Vision Problems After Spine Surgery with Controlled Hypotension

Ischemic optic neuropathy is the most frequently reported cause of postoperative visual loss following general anesthesia.^1,2 The following discussion, based on a review of The Doctors Company claims and a study of the medical literature, is intended to promote an awareness of the ION syndrome and to provide an understanding of current theories about its etiology and treatment.

The Doctors Company has noted an increased incidence of claims involving postoperative blindness or severe visual impairment following spine surgeries in which controlled hypotension was utilized. Most cases have involved an eventual ophthalmologic diagnosis of ischemic optic neuropathy.

Claims

Examples The following two cases are composites, incorporating details from 12 The Doctors Company claims.

• A 32-year-old female, 5’4" and 218 lbs, was scheduled for posterior lumbar fusion at L3-S1. The patient had consented to having general anesthesia with controlled hypotension. An arterial line was placed after giving light sedation. Anesthesia was then induced with propofol and maintained with desflurane, air, and oxygen.
  
  The patient 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 to 55 mmHg for a 4-hour portion of the 8-hour case, after which the systolic pressure was allowed to rise to 100 to 120 mmHg. 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 3500 cc, and this was replaced intraoperatively with 4 units of autologous blood and 8 liters of crystalloid. Postoperative hematocrit was 24.5%.
  
  Upon waking in the recovery room, the patient complained of blurry vision. An ophthalmologic consult was obtained, and a fundoscopic examination and an MRI of the brain were normal.
  
  Visual field defects were noted bilaterally. Vision in both eyes had been normal preoperatively, but after surgery, vision tested initially at 20/200. Over several days, vision in the left eye improved 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 a bone graft. An arterial line and CVP monitoring were used. After propofol induction, anesthesia was maintained with oxygen, nitrous oxide, and Forane. The patient was placed prone and his head was supported only by Halo tongs. During the 9-hour procedure, controlled hypotension was induced with hydralazine and labetolol, keeping the mean blood pressure 50 to 60 mmHg 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 2,750 cc blood loss was 10 liters of crystalloid, 1 liter of colloid, and 750 cc of cell saver blood. The post operative hematocrit was 26%. Upon waking in the recovery room, the patient stated that he could not see. An ophthalmology consult confirmed there was no light perception bilaterally, and ION was diagnosed. The patient never regained his vision.

What Is ION?

Most anesthesiologists are aware that central retinal artery occlusion can follow improper head positioning when pressure is put on the eyes of patients who are placed in the prone position. Not all anesthesiologists, however, are familiar with ischemic optic neuropathy. This syndrome 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 This has been reported following cardiopulmonary bypasses, radical neck dissections, and abdominal and hip procedures. ^{2, 3,6} In many cases, extensive blood loss and periods of hypotension were believed to be etiologic factors.^2-6 Incidents of ION occurring after spine surgery are well documented.^1,3-7

Postoperative ION may be unilateral or bilateral, with 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 during the immediate recovery period. Most delays are caused when patients assume their vision problems are a temporary part of normal recovery or believe that their eyes have been patched. In a few cases, patients initially had normal vision, but developed symptoms during the first 12 postoperative days.^2,4,6 Ophthalmologic exams initially revealed swelling of the optic discs in some patients, but were normal in others.^2,3,6,8

What Causes ION?

In most postoperative cases reported, relative hypotension and anemia have contributed to the development of ischemic optic neuropathy.^1-6 A review of the literature involving six patients who developed ION after general anesthesia found that all six had hemoglobin counts less than 8.0 g/dl recorded at least once. In addition, all six 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: "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; 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 case studies include the presence of hypertension, diabetes, atherosclerotic cardiovascular disease, and a history of smoking. These factors may all cause preoperative abnormalities in the ophthalmic blood vessels.^2-7 Another striking similarity in many cases is a long operating time—averaging nearly 7 hours in one series.⁴ Cases that involve long operating times have a tendency for greater blood loss and more prolonged periods of hypotension. Some evidence also supports the hypothesis that ION 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

What Has Changed?

Controlled hypotension for spine surgery has been used safely for decades, and the mean blood pressures used in the cases reviewed were within well accepted limits of autoregulation. So what is causing the sudden, increased incidence of ischemic optic neuropathy?

One possibility is the change in thinking regarding transfusion. Since 1986, concerns about the spread of HIV have resulted in more conservative recommendations regarding transfusion.^2,5,6 In the past, a hemoglobin level of 10 g/dl was a commonly used threshold for intraoperative blood transfusion.⁵ Now, the Transfusion Practice Committee of the American Association of Blood Banks recommends using 8 g/dl, the National Institutes of Health Consensus Conference on Perioperative Blood Transfusion suggests 7 g/dl, and the American College of Physicians advocates waiting for a deterioration in vital signs or until the patient develops symptoms before giving blood.^5,6

In addition, patients are now likely to be maintained at lower average intraoperative hemoglobin levels than they were previously. As Brown et al concluded: "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

Another change that may be linked to the increased incidence of ION is the advent of newer anesthetic agents that may not be as effective cerebral dilators as agents popular in decades past.⁹ The impact of changes in agents that are commonly used to induce controlled hypotension also has yet to be delineated.

Recommendations

It is difficult to make risk management recommendations for a syndrome about which so much remains unknown. In most ION cases, the anesthesia practices are within published guidelines and well within current standards of care. Still, the increased incidence of unfortunate outcomes may prompt consideration of using alternative techniques. For example, the independent association of blood loss with development of ION leads some authors to conclude that the transfusion practice for longer spine surgeries should be more aggressive—utilizing cell saver or predonated autologous blood.^2-4

Every case requires that the anesthesiologist, in conjunction with the surgeon, carefully weigh the risks and benefits of the controlled hypotensive technique.¹ A review of The Doctors Company claims involving postoperative ION prompts the following risk management suggestions:

• Limit periods of extreme controlled hypotension to crucial parts of the procedure, and allow the pressure to rise when increased blood loss is tolerable.
• Use staging for unusually long surgeries that require multiple approaches.⁴
• Use the patient’s resting blood pressure to help decide what percentage drop will be tolerable during deliberate hypotension instead of using the same target pressure for each case.⁹

In addition, special consideration should be given to deciding how much to lower the blood pressure of patients with preexisting hypertension, atherosclerotic cardiovascular disease, diabetes mellitus, or a history of smoking. Once a blood pressure target is determined by the anesthesiologist, an accurate arterial line reading during the hypotensive period will help ensure that the pressure does not drop below the acceptable value. Frequent checks of the patient’s face should be made to ensure the absence of pressure against the eyes. Good documentation of this can help prove that every attempt was made to avoid elevating intraocular pressure.

Some evidence suggests that non-postsurgical ION, treated soon after diagnosis with vasopressors 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.

Conclusion

New research and case reviews will no doubt generate considerably more literature and risk management recommendations on ischemic optic neuropathy. Without further study, it is impossible to determine the influence, if any, of likely contributing factors. Clearly, much remains to be learned about this syndrome.

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