Download N Jaca - Post-operative visual loss

18 May 2012
No. 15
Post-operative visual loss
Dr Nokwanda Jaca
Commentator: Dr N Moodley
Moderator: Dr J Reddy
Department of Anaesthetics
CONTENTS
INTRODUCTION ................................................................................................... 3
PREVALENCE AND INCIDENCE......................................................................... 3
BLOOD SUPPLY OF THE EYE. ........................................................................... 4
TYPES OF POVL .................................................................................................. 6
Ischemic Optic Neuropathy ............................................................................. 6
Central Retinal Artery Occlusion (CRAO) ....................................................... 9
Cortical Blindness .......................................................................................... 10
INFORMED CONSENT ....................................................................................... 10
RISK FACTOR STRATIFICATION ..................................................................... 11
THE CURRENT THINKING ................................................................................ 12
CONCLUSION .................................................................................................... 15
REFERENCES.................................................................................................... 16
Page 2 of 17
INTRODUCTION
Peri-operative visual loss (POVL) is an extremely rare, unexpected and
devastating complication that patients can sustain after general anaesthesia and
non-ocular surgeries.2
The risk of POVL varies according to the nature and approach of surgical
procedures, from the Nationwide Inpatient Sample (NIS), highest incidence of
POVL is amongst prone positioned spinal and cardiac procedures.2
According to POVL Registry the patients at highest risk for developing POVL are
those undergoing prolonged duration of procedures (>6hrs) with substantial blood
loss (>1000ml).2
The most common causes of visual loss are Ischemic optic neuropathy (ION),
Central retinal artery occlusion (CRAO) and Cortical blindness (CB), there are
also rare causes like orbital compartment syndrome, pituitary apoplexy, orbital
lobe infarction but this article will only focus on the more common causes of this
devastating complication.10
Specific pathogenesis and is unknown; much controversial surrounding the patient
and surgical risk factors and limited treatment options makes the general outcome
of POVL to be very poor therefore prevention is of utmost importance.3,10
PREVALENCE AND INCIDENCE
The incidence of POVL in general surgery is very low (0.0008-0.0016%), however
the incidence rises with surgical procedures like spinal and cardiac surgery. 11 Two
large retrospective studies estimated incidence of ION to be ~1/60 000-1/125 000
of all anaesthetics.4
Two large studies conducted through NIS (largest inpatient database in America)
reported an overall incidence of visual disturbances after spine surgeries of
0.094% between1993-2002, and also from 1996-2005 a second study reported an
incidence of POVL in various surgical procedures as follows: 8.64/10000 in
cardiac surgeries, 3.09/10000 in cases of spinal fusion (5.36/10000 through the
posterior approach), 1.08 And 1.86/10000 in knee and hip surgery respectively,
and 0.12/10000 in appendicectomy.10
Additional large-scale studies of POVL after spine surgery have demonstrated
incidence rates varying from 0.094% to 0.2% and similar studies following cardiac
surgery have shown incidence rates ranging 0.09% to 0.113%.3
Page 3 of 17
BLOOD SUPPLY OF THE EYE.
The ophthalmic artery is the major blood supply of the orbit. It arises from the
Internal Carotid Artery (first branch of the ICA) as the ICA is emerging from the
cavernous sinus on the medial side of the anterior clinoid process. It enters the
orbital cavity through the optic foramen, below and lateral to the optic nerve. The
ophthalmic artery passes over the nerve (in 85% of cases) to reach the medial
wall of the orbit.17
The artery then proceeds forward horizontally, beneath the lower border of the
superior oblique muscle, and divides into 2 terminal branches, frontal and dorsal
nasal. As the artery crosses the optic nerve, it is accompanied by the nasociliary
nerve and is separated from the frontal nerve by the superior rectus muscle and
the superior levator palpebral muscle. The ophthalmic artery rarely arises from the
middle meningeal artery. Most branches of the ophthalmic artery arise in the
posterior one third of the orbit and pass anteriorly. The branches of the ophthalmic
artery are divided into an orbital group, distributing vessels to the orbit and
surrounding parts, and an ocular group, distributing vessels to the muscles and
bulb of the eye.
Orbital group
The orbital group consists of the following (distributing vessels to the orbit and
surrounding parts.)
 Lacrimal artery
 Supraorbital artery
 Posterior ethmoidal artery
 Anterior ethmoidal artery
 Internal palpebral artery
 Frontal artery
 Nasal artery Anatomy of arterial supply, orbit.
Ocular group
The ocular group consists of the following (distributing vessels to the muscles and
bulb of the eye.)
 Long ciliary artery
 Short ciliary artery
 Anterior ciliary artery
 Central retinal artery
 Muscular artery
Page 4 of 17
The Arterial Supply of the Eye
1. Ophthalmic artery 2. Central Retinal Artery 3. Ciliary Artery
4. Long Posterior Ciliary Artery (2) 5. Short Posterior Ciliary Artery (20)
6. Recurrent Branches 7. Anterior Ethmoidal Artery
8. Posterior Ethmoidal Artery 9. Superior Oblique Muscle (Orientation)
The Venous System
Vortex veins
The vortex veins provide drainage for the uveal tract (choroid, ciliary body, and
iris). They pierce the sclera obliquely and open posterior to the equator. The
superior vortex veins (lateral and medial) drain into the superior ophthalmic vein or
its muscular or lacrimal branches. The 2 inferior vortex veins (lateral and medial)
drain into the inferior ophthalmic vein.
Superior ophthalmic vein
The superior ophthalmic vein is the main venous channel for the superior orbit; it
drains to the cavernous sinus. The course of the superior ophthalmic vein begins
at the inner angle of the orbit. It pursues the same course as the ophthalmic artery
and receives tributaries corresponding to the branches of that vessel. It passes
between the 2 heads of the lateral rectus muscle, through the medial part of the
superior orbital fissure, and ends in the cavernous sinus.
Inferior ophthalmic vein
The inferior ophthalmic vein begins at the floor and medial wall of the orbit, travels
backward, and divides into 2 branches. It provides a channel for inferior drainage.
Page 5 of 17
The Venous Drainage Of The Eye
1. Superotemporal and 2. Superonasal Vortex Vein both drain into the superior
ophthalmic artery (not shown)
3. Inferonasal and 4. Inferotemporal Vortex vein both drain into the inferior
ophthalmic artery (not shown)
5. Cavernous Sinus 6. Optic nerve (orientation)
TYPES OF POVL
The most common causes of POVL are Ischemic Optic Neuropathy (ION), Central
Retinal Artery Occlusion (CRAO) and Cortical Blindness (CB).
Ischemic Optic Neuropathy
ION has been mostly reported in adults after a variety of surgical procedures and
less often in children7. The most common types of ION are anterior ischemic optic
neuropathy (AION) and posterior ischemic neuropathy (PION). The type of ION
varies depending on the surgical procedure done, with AION occurring most often
after cardiac surgery and PION occurring most after prone- positioned spine
surgery and radical neck dissection.3 Most of the cases with ION reported from
ASA POVL Registry presented with bilateral visual disturbance which is
suggestive of systemic event.12 However unilateral involvement has been
described.11 It is appropriate to divide cases into AION and PION, as the anterior
and posterior optic nerve differ anatomically, and these two entities differ
pathophysiologically.6
ION generally presents with painless visual loss, visual field deficits, afferent pupil
defect or nonreactive pupil, and no light perception. Colour vision is decreased or
absent.4,2 Visual loss typically presented within the first 24–48 h, and frequently
noted upon recovery after surgery. Later onset (3-10 days) of visual loss has been
Page 6 of 17
described, particularly in sedated patients who remained mechanically ventilated
after operation.2
In contrast, orbital compartment syndrome is associated with painful loss of vision,
acute periorbital oedema, conjuctival chemosis and oedema; which also probably
occurs as a result of raised intra ocular pressure secondary to direct pressure on
global and periorbital structures due to abnormal head position during prolonged
prone position.10 This is an ophthalmic emergency which requires urgent
decompression of the eye
Anterior Ischemic Optic Neuropathy (AION)
AION is the most common acute optic neuropathy affecting patients aged 50
years and older, accounting for 90% of the cases of ION. 11 AION is caused by
occlusion or relative hypoperfusion of anterior optic nerve head by the posterior
ciliary arteries, with diffuse or focal disc oedema with or without peripapillary flame
shaped haemorrhages or splinter haemorrhages at the optic disc margin on
fundoscopy.10 Inferior altitudinal visual field disturbances maybe present with
AION owing to the optic disc oedema. Whereas MRI is normal although some
reports described nerve enlargement or perineural enhancement suggestive of
oedema, but on follow up (days up to weeks), both AION and PION show disc
pallor so cannot be differentiated based on fundoscopic examination.10,12
Blood flow to the anterior optic nerve is autoregulated by endovascular and
metabolic factors similar to cerebral circulation. Autoregulation is effective over a
critical range of perfusion pressure –which is not clearly defined in humans.
Diseases of the circulatory system (hypertension, diabetes mellitus, and
atherosclerosis) damage autoregulation and therefore increase the critical
perfusion pressure below which autoregulation of the anterior optic nerve fails.13
Perfusion pressure of the anterior optic nerve is the difference between the ciliary
artery and venous drainage i.e. MAP - IOP. Increased IOP may substantially
reduce the perfusion pressure of the anterior optic nerve.13
There are two forms of AION: Arteritic and Non-arteritic. Making an immediate
distinction is critical to prudent management because in arteritic AION treatment
with systemic corticosteroids, followed by oral steroids is required to prevent
development of bilateral blindness until the ESR and CRP are under control.11,3,10
The arteritic form of AION, associated with giant cell arteritis (GCA), often
presents in the elderly with an elevated erythrocyte sedimentation rate (ESR) and
C-reactive protein (CRP), and systemic symptoms such as weight loss and jaw
claudication. It is important to note that inflammatory markers are often extremely
elevated after general surgery. Because of this, in the absence of other features of
GCA such as systemic symptoms or abnormal temporal arteries, it is not
advisable to check ESR and CRP in a patient who wakes up from surgery with
visual loss. If these are checked, an elevated ESR alone is not enough to
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diagnose arteritic AION in the postoperative period.3
diagnosing arteritic AION is the temporal artery biopsy.
The gold standard for
Non-arteritic AION usually presents in eyes with structural crowding of the optic
nerve head so that the physiological cup is either very small or absent (disk at
risk). This configuration is thought to predispose to infarction of the optic nerve
head because axons in the optic nerve pass through a narrower opening . 11,7 The
use of steroids in this form of AION is controversial, although there have been
reports of improvement after steroids were given, which could also be a
coincidence.10
Posterior Ischemic Optic Neuropathy (PION)
Posterior ischemic optic neuropathy (PION) is much less common than the
anterior variety. PION is caused by ischemia to the retrolaminar portion of the
optic nerve, which is supplied by the surrounding pial capillary plexus and the
optic disc initially appears normal despite visual loss, with optic nerve pallor and
atrophy ensuing only after 4‑6 weeks. PION shows gadolinium enhancement
and/or restricted diffusion on MRI.11,12 Visual loss almost always is apparent
within the first 24 hours after surgery with PION.6
There are three types of PION: peri-operative, arteritic, and nonarteritic; and the
peri-operative type is the most common. The pial vessels that supply the posterior
optic nerve lack an autoregulatory mechanism, and are therefore prone to
ischemia during periods of systemic hypotension and when the blood oxygen
carrying capacity is decreased.3
Distension of ophthalmic veins, with accompanying facial oedema, due to internal
jugular vein ligation has been proposed as a potential mechanism for PION
development after radical neck distension. The venous distension could cause
compression of the orbital apex, resulting in reduced perfusion and further anoxia
of the posterior aspect of the optic nerve.3
Pathogenesis of ION
The pathogenesis of postoperative ION remains undefined.3 Hypotension,
peripheral vascular disease and anaemia are commonly implicated in the
development of ION, whereas excessive external pressure over the eye,
uncontrolled hypertension, diabetes mellitus, morbid obesity peripheral vascular
disease and blood transfusion have been associated with CRAO. Other factors
associated with ION include excessive blood loss, hemodilution, and increased
intraorbital/intraocular pressure use of head low position during surgery and
smoking.10
Blood loss, with or without arterial hypotension, has been shown to cause the
release of endogenous vasoconstrictors due to the activation of the sympathetic
nervous system, which can produce choroidal and optic nerve ischemia. The use
of vasoconstricting agents to correct intraoperative hypotension has also been
suggested to promote optic nerve ischemia, however there have been cases of
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ION reported to reasonable pressures SBP >90mmHg and minimal blood loss
<500ml.3
Central Retinal Artery Occlusion (CRAO)
Central retinal artery occlusion (CRAO) has been well documented in children and
adults following trauma, embolic, thrombotic or vasospastic episodes. 3 CRAO also
presents as postoperative sudden severe visual loss on awakening with absent
sluggish pupillary reflex and relative afferent papillary defect. On fundoscopic
examination, the classical findings are: white ground-glass appearance of retina,
attenuated arterioles with preserved choriocapillaries, afferent pupillary defect and
the classical cherry red spot at the macula.10,3
CRAO after surgery is typically observed following external ocular compression
and improper patient positioning or its unintended movement when on a
horseshoe headrest is a hazard that can place the eye in contact with the
headrest.7
Pressure within the orbit can also be increased internally after
retrobulbar haemorrhage, associated with vascular injuries during sinus or nasal
surgery.2
When compared with cases of ION patients who develop CRAO were found to
have lower anaesthetic durations and estimated blood loss.3 Majority of cases with
were reported to have periocular trauma evidenced by ipsilateral decreased
supraorbital sensation, ophthalmoplegia, corneal abrasion, ptosis, or unilateral
erythema, unilateral visual loss, no light perception and afferent pupil defect.3,2
Early orbital computed tomography (CT) or magnetic resonance imaging (MRI)
showed proptosis and extraocular muscle swelling in some patients.7 Extensive
pressure on the globe may raise IOP above the SBP leading to retinal ischemia.
Animal experiments have shown that retina can tolerate ischemia for 95 min and
still fully recover although it suffers permanent damage after 105 min. Majority of
CRAO cases occur after prone position positioned patients, or in those positioned
supine with excessive ocular pressure secondary to an anaesthetic mask.
Prognosis is very poor and there is no Class I data on the effective treatment for
CRAO that exists, and the accompanying blindness is often permanent but there
is treatment that has been attempted and studies are still being done to test
efficacy.3,2
The attempted treatment strategies: ocular massage which can lower the IOP and
possibly dislodge embolus, ivi acetazolamide can be given to increase retinal
blood flow and 5% CO2 in O2 inhaled to enhance dilatation and increase O2
delivery, fibrinolysis via ophthalmic artery within 6-8hr of CRAO has been
associated with visual improvement. Localised application of hypothermia has
been used in animal studies and was shown to decrease injury after ischemia. 7 It
has been suggested that the use of a foam headrest with orbital cutouts may
prevent postoperative CRAO development.3 Avoid the us the of goggles with
headrest because the goggles move and compress the eyes.2
Page 9 of 17
Cortical Blindness
Cortical blindness results from the destruction or denervation of the primary visual
cortex. The parieto-occipital region of the brain is a watershed zone for the middle
cerebral and posterior cerebral arteries, and may undergo infarction during
periods of systemic hypotension. Stroke after general surgery is very rare,
although the risk appears to be increased after cardiac or vascular surgery,
especially CABG. The majority of postoperative strokes are ischemic or embolic in
nature.3
Risk factors for developing postoperative stroke include: hypertension, diabetes
mellitus, renal insufficiency, smoking history, COPD, peripheral vascular disease,
cardiac disease, and/or systolic dysfunction. Patients with symptomatic carotid
stenosis maybe at increased risk of postoperative stroke, including cortical
blindness, and may benefit from carotid revascularization prior to undergoing
surgery.3
These patients presents with reduced vision with normal pupil reaction, intact
corneal reflexes, and normal eye movement. Bilateral complete vision loss is rare,
and is usually seen in association with other neurologic symptoms associated with
vertebrobasilar strokes, such as ataxia, hemisyndrome, diplopia, and nausea.3
The diagnosis should include a detailed neurologic examination and brain
computed tomography (CT) or MRI to evaluate the lesion. The prognosis of
postoperative parieto-occipital stroke ranges from total permanent blindness to
brief periods of transient ischemic attacks with full recovery of visual acuity. 3
INFORMED CONSENT
Should we however inform all patients of the risk given the incidence of postoperative visual loss is rare but devastating complication?
The American Society of Anaesthesiologists’ practice advisory for peri-operative
visual loss associated with spinal surgery suggests that a physician “consider”
disclosing the risk of POVL to high-risk patients.
The advisory does not address which physician is responsible for disclosure, nor
does it address the timing of such disclosure?4
The informed consent process is complex. It often involves the physician’s
judgment of what a reasonable patient would want to know regarding rare but
catastrophic risks. The physicians are expected to inform the patient of the most
common risks and benefits, as well as those rare but devastating events that have
the potential for significantly impacting patients’ lifestyle. Some physicians weigh
the risks based on the frequency of occurrence and do not discuss extremely rare
risks and complications, despite the significant impact of such risks if they occur. 4
There are no practice guidelines by either the American College of Surgeons or
the American Society of Anaesthesiologists regarding the best method of
Page 10 of 17
discussing the potential for POVL with patients. Because the patient is cared for
by at least two physicians the anaesthesiologist and surgeon and no exact
aetiology for the visual loss has been determined, this remains a shared fear and
responsibility of both physicians. As a result, which physician should be
responsible for disclosure to the patient, and the setting and timing for this
disclosure, remains a controversial matter.4
Patients who had undergone prolonged prone positioned spinal procedures were
surveyed to help develop a national consensus on the disclosure of the risk of
POVL associated with high risk surgery. The results showed that most of the
patients preferred to be informed by the surgeon, a day before the operation and
face to face.
However the study had potential limitation that it only focused on the specific risk
of POVL associated with prolonged prone spinal surgery. The results cannot be
extrapolated to preferences of patients who undergo other procedures and nonresponders were not contacted therefore the responders were not compared with
non-respond who might have had different opinions.4 However in an era in which
a patient-centred model of care focuses on the patient’s involvement in his or her
own health care it is appropriate that we include the patient’s preference when
examining the complicated issue of disclosure of POVL before high-risk
procedures such as prone spinal surgery. 4
RISK FACTOR STRATIFICATION
Previous studies of ION have been hindered either by small numbers of similar
patients with ION from single institutions, or by lack of detailed peri-operative data
from national inpatient databases. The American Society of Anaesthesiologists
(ASA) POVL Registry database contains the largest collection to date of ION
cases associated with spine surgery with detailed anaesthetic and postoperative
data.6
An analysis of the initial 83 ION cases reported to the ASA POVL Registry
demonstrated that these cases were characterized by prolonged duration in the
prone position and large blood loss; however, the lack of a control group
prevented identification of risk factors.
ION cases associated with prone spine surgery from the ASA POVL Registry in a
multi-institutional case-control study to identify risk factors for this devastating
peri-operative complication.6
A subset of patient and peri-operative factors from the data available from the
ASA POVL Registry was compared between ION cases and control subjects and
these factors were hypothesized to be possibly associated with ION. Patient
preexisting conditions included age, sex, and the following comorbidities:
hypertension, diabetes, smoking,
atherosclerosis (any coronary artery
disease/myocardial infarction, or
Page 11 of 17
cerebrovascular disease), and obesity (defined by either clinical assessment or
body mass index>30.6
Other patient factors examined included fusion location (lumbar vs. Non-lumbar),
indication for surgery (tumour, trauma, or other), and clinic blood pressure.
Predetermined procedural factors included type of surgical frame, number of
levels of fusion, and the headrest type.6
Potentially modifiable intraoperative procedural factors included anaesthetic
duration and estimated blood loss (EBL).
Potentially modifiable intraoperative management factors included decrease in
blood pressure (measured as reduction for a minimum of 30 consecutive or nonconsecutive min in the following ranges: 0–20% below baseline; 21–40% below
baseline; and >40% below clinic baseline for either systolic blood pressure or
mean arterial pressure), lowest hematocrit, fluid management variables (total
volume replacement [all blood products, crystalloid, and colloid], total nonblood
product replacement [crystalloid and colloid], total volume replacement:EBL ratio,
and colloid [hydroxyethyl starch or albumin] as % of total nonblood replacement),
and use of vasopressors.6
In the analysis, male sex, obesity, diabetes, use of the
Wilson frame, anaesthesia duration, EBL, and blood pressure more than 40%
below baseline values for >30 min were associated with a significantly increased
risk of ION. There were no statistically significant associations of case/control
status with age, ASA physical status, other preexisting conditions, type of
headrest, number of levels fused, or with indication for surgery (tumour, trauma, or
other diagnosis).6
This study demonstrates that obese and male patients have an increased risk of
developing ION after major spinal surgery in the prone position. Avoidance of the
Wilson frame and minimizing the anaesthetic duration and EBL may decrease the
risk of developing ION. Use of colloid along with crystalloid may decrease the risk
of developing ION.
THE CURRENT THINKING

Statements reported by American Society of Anaesthesiologists Task Force
on Peri-operative Visual Loss7

Preoperative Patient Evaluation and Preparation
- Although the consultants and specialty society members agree that there are
identifiable preoperative risk factors, at this time the Task Force does not
believe that there are identifiable preoperative patient characteristics that
predispose patients to peri-operative ION.
Page 12 of 17
- The Task Force also believes that there is no evidence that an ophthalmic or
neuro-ophthalmic evaluation would be useful in identifying patients at risk for
peri-operative visual loss.
- The Task Force believes that the risk of peri-operative ION may be increased
in patients who undergo prolonged procedures, have substantial blood loss,
or both.
- Consider informing patients in whom prolonged procedures, substantial blood
loss, or both are anticipated that there is a small, unpredictable risk of perioperative visual loss.
- Because the frequency of visual loss after spine surgery of short duration is
very low, the decision to inform patients who are not anticipated to be “high
risk” for visual loss should be determined on a case-by-case basis.7
 Intraoperative Management
Blood Pressure Management
- Systemic blood pressure should be monitored continually in high-risk
patients.
- The Task Force believes that the use of deliberate hypotensive techniques
during spine surgery has not been shown to be associated with the
development of peri-operative visual loss; therefore, the use of deliberate
hypotension for these patients should be determined on a case-by-case
basis.7
Management of Intraoperative Fluids
- Central venous pressure monitoring should be considered in high-risk
patients.
- Colloids should be used along with crystalloids to maintain intravascular
volume in patients who have substantial blood loss.
Management of Anaemia
- Haemoglobin or hematocrit values should be monitored periodically during
surgery in high-risk patients who experience substantial blood loss.7
- The Task Force believes that there is no documented lower limit of
haemoglobin concentration that has been associated with the development of
peri-operative visual loss.7
- Therefore, the Task Force believes a transfusion threshold that would
eliminate the risk of peri-operative visual loss related to anaemia cannot be
established at this time.7
Use of Vasopressors
- The Task Force consensus is that there is insufficient evidence to provide
guidance for the use of alpha-adrenergic agonists in high-risk patients during
spine surgery. Therefore, the decision to use alpha-adrenergic agonists
should be made on a case-by-case basis.7
Page 13 of 17
Patient Positioning7
- The Task Force believes that there is no pathophysiologic mechanism by
which facial oedema can cause peri-operative ION.
- There is no evidence that ocular compression causes isolated peri operative
anterior ION or posterior ION. However, direct pressure on the eye should be
avoided to prevent CRAO.
- The high-risk patient should be positioned so that the head is level with or
higher than the heart when possible.
- The high-risk patient’s head should be maintained in a neutral forward
position (e.g., without significant neck flexion, extension, lateral flexion, or
rotation) when possible.7

Staging of Surgical Procedures
- Although the use of staged spine surgery procedures in high-risk patients
may entail additional costs and patient risks (e.g., infection,
thromboembolism, or neurologic injury), it also may decrease these risks and
the risk of peri-operative visual loss in some patients.
- Therefore, consideration should be given to the use of staged spine
procedures in high-risk patients.7

Postoperative Management
- The consensus of the Task Force is that a high-risk patient’s vision should be
assessed when the patient becomes alert (e.g., in the recovery room,
intensive care unit, or nursing floor).
- If there is concern regarding potential visual loss, an urgent ophthalmologic
consultation should be obtained to determine its cause.
- Additional management may include optimizing hemoglobin or hematocrit
values, hemodynamic status, and arterial oxygenation.
- To rule out intracranial causes of visual loss, consider magnetic resonance
imaging.
- The Task Force believes that there is no role for antiplatelet agents, steroids,
or intraocular pressure-lowering agents in the treatment of peri-operative
ION.7
Page 14 of 17
CONCLUSION
There are no definite clinical trials to show a direct causal relationship between
some patient related factors and intraoperative situations with the occurrence of
POVL. But on review of literature some factors may be associated with
occurrence of POVL like preoperative anaemia and vascular risk factors like
hypertension, glaucoma, carotid artery disease, smoking, obesity and diabetes.
The literature also suggests association of perioperative visual loss with prolonged
procedures, substantial blood loss or both. Intra operatively hypotension, blood
loss, anaemia, hemodilution, facial oedema, pressure on the eye, use of
vasopressors, prone and head down positions, substantial fluid resuscitation,
increased venous pressures, and prolonged surgery have been proposed for
postoperative visual loss; but of these prolonged surgical duration and substantial
blood loss have been present in majority of the patients who have experienced
postoperative visual loss.10
So despite postoperative visual loss being a well‑known complication after
non‑ocular surgeries, there is dearth of level I evidence to directly relate some
causal factors to its occurrence resulting in inability on our part to reduce its
incidence and also managing such complications.10
No effective treatment for ION exists, once established, hence prevention is
crucial. Despite this, studies to date have only succeeded in demonstrating that
minimizing one risk factor for the development of ION may merely serve to
introduce another.12
Although correction of hemodynamic disturbances may be beneficial. The
guidelines for transfusion are controversial and unstandardized. The ASA
concluded that transfusion is rarely indicated when the haemoglobin concentration
is higher than 10 g/dl, and almost always indicated when the haemoglobin
concentration is less than 6 g/dl. A more meticulous management of perioperative systemic hypotension and earlier correction of anaemia may decrease
the risk of PVL, especially in patients with a disk at risk.11
Whether patients should be informed of ION, especially those undergoing higherrisk cardiac surgery and complex instrumented spinal fusion surgery, is
controversial. The Task Force recommendation is to consider informing those
undergoing prolonged spine fusion surgery with large anticipated blood loss.2
Page 15 of 17
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