Episode #16 Postoperative Vision Loss

Hello and welcome back to the Anesthesia Patient Safety Podcast.  My name is Alli Bechtel and I am your host. Thank you for joining us for another show.

The Special 35^th Anniversary Jade Edition APSF Newsletter is live and there is so much to talk about!!  In creating this special Newsletter, the APSF Editorial Board put on their reading glasses and read through 35 years of APSF Newsletter articles (and this was done prior to the onset of the Covid-19 pandemic) before voting on the top 10 most impactful articles to include in this newsletter and review through the lens of What then and What now with the help of our current editorial team and past editors.

Today, we are going to head into the operating room to talk about a devastating postoperative complication and what we can do about it.

Before we dive into today’s episode, we’d like to recognize Merck, a major corporate supporter of APSF. Merck has generously provided unrestricted support as well as research and educational grants to further our vision that “no one shall be harmed by anesthesia care”. Thank you, Merck – we wouldn’t be able to do all that we do without you!”

We will start off today by looking at the #3 article, Induced Hypotension Tied to Possible Vision Impairments. This article first appeared in the Summer 1998 Newsletter. You can find the article from the APSF.org homepage and clicking on the Newsletter heading, 4^th one down is Newsletter archives. From here, scroll down to 1998 and click on Summer 1998. It is the 2^nd article in the list on the left.

The article was written by Lofsky and Gorney. The article starts with 2 cases that are a composite of several cases submitted for claims and the goals for this article were to bring awareness about Ischemic Optic Neuropathy and provide knowledge about etiology and treatment.

Let’s start with the cases.  The first is case is a female patient, 32 years old, 5’4” and 218lbs who underwent a posterior lumbar fusion L3-S1 with general anesthesia and controlled hypotension. A pre-induction arterial line was placed before a propofol induction followed by maintenance with desflurane, air, and oxygen. She was positioned prone with foam donuts and face position was checked every 45 minutes throughout the 8 hour case. For 4 hours, controlled hypotension was accomplished with Labetalol to maintain MAPs between 50-55mmHg. After that, the systolic blood pressures were allowed to rise to 100-120mmHg. Several times during the procedure, arterial blood gases demonstrated a mild metabolic acidosis that was treated with IV bicarbonate. Fluid totals included EBL of 3500mls with 4 units autologous blood and 8L crystalloid administered. Postop HCT was 24.5%. In the PACU, the patient complained of blurry vision. Ophthalmologic consult revealed normal fundoscopic exam and normal MRI, but visual field defects were present bilaterally and vision was found to be 20/200. Vision in the left eye improved to 20/100 over the next week, but did not improve in the right eye. The diagnosis was bilateral ischemic optic neuropathy.

The second case is that of a 42 year old man who is 5’9 and weighs 235lbs who underwent spinal fusion with instrumentation and bone graft. Additional monitoring included an arterial line and CVP. Propofol was used for induction and maintenance included oxygen, nitrous oxide and isoflurane. The patient was positioned prone with a custom foam face rest. The procedure last 9 hours and controlled hypotension involved keeping the MAPs 50-60mmHg with Hydralazine and Labetalol for 5 hours. After a couple hours, the arterial line damped out and the non-invasive blood pressure cuff was cycled every 2 minutes for the rest of the case. Fluid totals included 2750mls EBL with 10L crystalloid, 1L colloid, and 750mls cell-saver administered. The postoperative hematocrit was 26%. In the PACU, the patient reported that he could not see. Ophthalmology consult revealed no light perception bilaterally and ultimately a diagnosis of bilateral ischemic optic neuropathy was made and the patient never regained vision.

Just talking about these 2 cases has my pulse racing…I don’t know about you. This is an absolutely devastating complication.  We definitely need more information so let’s continue to learn more about ischemic optic neuropathy. First, what is it? It is the most frequently reported cause of postop vision loss after general anesthesia. Another important cause of postop vision loss is central retinal artery occlusion which can occur due to poor head positioning in the prone position leading to pressure on the eyes.

Ischemic optic neuropathy occurs from infarction of the optic nerve as a result of decreased oxygen delivery by one or more of the small arterioles that supply the nerve head. This can occur during cardiopulmonary bypass cases, radical neck dissection, abdominal, and hip procedures as well as spine surgery as a result of lots of blood loss and longer periods of hypotension. Postop ischemic optic neuropathy can be unilateral or bilateral and symptoms may occur immediately or on postop days 1-12 and include no light perception, color vision deficits, visual field defects, and decreased visual acuity. Ophthalmologic exams may reveal swelling of the optic discs, but may also be normal.

So, what causes ischemic optic neuropathy or ION? These cases often involve relative hypotension and anemia, often with hemoglobin less than 8g/dL recorded at least once upon review of the record as well as decreased mean arterial pressures from 20-24% of the preop values for long periods of time. It appears that significant anemia alone is unlikely to cause ION, but the combination of anemia plus hypotension may lead to the development of ION and postop vision loss. Another contributing factor may be the prone position since CVP may be elevated due to compressing the abdomen leading to decreased venous drainage from the ophthalmic veins and this is likely exacerbated in obese patients in the prone position. In addition, maintaining Trendelenburg position for long periods of time may decrease venous outflow and facilitating local capillary bed stasis in the eyes. This complication is also more likely to occur during longer procedures of about 7 hours or more and these may be cases where we are more likely to see increased blood loss as well as hypotension. There are several patient risk factors that we need to be aware of including HTN, diabetes, atherosclerotic cardiovascular disease, and smoking history. Some patients may also have congenitally small optic discs and this puts them at further increased risk since the nerve fibers have less room to expand during periods of hypoxia.

We are learning so much about ION today. Since controlled blood pressure has been used safely with MAPs within accepted limits of autoregulation, why the increased incidence of this complication back in 1998? It may have been due to changes in practice related to more conservative thresholds for blood transfusion. The threshold had decreased from 10g/dL to 7-8g/dL in addition to observation of changes in the patient’s vital signs or symptoms. Thus, during these long spine cases that were becoming more complex, we started to have patients that were managed with the same controlled hypotension, but with a lower hemoglobin level before a blood transfusion was initiated. There was also some thought that the new volatile anesthetics were not as good at cerebral vasodilation as older agents.

So, what could be done to prevent it…back in 1998? It was difficult since the overall anesthesia practices were safe and within standards for care…but obviously some patients were being harmed.  Due to the association between blood loss and ION, some anesthesia professionals advocated for a lower threshold to transfuse and increased use of cell saver or pre-donated autologous blood in order to prevent anemia. The author advocates for communication between the surgeon and anesthesiologist to weigh the risks and benefits of controlled hypotension. In addition, there were several risk management considerations including limited periods of extreme controlled hypotension to only the most critical time and allowing the blood pressure to increase as soon as possible. Surgeons may consider staging the longest procedures that require multiple approaches. Anesthesia professionals may consider the patient’s resting blood pressure to determine a safe limit for controlled hypotension that is tailored for each patient. Other special considerations may include determining a safe limit for controlled hypotension in patients with significant risk factors including HTN, atherosclerotic cardiovascular disease, diabetes, and smoking history and make sure that the arterial line provides an accurate reading so that the blood pressure does not drop below a certain cutoff to help keep the patient safe. And don’t forget to the check the patient’s face to avoid pressure on the eyes which may increase intraocular pressure. It may be possible to improve outcomes and vision following the development of ION with vasopressors to raise blood pressure, volume replacement and blood transfusion, but more studies are needed. An ophthalmologic consultation is also recommended to help with diagnosis and management.

That was a very informative trip back in time to learn about the What then for ischemic optic neuropathy?

It is time to go back to the future and learn about What now!! Buckle up.  Here we go!

In the Jade Edition Newsletter, the What Now article is Postoperative Visual Loss by Lorri Lee.  One of the great things about the APSF is the ability to bring together different medical specialties and the healthcare industry to work together towards improved patient safety.  Postop Vision loss is an area that highlights this collaboration. In 1998, the APSF pointed out the apparent increase in postop vision loss cases after spine surgeries in the prone position that we just talked about…these were more complex spine cases with increased blood loss and increased operating time with the use of controlled hypotension. Before this time, most cases of postop vision loss were thought to be due to cortical blindness caused by infarction in the visual cortex or central retinal artery occlusion due to compression of the globe. By the mid to late 1990s, there were more cases of ischemic optic neuropathy from damage to the optic nerve that we talked about earlier in the show, but there was a general lack of awareness about this condition. The authors of the 1998 article, Lofsky and Gorney, worked with The Doctors Company professional liability company and they were able to use this experience to identify a new trend in perioperative complication associated with anesthesia care and they were able to do this way before enough data would have been available in a national database since the national data revealed an incidence of 0.017% from 1996 until 2005. The ASA Closed Claims Project and the ASA Committee on Professional Liability started working on getting more information and created the ASA postop vision loss or POVL Registry for voluntary submission of anonymized data from cases in order to quickly gather large volumes of data. A short time later, the registry had gathered enough information to publish preliminary results in the APSF Newsletter and the ASA Newsletter to help provide additional information about this complication and continue to ask for case submissions.

Let’s fast forward from 1998 to 2006.  By this time, the Registry had 93 cases of POVL following spine surgery and 83 of these cases were found to be due to ION and 10 cases were from CRAO. Cases of central retinal artery occlusion were all unilateral vision loss with the majority having periocular trauma and none were done with Mayfield Pins. Over 50% of the ION cases involved bilateral vision loss and about 20% were done in Mayfield Pins and only 1 out of 83 had evidence of periocular trauma. In addition, there was higher amounts of blood loss, volume administered, and procedure time for the cases of ION compared to central retinal artery occlusion. With this new information, the ASA Committee on Standards and Practice Parameters published the first practice advisory that was then updated in 2012 and 2019 with the help of neuro-ophthalmologists, anesthesiologists, neurosurgeons, and orthopedic spine surgeons. One of the controversial topics that came out of this and subsequent meeting was the questions of consenting patients for this complication. By 2014, the APSF had developed 2 educational videos about consenting patients for POVL for surgeons and anesthesia professionals. More information about this complication was published in 2012 by members of the Society for Neuroscience in Anesthesiology and Critical Care as part of the POVL Study Group which found 6 risk factors associated with ION after surgery in the prone position including Male Sex, Obesity, Wilson Frame Use, longer anesthesia duration, greater blood loss, and lower percent of colloid used in non-blood fluid administration. Don’t worry I will also include these risk factors in the show notes. I will also include a link to the updated ASA practice advisory for POVL that included data from that study in the show notes.

We have learned a lot about ION following spine surgery. The etiology is likely elevated venous pressure in the prone position for a long time and contributes significantly to the development of this complication. Anything that further increases venous pressure or worsens venous congestion such as obesity or use of the Wilson frame are risk factors. This was a massive undertaking, building the registry, collecting data, analysis, and publication, and further review has led to increased awareness of this complication as well as changes in practice and a 2.7-fold decreased in ION cases after spinal fusion surgery from 1998 to 2012. This successful improvement in patient safety may be due to decreased practice of controlled hypotension, decreased use of the Wilson frame, and perhaps shorter operative times along with the increase in minimally invasive techniques with lower blood loss for spinal fusion surgery.

Our work is not quite done though. Further research is needed to help answer some lingering questions such as “Is everyone vulnerable to this complication given similar perioperative surgical events and anesthetic management, or do certain unique anatomic, physiologic, and genetic factors contribute to this injury?” and “What are the best treatment options?” So far, neuro-ophthalmology professionals often recommend normalizing blood pressure, avoidance of significant anemia, and Head-up positioning in the presence of facial edema.

Well, there you have it…the tale of recognizing an increasing complication, working to learn so much more about it, and disseminating this knowledge along with new practice advisories to help improve patient safety and decrease the incidence of ischemic optic neuropathy following spinal fusion surgery.

Thank you so much for joining us today on this journey towards improved patient safety. We can’t wait to crack open the Jade Edition Newsletter again in a future show!!

If you have any questions or comments from today’s show, please email us at [email protected].

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Until next time, stay vigilant so that no one shall be harmed by anesthesia care.

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