acutely after surgery it is typically secondary to installation of irritant substances into the eye. Many substances may be inadvertently splashed into the eye, with acidic or alkaline substances having the greatest potential to cause irritation. Skin preparations including alcohol-based compounds and chlorhexidine can cause chemical keratitis when applied around the face if pooling is allowed to occur around the eye. Povidone–iodine (Betadine) is relatively innocuous when in contact with the eye. Treatment requires consultation.
Seeing red: An unusual ocular injury is hemorrhagic retinopathy (Valsalva retinopathy) caused by forceful exhalation against closed glottis causing the affected individual to see “red.” This may also occur from “bucking” during mechanical ventilation if the patient attempts to exhale while a mandatory positive pressure breath is being delivered. Fundoscopic examination will reveal hemorrhage and the lesion should be suspected for patients complaining of “seeing red” or reddish discoloration of vision after general anesthesia. Ophthalmological consultation is prudent, but treatment is usually supportive.
Diplopia: Diplopia (double vision) may occur after surgery. Residual neuromuscular blockade may interfere with extraocular muscle movement, causing diplopia. Aggressive hydration with crystalloid solutions has been implicated in transient postoperative diplopia in cardiac surgery patients.[5] Diplopia in a single eye is indicative of an ocular cause (retinal detachment, lens dislocation), and treatment requires ophthalmological consultation. Diplopia in both eyes suggests an extraocular muscle etiology. Raising the head of the bed to facilitate edema resolution and ensuring adequate neuromuscular blockade reversal is adequate for most patients.
Blindness: Transient blindness may occur from systemic absorption of glycine used in irrigation solutions during transurethral prostate resection or procedures on the uterus, since glycine acts as an inhibitory neurotransmitter of the retina. Treatment is supportive and includes correction of other electrolyte abnormalities that may accompany irrigation solution absorption. Permanent blindness may occur after surgery owing to damage to the eye, optic nerve, or visual cortex of the brain. Cortical blindness has occasionally been reported owing to embolic cerebrovascular accident,[6–10] and patients may present with bilateral blindness without visual abnormalities of the external eye or retina. Patients with cortical blindness may not report their blindness and may deny being blind when questioned.
Central retinal vein or artery occlusion may occur after surgery, particularly if pressure is exerted upon the globe during the procedure. Procedures performed in prone or lateral position carry increased risk. Often there may be signs of external ocular trauma.[11,12] Although the eyes are vulnerable to compression injury any time the procedure is performed in other than supine position, direct ocular compression is an atypical cause of postoperative blindness.
Most postoperative visual loss (POVL) is due to injury of the optic nerve. The etiology is still incompletely understood, but disturbances in nerve perfusion appear to be responsible. Anterior ischemic optic neuropathy (AION) occurs within the intraorbital portion of the optic nerve. Perioperative AION is most commonly seen after procedures requiring cardiopulmonary bypass and among patients with risk factors for vascular disease. It is typically monocular and only a portion of the visual field may be affected. Although pressure on the globe could theoretically be causal, AION is most often seen after surgery in the supine position. Perioperative posterior ischemic optic neuropathy (PION) occurs because of ischemia of the optic nerve after it has exited the orbit. Spine surgery in the prone position is particularly high risk. Pressure on the globe is not believed to be able to cause PION. The American Society of Anesthesiologists Task Force of Postoperative Visual Loss found no evidence to implicate pressure on the globe as causing perioperative AION or PION, although it is a substantiated risk factor for central retinal artery occlusion.[13] Compared with AION, patients experiencing PION tend to be younger, healthier, and undergoing procedures that are longer and associated with greater blood loss. However, hypotension and anemia do not seem to be causative,[14] and disturbances in microperfusion and venous drainage from intravascular volume expansion may be associated. Although spine surgery in the prone position and cardiac procedures requiring cardiopulmonary bypass are considered higher risk, POVL may occur after any surgical procedure, and there is some more recent evidence that total hip replacement and, to a lesser extent, total knee replacement procedures also carry increased risk for visual loss.[15]
Retinal changes may be seen fundoscopically earlier in the course of AION than PION. Treatment of POVL requires ophthalmological consultation, and cases of POVL occurring in the United States should be reported to the ASA POVL Registry (http://depts.washington.edu/asaccp/projects/postoperative-visual-loss-registry).
Posterior reversible encephalopathy syndrome (PRES) is a rare syndrome characterized by visual loss associated with headaches, confusion, and seizures. Magnetic resonance imaging reveals edema in the occipital lobes and sometimes parietal lobes and pons. PRES is classically associated with malignant hypertension and eclampsia, but has been associated with nephrotic syndrome, immunosuppressant medications used in organ transplantation (especially cyclosporine and tacrolimus), sepsis, and systemic lupus erythematosus.[16] The incidence and exact pathophysiology of PRES is not known, but there have been an increasing number of reports of PRES presenting in the PACU in both print literature and presentation at national anesthesiology meetings. Several of these early reports have occurred in patients with seemingly mild elevations of systemic blood pressure. Visual disturbance associated with altered mental status and seizures should raise suspicion for PRES. While a CT scan without contrast may be clinically appropriate to exclude subarachnoid hemorrhage, it is important to note that the CT scan is normally unremarkable in patients with PRES. Magnetic resonance imaging should be obtained. Blood pressure reduction of 20% to 25% is indicated when PRES is identified. Short-acting agents that can be administered by intravenous infusion (see Chapter 3) and continuous blood pressure monitoring by arterial line should be instituted.
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