Recovery from anesthesia after nonocular surgery with loss of vision is a devastating experience for both the patient and health care provider. The incidence of perioperative vision loss in nonocular surgeries is lowest for appendectomy 0.12/10,000 and can be as high as 8.64/10,000 following cardiac surgeries.1 In a retrospective study of 501,342 noncardiac surgeries, only 4 patients (0.0008%) developed vision loss for longer than 30 days without direct surgical trauma to optic or cerebral tissues (2 ischemic optic neuropathies and 2 occipital infarctions).2
The most common site of permanent injury to the visual pathways for nonocular surgeries under general anesthesia is one or both optic nerves, with ischemia postulated to be the causal mechanism. Anterior ischemic optic neuropathy is more prevalent among cardiac surgery patients, which manifests as disc edema upon funduscopic examination.2 Posterior ischemic optic neuropathy will usually result in a normal acute funduscopic examination and is most likely to occur in patients who undergo spine and neck procedures.2
Occipital seizures can result in visual symptoms or vision loss and may be an ictal or postictal phenomenon.3 Visual symptoms of occipital seizures may include the sensing of bright colors, dark rings, spots, or simple continuous geometric forms as well as flashing or visual hallucinations. In contrast, ictal or postictal vision loss usually appears at the onset of occipital seizures and before the other visual manifestations occur. The duration of vision loss from occipital seizures can vary from minutes to days, with vision loss potentially becoming permanent if treatment is delayed.1,4 We describe a patient who awakened with postoperative vision loss and experienced occipital seizures after a Whipple procedure.
Consent for Publication
The local IRB reviewed the case report and gave permission to the authors for publishing this report. Written consent was obtained from the patient.
A 71-year-old woman with pancreatic adenocarcinoma presented for pancreatoduodenectomy (Whipple procedure).The patient’s medical history included chronic hypertension controlled with amlodipine, asymptomatic bilateral carotid stenosis of 30% to 40% (diagnosed within the preceding year), and complex partial seizures during the past 5 years that were pharmacologically well controlled by phenytoin ER (extended release) 100 mg every 8 hours. The patient reported only one seizure episode during the past 5 years that occurred 1 year ago without leaving any neurologic deficits. The patient had no recollection of that event. She was told the seizure activity lasted for only a few minutes during which time she displayed typical automatisms such as lip smacking. A recent ophthalmologic checkup was unremarkable, and the patient was able to read with eyeglasses and denied any history of vision loss or glaucoma/retinal problems.
Preoperatively the patient’s vital signs and preoperative laboratory values were within normal limits (blood pressure: 132/82 mm Hg, pulse rate: 76/min) and had normal blood counts and chemistry panel levels on the day of surgery (hemoglobin: 10.8 g/dL, hematocrit: 34.5%). The patient was continued on her daily maintenance dose of phenytoin ER, she took her regularly prescribed dose the morning of surgery, and she was given a subsequent dose of phenytoin as scheduled after 8 hours of her morning dose. Following informed consent, midazolam 2 mg IV and fentanyl 50 μg IV were given. Preoperatively, an epidural catheter was placed at T5/T6 level without any complications. Following a test dose injection of 1.5% lidocaine with 1:200,000 epinephrine 5 mL through the epidural catheter, no signs of systemic toxicity were noticed. A solution of bupivacaine 0.075% plus fentanyl 5 μg/mL was administered intraoperatively through epidural catheter at 10 mL/h. A bolus of 10 mL was given through epidural catheter after anesthetic induction and before surgical incision.
In the operating room, standard American Society of Anesthesiologists monitors were placed; anesthesia was induced with etomidate 16 mg, fentanyl 250 μg, and vecuronium 10 mg; and the trachea was orally intubated with a 7-mm cuffed endotracheal tube. Induction of anesthesia and intubation were uneventful, and there were only 2 brief episodes of hypotension intraoperatively. The lowest blood pressure (86/48 mm Hg) was treated with phenylephrine 40 μg IV and intravenous lactated Ringer’s solution. Total estimated blood loss was 850 mL; total fluid input was 4500 mL of lactated Ringer’s solution, 1000 mL of 6% hetastarch, and 2 units of packed red blood cells. Intraoperatively, end-tidal CO2 ranged from 31 to 36 mm Hg, pH from 7.35 to 7.41, Pao2 from 386 to 392 mm Hg, and Paco2 from 39 to 41 mm Hg. At the end of the case, tactile assessment of the train-of-four (TOF) response to ulnar nerve TOF stimulation showed a fade. Muscle relaxation was reversed with neostigmine 4 mg and glycopyrrolate 0.4 mg. TOF ratios before and after administration of reversal drugs were >0.7 and >0.9, respectively. The patient was responding to verbal commands before the removal of the endotracheal tube with Sao2 values of 99% on facemask after extubation.
In the postanesthesia care unit, the patient complained of vision loss in both eyes. The patient denied having headache, eye pain, weakness or numbness in arms and legs; had no limb tingling or slurred speech; and was awake, alert, and oriented. Neurology and ophthalmology consultations were immediately obtained and documented normal pupillary light reflexes and funduscopic examinations; however, the patient had no perception of light. On physical examination, visual acuity in both eyes was limited. The patient’s mental status, coordination, cranial nerve function, motor function, deep tendon reflexes, and serum concentrations of hemoglobin, hematocrit, and electrolytes were all unremarkable. A magnetic resonance angiogram of the head and neck without contrast showed a hypoplastic distal right vertebral artery with no significant abnormality. Magnetic resonance imaging of the brain without contrast showed no acute infarct.
The patient was transferred to the intensive care unit (ICU) for observation and further workup. The patient displayed fluctuating level of alertness, with episodic conjugate deviation of the eyes inferiorly to the left, along with jerky eye movements, suggesting a possibility of seizure occurrence. An EEG showed a 2.5-minute event of medium voltage, 3 Hz, sharp and wave complexes over the right frontotemporal and occipital areas. This seizure activity was considered epileptiform in nature. The free serum phenytoin concentration was subtherapeutic (<0.5 µg/mL, normal range 10–20 μg/mL).Therefore, the dose of phenytoin was increased to 100 mg every 8 hours, and treatment with levetiracetam (Keppra) was started (loading dose 750 mg, maintenance doses 500 mg every 12 hours). This treatment resulted in resolution of her seizure activity on EEG, resolution of her jerky eye movements, and gradual recovery of her vision to baseline per ophthalmological examination over the following 3 days.
The patient’s fluctuating level of alertness, as well as the episodic conjugate deviation of her eyes inferiorly to the left, along with jerky eye movements suggested the possibility of seizure and prompted an EEG in the ICU. Visual field defects are rarely associated with epilepsy; occipital seizures constitute only 8% of total seizures in the epileptic population.5 Visual hallucinations are the most common manifestation of occipital lobe epilepsy.6 In the Montreal Neurological Institute series, almost 75% of the patients with occipital lobe epilepsy had visual auras. However, other studies have reported a lower frequency.6
We excluded other potential causes of vision loss in our patient. Because portal vein reconstruction had been performed, cerebral embolism had to be ruled out. Magnetic resonance imaging and magnetic resonance angiogram of the head without contrast revealed no acute infarctions or changes. The arteries of the posterior circulation showed good flow and did not suggest that there might be reduced blood flow to the occipital lobes. Local anesthetic toxicity can also result in seizures. The patient did not exhibit signs of central nervous system toxicity following epidural injection of a test dose of local anesthetic after placement of the epidural catheter. An ophthalmologist evaluated the patient and found no apparent pupillary defect or changes suggestive of central retinal artery occlusion or optic disc swelling or atrophy.
There are several factors that can increase the chance of seizure activity in patients with a known seizure disorder, including changes in antiepileptic drug levels, fatigue, stress, sleep deprivation, menstruation, electrolyte disturbances, and excessive alcohol intake.7,8 Several situations arise in the perioperative period that can influence antiepileptic drug levels, including preoperative medication noncompliance, changes in dosing schedule, and altered gastrointestinal absorption and motility. Decreased antiepileptic drug serum levels may contribute to perioperative seizure activity.8 The free phenytoin level was well below therapeutic range indicating previous noncompliance. In our case, the patient had seizure activity that started intraoperatively or in the postanesthesia care unit; however, EEG seizure activity was noticed in the ICU where further workup was done.
A retrospective study examined the incidence of postoperative seizures in patients with epilepsy undergoing general anesthesia and reported that seizures were observed in 2% of the patients and that there were no adverse effects occurring after cessation of general anesthesia.9 In a 6-year retrospective study from 2002 to 2007 of 641 patients with a documented seizure disorder, 22 (3.4%) patients experienced perioperative seizure activity.10 Among the 22 patients, 6 had documented subtherapeutic antiepileptic levels. The incidence of seizures did not appear to be affected by the type of anesthesia or surgical procedure.10 In our patient, the free phenytoin level was subtherapeutic (<0.5 μg/mL); this likely contributed to her postoperative seizure activity.
The duration of postictal blindness has been reported to vary from <1 minute up to a period of several days (status epilepticus amauroticus) and, in some instances, can become permanent.4 Incidence of ictal blindness varies depending on the etiology and ranges from 0.3% to 1% after a diagnostic angiogram and can be as high as 15% in patients with preeclampsia.11 The onset of ictal blindness in adulthood nearly always indicates symptomatic epilepsy,12 whereas, in children, it is usually a manifestation of benign occipital epilepsy.13 Vision loss is usually sudden in onset, bilateral, symmetrical, and can be severe up with to limited or no light perception, with eye movements, pupillary reflex, and funduscopic examination appearing normal. Because the possible causes of cerebral blindness are numerous, it is important to rule out any nonorganic cause of blindness by using an optokinetic nystagmus and mirror test that can be quickly performed at bedside.14
Our patient’s seizure-related blindness is a rare but well-documented cause of bilateral loss of vision. The mechanism of seizure-related blindness is hypothesized to be due to either neurotransmitter depletion or active inhibition of the visual cortex. This blindness may be associated with encephalopathy, neurobehavioral abnormalities, and vertical gaze palsy. None of these were present in our patient. Fortunately, most patients with postoperative blindness associated with occipital seizure activity will recover their vision within 48 hours. Patients who develop status epilepticus postoperatively may, however, develop occipital lobe anoxia and permanent vision loss.15
Unexplained postoperative blindness may be an epileptic phenomenon. Even persistent postoperative blindness may represent status epilepticus amauroticus. An EEG evaluation should be included in the workup of all patients who present with acute postoperative blindness and in whom the cause remains ambiguous. Therapeutic serum concentrations of antiepileptic medications should be confirmed preoperatively.
Special thanks to Dr Mark Warner, MD, Mayo Clinic Rochester, MN (Former ASA President), for reviewing our case report.
Name: Lakshman Gollapalli, MD.
Contribution: This author helped write the manuscript.
Name: Aashish J. Kumar, MD.
Contribution: This author helped write and edit the manuscript.
Name: Kunal Sood, MD.
Contribution: This author helped edit and proofread the manuscript.
Name: Rudram Muppuri, MD.
Contribution: This author helped write the manuscript.
This manuscript was handled by: Hans-Joachim Priebe, MD, FRCA, FCAI.
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