Postoperative Visual Loss (POVL)
ION in Spine Cases?
Recently The Doctors’ Company has noted an increasing incidence in the number of claims involving postoperative blindness or severe visual impairment following spine surgeries in which controlled hypotension was utilized. One case, presented at a claims panel, involved a patient whose head was supported only by Halo tongs, excluding improper face padding as an etiology. Most of the cases involved an eventual ophthalmologic diagnosis of ischemic optic neuropathy. TDC presents the following discussion so that anesthesiologists are aware of this syndrome and understand current theories about its etiology and treatment.
The following two cases are composites, incorporating details from 12 similar claims:
A 32-year-old female, 5’4 and 218 lbs., was scheduled for posterior lumbar fusion at L3-S1. She was consented for general anesthesia with controlled hypotension. An arterial line was placed after light sedation. Anesthesia was then induced with propofol and maintained with desflurane, air and oxygen. She was placed face down on foam donuts and her face position was checked every 45 minutes as documented in the anesthesia record. Labetolol was used to keep the mean arterial pressure 50-55 mmHg for a 4-hour portion of the 8-hour case, and the systolic pressure was then allowed to rise to 100-120mmHg. Arterial blood gases taken several times during the procedure demonstrated mild metabolic acidosis which was treated each time with intravenous bicarbonate.
Estimated blood loss was 3500cc and this was replaced intraoperatively with 4 units of autologous blood and 8 liters of crystalloid. Postoperative hematocrit was 24.5%. On arising in the recovery room, the patient complained of “blurry vision.” Ophthalmologic consult was obtained and fundoscopic examination and MRI of the brain were normal. Visual field defects were noted bilaterally. Vision in both eyes had been normal preoperatively, but was initially 20/200 after surgery. Vision in the left eye improved over several days to 20/100 but the right eye remained severely impaired. The diagnosis was bilateral ischemic optic neuropathy.
A 42-year-old truck driver, 5’9 and 235 lbs., presented for spinal fusion with instrumentation and bone graft. Arterial line and CVP monitoring were used. After propofol induction, anesthesia was maintained with oxygen, nitrous oxide and Forane. He was placed in the prone position on a custom made foam face rest. During the 9-hour procedure, controlled hypotension was induced with hydralazine and labetolol keeping the mean blood pressure 50-60mmHg for 5 hours. Midway during this period, the arterial line “damped-out” and the automatic blood pressure cuff was cycled every 2 minutes for the remainder of the case.
Fluid replacement for the estimated 2750cc blood loss was 10 liters of crystalloid, 1 liter of colloid and 750cc of cell saver blood. Postoperative hematocrit was 26%. On awakening in the recovery room the patient stated he could not see. An ophthalmology consult confirmed no light perception bilaterally and the diagnosis of ischemic optic neuropathy was made. The patient never regained vision.
What is ION?
Ischemic optic neuropathy (ION) is the most frequently reported cause of postoperative visual loss following general anesthesia.1,2 Most anesthesiologists are aware that central retinal artery occlusion can follow improper head positioning with pressure on the eyes in the prone position. Not all anesthesiologists, however, are familiar with ION. Ischemic optic neuropathy results from an infarction of the optic nerve due to decreased oxygen delivery by one or more of the small arterioles supplying the nerve head.2,3 It has been reported following cardiopulmonary bypass, radical neck dissection, abdominal and hip procedures.2,3,6 In many of the cases, there was extensive blood loss and periods of hypotension, believed to be etiologic factors.2-6 Incidents of ION following spine surgery have been well documented in the literature.1,3-7
Postoperative ION may be unilateral or bilateral and includes symptoms ranging from no light perception to color vision deficits, visual field defects and decreased visual acuity.2,4,5 The diagnosis is not always apparent in the immediate recovery period. Most of the delays are caused by patients assuming the vision problems are a temporary part of normal recovery, or thinking that their eyes have been patched. A few patients with initially normal vision developed symptoms on postoperative days one through twelve.2,4,6 Ophthalmologic exams initially revealed swelling of the optic discs in some patients and were normal in others.2,3,6,8
What causes ION?
Contributing factors to the development of ischemic optic neuropathy in most postoperative cases reported are relative hypotension and anemia.1-6 A review in the anesthesia literature involving 6 patients who developed ION after general anesthesia found that all 6 had hemoglobin counts less than 8.0g/dl recorded at least once, and all had episodes of decreased mean blood pressure ranging from 24% to 46% of preoperative levels for extended periods of time.6 Brown et al concluded that “although severe anemia alone may not cause ION, even a short episode of hypotension in an already anemic patient may predispose that patient to ION-induced vision loss.”6 Some authors have speculated that the prone position itself may elevate central venous pressure by compressing the abdomen, indirectly retarding venous drainage through the ophthalmic veins.7 This might be exacerbated in obese patients. Keeping the head in a prolonged down-tilt position could also decrease venous outflow from the cranium, causing local capillary bed stasis in the eyes.7
Patient risk factors identified in some studies include the presence of hypertension, diabetes, atherosclerotic cardiovascular disease and smoking history, possibly due to preoperative abnormalities in the ophthalmic blood vessels.2-7 Another striking factor in many cases is the long operating room times, averaging nearly 7 hours in one series.4 Cases with long operating room times do tend to have greater blood loss and more prolonged periods of hypotension.
There is some evidence that ischemic optic neuropathy may occur more frequently in patients with congenitally small optic discs, possibly because the nerve fibers have less room to expand in response to hypoxia.2 Clearly there is still much to be learned about this syndrome. There are several possible contributing factors and the contribution of each of them, if any, is impossible to determine without further study.
What has changed?
Controlled hypotension for spine surgery has been used safely for decades. The mean blood pressures used in these cases are within well accepted limits of autoregulation. Why would the incidence of ischemic optic neuropathy be increasing suddenly? One possibility suggested is the changing thinking regarding transfusion. Since 1986, concerns about the spread of HIV have made recommendations regarding transfusion more conservative.2,5,6 In the past, a hemoglobin level of 10g/dl was the threshold used by many for intraoperative blood transfusion.5 More recently, the Transfusion Practice Committee of the American Association of Blood Banks recommends using 8g/dl, the National Institutes of Health Consensus Conference on Perioperative Blood Transfusion suggests 7g/dl, and the American College of Physicians recommends awaiting a deterioration in vital signs or the patient’s developing symptoms.
Patients are likely now to be maintained at lower average intraoperative hemoglobin levels than previously. As Brown et al concludes, “Current practice of lower acceptable hemoglobin concentrations associated with more extensive surgeries, and therefore greater potential for blood loss and hypotension, may be predisposing a larger portion of the anesthetic patient population to temporary or permanent vision loss than appreciated previously.”6 Other changes include the advent of newer anesthetic agents that may not be as effective cerebral dilators as agents popular in decades past.9 The agents commonly used to induce controlled hypotension have also changed in recent years. The impact of these changes has yet to be delineated.
What can be done to prevent it?
Obviously it is difficult to make risk management recommendations for a syndrome about which so much remains unknown. The anesthesia practices demonstrated in most of the cases of ischemic optic neuropathy are reportedly safe and well within current standards of care. Still, the unfortunate outcomes in these cases may prompt consideration of alternative techniques. The independent association of blood loss with development of ischemic optic neuropathy has led some authors to conclude that in longer spine surgeries perhaps transfusion practice should be more aggressive, utilizing cell saver or pre-donated autologous blood.2-4
In any given case the anesthesiologist, in conjunction with the surgeon, needs to carefully weigh the risks and benefits of the controlled hypotensive technique.1 Risk management suggestions include considering limiting periods of extreme controlled hypotension to crucial parts of the procedure and allowing the pressure to rise when increased blood loss is tolerable. Surgeons have suggested that staging might be appropriate for unusually long surgeries requiring multiple approaches.4 In arriving at an acceptable level of deliberate hypotension, it has been suggested that the patient’s resting blood pressure be used in deciding what percentage drop will be tolerable as opposed to using the same target pressure for each case.9
Special consideration should be given to deciding how much to lower the blood pressure of patients with pre-existing hypertension, atherosclerotic cardiovascular disease, diabetes mellitus or history of smoking. Once a blood pressure target has been determined by the anesthesiologist, an accurate arterial line reading during the hypotensive period can assure that the pressure does not drop below the acceptable value. Good documentation of periodic checks of the patient’s face to assure the absence of pressure against the eyes can help prove that every attempt was made to avoid elevating intraocular pressure.
There is some evidence that non-postsurgical ION treated early after diagnosis with pressors to aggressively raise blood pressure, volume replacement and transfusion can result in at least partial restoration of vision.1,2,8 Whether this will benefit postsurgical patients has yet to be determined. Prompt ophthalmologic consultation is highly recommended.
How do I find out more about this?
The articles used in compiling this discussion are listed under References. We expect that new research and case reviews will generate considerably more literature on this subject in the near future.
Dr. Lofsky is a practicing anesthesiologist in Santa Monica, CA. She is a member of The Doctors’ Company Board of Directors and is a diplomate of the American Board of Anesthesiology and of the American Board of Internal Medicine.
Dr. Gorney is a plastic surgeon in San Francisco, CA. He is a founding member of TDC and the Medical Director of The Doctors’ Company.
1. Stevens WR, Glazer PA, Kelley SSD, Leitman TM, Bradford DS: Ophthalmologic Complications After Spinal Surgery. Spine 22(12):1319-1324, 1997.
2. Williams EL, Hart WM, Tempelhoff R: Postoperative Ischemic Optic Neuropathy. Anesthesia and Analgesia 80:1018-1029, 1995.
3. Katz DM, Trobe ID, Cornblath WT, Kline LB: Ischemic Optic Neuropathy After Lumbar Spine Surgery. Arch Opthalmol 112:925-931, 1994.
4. Myers MA, Hamilton SR, Bogosian AJ, Smith CH, Wagner TA: Visual Loss as a Complication of Spine Surgery. Spine 22(12): 1325-1329, 1997.
5. Lee AG: Ischemic optic neuropathy following lumbar spine surgery. J Neurosurg 83:348-349, 1995.
6. Brown RH, Shauble JF, Miller NR: Anemia and Hypotension as Contributors to Perioperative Loss of Vision. Anesthesiology 80:222-226, 1994.
7. Dilger JA, Tetzlaff JE, Bell GR, Kosmorsky GS, Agnor RC, O’Hara JF: Ischaemic optic neuropathy after spinal fusion. Canadian Journal of Anaesthesia 45(1):63-66, 1998.
8. Connolly SE, Gordon KB, Horton JC: Salvage of Vision After Hypotension-induced Ischemic Optic Neuropathy. American Journal of Ophthalmology 117:235-242, 1994.
9. Drummond JC: The Lower Limit of Autoregulation: Time to Revise Our Thinking? Anesthesiology 86(6): 1431-1433, 1997.
[Editor’s Note: Reprinted by permission of The Doctors’ Company. All rights reserved.]