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eects, pain therapy, sleep deprivation, and the lack of easily available biomarkers. More concerning, we are probably missing a large cohort of patients suering “covert”
stroke that while not clinically evident may have implications for long- term neurologic disability such as dementia
and cognitive deterioration.20 Preliminary results from
the NeuroVISION trial21 suggest an incidence of covert
stroke, as diagnosed by postoperative MRI, of greater than
10% for noncardiac surgery patients. We are clearly recognizing just a fraction of the perioperative strokes occurring
in our patients.
Given the low incidence of clinically apparent stroke
in the noncardiac surgery population,8 associations with
perioperative stroke have been extensively studied using
large retrospective databases. ere are clear patient and
surgical risk factors, which are summarized in Box 64.2.
Perioperative events that may inuence the incidence
of stroke are less well supported in the literature and
are more conjectural are shown in Box 64.2. Preexisting
atrial brillation is clearly associated with perioperative
stroke,22 but recent evidence supports that the onset of
perioperative atrial brillation, rather than merely representing a transient response to perioperative stressors,
is associated with an increased long- term risk for stroke,
particularly in noncardiac surgery patients.23 e eect
of intraoperative hypotension on perioperative stroke
remains unclear but is highly relevant to our practice. e
ubiquity of intraoperative hypotension24 and the low frequency of perioperative stroke evident at emergence
18,25,26
would argue against a signicant role of transient intraoperative hypotension on postoperative stroke. Even the
neurologic literature supports this assumption.25 Recent
data, however, would support a small but signicant association between intraoperative hypotension and postoperative stroke, particularly for strokes occurring in the
immediate postprocedure interval. In a retrospective
case- control study of 48,000 noncardiac surgery patients,
Bijker et al.27 found an association between the duration of hypotension, dened as mean pressure decreased
30% below baseline pressure, and perioperative stroke.
e eect size was so small that the authors suggested
that perhaps intraoperative hypotension identied those
patients at risk for unrecognized perioperative hypotension and that this interval may be more important in the
pathogenesis of perioperative stroke risk.27 ese ndings
are consistent with recent studies supporting a more general association between intraoperative hypotension and
perioperative 30- day mortality28 and morbidity29 in noncardiac surgery patients.
Unfortunately there are no denitive guidelines for
the perioperative management of patients at risk for
stroke. ere are data, however, regarding the timing of
elective surgery following stroke. Jorgensen etal.30 using
the Danish nationwide cohort (all patients ≥ 20 years
undergoing noncardiac surgery, n= 481,183 surgeries)
evaluated the incidence of perioperative major adverse
cardiovascular events (MACE— ischemic stroke, acute
myocardial infarction, and cardiovascular death) versus the time elapsed from an ischemic stroke. ere was
an increased risk of MACE (odds ratio 4.03 relative to
control nonstroke patients), recurrent stroke (calculated
independently, odds ratio 67.60), and mortality (30- day
all cause, odds ratio 3.07) when elective surgery was performed within 3months of stroke. is increased risk for
postoperative stroke was true for minor, intermediate, and
major surgical procedures and extended temporally as far
as 9months following a stroke. Patients with any history
of ischemic stroke (including remote) had an increased
risk of 30- day MACE, ischemic stroke, and all- cause mortality, supporting a history of ischemic stroke as a marker
for perioperative cardiovascular complications. is paper
was subsequently criticized for not using true controls
(i.e., patients not undergoing surgery),31 as there is a recognized elevated risk for recurrent stroke in the immediate
poststroke period which decreases over time. In response
to this concern, the authors compared their study population to nonsurgical stroke patients in the Danish national
cohort and demonstrated a marked increase in recurrent
stroke in the surgical population relative to nonsurgical
controls,31 supporting that the perioperative period presents unique risks to patients with a history of recent or
remote stroke.
As for our case presentation, this patient presents several risk factors for perioperative stroke including advanced
age,18 female gender,18 a history of atrial brillation,22 and
general anesthesia for her hip replacement.
32,33
It is important to note that joint replacement surgery is the only surgical population for whom there are data to support that
regional anesthesia may be associated with a lower incidence
of stroke than general anesthesia.
32,33
If our patient should
present with a focal neurologic decit in the perioperative
period, it is critical that early recognition and evaluation
occur rapidly. See Box 64.3 for suggestions for the management of perioperative stroke. In terms of acute intervention,
there are few data to guide clinical management for the
postoperative patient. While there are reports of systemic
thrombolysis following total hip arthroplasty,
33,34
postop-
erative patients may be uniquely suited for endovascular
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for primary ICH are poor with a 30- day mortality of
BOX 64.3 MANAGEMENT SUGGESTIONS
FORPERIOPERATIVESTROKE
1. Emergent notication of Hospital StrokeTeam
40%,36 and survivors generally have a poor functional outcome.37 In 2001 Hemphill etal.38 developed a clinical grading scale for predicting outcomes that is still used today.
Independent predictors for 30- day mortality accord-
2. Emergent head CT without contrast (r/ oICH)
3. Determine time patient was “last normal”
4. Consider MRI of head if “last normal” time unclear
(salvageable penumbra?)
5. Maintain oxygen saturations≥92%
ing to this ICH scale include low presenting GCS score,
age ≥80years, large ICH volume (≥30 mL vs. < 30 mL),
infratentorial location, and intraventricular involvement.
38
Patient management is based on recommendations
from the American Heart Association and American
Stroke Association39 and much of the evidence in support
of these recommendations is admittedly incomplete. In
6. Permissive hypertension (consider upper limits of
185mmHg systolic and 105mmHg diastolic)
7. ECG (evaluate for atrial brillation)
the largest retrospective study of patients suering oral
anticoagulant- associated ICH, correcting INR (international normalized ratio) to ≤ 1.3 and controlling systolic
blood pressure ≤ 160 mmHg within 4 hours of admis-
8. INR, PTT, and platelet count (to assess for rtPA eligibility)
9. Normoglycemia
sion were the most signicant interventions for reducing hematoma extension and 30- day mortality.40 Clinical
attention should thus be focused on preventing extension
of hemorrhage through blood pressure control and reversal of anticoagulation. For those patients with evidence
therapy, thus avoiding the risk of catastrophic hemorrhage
following systemic thrombolysis. For our postoperative
patient, the most important (and dicult) step is the rec-
of intracranial hypertension, management of intracranial
pressure should also be a priority. See Table 64.1 for a
list of perioperative considerations for ICH patients. For
ognition that an acute stroke may be in progress. Immediate
notication of the hospital stroke team should follow, and
this group of specialty neurologists and neurointerventionalists can assist in the management of the postoperative
patient withAIS.
HEMORRHAGICSTROKE
Although hemorrhagic stroke represents only 10%– 15%
of strokes in total,10 and less than 10% of perioperative
strokes,35 it remains relevant to anesthesiologists because
of the prevalence of hypertension in the general population and the large number of patients on oral anticoagulant therapy who may present for surgical decompression.
Most cases of intracranial hemorrhage (ICH) are primary
in origin, meaning they result from chronic hypertension
and/ or amyloid angiopathy. Secondary causes result from
vascular abnormalities such as cerebral aneurysms or arteriovenous malformations or conditions such as ischemic
stroke with secondary hemorrhagic conversion and are not
included in this discussion. Unlike the interventions available to improve outcomes for ischemic stroke, patient care
for primary ICH remains focused on minimizing secondary injury and as such is primarily supportive. Outcomes
TABLE64.1 MANAGEMENT OFHEMORRHAGICSTROKE
Management
Recommendations
Reversal of
anticoagulant or
antiplatelet therapy
Blood pressure
management
Intracranial pressure In setting of intracranial
Glucose management Maintain serum
Temperature
Management
Clinical Applications
As rapidly as
possible— for patients
on oral anticoagulants
consider Vitamin K,
prothrombin complex
concentrates (PCC),
rFVIIa, fresh frozen
plasma
When intracranial
pressure is felt to be
normal SBP should
be rapidly reduced to
140–160mmHg
hypertension, ICP
measurement should
be considered prior
to aggressive blood
pressure reduction
glucose < 180 mg/ dL
Avoid hyperthermia 39
References
39, 40
39
37
39
ACUTESTROKE 467
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more information see the excellent review of the subject
by Fogarty Mack.
CONCLUSION
37
While the importance of emergent intervention for acute
coronary syndrome is recognized by the lay public and the
new intern, we have been slow to convey the signicance and
opportunities for intervention for AIS. Fortunately our understanding of AIS and endovascular technology is progressing
rapidly, providing hope for what was once a devastating diagnosis. Anesthesiologists are critical to the care of patients suffering nonoperative or perioperative AIS, but we have much
to do in terms of determining optimal anestheticcare.
CASE- BASED LEARNING DISCUSSION
1. What are some reasons that stroke is dicult to
recognize in the perioperative setting?
2. What risk factors does our patient have for
perioperative stroke? In general, what known risk
factors for perioperative stroke are modiable? Which
risk factors are not modiable?
3. Would a regional technique have been preferable for
this patient? What are the pros and cons in support
of your response? Is there evidence to support one
technique over another?
4. What are the eligibility time frames (from last
known normal to stroke recognition) for systemic
thrombolysis? Is this window of eligibility dierent
for endovascular intervention? As a postoperative
patient, is this woman eligible for systemic
thrombolysis?
5. What is your management plan when you are asked to
evaluate this patient in the PACU? What studies need
to be done? What are your hemodynamicgoals?
REFERENCES
1. Prabhakaran S, et al. Acute stroke intervention: a system-
atic review. Journal of the American Medical Association.
2015;313(14):1451– 62.
2. World Health Organization. e top 10 causes of death. http://
www.who.int/ mediacentre/ factsheets/ fs310/ en/ (accessed Jan
3,2016).
3. Tissue plasminogen activator for acute ischemic stroke. e National
Institute of Neurological Disorders and Stroke rt- PA Stroke Study
Group. New England Journal of Medicine. 1995;333(24):1581– 8.
4. Berkhemer OA, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. New England Journal of Medicine.
2015;372(1):11– 20.
5. Goyal M, et al. Randomized assessment of rapid endovascular
treatment of ischemic stroke. New England Journal of Medicine.
2015;372(11):1019– 30.
6. Campbell BC, etal. Endovascular therapy for ischemic stroke with
perfusion- imaging selection. New England Journal of Medicine.
2015;372(11):1009– 18.
7. Saver JL, et al. Stent- retriever thrombectomy aer intravenous tPA vs. t- PA alone in stroke. New England Journal of Medicine.
2015;372(24):2285– 95.
8. Mashour GA, et al. Perioperative stroke and associated mortality aer noncardiac, nonneurologic surgery. Anesthesiology.
2011;114(6):1289– 96.
9. Saver JL, Time is brain— quantied. Stroke. 2006;37(1):263– 6.
10. Mozaarian D, et al. Heart disease and stroke statistics— 2015
update:a report from the American Heart Association. Circulation.
2015;131(4):e29– 322.
11. Hacke W, et al. rombolysis with alteplase 3 to 4.5 hours
aer acute ischemic stroke. New England Journal of Medicine.
2008;359(13):1317– 29.
12. Grotta JC, Hacke W. Stroke neurologist’s perspective on the new
endovascular trials. Stroke. 2015;46(6):1447– 52.
13. Talke PO, et al. Republished: Society for Neuroscience in
Anesthesiology and Critical Care expert consensus statement:anesthetic management of endovascular treatment for acute ischemic
stroke. Stroke. 2014;45(8):e138– 50.
14. Geeganage CM, Bath PM. Relationship between therapeutic
changes in blood pressure and outcomes in acute stroke:a metaregression. Hypertension. 2009;54(4):775– 81.
15. Jauch EC, etal. Guidelines for the early management of patients with
acute ischemic stroke:a guideline for healthcare professionals from
the American Heart Association/ American Stroke Association.
Stroke. 2013;44(3):870– 947.
16. Maier CM, etal. Optimal depth and duration of mild hypothermia
in a focal model of transient cerebral ischemia:eects on neurologic outcome, infarct size, apoptosis, and inammation. Stroke.
1998;29(10):2171– 80.
17. Villwock MR, et al. Trends in mortality following mechanical
thrombectomy for the treatment of acute ischemic stroke in the
USA. Journal of Neurointerventional Surgery. 2016;8(5):457–60.
18. Sharifpour M, etal. Incidence, predictors, and outcomes of perioperative stroke in noncarotid major vascular surgery. Anesth Analg.
2013;116(2):424– 34.
19. Ng JL, et al. Perioperative stroke in noncardiac, nonneurosurgical
surgery. Anesthesiology. 2011;115(4):879– 90.
20. Vermeer SE, etal. Silent brain infarcts:a systematic review. Lancet
Neurology. 2007;6(7):611– 9.
21. Mrkobrada M, e neurovision pilot study. Stroke.
2013;444:ATMP9.
22. Bateman BT, et al. Perioperative acute ischemic stroke in noncardiac and nonvascular surgery:incidence, risk factors, and outcomes.
Anesthesiology. 2009;110(2):231– 8.
23. Gialdini G, etal. Perioperative atrial brillation and the long- term
risk of ischemic stroke. Journal of the American Medical Association.
2014;312(6):616– 22.
24. Bijker JB, etal. Incidence of intraoperative hypotension as a function of the chosen denition:literature denitions applied to a retrospective cohort using automated data collection. Anesthesiology.
2007;107(2):213– 20.
25. Limburg M, et al. Ischemic stroke aer surgical procedures:clinical features, neuroimaging, and risk factors. Neurology.
1998;50(4):895– 901.
26. Didier TJ, In- hospital versus postdischarge management. Journal of
Neurosurgical Anesthesiology. 2012;24:4730– 4474.
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27. Bijker JB, et al. Intraoperative hypotension and perioperative
ischemic stroke aer general surgery: a nested case- control study.
Anesthesiology. 2012;116(3):658– 64.
28. Monk TG, et al. Association between intraoperative hypotension
and hypertension and 30- day postoperative mortality in noncardiac
surgery. Anesthesiology. 2015;123(2):307–19.
29. Walsh M, et al. Relationship between intraoperative mean arterial
pressure and clinical outcomes aer noncardiac surgery: toward
an empirical denition of hypotension. Anesthesiology.
2013;119(3):507– 15.
30. Jorgensen ME, etal. Time since stroke and risk of adverse outcomes
aer surgery— reply. Journal of the American Medical Association.
2014;312(18):1930– 1.
31. Powers WJ, Time since stroke and risk of adverse outcomes
aer surgery. Journal of the American Medical Association.
2014;312(18):1930.
32. Basques BA, et al. General compared with spinal anesthesia for
total hip arthroplasty. Journal of Bone and Joint Surgery- American
Volume. 2015;97(6):455– 61.
33. Mortazavi SM, et al. Perioperative stroke aer total joint arthroplasty: prevalence, predictors, and outcome. Journal of Bone and
Joint Surgery- American Volume. 2010;92(11):2095– 101.
34. Ezzet KA, Reversal of acute ischemic stroke aer THA using tissue
plasminogen activator. Orthopedics. 2013;36(5):e676– 8.
35. Selim M, Perioperative stroke. New England Journal of Medicine.
2007;356(7):706– 13.
36. van Asch CJ, etal. Incidence, case fatality, and functional outcome of
intracerebral haemorrhage over time, according to age, sex, and ethnic origin:a systematic review and meta- analysis. Lancet Neurology.
2010;9(2):167– 76.
37. Fogarty Mack P, Intracranial haemorrhage: therapeutic interventions and anaesthetic management. British Journal of Anaesthesia.
2014;113(Suppl 2):ii17– 25.
38. Hemphill JC 3rd, etal. e ICH score:a simple, reliable grading
scale for intracerebral hemorrhage. Stroke. 2001;32(4):891– 7.
39. Morgenstern LB, etal. Guidelines for the management of spontaneous intracerebral hemorrhage:a guideline for healthcare professionals from the American Heart Association/ American Stroke
Association. Stroke. 2010;41(9):2108– 29.
40. Kuramatsu JB, etal. Anticoagulant reversal, blood pressure levels,
and anticoagulant resumption in patients with anticoagulationrelated intracerebral hemorrhage. Journal of the American Medical
Association. 2015;313(8):824– 36.
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65.
POSTOPERATIVE VISUALLOSS
LorriA.Lee
CLINICALCASE
an irrigant for urologic procedures, and is not discussed
further.
A 62- year- old male with a BMI of 36 weighing 140kg,
hypertension, coronary artery disease s/ p coronary stents
Acute Angle Closure Glaucoma
×2 one year ago on clopidogrel and s/ p L1–3 posterior
spinal instrumentation and fusion 3years ago fell from a
rooop while cleaning gutters. He sustained le rib fractures and a T12 three- column burst fracture with breakage of his rods below. He now presents for a T10 to L5
spinal fusion with multimodal neuromonitoring including
motor and somatosensory evoked potentials and electromyography. e surgeon estimates the procedure will take
approximately 6– 7 hours and that he will lose approximately 1,000 to 1,500 mL blood. e plan is to provide
total intravenous anesthesia with large bore intravenous
access and direct arterial blood pressure monitoring. He
has been o of his clopidogrel for 5days and is neurologically intact.
Acute angle closure glaucoma in the perioperative phase is
very rare (approximately 1 in 25,000 cases) and has been
associated with extreme emotional distress and numerous
sympathomimetic or anticholinergic medications adminis-
tered for anesthesia to patients with narrow angles between
their iris and trabecular meshwork (irido- corneal angle).
1– 3
e increased sympathetic tone is thought to cause com-
plete obstruction or closure of this angle by contraction of
the iris dilator muscles with pupillary dilation that prevents
drainage of aqueous humor via the trabecular meshwork
and Schlemm canal lying within the angle. Several other
mechanisms for acute angle closure glaucoma also exist,
but this mechanism is the most commonly suggested in
the perioperative period. e prone position has also been
RARER CAUSES OFPOSTOPERATIVE VISUAL
LOSS:MEDICAL/ SURGICAL EMERGENCIES
ere are two main division of postoperative visual loss
(POVL); namely POVL with pain and POVL without
pain. Understanding this cardinal sign and the dierential
that goes with each is essential.
suggested to predispose to this condition in susceptible
patients with narrow angles. e buildup of aqueous humor
causes a rise in intraocular pressure greater than 21mmHg
and, if the pressures are very high, can result in acute loss of
vision within several hours. Risk factors for acute angle clo-
sure glaucoma in the community include Asian and Inuit
Eskimo ethnicity (narrower angles), hypermetropia (nar-
rower angles), female sex (shallower anterior chambers) and
the elderly (anterior chamber depth decreases with age).
VISION LOSS WITHPAIN
Any POVL requires an emergent or urgent ophthalmologic (preferably neuro- ophthalmologic) consultation, but
some POVL diagnoses are considered medical or surgical
emergencies. ese POVL diagnoses that require prompt
intervention to limit further loss of vision and to minimize
permanent loss of vision are very rare and include acute
angle closure glaucoma, retrobulbar hematoma, and pituitary apoplexy (Table 65.1).1 Glycine- induced visual loss is
exceedingly uncommon, as glycine is rarely used today as
Patients present with unilateral or bilateral pain, headaches,
blurred vision with halos, and nausea and vomiting. Exam
reveals xed and mid- dilated pupils, injected conjunctiva,
edematous corneal epithelium, and increased intraocular
pressure greater than 21mmHg (Table 65.1). It is consid-
ered a medical emergency requiring urgent therapy with
medications for lowering intraocular pressure followed by
more denitive surgical intervention with a peripheral iri-
dotomy. Medications (dilated exam) or conditions (dark
room, eye patches) that dilate the pupil are contraindicated,
as they can worsen the angle closure.
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TABLE65.1 MEDICAL AND SURGICAL OCULAR EMERGENCIES WITHVISUAL LOSS WITHPAIN
Diagnosis
Acute Angle
Closure
Glaucoma
Retrobulbar
Hematoma
Most Commonly
Associated Procedures
EtiologySuggested Risk
Factors
Any type of surgery Sympathomimetic
or anticholinergic
medications
with mydriatic
effect. Iris dilator
muscles contract
and obstruct the
drainage canal
for aqueous
humor in the
iridocorneal angle;
prone position;
Asian or Inuit
Eskimo ethnicity,
hypermetropia,
female sex, elderly,
baseline narrow
angle or shallow
anterior chamber.
Periorbital surgery or
trauma; endoscopic
sinus surgery;
oribital oor fracture
repair high risk; any
procedure with strong
Valsalva, hypertension,
anticoagulation
Surgery, trauma,
anticoagulation,
hypertension,
straining/ Valsalva
(coughing,
wretching, vomiting,
sneezing)
Presentation and
Ophthalmologic
Examination Findings
Unilateral > bilateral.
May have delayed
onset more than 12
hours postoperatively;
painful red eye and
ipsilateral headache;
nausea/ vomiting; halos
with blurred vision;
conjunctival erythema,
corneal epithelial
edema, xed and middilated pupil, intraocular
pressure > 21mmHg.
Unilateral. Usually within
24 hours postoperatively
but can occur 9days
after surger y/ trauma.
Very painful (stabbing)
pressure with nausea,
vomiting, visual ashes,
double vision, amaurosis
fugax, hemianopsia,
paralysis or weakness
of extraocular muscles,
erythematous eye with
marked proptosis, eyelid
bruising, relative afferent
or absent pupillary
defect
Workup/ Urgency
History including symptoms,
ophthalmologic examination
including external eye,
intraocular pressure and
funduscopic examination
(NOT DILATED)
Urgency:Permanent loss of
vision can occur within a few
hours of onset of symptoms.
History including symptoms,
ophthalmologic examination.
Imaging may delay denitive
therapy.
Urgency:Permanent visual
loss can occur within a few
hours of onset of symptoms.
Treatment/ Prognosis
Medications to lower
intraocular pressure
(beta blocker eye gtts,
acetazolamide, etc.);
peripheral iridotomy for
medication- resistant
cases; anterior chamber
paracentesis; avoid dark
rooms, eye patches, or
anything that will cause
pupillary dilation.
Prognosis:Good if
intraocular pressure can be
quickly controlled
If visual loss present,
surgical emergency
with lateral canthotomy
or inferior cantholysis
at bedside using local
anesthesia followed
by denitive surgical
treatment in the operating
room.
Prognosis:Depends on
time from symptoms to
decompression— usually
good if done within 1–2
hours of symptoms.
Pituitary
Apoplexy
SOURCE:Adapted with permission from:Lee LA, Newman NJ. Postoperative visual loss after anesthesia for nonocular surgery. In:UpToDate, Post TW (Ed), UpToDate, Waltham, MA.
(Accessed on [DATE].) Copyright © 2016 UpToDate, Inc. For more information visit www.uptodate.com.
Retrobulbar Hematoma
Retrobulbar hematoma is considered a surgical emergency
and is associated with facial or periorbital surgery or trauma
including endoscopic sinus surgery, plastic surgery, and
Any procedure—
cardiac, prostate,
pregnancy
Profound shock,
hypertension,
anticoagulation,
pituitary gland
stimulation, head
trauma, irradiation
Onset may occur from
immediate postoperative
period to 3months
later; severe headache,
nausea, vomiting,
altered mental status,
possible Addisonian
crisis from loss of
hormones; blurred vision
to blindness; paralyzed
or weak extraocular
muscles, often dilated
xed pupil from cranial
nerve III involvement
retrobulbar injections. Although it is rare overall, it is the
most common cause of vision loss associated with repair
of orbital oor fractures, occurring in slightly more than
3% of cases.
History including symptoms,
ophthalmologic examination
including external eye, and
funduscopic examination;
electrolytes, hormone levels,
CT or MRI head
Urgency:Permanent visual
loss or cerebral ischemia
can occur if decompression
delayed, though signicant
visual improvement has been
reported as late as 1week
post symptom onset.
1,4,5
Less commonly, it can be caused by severe
If visual loss or altered
mental status present,
need urgent surgical
decompression with
hormone/ corticosteroid
replacement.
Prognosis:Good if surgical
decompression done early
with symptoms of visual
loss or altered mental
status.
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wretching, vomiting, coughing, or straining, particularly
if the patient is anticoagulated. e cause of the vision loss
is compression of the optic nerve or central retinal artery
occlusion by the expanding hematoma, which can result in
permanent vision loss within hours. Marked proptosis from
the hematoma, a pressure sensation, and painful loss of vision
are prominent distinguishing features. Patients will also
oen have nausea, vomiting, double vision, visual ashes,
anterior ischemic optic neuropathy (AION), posterior
ischemic optic neuropathy (PION), central retinal artery
occlusion (CRAO), and cerebral or cortical visual loss
(CVL), also known as cortical blindness (Table 65.2). With
the exception of cortical blindness, recovery of vision with
these POVL diagnoses is poor and denitive treatment has
not been identied. Care is directed at restoring normal
physiologic parameters for all of these ischemic events.
1,7
amaurosis fugax, hemianopsia, and occasionally paralysis
or weakness of the extraocular muscles (ophthalmoplegia).
Pupillary light reexes may demonstrate a relative aerent or
absent pupillary defect. Treatment should be immediate and
focused on surgical intervention, as vision loss can be permanent by as early as 1 to 2 hours. Emergent lateral canthotomy
or inferior cantholysis under local anesthesia at the bedside
is the preferred treatment, followed by more denitive surgical decompression in the operatingroom.
Pituitary Apoplexy
Pituitary apoplexy results from hemorrhage or infarction
within the pituitary gland and is oen associated with a pituitary tumor.
1,6
It can be caused by states of profound shock,
hypertension, hormonal manipulation, localized radiation
to the pituitary gland, trauma, and anticoagulation. Risk
factors for pituitary apoplexy are found in less than half of
patients in large series. is condition may be life threatening, with associated acute loss of hormonal production with
an Addisonian crisis. Patients oen have a diuse headache
and nausea and may have visual acuity or visual eld decits
along with paralysis or weakness of the extraocular muscles.
Workup includes a CT or MRI of the head, electrolytes, and
hormone levels. Urgent surgical decompression may be indi-
Anterior and Posterior Ischemic Optic Neuropathy
e exact mechanism for AION and PION is primarily speculative and based on case reports, large case series,
and case- control studies, where a variety of associated factors have been implicated. Interstitial edema formation and
hypoperfusion from reduced inow, obstructed outow, or
both are thought to be precipitating events for injury to the
optic nerve.
1,7,8
Anterior ischemic optic neuropathy is associated with injury to the optic nerve head anterior to the
lamina cribrosa, which is a thin layer of mesh- like connective tissue that separates the intraocular from the retrobulbar spaces and pressures.
8,9
It is more commonly associated
with cardiac bypass procedures and major vascular procedures. Posterior ischemic optic neuropathy occurs posterior
to the lamina cribrosa. Posterior ischemic optic neuropathy
appears to be more commonly associated with procedures
that are associated with increased venous pressure in the head
for prolonged periods such as prone spine surgery, bilateral
radical head and neck surgery, and robotic and laparoscopic
procedures in steep head- down position. Histopathologic
examination of the optic nerves of patients who have developed PION and subsequently died have revealed either central or peripheral hemorrhagic infarction.
10,11
cated for some cases with visual loss or altered mental status along with medical therapy including hormone/ steroid
replacement. Improvement of vision has been reported with
decompression as late as 1 week aer symptomsonset.
Central Retinal Artery Occlusion
Central retinal artery occlusion can occur from thromboembolic phenomenon or direct compression of the globe. e
COMMON CAUSES OFPOVL:VISION LOSS
WITHOUTPAIN
PATHOPHYSIOLOGY OFDISEASESTATE
Mechanism
injury is almost always unilateral and is diagnosed by the distinctive presence of a cherry- red spot at the macula, where
the choriocapillaris provides blood supply superimposed
on the wider background of a pale ischemic retina that was
previously supplied by the central retinal artery prior to its
occlusion. e funduscopic ndings in CRAO have been
replicated in animals with compression of the globe.
12
Most diagnoses for POVL aer nonocular surgery fall into
four major categories unless there is preexisting recent facial
trauma, medical conditions, or at- risk ophthalmologic
anatomic features that predispose patients to certain ophthalmologic complications. ese four categories include
Cerebral VisualLoss
Cerebral visual loss can be caused by thromboembolic phenomenon in the posterior cerebral arteries or profound
472 SECTION A. CEREBRAL ORIGIN
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TABLE65.2 MORE COMMON CAUSES OFPOVL:LOSS OFVISION WITHOUTPAIN
Diagnosis
Anterior
Ischemic
Optic
Neuropathy
Posterior
Ischemic
Optic
Neuropathy
Most Commonly
Associated
Procedures
Cardiac, prone
spine, major
vascular, head
and neck
Prone spine,
head and
neck, cardiac,
laparoscopic or
robotic steep
Trendelenburg
position for
prolonged
periods
Etiology- Suggested Risk
Factors
Vascular disease,
hypotension, anemia,
small optic nerve cupto- disc ratio
Elevated venous
pressure in head for
prolonged duration,
hypotension, anemia,
Wilson spine frame,
obesity, male sex, blood
loss, lower percent
of colloid in uid
administration
Presentation and Ophthalmologic
Examination Findings
Bilateral > unilateral; onset
may be delayed 1–3days
postoperatively; may progress
over few days; altitudinal eld
cuts, scotoma to complete loss
of vision with no light perception;
relative afferent pupillary defect.
Funduscopic Examination:Early
exam with peripapillary ameshaped or splinter hemorrhages,
optic disc edema, narrowed
retinal vessels. Late exam
several weeks to month postinjury with normal fundus except
for optic disc pallor.
Bilateral > unilateral; onset is
immediate on awakening from
anesthesia with no progression
of severity of decit; altitudinal
eld cuts, scotoma to complete
loss of vision with no light
perception; relative afferent
pupillary defect.
Funduscopic Examination:Early
exam:normal; Late exam
several weeks to months postinjury:optic disc pallor.
Workup
History with
symptoms and
ophthalmologic
examination
including pupillary
light reexes,
external eye
and dilated
funduscopic
examinations.
History with
symptoms and
ophthalmologic
examination
including pupillary
light reexes,
external eye
and dilated
funduscopic
examinations
Treatment/ Prognosis
No proven benecial
treatment.
Theoretical treatment to
optimize oxygen delivery
including normalizing blood
pressure and cardiac output,
oxygenation. Head elevation
to decrease edema as blood
pressure permits.
Prognosis:Permanent loss
of vision with slight chance
of vision recovery, but not to
baseline.
No proven benecial
treatment.
Theoretical treatment to
optimize oxygen delivery
including normalizing blood
pressure and cardiac output,
oxygenation. Head elevation
to decrease edema as blood
pressure permits.
Prognosis:Permanent loss
of vision with slight chance
of vision recovery, but not to
baseline.
Central
Retinal Artery
Occlusion
Cerebral
Visual Loss
SOURCE:Adapted with permission from:Lee LA, Newman NJ. Postoperative visual loss after anesthesia for nonocular surgery. In:UpToDate, Post TW (Ed), UpToDate, Waltham, MA.
(Accessed on [DATE].) Copyright © 2016 UpToDate, Inc. For more information visit www.uptodate.com. Lee LA, etal. Postoperative ischemic optic neuropathy. Spine. 2010;35(9
Suppl):S105– 16.
Prone spine,
cardiac, head
and neck, facial
injections
Spinal fusion,
cardiac,
nonfusion
orthopedic (hip,
femur, knee)
Primarily globe
compression
perioperatively (prone
position, horseshoe
headrest), but also
embolic causes; GA
with nitrous oxide
within 2months of
having an intraocular
gas bubble placed for
retinal surgery.
Profound, prolonged
hypotension; emboli
(air, fat, cement, etc.);
atherosclerotic disease
Unilateral; immediate onset of
symptoms with awakening from
anesthesia with no progression
of symptoms; profound loss of
vision in affected eye; may have
periorbital signs of trauma if
caused by globe compression;
Funduscopic Examination:Cherry
red spot at macula; ischemic,
white retina; narrowed retinal
arterioles.
Onset immediate on awakening
from anesthesia; may be
bilateral with total or near- total
blindness with preserved small
islands of central vision or may
be unilateral with contralateral
homonymous hemianopsia.
Pupillary light reexes and
funduscopic examination normal
History with
symptoms and
ophthalmologic
examination
including pupillary
light reexes,
intraocular
pressure
measurement,
external eye
and funduscopic
examinations
History with
symptoms and
ophthalmologic
examination
including pupillary
light reexes,
external eye
and funduscopic
examinations.
CT or MRI head
No proven benecial
treatment. May use inhaled
oxygen with 5% carbon
dioxide. Consider risk to
benet ratio for directed intraarterial thrombolysis.
Prognosis:Poor, may have
slight recovery.
Optimize oxygen delivery
with normalization of
blood pressure, cardiac
output, cerebral blood ow,
oxygenation.
Prognosis:Variable— most do
not recover to baseline
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hypoperfusion resulting in watershed infarctions in the
parieto- occiptal territory. It is associated with cases with
high thromboembolic loads and/ or hypoperfusion such as
cardiac bypass procedures, instrumented spine surgery, and
lower extremity joint replacement surgery.
1,7
AION is associated. Smaller case- control studies examining POVL have been limited by small numbers, combining multiple disparate ophthalmologic diagnoses such
as ION, CRAO, and cortical blindness into one group,
and/ or combining multiple disparate types of operations
into onegroup.
RISK AND PREVENTION
e incidence of any POVL based on the nationwide
inpatient sample varies from 0.12 per 10,000 patients for
low- risk procedures such as appendectomy to higher risk
procedures such as spinal fusion at 3 per 10,000 patients
and cardiac surgery at 8.6 per 10,000 patients.13 e incidence varies between institutions with multicenter tertiarycare institutions for spinal surgery reporting an incidence
as high as 1 in 500 patients.14 ese dierences are probably related to the types of procedures being performed
and local institutional practice patterns as well as a possible
contribution from unidentied geographic and genetic risk
factors.
e largest case- control study to date for prone spinal
fusion surgery, which is considered high risk for POVL,
combined both AION and PION cases aer preliminary
analysis found no dierences in the preoperative or intraoperative characteristics between the two groups.15 is
study examined 80 cases of ION aer prone spinal fusion
surgery and matched each case to four control prone spinal
fusion cases without ION. e six risk factors identied for
ION included male sex, obesity, use of the Wilson frame
(which places the head considerably lower than the heart),
duration, blood loss and decreased use of colloid in the
uid administration. ere were no dierences between
POVL cases and controls in the percent of patients with
vascular disease, the lowest hematocrit, or with a 40%
reduction from baseline blood pressure for 30 minutes.
Anterior and Posterior Ischemic Optic Neuropathy
Anterior ischemic optic neuropathy is one of the most common causes of spontaneous loss of vision outside of the surgical arena, typically occurring in the sixth decade of life and
frequently associated with some atherosclerotic risk factors.
Spontaneously occurring PION is far less common in the
community. It is unclear whether there is any overlap in the
clinical, anatomic, or genetic risk factors for the spontaneous forms of ION that predispose to the development of
ION in the perioperative setting. Asmall cup- to- optic- disc
ratio measured in the fundus is a risk factor for spontaneously occurring AION,8 but its presence in perioperative
AION is inconsistent.
Perioperative AION is most common in cardiac, prone
spinal fusion, major vascular, and head and neck procedures. Perioperative PION is most common in prone spi-
Asimilar case- control study of this size has not yet been
performed for cardiac bypass surgery. Prevention of ION
is aimed at avoiding use of the Wilson surgical frame when
possible, minimizing blood loss with use of antibrinolytics, topical hemostatic agents, good surgical hemostasis
with the electrocautery, keeping the head neutral and level
or higher than the heart to minimize venous congestion,
and using more colloid in the uid administration. Most
clinicians still recommend avoiding signicant hypotension or anemia in procedures at high risk for this ischemic
injury, as this study was not a randomized controlled trial.
Staging of very prolonged prone spine procedures has been
recommended as another potential strategy for risk reduction for ION, though potentially prolonged hospital stays,
increased risk of infection and deep venous thrombosis,
and increased costs should be considered when making
these decisions.
nal fusion, bilateral head and neck, and laparoscopic or
robotic steep head- down procedures for prolonged periods of time. Posterior ischemic optic neuropathy occurs
more commonly than AION in procedures where there
is prolonged duration of elevated venous pressure in the
head. Factors that have been proposed to be contributory
to AION and PION from case reports and case series
overlap considerably and include blood loss, duration,
hypotension, anemia, vascular disease, high- dose vasoactive agents, and large- volume resuscitation.
1,7
However,
it is unclear whether these factors are causative or are
more commonly present in the procedures with which
Central Retinal Artery Occlusion
ough CRAO can be caused by emboli, the vast majority
of cases that occur perioperatively appear to be related to
direct globe compression, usually in the prone position. e
horseshoe headrest has been associated with this complication as early as 1954, when Hollenhorst reported on a series
of eight patients who developed unilateral blindness while
having prone suboccipital or cervical spine surgery with
their heads positioned in horseshoe headrests.12 e cases
that lasted 2 hours ranged from full recovery to recovery
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475
with a central scotoma. Cases that lasted 3 hours had some
preserved isles of vision. Cases that lasted 4 to 6 hours had
no recovery of vision. e horseshoe headrest shape has a
very narrow margin of safety around the eyes and requires
no movement of the head once it is positioned and checked.
For many procedures, movement of the head is common
and the one eye may come to rest on the edge of the horseshoe headrest. Checking the eyes regularly during these
procedures on this headrest is also dicult because of the
location of the surgeons and surgical equipment and operating room sta in the same vicinity. Most spine surgeons
today use Mayeld head pins for cervical spine surgery;
these pins suspend the head immobile with the face completely free of pressure. So foam cushions with cutouts for
the eyes and nose and endotracheal tube are frequently used
during prone spine surgery below the cervical level. Patients
can also develop CRAO from the eye resting on the foam
portion of this cushion, but regular checking of the eyes and
nose on this headrest can typically be easily accomplished.
pituitary apoplexy, where eye pain, headaches, nausea and
vomiting, and altered mental status may be prominent features.1 Some of these symptoms may be dulled in the immediate postoperative period with residual anesthetic and
opioids on board, or these symptoms may be caused by the
anesthetic and opioid medications, making denitive diagnosis more challenging. Ischemic optic neuropathy, CRAO,
and cortical blindness have distinctive ophthalmologic
exams with dierences between pupillary light reexes,
visual eld decits, and funduscopic ndings (Table 65.2).
Ischemic optic neuropathy is usually bilateral, reecting
the proposed systemic etiology of the injury, but may be
unilateral. Central retinal artery occlusion is almost always
unilateral, consistent with the head slightly shiing on the
headrest and one eye becoming compressed. Cortical blindness may be unilateral or bilateral. Both ION and CRAO
usually have abnormal pupillary light reexes, whereas cortical blindness has normal light reexes. Typically ION has
altitudinal eld cuts, scotoma, or no light perception, while
CRAO is usually associated with profound visual loss, oen
Cerebral VisualLoss
with no light perception.
1,7
Risk factors for cortical blindness include profound sys-
MANAGEMENT OFTHE PATIENT
temic hypoperfusion, procedures with a high embolic load
such as cardiac bypass, instrumented spinal fusion, orthopedic lower extremity joint or femur surgeries, and patients
with right- to- le shunts such as a patent foramen ovale.
Prevention of cortical blindness is aimed at avoidance of
hypoperfusion of the brain when possible. For signicant
right- to- le shunts, some clinicians have advocated closure
of patent foramen ovales preoperatively before procedures
at high risk for ION, though the risk- to- benet ratio is
unclear.
As previously noted, the rst step in management of a
patient with POVL is to obtain an urgent or emergent
ophthalmologic consultation. Based on the history and
external and funduscopic examination from the consultant,
they may recommend a CT or MRI if CVL or pituitary
apoplexy is suspected. Visual evoked potentials may be recommended for AION and PION at a later date for conrmation and prognosis.
For both AION and PION, there are no evidence-
based proven treatments. erapy is empiric and based
ASSESSMENT OFTHE PATIENT:PRESENTING
SIGNS AND SYMPTOMS
First and foremost, any patient presenting with loss of vision
should have an urgent ophthalmologic consultation, as some
causes are considered medical or surgical emergencies where
delay in care could result in permanent loss of vision. Abrief,
cursory history and exam of the patient should be sucient
for the ophthalmologic consultant. Prolonged delays for
medical record retrieval, family consultation, or literature or
textbook searches for ophthalmologic examination before
calling the consultant should be avoided, as vision loss for
certain diagnoses can occur in as little as 1 to 2hours.
Ischemic optic neuropathy, CRAO, and cortical blindness are associated with painless loss of vision, unlike
acute angle closure glaucoma, retrobulbar hematoma, and
on normalization of physiology including blood pressure,
cardiac output, and oxygenation.
1,7
For signicant facial
edema, elevation of the head while maintaining a normal
perfusion pressure may also be advised. Case reports have
described use of mannitol, high- dose steroids, and hyperbaric oxygen with variable success. Recovery of vision with
AION and PION is poor, with prognosis tied to severity
of visual loss on rst complaint. Patients very rarely recover
full baseline vision.
Perioperative CRAO also has no proven eective
therapy, but treatments with theoretical benet include
inhaled oxygen in 5% carbon dioxide and acetazolamide.1
Depending on the procedure and risk of harm with bleeding postoperatively, directed intra- arterial thrombolysis is
another potential treatment option with theoretical benet. Recovery of vision is also poor with this diagnosis.
POSTOPERATIVE VISUALLOSS 475
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