U.S. patent application number 14/486019 was filed with the patent office on 2014-12-25 for optic function monitoring process and apparatus.
The applicant listed for this patent is Donald Bernstein, Ricardo Bravo, Laurence M. McKinley. Invention is credited to Donald Bernstein, Ricardo Bravo, Laurence M. McKinley.
Application Number | 20140378789 14/486019 |
Document ID | / |
Family ID | 41507442 |
Filed Date | 2014-12-25 |
United States Patent
Application |
20140378789 |
Kind Code |
A1 |
McKinley; Laurence M. ; et
al. |
December 25, 2014 |
OPTIC FUNCTION MONITORING PROCESS AND APPARATUS
Abstract
A method and apparatus for monitoring optic function is
provided. The apparatus and method relies on two principle modes of
measuring the function of the optic nerve, namely, monitoring VEPs
for neural function, and monitoring at least one additional
parameter of optic function such as intraocular pressure, blood
flow or location of the eye to provide a multi-variable optic
function monitor. The method and apparatus is proposed for the use
to diagnose and potentially prevent the incidence of POVL and
anaesthesia awareness in patients during medical procedures.
Inventors: |
McKinley; Laurence M.;
(Escondido, CA) ; Bernstein; Donald; (Rancho Santa
Fe, CA) ; Bravo; Ricardo; (South Gate, CA) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
McKinley; Laurence M.
Bernstein; Donald
Bravo; Ricardo |
Escondido
Rancho Santa Fe
South Gate |
CA
CA
CA |
US
US
US |
|
|
Family ID: |
41507442 |
Appl. No.: |
14/486019 |
Filed: |
September 15, 2014 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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12500216 |
Jul 9, 2009 |
8862217 |
|
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14486019 |
|
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61079258 |
Jul 9, 2008 |
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Current U.S.
Class: |
600/301 ;
600/558 |
Current CPC
Class: |
A61B 3/0008 20130101;
A61B 3/1241 20130101; A61B 3/16 20130101; A61B 5/0205 20130101;
A61B 5/4041 20130101; A61B 5/7225 20130101; A61B 3/1233 20130101;
A61B 5/7282 20130101; A61B 5/412 20130101; A61B 3/0025 20130101;
A61B 5/4076 20130101; A61B 3/113 20130101; A61B 3/18 20130101; A61B
5/04842 20130101; A61B 5/6843 20130101; A61B 5/6803 20130101; A61B
5/6844 20130101; A61B 5/04001 20130101; A61B 5/4047 20130101; A61B
5/4821 20130101 |
Class at
Publication: |
600/301 ;
600/558 |
International
Class: |
A61B 5/00 20060101
A61B005/00; A61B 3/12 20060101 A61B003/12; A61B 3/16 20060101
A61B003/16; A61B 3/00 20060101 A61B003/00; A61B 5/0484 20060101
A61B005/0484; A61B 5/0205 20060101 A61B005/0205 |
Claims
1. An optic monitor comprising: at least one sensor band having an
inner surface designed to be securedly attached to at least the
outer surface of the eyelid; at least one optic function sensor
positioned on the inner surface of the sensor band, said at least
one optic function sensor being designed to stimulate and monitor
the function of at least one portion of the eye selected from the
group consisting of the optic nerve, the optic chiasm and the optic
cortex to produce signals, said signals forming a visual evoked
potential, the visual evoked potential being characterized by a
waveform, and output an optic function signal; and at least one
data processor in signal communication with the at least one sensor
band to collect and process the optic function signal from the at
least one sensor such that changes in the waveform of the visual
evoked potential over time are monitored for an adverse change in
optic function, wherein the processing includes an analysis of at
least the temporal interval (TL1) between the onset of stimulation
(t.sub.0) and the absolute magnitude of the second measured maximum
visual evoked potential (EVP2) after stimulation, and at least one
aspect of the waveform of EVP2 selected from the group consisting
of the vertical distance (P2) between the maximum value of the
upslope of EVP2 to the nadir (N3) of the EVP2, the peak first
time-derivative of EVP2, the mean slope of EVP2, and combinations
thereof and communicating the output signals to a user.
2. The device of claim 1, further including a pressure sensor
positioned on the inner surface of the sensor band, said pressure
sensor being designed to monitor the intraocular pressure of the
eye and output a pressure signal.
3. The device of claim 1, further including a blood flow sensor
positioned on the inner surface of the sensor band, said blood flow
sensor being designed to monitor one of either retinal or optic
blood flow and output a blood flow signal.
4. The device of claim 1, wherein the at least one optic function
sensor stimulates the eye by producing a visual evoked potential in
at least one of the nasal or temporal halves of the optic
nerve.
5. The device of claim 4, wherein the at least one optic function
sensor is a light emitting diode.
6. The device of claim 2, wherein the pressure sensor is a
tonometer.
7. The device of claim 3, wherein the blood flow sensor is selected
from one of either a near-infrared spectrometer or a laser Doppler
velocimeter.
8. The device of claim 1, further comprising a location sensor
being designed to monitor the placement of said eye in relation to
the eye socket and output an eye location signal.
9. The device of claim 8, wherein the location sensor is a pressure
transducer.
10. The device of claim 1, further comprising a plurality of
preprogrammed thresholds for each of the output signals such that
the device gives an automated warning should the preprogrammed
thresholds be reached.
11. The device of claim 1, wherein the sensor band is incorporated
into an eye-cover.
12. The device of claim 1, wherein the eye-cover is a pair of
goggles.
13. The device of claim 1, wherein the stimulating and monitoring
the function of the eye further includes positioning at least two
sensors and two visual evoked potential stimulators proximate to
the eye.
14. The device of claim 1, wherein the adverse change is one of
either perioperative vision loss (POVL) or anesthesia
awareness.
15. The device of claim 1, wherein the at least one processor
produces an evaluation number from the waveform of the VEP, said
evaluation number being indicative of at least the level of optic
function.
16. The device of claim 1, wherein the at least one processor
further includes computing an anesthesia evaluation number from the
VEP waveform in accordance with an equation selected from the group
consisting of: P2/TL1, where P2 is the vertical distance between
the maximum value of the upslope of a second and largest maximum
visual evoked potential (EVP2) measured by the waveform to the
nadir (N3) of the EVP2, and TL1 is the temporal interval between
the onset of stimulation (t.sub.0) and the absolute magnitude of
the second evoked potential (EVP2); (P2/TL1).sup.n, wherein n is an
exponent between 0.333 and 3; (P2).sup.x/(TL1).sup.y, where P2 is
the vertical distance between the maximum value of the upslope of a
second and largest maximum visual evoked potential (EVP2) measured
by the waveform to the nadir (N3) of the EVP2, and TL1 is the
temporal interval between the onset of stimulation (t.sub.0) and
the absolute magnitude of the EVP2, and wherein x and y are an
exponents between 0.333 and 3; ((P2).sup.x/(TL1).sup.y).sup.n where
n is an exponent between 0.333 and 3;
((P2).sup.x/(TL1).sup.y).sup.n where n is an exponent between 0.5
and 2; (.delta.(EVP2)/.delta.t.sub.max)/TL1, where (EVP2) is a
second and largest maximum visual evoked potential,
.delta.(EVP2)/.delta.t.sub.max is the peak forward upslope of EVP2,
and TL1 is the temporal interval between the onset of stimulation
(t.sub.0) and the absolute magnitude of EVP2;
(.delta.(EVP2)/.delta.t.sub.max).sup.x/(TL1).sup.y, where (EVP2) is
a second and largest maximum visual evoked potential,
.delta.(EVP2)/.delta.t.sub.max is the peak forward upslope of EVP2,
TL1 is the temporal interval between the onset of stimulation
(t.sub.0) and the absolute magnitude of EVP2, and wherein x and y
are an exponents between 0.333 and 3;
((.delta.(EVP2)/.delta.t.sub.max).sup.x/(TL1).sup.y).sup.n where n
is an exponent between 0.333 and 3;
(.delta.(EVP2)/.delta.t.sub.mean)/TL1, where (EVP2) is a second and
largest maximum visual evoked potential,
.delta.(EVP2)/.delta.t.sub.mean is the mean slope of EVP2 and P2,
and TL1 is the temporal interval between the onset of stimulation
(t.sub.0) and the absolute magnitude of EVP2, and where P2 is the
vertical distance between the maximum value of the upslope of a
second and largest maximum visual evoked potential (EVP2) measured
by the waveform to the nadir (N3) of the EVP2;
(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(TL1).sup.y, where (EVP2)
is a second and largest maximum visual evoked potential,
.delta.(EVP2)/.delta.t.sub.mean is the mean slope of EVP2 and P2,
TL1 is the temporal interval between the onset of stimulation
(t.sub.0) and the absolute magnitude of EVP2, and wherein x and y
are an exponents between 0.333 and 3, and where P2 is the vertical
distance between the maximum value of the upslope of a second and
largest maximum visual evoked potential (EVP2) measured by the
waveform to the nadir (N3) of the EVP2;
(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.sup.z).sup.m
in (.mu.V/ms), where (EVP2) is a second and largest maximum visual
evoked potential, .delta.(EVP2)/.delta.t.sub.mean is the quotient
of P2 and the temporal interval occurring between the onset of the
upslope of EVP2 and P2, t.sub.1 is the absolute magnitude of EVP2,
P2 is the vertical distance between the maximum value of the
upslope of a second and largest maximum visual evoked potential
(EVP2) measured by the waveform to the nadir (N3) of the EVP2, and
wherein x and y are an exponents between 0.333 and 3;
((.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.sup.z).sup.m).-
sup.n where n is an exponent between 0.333 and 3;
.delta.(EVP2)/.delta.t.sub.max/t.sub.1/P.sub.2 in (.mu.V/ms), where
(EVP2) is a second and largest maximum visual evoked potential,
.delta.(EVP2)/.delta.t.sub.max is the peak forward upslope of EVP2,
t.sub.1 is the absolute magnitude of EVP2, and P2 is the vertical
distance between the maximum value of the upslope of a second and
largest maximum visual evoked potential (EVP2) measured by the
waveform to the nadir (N3) of the EVP2;
.delta.(EVP2)/.delta.t.sub.max/t.sub.1/P2 in (.mu.V/ms), where
(EVP2) is a second and largest maximum visual evoked potential,
t.sub.max .delta.(EVP2)/.delta.t.sub.max is the peak forward
upslope of EVP2, t.sub.1 is the absolute magnitude of EVP2, P2 is
the vertical distance between the maximum value of the upslope of a
second and largest maximum visual evoked potential (EVP2) measured
by the waveform to the nadir (N3) of the EVP2, and wherein x, y and
z are an exponents between 0.333 and 3;
(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.sup.z).sup.m
in (.mu.V/ms), where (EVP2) is a second and largest maximum visual
evoked potential, .delta.(EVP2)/.delta.t.sub.mean is the mean slope
of EVP2 and P2, t.sub.1 is the absolute magnitude of EVP2, P2 is
the vertical distance between the maximum value of the upslope of a
second and largest maximum visual evoked potential (EVP2) measured
by the waveform to the nadir (N3) of the EVP2, and wherein x, y, z
and m are an exponents between 0.333 and 3;
((.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.sup.z).sup.m).-
sup.n where n is an exponent between 0.333 and 3;
(.delta.(EVP2)/.delta.t.sub.max).sup.x/(t.sub.1.sup.y/P2.sup.z).sup.m
in (.mu.V/ms), where (EVP2) is a second and largest maximum visual
evoked potential, .delta.(EVP2)/.delta.t.sub.max is the peak
forward upslope of EVP2, t.sub.1 is the absolute magnitude of
EVP2), P2 is the vertical distance between the maximum value of the
upslope of a second and largest maximum visual evoked potential
(EVP2) measured by the waveform to the nadir (N3) of the EVP2, and
wherein x, y, z and m are an exponents between 0.333 and 3; and
((.delta.(EVP2)/.delta.t.sub.max).sup.x/(t.sub.1.sup.y/P2.sup.z).sup.m).s-
up.n where n is an exponent between 0.333 and 3.
17. The device of claim 16, wherein the at least one processor
further computes a dimensionless anesthesia evaluation index,
obtained by dividing the anesthesia evaluation number by a static
control value defined as the value of the anesthesia evaluation
number measured at a time before the induction of anesthesia.
18. The device of claim 1, wherein the at least one processor
further computes two anesthesia evaluation numbers from the VEP
waveform in accordance with the equation, (P2).sup.x/(TL1).sup.y,
where P2 is the vertical distance between the maximum value of the
upslope of a second and largest maximum visual evoked potential
(EVP2) measured by the waveform to the nadir (N3) of the EVP2, and
TL1 is the temporal interval between the onset of stimulation
(t.sub.0) and the absolute magnitude of the EVP2, and wherein x and
y are an exponents between 0.333 and 3; computing a third
anesthesia evaluation number according to the equation
((P2).sup.x/(TL1).sup.y).sup.n where n is an exponent between 0.333
and 3; and further comprising computing a dimensionless anesthesia
evaluation index obtained by dividing the third anesthesia
evaluation number by a static control value defined as the value of
the third anesthesia evaluation number measured at a time before
the induction of anesthesia.
19. The device of claim 16, wherein the at least one processor
further calibrates the anesthesia evaluation number by measuring
the anesthesia evaluation number prior to the administration of an
anesthesia.
Description
CROSS-REFERENCE TO RELATED APPLICATIONS
[0001] The current application is a continuation of U.S. patent
application Ser. No. 12/500,216, filed Jul. 9, 2009, which claimed
priority to U.S. Provisional Application No. 61/079,258, filed Jul.
9, 2008, the disclosures of which are incorporated herein by
reference.
FIELD OF THE INVENTION
[0002] The invention is directed to a method and apparatus for
monitoring optic function in consciousness-altered patients; and
more particularly to method and apparatus for the real-time
monitoring of optic function for evaluating potential optic damage
or unintended interoperative awareness.
BACKGROUND OF THE INVENTION
[0003] The use of some form of anesthesia, or "reversible lack of
awareness", can be dated as far back as the Greek and the Persian
empires. However, it was not until the 19.sup.th century that
modern narcotic anesthesia agents would be discovered. The
introduction and the development of effective anesthetics in the
19th century was, with Listerian techniques, one of the keys to the
development of successful surgical protocols.
[0004] Although anesthesia has made modern surgical procedures
possible the process has, from the beginning, been fraught with
danger. For example, the first chloroform surgeries were performed
in late 1847, and the first fatality directly attributed to
chloroform anesthesia was recorded mere months later in January
1848. The framed physician John Snow published a classical study of
chloroform deaths as early as 1858. Indeed, medical literature is
replete with the names of prominent figures in medicine that wrote
about the dangers of anesthesia. Harvey Cushing, generally
considered the father of modern neurosurgery, lost a patient who
aspirated gastric contents during ether anesthetic. He later wrote
that this event almost caused him to leave medical school. As a
result, anesthesiologists the world over have long been concerned
with and involved in studies related to anesthesia safety. Many
prominent anesthesiologists in the United States began to collect
statistics of anesthetic morbidity and mortality as early as the
1930's. However, the dangers of anesthesia are not purely
historical. Indeed, it was not until 1983 that a modern system of
reporting was implemented so that anesthesiologists could develop
statistics and define the parameters of future studies.
[0005] The results of these studies have been to create standards
and protocols for how anesthesia is administered and how a patient
is monitored while under anesthesia. For example, under current
protocols patients being treated under general anesthetics must be
monitored continuously to ensure the patient's safety. For minor
surgery, this generally includes monitoring of heart rate (via ECG
or pulse oximetry), oxygen saturation (via pulse oximetry),
non-invasive blood pressure, inspired and expired gases (for
oxygen, carbon dioxide, nitrous oxide, and volatile agents). For
moderate to major surgery, monitoring may also include temperature,
urine output, invasive blood measurements (arterial blood pressure,
central venous pressure), pulmonary artery pressure and pulmonary
artery occlusion pressure, cerebral activity (via EEG analysis),
neuromuscular function (via peripheral nerve stimulation
monitoring), and cardiac output. In addition, the operating room's
environment must be monitored for temperature and humidity and for
buildup of exhaled inhalational anesthetics, which might impair the
health of operating room personnel. While these protocols have
resulted in significant improvements in anesthesia related
mortality, they have not eliminated all of the risks associated
with anesthetized and otherwise consciousness altered
individuals.
[0006] For example, one risk that has become more prevalent over
time is perioperative visual loss. Perioperative visual loss (POVL)
broadly refers to permanent impairment or total loss of sight
associated with general anesthesia. The relevant perioperative
period generally includes a time from the immediate preoperative
assessment through discharge from the acute healthcare facility,
and is indicated for patients who, within seven days following
non-ophthalmological surgery, began to develop visual impairment
and/or blindness. Despite the data and the in-depth demographic
studies available, the mechanism of perioperative ischemic optic
neuropathy is still theoretical and, thus, up until this time,
monitoring and prevention strategies could not be effectively
defined.
[0007] Another potentially disturbing complication can be
`anesthesia awareness`. In this situation, patients paralyzed with
muscle relaxants may awaken during their anesthesia, due to
decrease in the levels of drugs providing sedation, lack of
awareness and/or pain relief. If the anesthesia provider misses
this fact, the patient may be aware of his surroundings, but be
incapable of moving or communicating that fact.
[0008] Neurological monitors are becoming increasingly available
which may help decrease the incidence of POVL and awareness. One
exemplary monitor that is currently available is the BIS monitor,
manufactured by Aspect Medical Systems of Natick, Mass. The BIS
device monitors EEG-based brain function to reduce the incidence of
recall or awareness of a patient while under anesthesia. During
function the BIS monitor uses proprietary algorithms to monitor
brain activity and give the anesthesiologist a series of empiric
numbers upon which to assess the patient's level of consciousness.
While monitoring EEG-based brain activity has been shown to be of
some benefit in allowing for quicker recovery from anesthesia,
studies have indicated that the EEG measurements can be
dramatically impacted even when the patient is not under
anesthesia. For example, in a study published in 2008 it was shown
that BIS scores could be changed by as much as 20 basis points
simply by the administration of muscle relaxants to
non-anesthetized patients. (Lu, et al., Int. Anesthesia Res. Soc.,
107:4, 2008, the disclosure of which is incorporated herein by
reference.) Likewise, a study published in the New England Journal
of Medicine showed that awareness under anesthesia occurred in
patients even when the BIS values were within target ranges.
(Avidan, M. S., et al., New England Journal of Medicine, 358, 1097,
2008, the disclosure of which is incorporated herein by
reference.)
[0009] A second device being marketed for use as an anesthesia
monitor is the BAER system, which stands for Brain Auditory Evoked
Response. These monitors have been used successfully in the past to
evaluate brain injury; however, recently it has been suggested that
such a technique could be used to monitor the depth of anesthesia.
Recent studies have openly questioned this assumption. However,
some studies on the efficacy of the system have shown that there is
no correlation between the potentials measured by the BAER system
and level of anesthesia.
[0010] In summary, despite the widespread marketing of these new
monitoring devices many case reports exist in which awareness under
anesthesia has occurred despite apparently adequate anesthesia as
measured by such neurologic monitors. Accordingly, a method and
apparatus for monitoring a patient under anesthesia that could
provide better data concerning both POVL and Anesthesia Awareness
is needed to provide surgeons with adequate information to enable
real-time prevention of these serious conditions.
SUMMARY OF THE INVENTION
[0011] The current invention is directed to a method and apparatus
for monitoring in real-time optic nerve function for use in
consciousness-altered individuals.
[0012] In one embodiment, the method/apparatus includes the
placement of at least one optic function sensor proximate to the
eye that is designed to stimulate and monitor the function of at
least one of the optic nerve or the optic cortex. In such an
embodiment, the at least one optic function sensor may stimulate
the eye by producing a visual evoked potential in at least one of
the nasal or temporal halves of the optic nerve, such as by a light
emitting diode or other suitable mechanism.
[0013] In another embodiment, the method/apparatus includes the
placement of at least one pressure sensor proximate to the eye that
is designed to monitor the intraocular pressure of the eye. In such
an embodiment the pressure sensor may be a tonometer.
[0014] In yet another embodiment, the method/apparatus includes the
placement of a blood flow sensor proximate to the eye that is
designed to monitor one of either retinal or optic blood flow. In
such an embodiment, the blood flow sensor may be selected from one
of either a near-infrared spectrometer or a laser Doppler
velocimeter.
[0015] In still another embodiment, the one or more of the above
sensors are integrated into a sensor band. In such an embodiment
the sensor band may be incorporated into an eye-cover.
[0016] In still yet another embodiment, the eye-cover may take the
form of a pair of goggles.
[0017] In still yet another embodiment, the method/apparatus of the
current invention further includes analyzing the output from the
visual evoked potential curves using one of the following
mathematical formulas:
AI-1=P2/TL1 in(.mu.V/ms)
AI-2=(AI-1).sup.n in(.mu.V/ms)
AI-3=(P2).sup.x/(TL1).sup.y in(.mu.V/ms)
AI-4=(AI-3).sup.n in(.mu.V/ms)
AI-5=(.delta.(EVP2)/.delta.t.sub.max)/TL1 in(.mu.V/ms)
AI-6=(.delta.(EVP2)/.delta.t.sub.max).sup.x/(TL1).sup.y
in(.mu.V/ms)
AI-7=AI-6.sup.n in(.mu.V/ms)
AI-8=(.delta.(EVP2)/.delta.t.sub.mean)/TL1 in(.mu.V/ms)
AI-9=(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(TL1).sup.y
in(.mu.V/ms)
AI-10=(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.sup.z).s-
up.m in(.mu.V/ms)
AI-11=AI-10.sup.n in(.mu.V/ms)
AI-12=.delta.(EVP2)/.delta.t.sub.max/t.sub.1/P2
in(.mu.V.sup.2/ms.sup.2)
AI-13=(.delta.(EVP2)/.delta.t.sub.max).sup.x/t.sub.1.sup.y/P2.sup.z
in(.mu.V.sup.2/ms.sup.2)
AI-14=(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.sup.z).s-
up.m in(.mu.V.sup.2/ms.sup.2)
AI-15=AI-14.sup.n in(.mu.V/ms)
AI-16=(.delta.(EVP2)/.delta.t.sub.max).sup.x/(t.sub.1.sup.y/P2.sup.z).su-
p.m in(.mu.V.sup.2/ms.sup.2)
AI-17=AI-16.sup.n in(.mu.V/ms)
AI-D=((AI-1)(AI-17))/(CV(AI-1)CV(AI-17))
wherein in each of the above equations the exponents have a value
from 0.333 to 3 and preferably from 0.5 to 2.
BRIEF DESCRIPTION OF THE DRAWINGS
[0018] The description will be more fully understood with reference
to the following figures and data graphs, which are presented as
exemplary embodiments of the invention and should not be construed
as a complete recitation of the scope of the invention,
wherein:
[0019] FIG. 1 provides a schematic of an exemplary embodiment of
the method and apparatus of current invention;
[0020] FIG. 2 provides a schematic of the neural anatomy of the
eye;
[0021] FIGS. 3a and 3b provide exemplary waveforms from visual
evoked potentials in accordance with the current invention;
[0022] FIG. 4 provides an exemplary waveform from a visual evoked
potential in accordance with the current invention;
[0023] FIG. 5 provides an exemplary waveform from a binocular
visual evoked potential in accordance with the current
invention;
[0024] FIG. 6 provides a schematic diagram of an active eye support
apparatus in accordance with one exemplary embodiment of the
current invention;
[0025] FIG. 7 provides a schematic diagram of an exemplary optic
nerve function goggle apparatus in accordance with the current
invention;
[0026] FIG. 8 provides an MRI of showing an embolus or
hypoperfusion of the visual cortex associated with cortical
blindness;
[0027] FIG. 9 provides a schematic diagram of the blood vessels
associated with the eye;
[0028] FIG. 10 provides schematic diagrams showing one exemplary
method of placing electrodes for using in monitoring visual evoked
potentials in accordance with the current invention;
[0029] FIG. 11 provides waveforms taken while monitoring the P100
cortical response while under anesthesia; and
[0030] FIG. 12 provides a normal flash VEP waveform along with
labels for important components of the VEP waveform.
DETAILED DESCRIPTION OF THE INVENTION
[0031] The current invention is directed to a method and apparatus
for the real-time monitoring of optic nerve function. The invention
recognizes that although great advance have been made in preventing
fatalities in consciousness altered patients, it is very difficult
to accurately monitor the more subtle ongoing stresses that can
occur in consciousness altered individuals, such as those under
anesthesia, and that as such a need exists for a monitoring system
that can accurately monitor, and potentially prevent injury by
providing data on the function of a patient's optic nerve. For
example, the method and apparatus of the current invention would
allow a surgical team to monitor the function of the optical nerve
in real-time during surgery, thereby providing information on the
status of the patient. In addition, the current invention
specifically recognizes that the function of the optic nerve can be
used as a diagnostic tool for common anesthesia induced injuries,
including, for example, POVL and anesthesia awareness.
[0032] The method and device of the current invention is able to
monitor such function for two principal reasons. First, unlike
conventional monitors, such as BIS, which monitor activity in only
a portion of the brain (the cerebrum for BIS and the midbrain for
BAER), the device and method of the current invention monitors
activity in multiple parts of the brain simultaneously.
Specifically, because it examines visual evoked potentials, the
current technique must look at activity across three neurological
systems--the peripheral nerves, the midbrain and the cortex. This
is because visual evoked potentials are impacted by the function
optic nerve (a peripheral nerve) and also the optic chiasma (a
midbrain structure). Second, current techniques are designed to
watch physiological variables and look for stability and constancy.
The current invention is designed to watch for change in
neurological activity, and more particularly to watch for a trend
of change indicative of an impending adverse event.
[0033] As discussed above, in one embodiment the current invention
is directed to a method/apparatus for monitoring optic nerve
function. FIG. 1 provides a schematic diagram of the proposed
apparatus in combination with a flowchart showing the method of the
current invention. As shown, in one embodiment the optic nerve
function monitoring method/apparatus of the current invention
comprises the placement and monitoring of at least a sensor capable
of providing information on the function of the optic nerve and
optic cortex via visual evoked potentials (10), and optionally at
least one of three additional optic nerve sensors: a sensor for
monitoring the intraocular pressure of the eye (12), a sensor for
monitoring retinal blood flow (14), and a sensor for measuring the
location and movement of the eye (15). A description of each of the
sensors and their function in monitoring optic nerve function is
provided below. In general though the sensors (10, 12, 14, 15) are
placed either individually or together against the closed lid of
the patient's eye (16). Leads (18) connect the sensors (10, 12, 14,
15) to a remote monitor (20) that can communicate the signal
information to a trained physician (22) for evaluation.
[0034] Visual Evoked Potential Sensor
[0035] As shown in FIG. 1, the optic nerve function monitoring
apparatus/method of the current invention at least comprises a
visual evoked potential (VEP) sensor (10). However, to understand
the structure and function of this sensor in the current invention
it is necessary to understand how the optic nerve functions. In
this discussion reference will be made to the schematic of the eye
provided in FIG. 2. Specifically, as shown, for a human to see
light has to be reflected from an object at an angle so that it
strikes the eye and is refracted by the cornea and the lens, and
then projects an image on the retina. The optical property of the
lens in the eye turns the image upside down and reverses the object
(turning it left for right). It is projected onto the retina. The
right half of the visual field is projected into the nasal half of
the right retina and onto the temporal half of the left retina. The
information is then sent on to the left cerebral hemisphere. This
schematic is reversed for the left half of the visual field.
[0036] The retina itself contains two types of photoreceptor cells.
Rods are used for low light vision, such as night vision, and the
cones provide high visual acuity and the ability to see colors.
Their highest density is found in the vicinity of the fovea
centralis, which is located within the macula. The macula is found
within the retina and is specialized to provide high visual acuity.
The other cells in the eye include receptor cells and bipolar
cells, which transmit visual signals to the ganglion cells. The
rods and cones connect to the ganglion cells and process
information about color and the contrast of images that fall on the
retina. Action potentials are generators by these ganglion cells
and provide highly processed information about visual images, which
are passed onto the thalamus and brain stem.
[0037] The axons of the ganglionic cells from the inner surface of
the retina come together and then exit the optic disc. Here they
become myelinated and form the optic nerve. The optic nerve fibers
then pass the optic chiasm, which is found anterior to the Sella
turcica, which is directly above the pituitary gland at the base of
the brain. The optic fibers partially cross at the chiasm. Fibers
from the left and right nasal halves cross. The temporal portions
do not cross at the chiasm, but remain on their same original
side.
[0038] Once the optic fibers pass the chiasm, they become the optic
tracks and they continue onto the lateral geniculate body (LGB)
where a large number of optic fibers terminate. Each LGB gains
input from the retina in a topographic pattern representing the
contralateral visual half field. Visual input from the optic tracts
and various other projections from the visual cortex and neurons
connect with the superior colliculus. The superior colliculus aids
in eye movement and then sends visual input in two directions, one
to the pons via the tectopontine tract, which relays information to
the cerebellum and, two, to the spinal cord via the tectospinal
tract. These tracts control head and neck movements in response to
visual stimuli.
[0039] The pretectal area is found rostral to the superior
colliculus. This is an important site for the mediation of
pupillary reflexes. Pretectal neurons reach the Edinger-Westphal
nucleus in the mesencephalon. Neurons from the LGB form fibers that
create the Geniculocalcarine tract, also known as the optic
radiations. These fibers reach all of the way to the occipital
lobe.
[0040] The current invention recognizes that VEPs provide an
extremely powerful tool to monitor the function of these
complicated neural structures, as they provide a check on the
integrity of the visual pathways. In other words, using VEPs it is
possible to monitor whether and how the neural structures, such as
the optic nerve, chiasm and cortex are carrying electrical signals
and any change in those signals. In order to monitor the function
of these structures in real-time, the current invention proposes
the placement of at least two LEDs, or other equivalent
light-emitting device, proximate to the eye. These devices are well
known and any of the prior art devices may be used with the current
invention. (See, e.g., Celsia, G., et al., American J. of EEG
Tech., 25:93-113 (1985 and Erwin, C. W., American J. of EEG Tech.,
20:161-184 (1980), the disclosures of which are incorporated herein
by reference.) One of the LEDs is provided to stimulate the nasal
half of the optic nerve, and the other to stimulate the temporal
half of the optic nerve. In addition, a sufficient number of signal
receiving electrodes must be placed on the patient to allow for the
monitoring of the neural activity generated in response to the
LED-generated stimulus. Using such a sensor design it is possible
to monitor the function of the two critical structures in the
eye--the optic nerve and the optic cortex. In an alternative
embodiment, it is also possible to monitor the function of the
optic chiasma by the inclusion of an additional LEDs to stimulate
the entire surface of the retina periphery to periphery, i.e., from
the nasal to the temporal side.
[0041] However, while the above provides a bare description of the
minimum apparatus required to perform VEP monitoring on a patient,
there are a number of different parameters that must be considered
in determining the appropriate method of measuring visual evoked
potentials to use in accordance with the current invention,
including, for example, the type of stimulus, the field of
stimulation, the rate of stimulation, what parameters to monitor
and record, and the details of how to take a measurement. Each of
these parameters will be discussed in detail below. For additional
information on standard VEP parameters that can be used in
accordance with the current invention see Odom, J. V., et al.,
Documenta Optha., 108:115-123 (2004), the disclosure of which is
incorporated herein by reference.)
[0042] Types of Stimulation
[0043] First, to fully monitor the function of optical nerve, the
current invention preferably monitors two different types of visual
evoked potentials resulting from two different types of stimulus.
Schematics of both of these stimuli and associated waveforms are
provided in FIGS. 3a and 3b. The first type of stimulus is
patterned stimulus (FIG. 3a), such as, for example, alternating
checkerboard pattern consisting of sharply defined light and dark
squares. Also used are sine wave grating patterns that have dark
stripes and a changing brightness between the stripes, such as,
bars with well-defined borders or random dots. The visual evoked
potential due to a pattern is a result of the density of light and
dark contrast in the stimulus. The second type of stimulus is
diffuse light (FIG. 3b) used in flash visual evoked potentials. The
visual evoked potential waveform from this stimulus comes from the
changes in luminescence appreciated by the eye.
[0044] For the stimulus, contrast borders should be clear and well
defined. A blurring of borders degrades the visual evoked potential
pattern. If the check size is too small, the amplitude may be
reduced and the latency may increase. The luminance of a patterned
light stimulus is measured with a spot photometer. Light and dark
elements are measured, the mean is figured, and this is called the
mean luminance. Luminance is measured as candela per square meter
(cd/m). The depth of contrast is the difference between the
luminance of the light and dark elements divided by their sum,
which is expressed as contrast=Lmax-Lmin/Lmax+Lmin. This makes the
maximum contrast a value of one and the minimum contrast is a value
of zero. For the current invention, a contrast of stimulus set at
0.5 or a 3:1 ratio between minimum and maximum is preferred.
[0045] Field of Stimulation
[0046] Although these stimuli may be applied to the eye in a number
of suitable ways, in one preferred embodiment a hemifield
stimulation is provided. To understand what is meant by
"hemifield", it is necessary first to understand how a person's
"field of vision" is defined. When a stimulus pattern extends
beyond both sides of a fixation point (e.g. a dot in the middle of
a television screen or checkerboard pattern or a light emitting
diode in the middle of a pattern), this is called full field
stimulation. A hemifield is one of two halves of a sensory field,
i.e., the parts of each visual hemifield that can be seen with both
eyes. Although there are a number of ways to accomplish hemifield
stimulation, any of which might be used in the current invention,
in one preferred embodiment half of the visual stimulation pattern
is shown either to the right or left of the visual fixation point,
and in another preferred embodiment using the entire stimulus
pattern the fixed point is positioned in the left or right margin
of the pattern.
[0047] Rate of Stimulation
[0048] In terms of the rate of stimulation, the typical visual
evoked potential in the lab consists of checkerboard pattern
reversals at a stimulus rate of two per second. Slower rates of
stimulation produce no change in the visual evoked potential where
increasing the stimulation rate to four per second may increase the
latency of a transient visual evoked potential. Meanwhile, uniform
steady state response is usually seen with weights that are six or
eight stimuli per second.
[0049] Recording Parameters
[0050] As discussed above the stimulus in a visual evoked potential
may vary; however, in the parameters for recording the various
visual evoked potentials are similar for all visual evoked
potential types. Specifically, there should be four channels for a
complete examination, but fewer channels are required, if only
testing the prechiasmal portion of the optic nerve. The American
EEG Society Guidelines recommend the following electrode
placements, which may be used in conjunction with the current
invention: [0051] MO: Midline Occipital, 5 cm above inion; [0052]
MF: Midline Frontal, 12 cm above nasion; [0053] RO: Right
Occipital, 5 cm right of MO; and [0054] LO: Left Occipital, 5 cm
left of MO.
[0055] Using these electrodes, the following montage for pattern
reversal visual evoked potentials is recommended: [0056] Channel
No. 1: RO-MF; [0057] Channel No. 2: MO-MF; [0058] Channel No. 3:
LO-MF; and [0059] Channel No. 4: MF-A1.
[0060] The actual electrodes should be preferably placed on the
scalp in the occipital region in the midline and laterally.
Reference electrodes can be preferably placed on the earlobes,
frontal, or central scalp.
[0061] Measurement Parameters
[0062] The low frequency filter should be preferably set at 0.2 to
1.0 hertz and the high frequency filter should preferably be set at
200 to 300 hertz. If the high frequency filter is set at 100 hertz,
peak latency may be increased.
[0063] For transient visual evoked potentials, the analysis period
is 250 milliseconds for normal adults and up to 500 milliseconds
for infants or an abnormally delayed visual evoked potential at any
age. Before visual evoked potential testing with an awake and alert
patient, they should be seated in a comfortable chair in a quiet
room. The patient needs to be alert. The patient's visual acuity
must be greater than 20/200 or an alteration of visual evoked
pattern will occur.
[0064] A typical transient visual evoked potential produced by
checkerboard reversal patterns at two per second is reproduced in
FIG. 4. As shown the visual evoked potential usually consist of an
N-75, P-100, N-145. The waveform starts with a small negative at 60
to 80 milliseconds (N-75) then there is a larger positive occipital
peak at a latency of between 90 and 110 milliseconds with amplitude
of approximately 10 .mu.V (microvolts). This peak is at P-100. The
N-145 is a negative wave following the P-100. The visual evoked
potentials should be recorded at least two times and should
replicate within 2 to 3 milliseconds to be considered a valid
study.
[0065] Using the above methodology in accordance with the current
invention it is possible to obtain information about the function
of the optical nerve of the individual in real-time. In turn,
obtain information about the health of the individual. For example,
it is well known that many disorders can affect an individual's
visual evoked potential. A listing of disorders and possible
affects are provided in Table 1, below.
TABLE-US-00001 TABLE 1 Abnormal Full Field Monocular Visual Evoked
Potentials Best Eye Worst Eye Abnormality Location Absent VEP
Absent VEP Bilateral prechiasmal, chiasmal, or retrochiasmal lesion
Increased Absent VEP Chiasmal lesion or latency bilateral optic
nerve lesion Normal Absent VEP Optic nerve or ocular lesion Normal
Increased latency Optic nerve lesion Normal Normal latency with
interocular Optic nerve lesion differences, i.e. the latency in the
worst eye is different than the latency in the best eye
[0066] In addition to the determining abnormalities in the function
of the optic nerve, which can, as discussed above, be identified
and diagnosed using visual evoked potentials, visual evoked
potentials can also be used to identify and diagnose a wide-variety
of broader disorders, as shown in Table 2, below.
TABLE-US-00002 TABLE 2 How Do Disorders Affect Visual Evoked
Potential Disorder Affect Alcoholism Increased latency is possible
Charcot-Marie-Tooth Delayed visual evoked potential Muscular
dystrophy Delayed visual evoked potential Chronic renal failure
Reduced amplitude and possible increase in latency Cataracts
Reduced amplitude and possible increase in latency Corneal
opacities Reduced amplitude and possible increase in latency
Diabetes Delayed visual evoked potential Downs Syndrome Low
amplitude with delayed visual evoked potential Endocrine
orbitopathy Delayed visual evoked potential Glaucoma Increase
latency of visual evoked potential Hysterical blindness Normal
visual evoked potentials Optic nerve trauma Decrease amplitude and
optic nerve tumors increased latency and decreased amplitude or may
have been completely absent Retrobulbar neuritis The affected side
may have increased latency and decreased amplitude Celesia G, et
al., American Journal of EEG Technology, 25: 93-113 (1985), the
disclosure of which is incorporated herein by reference.
[0067] During operation, as shown in FIG. 1, a visual evoked
potential sensor, such as a light emitting diode device is applied
over the eye. The eye may be optionally "taped shut" to ensure that
the sensor is not dislodged by the patient. Regardless, as shown in
FIG. 5, below, the intensity of the stimulus is enough to pass
through the eyelid and tape. Specifically, the upper tracing is
binocular with goggles, no tape, and the eye is shut. The lower
tracing is with Transpore.RTM. tape taping the eye shut. The
waveform amplitude and latencies are comparable, although there
appears to be a variation in the latency between the dominant and
the non-dominant eye of approximately 1.0 to 1.25 milliseconds.
Although any type of visual evoked potential sensor may be used,
the use of LED goggles, which are placed directly over the eyes,
have the advantage of producing a very large field of stimulation
and minimizes the affect of changes in direction of gaze. The
stimulation usually takes place through closed eyelids. Although a
number of different goggle designs can be used, in a preferred
embodiment the LED is be placed in the middle of the goggle because
having the LED placed laterally or medially would stimulate one of
only the nasal field or temporal field not both.
[0068] Although the above parameters and procedures may be
generally used, it should be understood that some modifications
must be made based on the demographic of the patient. For example,
Shaw, et al., showed that at lower levels of luminance there was a
significant difference between those under 40 and those over 40 in
the latency of P-100. This was very clear in those in their
fifties. At higher levels of luminance, there was no significant
increase in the latency at P-100. (Shaw N. A., et al.,
Electroencephalography and Clinical Neurophysiology, 48:237-241
(1980), the disclosure of which is incorporated herein by
reference.) There are a number of changes in visual function
associated with aging, which underlies the increase in the latency
of P-100. There was a decrease in pupillary diameter, increase in
opacity of the lens, which results in an essentially linear
decrease in the amount of light reaching the retina between the
ages of 20 and 60 years. (Corso J F, Journal of Gerontology,
26:90-105 (1971), the disclosure of which is incorporated herein by
reference.) Similarly, neuroaxonal dystrophy is described in the
central nervous system beginning at the age of 20 as becoming more
severe by the age of 50. (Sung J. H., Journal of Neuropathology and
Experimental Neurology, 23:567-583 (1964), the disclosure of which
is incorporated herein by reference.) There is also a demonstrable
loss of neurons in the striate cortex in the fifth decade. (Brody,
H., Journal of Comprehensive Neurology, 102:511-566 (1955), the
disclosure of which is incorporated herein by reference.)
[0069] In addition, there are more subtle changes, such as the loss
of dendrites and changes in neurotransmitter function. (Samorajski
T., of American Geriatric Society, 25:337-348 (1977) and Scheibel
M. E., et al., "Structural Changes in the Aging Brain: Volume I,
Clinical Morphologic and Neurochemical Aspects in the Aging Central
Nervous System", Ravencrest, N-.Y., 1975:11-37, the disclosures of
which are incorporated herein by reference.) There is increased
synaptic delay, which contribute to increased latency associated
with increasing age. (Wayner M J, Emers R, American Journal of
Physiology, 194:403-405 (1958), the disclosure of which is
incorporated herein by reference.) In short, it is important when
looking at visual evoked potentials to consider neurological
diagnoses, consider the age of the subject, and consider the level
of luminance used. (For a more detailed discussion see the
references above and Allison T., et al., Electroencephalography and
Clinical Neurophysiology, 58:14-24 (1984); Erwin C. W., American
Journal of EEG Technology, 20:161-184 (1980); Gilman S., et al.,
"Essential of Clinical Neuroanatomy and Neurophysiology", 1996, FA
Davis Company, Philadelphia; Skrandies W., Neuro. Report,
10:249-253 (1999); and Weale R. A., Trans. Opthal. Soc. UK,
95:36-38 (1975), the disclosures of which are incorporated herein
by reference.)
[0070] Intraocular Pressure Sensor
[0071] As shown in FIG. 1, another optional sensor that may be used
with the method/apparatus of the current invention is an
intraocular pressure (IOP) sensor (12). The intraocular pressure
sensor, like the VEP sensor is place against the closed and/or
taped eyelid of the patient and connected an external monitor. Any
pressure transducer sensor suitable for monitoring intraocular
pressure may be used, such as, for example, a tonometer. (See,
e.g., Amm M., et al., Ophthalmologe. 102(1):70-6 (2005), the
disclosure of which is incorporated herein by reference.)
[0072] As discussed above, in one embodiment of the invention the
IOP is measured via a tonometer. There are a number of different
types of tonometeric techniques that may be used with the current
invention, such as, for example, apponation tonometry, Goldmann
tonometry, dynamic contour tonometry, diaton tonometery,
non-contact tonometry, impression, tonometry, rebound tonometry,
Schiotz tonometry, and Perkins tonometer. However, in one preferred
embodiment, the invention uses transpalpebral tonometery, which
measures intraocular pressure through the eyelid by a diaton
tonometer. Transpalpebral tonometry requires no contact with the
cornea, therefore sterilization of the device and topical
anesthetic drops are not required and there is very little risk of
infection. (See, e.g. Davidson, R. S., et al., ASCRS/ASOA, Poster #
P-130 (2007); Theodore H. Curtis, et al., ASCRS/ASOA, Poster #
P-128 (2007); Lam A. K., et al., Ophthalmic Physiol Opt.
25(3):205-10. (2005); Henry D. Perry, Eyeworld Magazine (2006);
Nesterov A. P., et al., Vestn Oftalmol. 119(1):3-5 (2003); Sandner
D., et al., Graefes Arch Clin Exp Ophthalmol. 243(6):563-9 (2005);
and Troost A, et al., Br J. Ophthalmol. 89(3):280-3 (2005), the
disclosures of which are incorporated herein by reference.)
[0073] Although it is not essential to the operation of the optic
nerve function apparatus/method of the current invention, it is
preferred that the intraocular pressure be monitored as well,
because an increase in intraocular pressure can signal potentially
serious disorders. (See, e.g., U.S. Pat. No. 7,314,454, the
disclosure of which is incorporated herein by reference.) For
example, rising intraocular pressure is known to decrease ocular
perfusion pressure even where normal mean arterial pressure is
maintained. In turn, reduced ocular perfusion (or a decrease in
oxygenated blood) being supplied to the optic nerve can stress the
nerve ultimately resulting in substantial damage, such as, for
example, posterior ischemic optic neuropathy.
[0074] Moreover, significant changes in intraocular pressure are a
common side effect of anesthesia, particularly where patients are
placed into prone positions for long periods of time. For example,
in a study of awake volunteers, intraocular pressure increased in
an article by Cheng in 2001 from 13.5 millimeters of mercury, plus
or minus 2.01 in the sitting position, to 20 millimeters of
mercury, plus or minus 3.27 in the prone position. Cheng, M. D., et
al., Anesthesiology, 95:6, 1351-1355 (2001), the disclosure of
which is incorporated herein by reference.) Other studies have
shown that sequentially over time, intraocular pressure increases.
It increases by 100% after four hours. This may be due to a number
of issues. For example, the prone position increases
intraperitoneal pressure, central venous pressure, peak inspiratory
pressure, and intraocular pressure. Intraocular pressure has been
shown to increase in anesthetized patients who are supine in a head
down Trendelenburg position and in our study of awake inverted
volunteers, there was a considerable increase in intraocular
pressure over time. The mechanism for that increase may be related
to higher episcleral venous pressure. Freiberg, et al. in 1985
found 1 millimeter of mercury increase in intraocular pressure for
every 0.83 millimeters of mercury episcleral venous pressure. A
slightly head neutral or head up position may attenuate the
observed increase of intraocular pressure in the prone position.
However, beyond the position of the patient increased arterial
carbon dioxide tension can produce an increase in intraocular
pressure, demonstrated by Hvidberg in 1981. Increased intraocular
pressure may also be related to observed positive intraoperative
fluid balance. In an experiment carried out by Brucculeri in 1999,
healthy volunteers were given acute oral water loading, 14 ml per
kilogram, and the intraocular pressure increased. Martin, in 1999,
demonstrated that exercise-induced dehydration reduced intraocular
pressure. Decreased serum osmolality during dialysis increased
intraocular pressure in patients with renal failure. (See, Tawara
(2000), the disclosure of which is incorporated herein by
reference.) In another study performed by Evans in 1991, severely
burned patients were found to have very elevated intraocular
pressures in the range of 37.2 to 81.7 millimeters of mercury due
to extreme orbital congestion related to large amounts of
intravenous fluid.
[0075] Indeed, even elevations of central venous pressure (CVP)
have been shown to contribute to increased intraocular pressure.
(See, e.g., Kamming D., et al., British Journal of Anesthesia,
95:257-260 (2005), the disclosure of which is incorporated herein
by reference.) Although not to be bound by theory it is believed
that it is increased by reduced venous return in patients in the
head down position and obstruction of venous outflow, such as the
ligation of veins in radical neck surgery. Blood flow in the
posterior optic nerve is susceptible to increased venous pressure
because the arterial supply to the posterior optic nerve is derived
from small end vessels from the surrounding pia. Indeed, there are
case reports of ischemic optic neuropathy that occurred in patients
associated with increased venous and intracranial pressure after
radical neck operations with bilateral jugular vein ligation.
Turning the head to one side or the other can restrict venous
outflow. Central venous pressure can be increased if there is
direct pressure on the abdomen due to poor positioning on the
operating table during prone anesthetic. In a patient who is
correctly positioned and who has central venous pressure between
six to thirteen millimeters of mercury, this might not be seen as a
single significant factor in optical nerve trauma, such as, for
example, visual loss. However, CVP readings may not necessarily
reflect venous pressure inside the globe and there may be marked
venous congestion of the head and neck, even with a normal CVP
reading.
[0076] In short, it is important to remember that increased
intraocular pressure and concomitant reduced ocular blood flow that
results may be caused by a number of factors, which individually
may not seem significant, but cumulatively increase the risks to a
patient. Moreover, simply monitoring venous pressure often gives
inaccurate information on the physiology of the optic nerve because
an increase in intraocular pressure can lower ocular perfusion
pressure despite the maintenance of a normal mean arterial
pressure. Accordingly, an intraocular pressure sensor, such as that
described in the current invention, provides a more accurate
measurement of the stress on and function of the optic nerve than
do other types of monitoring.
[0077] Ocular Blood Flow Sensor
[0078] Finally, another optional sensor that can be used in
combination with the VEP and intraocular pressure sensors is a
blood flow sensor (14), which as with the VEP and IOP sensors is
attached or positioned near the surface of the closed and/or taped
eyelid of the patient. As discussed above in relation to the IOP,
one of the most serious stresses that can be placed on the optic
nerve during anesthesia is a reduction or loss in blood flow to the
optic nerve. Although the VEP and IOP sensors can provide
information on blood flow to the eye indirectly by measuring other
parameters such a neural function and IOP that are impacted by a
change in blood flow or perfusion, having a direct measurement of
blood flow to the eye and optic nerve would provide a more certain
measurement of this critical parameter.
[0079] Specifically, in one embodiment of the invention a blood
flow sensor is provided that can measure the function of the
choroidal arteries supplying the eye with blood, and in a most
preferred embodiment, that can measure the flow of blood to the
optic nerve itself. Even though choroidal blood flow is not
directly analogous to central retinal artery blood flow, it does
provide a baseline evaluation of perfusion of the optic disk and
the optic nerve head. As such, beyond providing a simple measure of
the function and general health of the eye, it can also be used in
preventing the possibility of iatrogenically induced ischemic optic
neuropathy.
[0080] Although any number of indirect methods can be used to
measure blood flow, in a preferred embodiment either laser Doppler
velocimetry or near-infrared spectroscopy can be used to make
instantaneous measurements of the flow of blood to and into the
eye. Laser Doppler Velocimetry (LDV) is a technique that fluid
mechanics and researchers use to make instantaneous velocity
measurements (magnitude and direction of fluid flow). (For a full
description see, Durst F., et al., "Principles and Practice of
Laser Doppler Anemometry", Academic Publishers, New York, 1976 and
Adrian R. J., Editor, Selected Papers on Laser Doppler Velocimetry,
Spine Milestone Series, MS 7,8, Spie Optical Engineering Press,
Bellingham, Wash., 1993, the disclosures of which are incorporated
herein by reference.) LDV utilizes the concept of the coherent wave
nature of laser light. The crossing of two laser beams of the same
wavelength produces a pattern. It produces areas of constructive
and destructive interference patterns. The interference pattern is
known as a fringe pattern and is composed of planar layers of high
and low intensity light. Velocity measurements are made when
particles seated in the flow pass through the fringe pattern
created by the intersection of a pair of laser beams. The particles
scatter light in all directions. The scattered light is then
collected by a stationary detector. The frequency of scattered
light is Doppler shifted and referred to as a Doppler frequency of
the flow. The technique is nonintrusive and can deliver
measurements independent of ambient conditions. It measures three
directional components and it can access any flow region with the
aid of fiberoptics. It has a range (dynamic range) from natural
convection to supersonic velocities.
[0081] In one such embodiment, the laser power source for the LDV
in accordance with the current invention is a helium/neon (HeNe) or
argon ion laser with a power of ten milliwatts. Lasers have
advantages over other radiation wave sources, including excellent
frequency stability, small beam diameter, and high focused energy.
Laser Doppler can be configured to act as flow meters or
anemometers by evaluating the velocity of reflected particles
entrained in a transparent flow field. In the current invention,
the LDV can be attached directly to the eye, or mounted in a set of
goggles that protect and support the eye, thereby allowing
real-time measurement of choroidal blood flow.
[0082] In another embodiment, near-infrared spectroscopy could be
used to monitor blood flow to the eye. Optical photons are
insufficiently ionized and unless light is concentrated to such a
high degree that it causes burning to the skin, optical radiation
is not a significant hazard. Accordingly, the diagnostic potential
of optical methods has been known since Jobsis, in 1977, who first
developed transmittance measurements of near infrared radiation and
showed it could be used to monitor the degree of oxygen related
metabolites. (Jobsis F. F., Science, 198:1264-1268 (1977), the
disclosure of which is incorporate herein by reference.) This led
to the development and increasingly widespread use of clinical near
infrared spectroscopy, which offers a safe, noninvasive means of
monitoring cerebral function at the bedside without the use of
radioisotopes. (Coke M., et al., "Medicine and Biological
Engineering and Computing", 26:289-294 (1988), the disclosure of
which is incorporated herein by reference.) Indeed, even tissues
contain a variety of substances whose absorption spectra at near
infrared spectroscopy wavelengths are well defined, including
oxygenated hemoglobin (HbO.sub.2), deoxyhemoglobin (Hb), and
tissues which are strongly linked to tissue oxygenation and
metabolism increasing the dominant absorption wavelengths limits
spectroscopic studies to less than approximately 1,000 meters.
[0083] Accordingly, using this technique it is possible to quantify
changes in tissue oxygenation can be evaluated in a noninvasive way
and quantifies changes in the concentration of deoxyhemoglobin and
oxygenated hemoglobin in units that are micromolar can be used to
study hemodynamic parameters, such as cerebral blood flow, and,
therefore, evaluate flow of the blood vessels in the eye (choroidal
blood flow). (Edwards A. D., et al., Lancet, 770 (1988) and Wyatt
J. S., et al., "EOR", 1086-1091 (1990), the disclosures of which
are incorporated herein by reference.) As such, a near-infrared
spectrometer could be incorporated into a sensor band or goggles
positioned proximate to the eye to provide a method to evaluate
blood flow in the choroidal system and the optic nerve head.
[0084] Location Sensor
[0085] In addition to monitoring physiological information about
the eye and optic nerve, as shown in FIG. 1, in another optional
embodiment a sensor may be included to measure the location and
movement of the eye (15). To understand the potential importance of
this sensor it is necessary to understand the stresses placed on
the eye during a typical surgery. When a patient is anesthetized
the patient's eye are taped or sewn shut and a protective device
placed over them because otherwise the eyes could open and dry
resulting in trauma. Also, during the surgery the patient is often
placed into downward angled or downward facing positions. The
result is that the eyes of the patient are susceptible to two types
of trauma. First, because of the presence of the tape and
protective device external pressures can inadvertently be applied
to eye if the patient's head rolls or moves relative to these
devices. In addition, if the patient is placed facing downward the
force of gravity can pull the eye downward out of the eye socket
fractionally. Although these direct or indirect forces might be
relatively small, the delicacy of the nerve and the weakness of the
vessels that supply blood to the optical structures, can lead to a
drop in circulation to the eye, which in turn can lead to damage to
the optic nerve or other structures.
[0086] The current invention recognizes that monitoring the
position and movement of the eye during surgery using a simple
pressure transducer can supply the treating physician with
important information about the force being placed on the eye, and
allow the physician to mitigate those forces, such as by
repositioning the patient, should they reach a dangerous threshold
level.
[0087] Any suitable pressure sensor capable of converting the
movement of the eye to an electrical signal that can be monitored
by an external device may be used in accordance with the current
invention. In one preferred embodiment, the pressure sensor is a
solid state MEMS pressure transducer that can be applied directly
to the closed eyelid of the patient. An example of a suitable
pressure sensor is described in U.S. Pat. No. 7,314,454, the
disclosure of which is incorporated herein by reference.
[0088] Although the above description has focused on an embodiment
comprising a passive eye position and movement sensor, it should be
understood that such a sensor can optionally be combined with an
active feedback system to neutralize the forces being felt by the
eye by actively fixing the position of the eye in its correct
anatomic location relative to the socket. Such an embodiment, shown
schematically in FIG. 6, incorporates a support mechanism (24) that
would be placed into contact with the outer surface of the eyelid
(16) to fix the eye into the correct anatomical placement and apply
appropriate pressure on the eye to ensure this placement is
maintained based on the signals supplied by the location sensor
(15). In accordance with the current invention any suitable support
mechanism and actuator capable of providing a force sufficient to
adjust the position of the eye, such as, for example, an air
bladder, hydraulic sleeve or electromechanical actuator. In
addition, the structure of the support mechanism itself may take
any form suitable for placement against the eyelid, including, for
example, a bladder, pad or contoured cup.
[0089] During operation the signal from the location/movement
sensor (15) is sent to a signal processor/controller (26) that then
activates the support mechanism (24) to neutralize the movement of
the eye to keep the eye in its proper anatomical placement within
the eye socket. In an alternative embodiment the active support
mechanism (24) is further supplied with a pressure sensor (28),
such as, for example, an electronic pressure transducer that would
monitor the pressure being applied to the eye by the active support
mechanism (24). In such an embodiment, safety thresholds and limits
can be preprogrammed into the controller (26) such that the
pressure being applied never exceeds a level that can be safely
tolerated by the eye.
[0090] Sensor Apparatus
[0091] Although the above discussion has focused on the construct
and operation of the individual sensors, it should be understood
that the current invention is also directed to an apparatus for
positioning and holding the sensor into position on a patient
during use. Although any construct capable of placing and holding
the sensor(s) in place proximate the patient's closed eye during
use may be used, in a preferred embodiment the sensors are
integrated into a pair of goggles (30) as shown in FIG. 7.
[0092] Although the goggles (30) can take a number of different
forms, there are a few necessary elements. First, as shown in FIG.
7 the goggles should have a main body (32) capable of covering both
eyes (34) sufficient to incorporate the package of sensors (36) in
a position proximate to the eyes of the patient. The goggles also
incorporate leads (38) or other means wired or wireless to transmit
the signals from the sensors (36) to an external monitor (40) that
can communicate the signals to a physician.
[0093] The goggles may be made of any suitable material. Preferably
the goggles are of a disposable one-use construction made from
surgical grade materials to ensure that the possibility of
cross-contamination between patients is avoided.
[0094] The above general statement of the invention will be better
understood with reference to the embodiments of the invention
provided in the examples detailed in the following sections. It
should be understood that these examples are only provided for
further detail of preferred embodiments of the invention, and the
scope of the invention is not to be considered to be constrained by
or to the those embodiments.
EXEMPLARY EMBODIMENTS
[0095] As discussed above, monitoring a patient's optic function
when in a state of altered consciousness can provide important
information to a physician about both the mental and physical state
of the individual at a time when the patient himself is unable to
communicate. However, beyond this general benefit to optic
monitoring, it is also possible to provide the physician
information that can help them diagnose, and potentially prevent,
the occurrence of anesthesia-induced disorders that are currently
difficult if not impossible to detect until after the patient has
regained consciousness.
[0096] Two examples of disorders that can be diagnosed using the
optic function monitor of the current invention are described in
the sections below.
Example 1
Post-Operative Visual Loss (POVL)
[0097] Post Operative Visual Loss (POVL) is a broad term that is
often discussed as a single condition; however, there are actually
a number of conditions that fall within this broad definition,
including, for example, posterior ischemic optic neuropathy (PION),
anterior ischemic optic neuropathy (AION), and central retinal
artery occlusion (CRAO). Currently there is a great deal of dispute
as to what factors play a role in causing POVL. As a result, there
is no known methodology for monitoring and preventing POVL in
real-time. Before providing a description of how the
apparatus/method of the current invention may be used to monitor,
diagnose and potentially prevent POVL, it is important to
understand the spectrum of disorders that fall within this broad
classification.
[0098] Corneal Abrasion and Scleral Injury
[0099] Corneal abrasion is the most common surgical and general
anesthesia-related eye complication. (See, e.g., Batra Y. K., et
al., Anesthesia and Analgesia, 56:363-365 (1977); Slocum N. C., et
al., Surgery Gynecology and Obstetrics, 86:729-732 (1948); and
White E. & Cross E., Anesthesia, 53:157-163 (1988), the
disclosures of which are incorporated herein by reference.) The
injury is usually the direct result of lagophthalmos (the
incomplete closure of the eye). General anesthesia reduces tear
formation and stability. If the eyelid does not cover the cornea,
the cornea may become dry, thus increasing the likelihood of
irritation, abrasion, or laceration. Uveal inflammation and
secondary infection increased after abrasions. The standard method
of preventing corneal abrasions is secure taping of the eye. One
alternative that has actually appeared in the literature is to have
the eyelids sewn shut prior to prone positioning of the patient.
(See, Cucchiara R. F. & Black S., Anesthesiology, 69:978-979
(1988), the disclosure of which is incorporated herein by
reference.)
[0100] When corneal abrasions are identified postoperatively, an
ophthalmological consultation is recommended and the usual
treatment is topical eye antibiotic. (See, Daughtery R. J.,
Clinical Pediatrics, 2002; 41:630, the disclosure of which is
incorporated herein by reference.) Topical anesthetics are to be
avoided, as they will delay corneal epithelialization and promote
keratitis. If anesthetic drops are used, an extension of the
abrasion may occur if the patient was to rub or scratch the
anesthetized eye. Although corneal abrasions can be relatively
benign, there are occasions where a corneal ulcer derived from an
abrasion can cause partial or complete visual loss on the involved
eye.
[0101] Central Retinal Artery Occlusion
[0102] Central retinal artery occlusion (CRAO) is the second most
common cause of postoperative blindness associated with prone
positioning and general anesthesia. (Stambough J. R., et al.,
Journal of Spinal Disorders, 5:363-365 (1992), the disclosure of
which is incorporated herein by reference.) Central retinal artery
occlusion is described as a stroke of the central retinal artery.
Central retinal artery occlusion after surgery is usually caused by
direct or indirect pressure on the eye, which increases intraocular
pressure, basilar spasm, or displacement of plaques from the
carotid artery may enter the central retinal artery (Hollenhorst
plaques). (Hollenhorst R. W., et al., Archives of Ophthalmology,
52:819-839 (1954), the disclosure of which is incorporated herein
by reference.) Perioperatively, central retinal artery occlusion
occurs associated with direct pressure from prone positioning. The
hallmark of this diagnosis is the cherry red spot on the center of
the macula. This is seen on funduscopic examination. CROA is
commonly reported secondary to prominent headrest and direct
orbital pressure, which increases intraocular pressure and
decreases retinal blood flow through the central retinal artery
producing the headrest syndrome coined by Katz DA in 2005. (Katz D.
A., et al., Spine, 30:E83-E85 (2005), the disclosure of which is
incorporated herein by reference.)
[0103] There are anatomic variations, which predispose towards the
occurrence of central retinal artery occlusion, including a small
nasal bridge, exophthalmus, a small cup to disc ratio, a narrow
cribrosus lamina, or microvascular anomalies in the eye. It is also
associated with osteogenesis imperfecta. An examination showed
evidence of external periorbital swelling or ecchymosis. Central
retinal artery occlusion is not painful, but there is secondary
irritation from the direct source, i.e. the sclera and associated
structures may be edematous, which is an obvious indication of
external compression. Intraocular pressure exceeds the perfusion
pressure of the central retinal artery producing ischemia of the
retina. Most patients will have unilateral loss of vision often
resulting in permanent amaurosis.
[0104] Blindness from central retinal artery occlusion is always
irreversible. However, Takeuchi, et al. reported a case of partial
visual loss associated with central retinal artery occlusion that
was treated aggressively with Dexamethasone, Paverine, and
Pentoxifylline. (West J., et al., British Journal of Ophthalmology,
74:243-244 (1990), the disclosure of which is incorporated herein
by reference.) After spine surgery, central retinal vein occlusion
has been reported in associated CRAO. It is always secondary to
increased intraocular pressure and a low flow state from primary
pathophysiology leading to CRAO. (Bradish C. F., et al., Spine,
12:193-194 (1987), the disclosure of which is incorporated herein
by reference.) To date, there are no consistently effective
treatments for central retinal artery occlusion.
[0105] Cortical Blindness
[0106] Cortical blindness is caused by an isolated cerebrovascular
accident that selectively affects the visual cortex in the
occipital lobes. It is usually associated with an embolus or
hypoperfusion of the visual cortex of the central nervous system,
such as that shown in the MRI provided in FIG. 8. (See, Drymalski
W. G., Postgraduate Medicine, 67:149-156 (1980), the disclosure of
which is incorporated herein by reference.) Many causes have been
associated with this condition including cardiac arrest, profound
hypotension, and air embolus. Another reported cause is difficult
intubation with prolonged hypoxia and cyanosis. The hallmark
finding in cortical blindness is the normal funduscopic examination
and the retention of pupillary reaction to light with the
associated decreased vision. Cortical blindness is usually
bilateral. Clinical features include failure to react to
threatening gestures, no response to optokinetic stimulation, and
consistent electroencephalogram changes to photic stimulation.
Patients present with Anton's Syndrome, an unusual condition in
which a patient who lost vision because of visual cortex ischemia
or infarct will deny blindness. This is also called anosognosia and
might be confused with hysterical conversion reaction.
[0107] The MRI picture shown in FIG. 8 demonstrates an infarct in
the left occipital lobe of a patient who had temporary cortical
blindness. The blindness manifested as a decreased ability to
concentrate, lethargy, and nonspecific visual impairment after an
elective right total knee arthroplasty. During the case,
hypotension or hemodynamic changes were not observed related to
anesthesia. Blindness subsequently was thought to be embolic as the
patient had a documented atrial septal defect. The visual
impairment was noted the day after surgery. Ophthalmologic
examination showed hemianopsia in the outer quadrant of the right
eye and the inner quadrant of the left eye. Neurologic and vascular
evaluations found no plaque in the carotid artery or source of
embolism.
[0108] Other abnormalities can also produce cortical blindness,
such as an air embolism in the sitting position during cervical
spinal osteotomy. (Stevens W. R., et al., Spine, 1997;
22:1319-1324, the disclosure of which is incorporated herein by
reference.) Air embolism during central venous catheterization in
combination with a rapid turning over of the patient or in
pediatric patients with septal defects may cause unilateral or
bilateral homonymous hemianopsia (the loss of half of the visual
field on the same side in both eyes). (See, Hoski J. J., et al.,
JBJS America, 75:1231-1232 (1993); Jaben S. L., et al., Clinical
Neuroophthalmology, 239-244 (1983); Wolfe S. W., et al., Spine,
17:600-605 (1992); and Yanagidate F., et al., Journal of
Anesthesia, 17:211-212 (2003), the disclosures of which are
incorporated herein by reference.) Homonymous hemianopsia acts like
a transient ischemic attack. Additionally, transient hemianopsia
may be considered a partial manifestation of cortical blindness.
Homonymous hemianopsia has been reported in patients who have
cardiac defects, such as atrial septal defects. Perioperative
echocardiograms with three-dimensional imaging can heighten the
diagnosis of atrial septal defects and the potential of embolic
phenomena. (See, Takahashi S., et al., Journal of Bone and Joint
Surgery, British, 85:90-94 (2003), the disclosure of which is
incorporated herein by reference.)
[0109] Ischemic Optic Neuropathy
[0110] Ischemic optic neuropathy (ION) results from infarction of
the intraorbital optic nerve. The infarction occurs as a result of
decreased oxygen delivery due to perioperative hemodynamic
derangements. There appear to be many subtle factors which, when
acting in concert, produce decrease in the amount of oxygenated
blood that comes to the optic nerve resulting in posterior ischemic
optic neuropathy.
[0111] Various risk factors and causes of factors have been
considered, including hypotension, increased venous pressure,
head-down operative position, increased cerebrospinal fluid
pressure, direct ocular compression (more important in central
retinal artery occlusion), and embolism. Also, the breakdown of the
autoregulation of the perfusion of the optic nerve and eyes that
have a greater risk due to poor autoregulation would be seen in
patients who have comorbidities, such as diabetes, elevation of
blood pressure, vasculitis, over the age of fifty, etc. Indeed, in
most of the instances of perioperative posterior ischemic optic
neuropathy, more than one hemodynamic parameter was altered,
suggesting that the mechanism causing infarction is produced by the
combination of factors, not one sole factor.
[0112] There would appear to be at least three basic ways
hemodynamic derangement leads to decreased oxygen delivery to the
optic nerve. There can be a decrease in arterial perfusion pressure
and an increase in resistance to blood flow or a decrease in blood
oxygen carrying capacity. When the cases evaluated by the American
Society of Anesthesiologists Postoperative Visual Loss Registry,
some of these factors were always present in patients who developed
posterior ischemic optic neuropathy. Combinations of anemia and
hypotension are seen in the majority of the cases. Perioperative
anemia and hypotension can lead to decreased blood oxygen carrying
capacity and decreased arterial perfusion pressure. Anemia can
result from uncorrected preoperative chronic anemia or due to
intraoperative blood loss and/or hemodilution. Hypotension can
result from hypovolemia or can be deliberately induced in some
cases to diminish blood loss during spinal surgery.
[0113] Even though perioperative anemia and hypotension existed in
many of these cases, those two factors are common in the
perioperative course of many surgical procedures, especially spine
surgery, cardiopulmonary bypass, etc. Only a small number of
patients actually develop posterior ischemic optic neuropathy. This
fact alone argues against hemodynamic factors as being the
exclusive reason for this problem to occur. Moreover, Myers, in
1997, actually compared patients who had sustained postoperative
visual loss after spine surgery to an unaffected control group and
showed quite clearly that perioperative hematocrit and blood
pressure were no different in the two groups. (Myers M. A., et al.,
Spine, 22:1325-1329 (1997), the disclosure of which is incorporated
herein by reference.)
[0114] Increased orbital venous pressure can lead to a decrease in
arterial perfusion pressure and may be involved in the pathogenesis
of this condition. Internal jugular vein ligation often part of a
radical neck dissection can cause rapid and severe increase in
venous pressure in the head and orbit, which results in massive
facial and orbital edema. (Balm A. J., Journal of Laryngol Otol,
104:154-156 (1990), the disclosure of which is incorporated herein
by reference.) A head down position often performed with spine
surgery results in facial and orbital edema with increased venous
pressure, especially after a prolonged surgery or associated with a
large volume of intraoperative fluid replacement. (Alexandrakis G.,
et al., American Journal of Ophthalmology, 27:354-355 (1999), the
disclosure of which is incorporated herein by reference.) The prone
position may contribute to increased orbital venous pressure from
increased abdominal venous pressure, especially in patients who are
overweight. Orbital venous pressure cannot easily be quantified. CT
scanning of the orbit demonstrates grossly dilated superior
ophthalmic veins and the dilatation of the venous plexus around the
optic nerve and venous engorgement of the orbital apex, so
positioning can be seen to have a contributing factor to the
pathogenesis of perioperative ischemic optic neuropathy. Yet, there
are case reports of patients who are not in a prone position who
have developed this complication. Radical neck dissections,
cesarean sections associated with anemia, nephrectomy, and
cardiopulmonary bypass. Again, it is believed that this is a
contributing factor, but it cannot be said to be an absolute
causative factor.
[0115] Increased cerebrospinal fluid pressure may decrease arterial
perfusion pressure and increase venous pressure, compressing the
optic nerve vasculature. Direct measurement of this mechanism is
lacking. However, after internal jugular vein ligation, the
cerebrospinal fluid pressure can increase 100% following the
unilateral ligation and 300% following bilateral ligation.
(Schweizer O., et al., Annals of Surgery, 136:948-956 (1952), the
disclosure of which is incorporated herein by reference.)
[0116] Dysfunction of the autoregulatory mechanism that maintains
perfusion of the optic nerve head can result in increased
resistance to blood flow. Autoregulation maintains a constant blood
flow with fluctuations in perfusion pressure by modulating the
resistance to blood flow through autonomic and vasoactive
substances. (Arnold A. C., Journal of Neuroophthalmology,
23:157-163, (2003), the disclosure of which is incorporated herein
by reference.) Proper autoregulation may be altered by
arteriosclerotic disease resulting in decreased blood flow.
Consequently, patients who experienced decreased perfusion pressure
with arteriosclerotic disease may be at a greater risk for
developing perioperative ischemic optic neuropathy. In one study,
twenty out of twenty-eight patients with perioperative posterior
ischemic optic neuropathy had one or more vascular risk factors for
arteriosclerotic disease (hypertension, diabetes, tobacco use,
hypercholesterolemia, coronary artery disease, congestive heart
failure, cardiac arrhythmia, or cerebrovascular disease). (Sadda S.
R., et al., American Journal of Ophthalmology, 132:743-750 (2001),
the disclosure of which is incorporated herein by reference.)
Unfortunately, in another study, no difference was found in the
number of arteriosclerotic risk factors in patients who developed
ischemic optic neuropathy after cardiopulmonary bypass as compared
to a control group (except those patients who had clinically severe
vascular disease or where clinically severe vascular disease was
not defined). (Nuttall G. A., et al., Anest Anal G, 93:1410-1416
(2001), the disclosure of which is incorporated herein by
reference.)
[0117] Direct ocular compression has been implicated in spinal
surgery where patients are in the prone position utilizing a face
support. However, direct ocular compression would tend to decrease
intraocular perfusion pressure and appears to be associated more
with central retinal artery occlusion than posterior ischemic optic
neuropathy. There are a number of cases where this ischemic optic
neuropathy has occurred in people who had their heads supported in
a Mayfield headrest (Mayfield pins) where there was no direct
ocular compression and the head was completely free.
[0118] Finally, it has been theorized that embolism could cause an
increase in resistance to blood flow, but there was no evidence to
support this mechanism occurring in posterior ischemic optic
neuropathy. (Rizzo J. F., American Journal of Ophthalmology,
103:808-811 (1987), the disclosure of which is incorporated herein
by reference.) Also, embolism has not been noted during the
funduscopic examination of patients with posterior ischemic optic
neuropathy nor did any of the histopathological examinations reveal
embolic phenomenon.
[0119] The case studies of perioperative ischemic optic neuropathy
(ION) are also confused. Specifically, the histopathology of ION
has been reported in three cases by Johnson in 1987, Marks in 1990,
and Schobel in 1995. Johnson, et al., in 1987, reported a clinical
pathological case of a fifty-nine year old woman who developed
posterior ischemic optic neuropathy (PION) after an exploratory
laparotomy, which was complicated by severe intraoperative
hemorrhage and hypotension. She subsequently died from sepsis nine
days after the onset of visual loss. Mild disk edema was found at
the clinical examination, but at autopsy, the retrobulbar optic
nerve was infarcted.
[0120] This case is included because it was thought that the disk
edema resulted from the close proximity of the infarction to the
optic nerve head. The gross neuropathological examination at
autopsy revealed bilateral symmetric fusiform swelling and
infarction with central intraparenchymal hemorrhage of the
intraorbital portion of the optic nerve, worse on the right side.
The remaining portion of the central nervous system was normal,
including retina and intracranial visual pathways. Using serial
sections, a composite diagram of the optic nerve was constructed.
The infarcted segment coursed longitudinally and extended from the
retrobulbar to the intracanicular portion bilaterally. The
immediate retrolaminar area was spared bilaterally. The infarction
predominantly affected the more central axial portion with sparing
of the nerve periphery anteriorly and broadening posteriorly. In
the mid-orbital section, the infarction extended into the periphery
circumferentially and narrowed again posteriorly, ending at the
optic canal.
[0121] Marks in 1990 reported a case of a sixty-seven year old man
who had bilateral posterior ischemic optic neuropathy who died from
sepsis fourteen days after a radical neck dissection that was
complicated by intraoperative hypotension and anemia. (Marks S. C.,
et al., Head and Neck, 12:342-345 (1990), the disclosure of which
is incorporated herein by reference.) The autopsy examination of
the brain showed a fresh cerebral infarction that did not involve
the occipital lobe. There was no indication of generalized cerebral
edema. There was diffuse ischemia or watershed zone infarction.
[0122] Nawa, et al., in 1992, subsequently reported the optic nerve
histopathology of this patient. (Nawa Y., Graefes Arch Clin Exp
Ophthalmol, 230:301-308 (1992), the disclosure of which is
incorporated herein by reference.) The gross examination showed
hemorrhagic infarction of the distal and proximal ends of the
intraorbital portion of both optic nerves. The intraocular,
intracanalicular, and intracranial portions were normal. The
central portion of the optic nerve was infarcted with sparing of
the peripheral fibers. Microscopic examination showed acellularity
of the fiber vascular pial septae, mild hemorrhage, glitter-cells
(swollen macrophages), infiltrate, and loss of myelin. A few small
thrombi in the paracentral pial vessels were found, but no emboli
were observed. No abnormalities were detected in either eye.
[0123] Finally, Schobel reported, in 1995, the clinicopathological
case of a forty-eight year old man with bilateral posterior
ischemic optic neuropathy, which occurred after bilateral neck
dissection for squamous cell carcinoma of the mouth. (Schobel G.
A., et al., Int J Oral Maxillofac Surg, 24:283-287 (1995), the
disclosure of which is incorporated herein by reference.) This
surgery was complicated by hypotension and blood loss. Six months
later, the patient had partial visual acuity of the left eye with a
severely constricted visual field. One year later, the patient died
from generalized metastasis and at autopsy there was no evidence of
cerebral infarction. The histopathology of the intraorbital optic
nerve showed complete loss of axons on the right and loss of the
peripheral axons with sparing of the central axons on the left. The
loss of peripheral axons appear to correspond to the constricted
visual field.
[0124] Based on this histopathology it would appear obvious that
hemodynamic derangement must play a role in the cause of ischemic
optic neuropathy, but all individuals are equally susceptible. The
fact that the intraorbital optic nerve is selectively infarcted and
the remaining central nervous system is spared suggests that there
is something unique about the optic nerve and it is more
susceptible to the effects of hemodynamic derangements in some
patients.
[0125] There are a number of unique facts about the blood supply of
the optic nerve, which will be discussed in reference to FIG. 9,
that it is now believed might make the optic nerve particularly
susceptible to such hemodynamic derangements. Firstly, it enters at
an oblique angle into the optic nerve and as it enters the
meningeal covering of dura and pia, the histological arrangement of
the blood vessel changes. The walls become less "muscular" and the
blood vessel becomes more fragile. The dura is known to have
redundancy and "bagginess" around the optic nerve. In the prone
position, the weight of the eye and muscular relaxation could cause
traction on the optic nerve. In this situation, traction on the
fragile central retinal artery would decrease the diameter of the
blood vessel and reduce the perfusion to the optic nerve.
[0126] When you consider the histopathology, it would appear that
there are two separate systems of blood supply to the optic nerve.
There is a pial plexus, which surrounds the periphery of the nerve
and penetrates the nerve a variable distance. The pial plexus is
derived from collateral branches arising from the ophthalmic
artery. The axial system is formed from small branches from the
central retinal artery. There appears to be considerable anatomic
variation in the number of anastomoses between the peripheral
centripetal system and the axial centrifugal system in the
intraorbital optic nerve because there are no anastomoses between
the two systems and endartery formation occurs creating a watershed
zone, which may be the reason that this section of the nerve is
more vulnerable. (Awai T., Jpn J Ophthalmol, 29:79-98 (1985), the
disclosure of which is incorporated herein by reference.)
[0127] Poiseuille's Law states that "the resistance to blood flow
is inversely proportional to the fourth power of the radius of the
vessel and is directly proportional to blood viscosity and the
length of the vessel". Here is the mechanism where the
autoregulation of perfusion of the optic nerve head is deranged.
One of the other factors is that, as will be discussed further
below, this condition appears to be associated with long
procedures, large amounts of blood loss, and replacement of blood
with crystalloid, as opposed to colloid, or whole blood, may be the
answer to the riddle of posterior ischemic optic neuropathy. A
decrease in gradient of blood flow in the optic nerve from the
prelaminar region to the optic chiasma was seen in the cat model.
(Weinstein J. M., et al., Invest Ophthalmol Vis Sci, 24:1559-1565
(1983), the disclosure of which is incorporated herein by
reference.) Such a gradient would make the nerve more susceptible
to the effects of hemodynamic derangement.
[0128] Anecdotal evidence for linking POVL to hemodynamic problems
can also be found by examining studies conducted on the results of
aging on the optic nerve. However, before reviewing the results of
the studies, it is important to understand the anatomy of the optic
nerve. As shown in FIG. 10, the optic nerve is a central nervous
system fiber tract invested by pia mater, arachnoid, and dura
mater, and is divided into bundles by fibrous glial septa, which
run the nutrient vessels. The central artery of the retina enters
the nerve about 1 cm from the nerve head. (Hayreh S. S., British
Journal of Ophthalmology, 47:651-662 (1962) the disclosure of which
is incorporated herein by reference.) The nerve near the globe
differs from the more proximal portion by containing the central
retinal vessels in the middle. It is also larger in cross-section
and has broader connective tissue components. The arteries within
the dural sheath have the thin muscle coat and internal elastica of
cerebral vessels, while those outside have sturdier structure of
systemic arteries with more muscle and elastic tissue, which makes
the optic nerve vulnerable to axial traction injuries (Poiseuille's
Law). The myelin is of the central type and is contributed by the
glia oligodendroglia. The other glial cells are microglia and
astrocytes. Nerve fibers cross the sclera at the cribriform plate
and become myelinated proximal to it.
[0129] Dolman in 1980 analyzed three hundred optic nerves from age
of birth to 96 years and compared the size of the nerves
calculating the area of cross-section. (Dolman C. L., et al.,
Archives of Ophthalmology, Volume 98, 2053-2058 (1980) the
disclosure of which is incorporated herein by reference.) The
longest and shortest diameters within the pia mater were measured
with a micrometer. The figures were averaged for each nerve and the
cross sectional area was calculated from the formula for
cross-sectional area (cross-sectional area=.pi.R.sup.2). The nerve
was seen to be round in the orbital portion and then became oval as
it entered the cranial cavity. There was a retrobulbar enlargement,
which was approximately one-eighth greater than at the midpoint of
the nerve. The cross-section diameters are demonstrated in Tables 3
and 4 below, and were smaller than diameters calculated by
Sylvester and Ari. However, the difference may be explained by the
fact that in the Dolman series, the nerves were trunk by the
paraffin treatment of the sections (see Table 1).
TABLE-US-00003 TABLE 3 Average Area of Cross Section of Optic
Nerves Dolman et al. Sylvester and Ari Age Area (sq. mm) Age Area
(sq. mm) 0-6 mo 2.8 0-6 mo 4.27 3-4 yr 5.4 3-4 yr 9.12 7-10 yr 6.25
7-10 yr 9.76 15-55 yr 6.75 Adult 9.93 60-96 6.75 -- --
[0130] This data shows that the optic nerve is quite small at
birth, but grows rapidly during the first years after which the
growth rate slows. The adult size is achieved at between 12 and 15
years. The size remains constant thereafter. Sylvester and Ari in
1961 used a special gauge and measured thirty premature and mature
infants, as well as 180 other patients. (Sylvester P. E., et al.,
Journal of Neurology, Neurosurgery, and Psychiatry, 24:45-59 (1961)
the disclosure of which is incorporated herein by reference.) Their
figures demonstrated a doubling in size of the optic nerve between
birth and the age of 3 to 4 years and then a much slower increase
in size. They believe that adult size was attained at age 12 years.
These anatomical changes are also seen in laboratory rats. There
was little change in the cross-sectional diameter between birth and
five days. Maximal change occurred between five and ten days. Very
little change occurred in diameter between ten and twenty days. The
adult optic nerve size in a rat is achieved at fifty days.
[0131] Observations were also made concerning the connective tissue
around the optic nerve. These are summarized in Table 4, below.
TABLE-US-00004 TABLE 4 Average Thickness of Fibrous Tissue
Components Thickness (.mu.m) Age Dura mater Pia mater Septa 1 mo
93.8 18.8 0.9 1 yr 187.6 46.9 9.4 4 yr 234.5 46.9 11.2 15-55 yr
375.2 46.9 14.1 60-96 yr 35.2 93.8 28.1
[0132] The thickness of the dura and pia mater were measured with a
micrometer. The dura mater doubled in thickness during the first
year and doubled again from that point on to adulthood. Pia mater,
fine at birth, doubles in thickness by one year and then gradually
becomes heavier. The septa, which divide the optic nerve, are
extensions of the pia mater and reach into the substance of the
nerve. The lamina cribrosa is very rich in elastic fibers. In
childhood and in the prime of life, the optic nerve is closely
packed with more than one million axons. (Hughes A., et al.,
Journal of Comp Neurology, 169:171-184 (1976) the disclosure of
which is incorporated herein by reference.)
[0133] Oppel in 1963 counted 1,186,172 myelinated fibers in the
optic nerve of a thirty-year-old healthy man; 21,351 were large and
69,984 were medium sized and 1,094,837 were small. (Oppel O.,
Albrecht Von Graefes Arch Klin Exp Ophthalmol, 166:18-27 (1963) the
disclosure of which is incorporated herein by reference.) From the
age of sixty onwards, many nerves display diminishing density of
axons. Brabec in 1977 reported the presence of swollen axons in the
nerve head at the level of the cribriform plate in individuals from
the age of forty-six on to eighty years. (Brabec F., Albrecht Von
Graefes Arch Klin Exp Ophthalmol, 200:231-236 (1977) the disclosure
of which is incorporated herein by reference.) The numbers
increased in aged persons. Swelling of axons may be due to
ischemia. The optic nerve at the level of the lamina cribrosa and
proximal to it is particularly apt to suffer ischemic damage in the
elderly because of insufficient perfusion through the posterior
ciliary arteries. (Hayreh S. S., AMALRICP, Editor of Proceedings of
the International Symposium on Fluorescein and Geography, Albi,
1969, Switzerland; S Karger A G, 510-530 (1971) the disclosure of
which is incorporated herein by reference.)
[0134] Glaucoma contributes to ischemia of the retrobulbar portion
of the optic nerve and initiates marked axonal swelling. (Lampert
P. W., et al., Invest Ophthalmol, 7:199-213 (1968) the disclosure
of which is incorporated herein by reference.) Dolman, in 1980,
demonstrated vascular degeneration, hyalinization of the
arterioles, intimal fibrosis, and elastosis of small arteries,
which were common in their series and were always associated with
the history and autopsy finding of vascular disease. (Dolman C. L.,
et al., Archives of Ophthalmology, Volume 98, 2053-2058 (1980) the
disclosure of which is incorporated herein by reference.) Thirty of
the three hundred subjects had focal scars with complete loss of
axons astrocytic gliosis and marked thickening of the septa. All of
those patients had generalized arterial sclerosis.
[0135] Likewise, Schnabel's cavernosa degeneration has been
attributed to several causes, but particularly to glaucoma and
vascular disease. (Henkind, 1976, Lampert, 1968, Virchow K, 1972
(cited), "Anatomy and Pathology of the Optic Nerve Head in
Glaucoma", Trans-Am Acad Ophthalmol Otolaryngol, 81:192-196 (1976)
the disclosure of which is incorporated herein by reference.)
Cavernosa degeneration involved a segment of the cross-section of
the nerve beginning at the cribriform plate and projecting
backwards for a distance of five millimeters. The nerve beyond that
showed tract degeneration.
[0136] In addition, with increasing age, the fibrous tissue
covering and intersecting the optic nerve broadens and coarsens,
and the elastic tissue multiplies. Eventually, the nerve is encased
in a sleeve of leptomeninges and wrinkled dura mater. The fibrous
septa encroach on the area occupied by the nerve fibers and yet the
nerve remains the same size. The fiber bundles become rarified as
age increases. Horgan and Zimmerman in 1962 suggested that the
condensation of fibrous tissue of the septa impeded the diffusion
of nutrients from the vessels to the axons and thus caused the
axonal depletion. (Horgan M. J., et al., Zimmerman L E, "The Optic
Nerve in Ophthalmic Pathology, Second Edition", Philadelphia, WB
Saunders Company, 1962; 577-580 the disclosure of which is
incorporated herein by reference.) However, Dolman, et al., did not
see a direct relationship between the width of the septa and the
density of the axons within the fiber bundles. (Dolman C. L., et
al., Archives of Ophthalmology, Volume 98, 2053-2058 (1980) the
disclosure of which is incorporated herein by reference.) They
postulated an alternative explanation based on the frequent
presence of swollen axons at the nerve head pointing to local
injuries sustained by the axons in this area. A block to axoplasmic
flow at this level had been postulated by Brabec in 1977. (Brabec
F., Albrecht Von Graefes Arch Klin Exp Ophthalmol, 200:231-236
(1977) the disclosure of which is incorporated herein by
reference.) Wirtschafer, in 1977, experimentally stopped axoplasmic
flow and produced axonal swellings filled with cell organelles in
the nerve head by proximal ligature of the optic nerve. In man, the
swelling of axons in this particular area may be due to anoxic
damage caused by faulty perfusion through aging sclerotic vessels
in a watershed zone caused either through glaucoma or simply old
age. (Wirtschafer J. D., et al., Invest Ophthalmol, 16:537-541
(1977), the disclosure of which is incorporated herein by
reference.) For additional information see the following additional
references Armaly M. F., et al., Invest Ophthalmol, 14:475-479
(1975); Birchow K., cited by Austin J. H., "Corpora Amylacea" in
Minckler J, Editor, Pathology of the Nervous System, New York,
1972, Volume 111:2961-2968; and Hayreh S. S., "The Pathogenesis of
Optic Nerve Lesions in Glaucoma", Trans-Am Acad Ophthalmol
Otolaryngol, 81:197-213 (1976), the disclosure of which are
incorporated herein by reference.)
[0137] Surgical Procedures Implicated
[0138] In short, there have been numerous studies on ION disorders
that have implicated any number of physiological conditions. (See,
e.g., Chutkow J. G., et al., Mayo Clin Proc, 48:713-717 (1973);
Harris A., et al., Ophthalmol, 116:1491-1495 (1998); Hayreh S. S.,
Indian Journal of Ophthalmology, 48:171-194 (2000); Johnson M. W.,
et al., Ophthalmology, 94:1577-1584 (1987); Lee L. A., et al.,
Anesthesiology, 95:793-795 (2001); Orgul S., et al., Sury
Ophthalmol 43, Supplemental 1, S17-S26 (1999); Roth S., et al.,
"Injuries to the Visual System and Other Sense Organs in Saidman L,
Editor", Anesthesia and Perioperative Complications, Edition Two,
St. Louis, Mosby, 1999; Sugarbaker E., et al., Cancer, 4:242-250
(1951); and Tobin N. A., Laryngoscope, 82:817-820 (1972), the
disclosures of which are incorporated herein by reference.)
Moreover, perioperative visual loss is known to occur in cases,
such as cardiopulmonary bypass, renal surgery where there were
large amounts of blood loss, head and neck surgery, and
neurosurgery. However, spine surgery seems to pose the greatest
risk for postoperative visual loss. (See, e.g., Huber J. F., et
al., Spine, 23:1807-1809 (1998) and Katz D. A., et al., Spine,
30:E83-E85 (2005), the disclosures of which are incorporated herein
by reference.) The risk of visual loss following spine surgery is
ten times greater than the risk of visual loss following
ophthalmological surgery. Complications are reported associated
with supine and lateral positioning, but there is a ten-fold
increase in eye injuries with prone spine surgical procedures.
Indeed, in 1948 Slocum reported the first case of blindness
resulting from the prone position during spine surgery. (Slocum N.
C., et al., Surgery Gynecology and Obstetrics, 1948, 86:729-732,
the disclosure of which is incorporated herein by reference. In
that case blindness was caused by malpositioning of the head on a
Bailey headrest. (Myers M. A., et al., Spine, 22:1325-1329 (1997),
the disclosure of which is incorporated herein by reference.) In
1954, Hollenhorst, et al. reported blindness caused by prone
positioning with the Mayfield horseshoe headrest. (Hollenhorst R.
W., et al., Archives of Ophthalmology, 52:819-830 (1954), the
disclosure of which is incorporated herein by reference.) These
authors expressed their opinion that increased intraocular pressure
was the principle pathophysiology resulting in visual loss. They
thought the problems were caused by periorbital pressure from the
horseshoe headrest. They went on to evaluate 198 patients who had
vision loss, which was described "as distant hemorrhage". They
established the association of hypoperfusion as being the key
etiological factor.
[0139] Despite the fact that there has been a long and growing body
of evidence that ophthalmological complications are associated with
a variety of surgical procedures and positions, there are some
remarkable conflicts in the data concerning incidents of
perioperative visual loss. For example, Roth, et al. reviewing
60,965 consecutive patients who underwent general anesthesia for
non-ophthalmological surgery found no patients with postoperative
visual loss. (Roth S., et al., Anesthesiology, 1996, 85:1020-7, the
disclosure of which is incorporated herein by reference.) Stephens
reviewed 3,450 spine surgeries in a nine-year period and found only
three patients who had postoperative visual loss for an incidence
of 0.087%. (Stephens W. R., et al., Spine 22:1319-24, 1997, the
disclosure of which is incorporated herein by reference.) Balm, et
al. evaluated 1,200 neck dissections and found only one patient,
0.08%, who had visual loss in the postoperative period. (Balm A.
J., et al., J. Laryngol. Otol. 104:154-6, 1990, the disclosure of
which is incorporated herein by reference.) Likewise, Maran in 1989
analyzed his nineteen year experience of radical neck dissection
reported no patients who had visual loss. (Maran A. G., et al., J.
Laryngol. Otol. 103:760-4, 1989, the disclosure of which is
incorporated herein by reference.) Despite these apparent low
incident rates, a recent survey by the Scoliosis Research Society
indicated that one eye complication occurred for every one hundred
spine procedures. Ischemic optic neuropathy is second only to
glaucoma as a cause of blindness. The incidence varies from 0.01%
to 1%. (See, e.g., Roth S., et al., cited above; Warner M E, 2001;
Williams EL, 1995; Kumar N, 2004). However, other studies indicate
that the incidence may be as high as 4.5%. (See, Shaw P. J., et
al., "Neuroophthalmological Complications of Coronary Artery Bypass
Graft Surgery", ActiNeural Scan-D 76:1-7 (1987), the disclosure of
which is incorporated herein by reference.)
[0140] It is possible that the acknowledge incidence rate is low
because of under reporting. Since the American Society of
Anesthesiology Visual Loss Registry was established in 1999, there
has been a growing awareness and an increase in reporting of this
complication, which suggests that it may actually be far more
common than was previously suspected. In general, the strength of
the data that has been collected so far is quite weak, hence the
great disparities on the percentage incidence of this complication.
However, by the last days of June of 2005, ninety-three cases of
perioperative visual loss associated with spine surgery had entered
the American Society of Anesthesiology Postoperative Visual Loss
Registry. They constituted that this was 72% of the total number of
one hundred thirty-one cases. From these results it was clear that
prone spine surgery is clearly the most common procedure associated
with postoperative visual loss. The analysis of the cases showed
that ischemic optic neuropathy was the cause of visual loss in 89%
of the ninety-three spine cases. Fifty-six cases were diagnosed as
posterior ischemic optic neuropathy and nineteen were diagnosed as
anterior ischemic optic neuropathy. Eight cases were diagnosed as
unspecified ischemic optic neuropathy. The results are summarized
in Table 5, below.
TABLE-US-00005 TABLE 5 POVL: Ophthalmic Lesion Associated with
Spine Surgery No light Perception Ophthalmic Lesion Cases (%) (%)
ION 83 (89) 47 (57) PION 56 (60) 34 (61) AION 19 (20) 8 (42) ION
unspecified 8 (9) 5 (63) CRAO 10 (11) 7 (70) AION: anterior
ischemic optic neuropathy CRAO: central retinal artery occlusion
ION: ischemic optic neuropathy PION: posterior ischemic optic
neuropathy
[0141] In a demographic analysis of the eighty-three spine surgery
cases, which had ischemic optic neuropathy, there were
significantly more males than females (72% males and 28% females).
The mean age was fifty years, plus or minus fourteen years, the
range being between sixteen and seventy-three years. Most patients
were seen as being relatively healthy with 64% of the patients
being rated in the American Society of Anesthesiology Physical
Status Levels as a Class I or Class II and 96% of the patients were
undergoing elective surgery. Coexisting diseases included
hypertension, diabetes, the use of tobacco, coronary artery
disease, cerebrovascular disease, elevated cholesterol or lipids,
and obesity. At least one of these factors was present in 82% of
all of the cases. In the 41% of the patients who were hypertensive,
thirteen were being treated with beta blockers, eleven used
angiotensin converting enzyme inhibitors, eleven used calcium
channel blockers, and eleven used diuretics, and five used other or
unknown medications. Not one patient had a preoperative history of
glaucoma.
[0142] All of the patients were positioned prone for a portion of
the procedure, except for two anterior spine procedures. Ten
procedures involved a supine lateral and prone position, i.e.
combined anterior and posterior procedures. Some of the patients
were positioned on the Wilson frame, some were positioned on a
Jackson table, and some were positioned on soft chest rolls. The
headrests that were used most commonly were foam pads, but there
were patients immobilized in Mayfield pins and/or donut/gel pads.
Eyes were checked routinely throughout the surgery and were
documented by the anesthesiologists in 51% of the cases.
[0143] Of the eighty-three patients who had ischemic optic
neuropathy, 66% had documented bilateral involvement for a total of
one hundred thirty-eight affected eyes. The median onset time of
reporting visual loss postoperatively was fifteen hours, the range
being from zero to one hundred sixty-eight hours following surgery.
One patient who was mechanically ventilated for two weeks
postoperatively reported complete blindness two days after his
extubation.
[0144] Full or partial eye opening was noted immediately post-op in
forty-three patients. The inability to open one or both eyes was
noted in twelve patients and the ability to open the eyes was
missing from the anesthesia records of twenty-eight patients.
[0145] There was associated periocular trauma in one case. Visual
fields were restricted in one hundred thirty-four of one hundred
thirty-eight affected eyes. Complete blindness with loss of light
perception occurred in sixty-four of the one hundred thirty-eight
affected eyes (forty-seven patients).
[0146] Posterior ischemic optic neuropathy was diagnosed in 67% of
all of the ischemic optic neuropathy cases. Anterior ischemic optic
neuropathy was diagnosed in 23% of the cases. Unspecified ischemic
optic neuropathy was diagnosed in 10% of the cases. There was some
degree of recovery of vision in 42% of the ischemic optic
neuropathy cases, although improvement was often clinically
insignificant, i.e. the patient could tell the difference between
light and dark or had a perception of hand motion only. Follow up
ophthalmological examinations appeared to be inconsistent in this
study group. It varied from an initial examination to one four
years post-op.
[0147] In the spine surgery cases where the patient had central
retinal artery occlusion, which numbered ten patients, the mean age
was 46 years (plus or minus thirteen years). Horseshoe headrests
were used in three cases, foam pads were used in two cases, and
miscellaneous headrests were used in five cases. Mayfield pins were
not used in any of the central retinal artery occlusion cases in
contrast to 19% of the ischemic optic neuropathy cases. Eye checks
were performed in six of the ten cases at intervals from thirty
minutes to only once during a ten-hour case. Mean anesthetic
duration and the mean blood loss were less in the central retinal
artery occlusion cases. Deliberate hypotension was utilized in four
of the ten central retinal artery occlusion cases. There were no
cases of bilateral central retinal artery occlusion, however, the
recovery of vision between central retinal artery occlusion and
ischemic optic neuropathy groups were not significantly different.
Periocular trauma was documented in seven of the ten central
retinal artery occlusion cases compared to only one of the
eighty-three ischemic optic neuropathy cases. These included
ipsilateral findings of decreased supraorbital sensation,
ophthalmoplegia, corneal abrasion, ptosis, and/or unilateral
erythema. (For additional information see, e.g., Horan F. T.,
Journal of Bone and Joint Surgery, British, 87:1589-1590 (2005);
Kumar R. N., et al., American Journal of Ophthalmology, 138:889-91
(2004); and Stambough J. L., et al., Journal of Spinal Disorders,
363-365 (1992), the disclosures of which are incorporated herein by
reference.)
[0148] Risk Factors
[0149] An eighteen-member panel of the American Society of
Anesthesiologists met, chaired by Mark A. Warner, M. D. of
Rochester, Minn., and submitted for publication on Nov. 2, 2005
their recommendations concerning postoperative visual loss.
(American Society of Anesthesiologists Postoperative Visual Loss
Registry, Analysis of 93 Spine Surgery Cases, Laurie Lee, M. D., et
al., Anesthesiology V. 105, No. 4, October 2006:652-659, the
disclosure of which is incorporated herein by reference.) Attached
in Appendix A are the tables of data that they generated and the
consensus that was developed from their deliberations. The panel
identified that preoperative anemia, vascular risk factors, such as
hypertension, glaucoma, carotid artery disease, smoking, obesity,
and diabetes, were associated with perioperative visual loss. Also
associated was substantial blood loss and prolonged surgical
procedures.
[0150] Procedures were thought to be prolonged when they exceeded
6.5 hours (range of 2 to 12 hours.) They also considered blood loss
to be substantial when it achieved a point of being 44.7% of the
estimated blood volume (the range was 10 to 200%.) They made
recommendations concerning blood pressure management, management of
intraoperative fluids, management of anemia, management of
vasopressors, patient positioning, and surgical procedures.
[0151] In the American Society of Anesthesiology Study in 2005,
eighty-three of the ninety-three cases were ischemic optic
neuropathy. It is more probable in males than females (72% male and
28% female). The mean age was fifty years, plus or minus fourteen
years. The range was sixteen to seventy-three years. The majority
of the patients were healthy, ASA Class I or II, and 96% were
undergoing elective surgery.
[0152] As mentioned, coexisting diseases included hypertension,
diabetes, tobacco use, coronary artery disease, cerebrovascular
disease, increased cholesterol, lipids, and obesity were present in
between 4 to 53% of the cases. At least one condition was present
in 82% of the cases. Of the 41% of the hypertensive patients,
thirteen used beta-blockers, eleven used angiotensin converting
enzyme inhibitors, eleven used calcium channel blockers, eleven
used diuretics, and five used something else. Not one patient had a
preoperative history of glaucoma.
[0153] In spinal cases, the following risk factors were found:
[0154] 89% of cases with ischemic optic neuropathy underwent
surgery for fusion with or without instrumentation for more than
one vertebral level in the thoracic, lumbar, or sacral region.
[0155] One-third (39%) had previous spine surgery. [0156] All of
the patients were positioned prone for a portion of the procedure,
except two had anterior spine procedures and ten had procedures,
which involved supine or lateral and prone positions. [0157]
Approximately one-third used a Wilson frame, one-third used the
Jackson table, and one-third used soft chest rolls. The headrests
most commonly used were foam pads, Mayfield pins with the Mayfield
headrest, and donut or gel pads. [0158] The majority of the cases
(94%) were greater than six hours or longer in duration. The median
blood loss was 2.0 liters. The range was 0.1 to 25 liters of blood;
82% of the cases had an estimated blood loss of 1.0 liters or
greater. [0159] Fluid management varied with colloid use in 30% of
the cases. Blood was replaced with a cell saver in 54% of the
cases. Packed erythrocytes were used in 57% of the cases. Whole
blood was used in 11% of the cases. [0160] Urine output was less
than 0.5 ml per kilogram in one-quarter of the cases. Postoperative
increased creatinine occurred in six cases and rhabdomyolysis
occurred in three cases. [0161] Blood pressure varied; in 33% of
the cases, the lowest blood pressures were greater than ninety
millimeters mercury, 20% had the lowest systolic blood pressure of
eighty milligrams of mercury or less, 6% of the cases had the
lowest mean arterial blood pressure, which was less than 20% below
baseline, and 34% of the cases had a systolic blood pressure 40% or
greater below the baseline. Deliberate hypotension was utilized in
27% of the cases.
SUMMARY
[0162] In summary, it is proposed that blood flow in the posterior
optic nerve is susceptible to increased venous pressure because the
arterial supply to the posterior optic nerve is derived from small
end vessels from the surrounding pia. There are case reports of
ischemic optic neuropathy that occurred in patients associated with
increased venous and intracranial pressure after radical neck
operations with bilateral jugular vein ligation. In the current
invention the conclusion has been drawn from this that high venous
pressure and interstitial tissue edema can compromise blood flow in
the optic nerve.
[0163] The histopathological studies of posterior ischemic optic
neuropathy in one patient associated with severe blood loss and in
two patients who had bilateral radical neck dissections
demonstrated central hemorrhagic infarction several millimeters
posterior to the lamina cribrosa all of the way up to several
millimeters anterior to the optic nerve canal. This is an area that
is supplied by the small pial blood vessels. Accordingly, although
not to be bound by theory, it is believe that ischemic optic
neuropathy might be caused by increased venous pressure and/or
interstitial fluid accumulation within a nondistensible space,
either the lamina cribrosa at the optic nerve head or the bony
optic canal. Furthermore, the increase in volume of the eye due to
venous engorgement increases the traction and the mass of the eye
as it "prolapses" or descends. This in turn provides traction and
alteration of the caliber of the blood vessels perfusing the optic
nerve, aggravating this watershed vascular supply in the optic
nerve structure.
[0164] The current invention recognizes that it is the combination
of these two mechanisms that is the probable origin of ischemic
optic neuropathy in surgical patients, and particularly in spinal
surgery patients. Specifically it should be recognized that: [0165]
ION always occurred without any evidence of vascular injury. Optic
nerve vasculature is uniquely vulnerable to hemodynamic alterations
in the prone position. [0166] 72% of cases were sine surgery in the
prone position. [0167] 89% of cases were associated with ischemic
optic neuropathy and were relatively healthy. [0168] Estimated
blood loss of 1,000 ml or greater and surgery lasting over six
hours was present in 96% of the cases.
[0169] As such, it is submitted that current techniques are
insufficient to monitor and diagnose potential cases of POVL in
real-time. Specifically, current standards do not provide
monitoring of the function of the optic nerve or the rate of
perfusion of blood into the optic nerve. Indeed, current
methodology only requires monitoring of the fluid and pressure of
the patient as a whole. However, as discussed above the optic nerve
is uniquely susceptible to damage while under anesthesia, and
particularly in a surgical environment. Accordingly, the current
invention, which allows for the monitoring of neurological optic
function through a VEP sensor and vascular function through a
combination of an intraocular pressure sensor and a blood flow
sensor, would uniquely allow for the monitoring and diagnosis of
the major risk factors of POVL in real-time.
[0170] More specifically, by providing a physician with real-time
information about hematological information about blood flow and
perfusion into the eye through the intraocular pressure and blood
flow sensors, in combination with an ability to monitor how the
optic nerve is function neurologically through the VEP sensor, the
current invention allows a physician to get a clear picture of the
ongoing function and health of the optic nerve. In a case where the
monitor of the current invention detects a decrease in blood flow
to the eye in combination with an alteration in neurological
function of the optic nerve, the physician would be alerted and
provided sufficient information to determine what, if any, counter
measures might be employed to prevent possible damage the optic
nerve.
[0171] Proposed Test Procedure
[0172] The current invention proposed the use of VEPs to monitor
optic function. In operation of the invention, goggles containing
light-emitting diodes (LEDs) will be placed on a patient in one of
either a sleeping, coma or sedated state. The LEDs will be
programmed to stimulate VEPs in the patient. Electrodes, either
gold cupsa, disposable subdermal needles or sticky leads, will be
placed on the patient's head, as shown in FIG. 10. In short, a
reference electrode is placed in the forehead (12 cm above the
nasion) and is labeled FPZ. A ground electrode is placed on the top
of the head. The active electrode is placed at the back of the head
at the mid-occipital (MO) scalp region. This MO electrode is placed
5 cm from the inion. In the preferred method, another electrode is
placed 5 cm to the right of the MO and another 5 cm to the left of
the MO. These two additional electrode are labeled left occipital
(LO) and right occipital (RO), as shown in the figure.
[0173] The LED goggles will be place over the patient's eyes and
using the VEPS generated from the stimulus the P100 cortical
response with be monitored. Changes in the P100 will be noted and
relayed to the surgeon and anesthesiologist. As discussed, patients
undergoing operation in the prone or supine position can be
vulnerable to visual impairments and blindness. Case studies have
shown that after undergoing a surgical procedure patients complain
of visual disturbances in one or both of the eyes. These
impairments can last a few hours up to a few days or longer.
Monitoring the visual pathways with the system should show changes
in the P100 response if the cortical response is degraded or
impaired while the patient is under anesthesia. These changes will
be used to alert the surgeon and anesthesiologist to make the
necessary adjustments to the medications or fluids being
administered, or to make positional adjustments to the patient's
head or body on the operating table, or to consider the possibility
of terminating the procedure to prevent the probability of a
service post-op complications.
Example 2
Anesthesia Awareness
[0174] Anesthesia awareness, or "unintended intra-operative
awareness" occurs during general anesthesia, when a patient has not
had enough general anesthetic or analgesic to prevent
consciousness. There are two states of consciousness that may be
present: [0175] Awareness. When patients seem to be vigilant and
cognizant responding to commands but with no postoperative recall
or memory of the events. [0176] Memorization and recall. When
patients can recall events postoperatively but were not necessarily
conscious enough for responding to commands.
[0177] The most traumatic case of anesthesia awareness is full
consciousness during surgery with pain and explicit recall of
intraoperative events. In less severe cases, patients may have only
poor recollection of conversations, events, pain, pressure or of
difficulty in breathing. The experiences of patients with
anesthesia awareness vary widely, and patient responses and
sequelae vary widely as well. This experience may be extremely
traumatic for the patient or not at all. Indeed, some patients
experience posttraumatic stress disorder (PTSD), leading to
long-lasting after-effects such as nightmares, night terrors,
flashbacks, insomnia, and in some cases even suicide.
[0178] Recently attempts have been made to manufacture awareness
monitors. Typically these monitor the EEG, which represents the
electrical activity of the cerebral cortex, which in theory is
active when awake but quiescent when anaesthetized (or in natural
sleep). However, none of these systems are perfect. For example,
they are unreliable at extremes of age (e.g. neonates, infants or
the very elderly). Secondly, certain agents, such as nitrous oxide,
ketamine or xenon may produce anesthesia without reducing the value
of the depth monitor. This is because the molecular action of these
agents (NMDA receptor antagonists) differs from that of more
conventional agents, and they suppress cortical EEG activity less.
Thirdly, they are prone to interference from other biological
potentials (such as EMG), or external electrical signals (such as
diathermy). Finally, because the cortex is active at all times
there is significant background. This means that the technology
does not yet exist which will reliably monitor depth of anesthesia
for every patient and every anesthetic.
[0179] It is well known that during surgery, the large amounts of
anesthetic gases used can affect the amplitude and latencies of
VEPs. Any of the halogenated agents or nitrous oxide will increase
latencies and decrease amplitudes of responses, sometimes to the
point where a response can no longer be detected. Indeed, several
studies have shown that changes in cortical responses can be
affected by several factors, including anesthetic agents and
surgical stimuli. (Chi, O., et al., Anesthesiology, 67:827-830
(1987), the disclosure of which is incorporated herein by
reference.) For example, Uhl, et al., have demonstrated a change in
latency and amplitude due to anesthesia. They demonstrated that the
P100 latency was prolonged by halothane. (Uhl, R. R., et al.,
Anesthesiology, 53:273-276 (1980), the disclosure of which is
incorporated herein by reference.) Likewise, Burchiel, et al.,
showed that the amplitude of the VEP was increased at high
concentration of enflurane (2.5-3.7%). (Burchiel, K. J., et al.,
Electroencephalo. Clin. Neurophysiol., 39:434 (1975), the
disclosure of which is incorporated herein by reference.) Chi, et
al. also showed that nitrous oxide anesthesia slightly increased
the latency of the VEP with no significant change in amplitude.
(See for example the time-lapse measurements taken in FIG. 11,
showing the decrease in number of peaks as a patient is placed
under anesthesia.)
[0180] Because the P100 cortical response is the biggest and most
consistent to monitor, it is proposed that in accordance with the
current invention using the optic function monitor described herein
can be used to measure the P100 cortical response from VEPs to
determine the awareness of a patient under anesthesia, and alert
the anesthesiologist to the need to make changes to the
concentration levels of the anesthesia. Although there are
variations in the P100 latency, amplitude and morphology among
individual patients, it is proposed that during surgery each
patient's P100 can be measured prior to administering anesthesia to
obtain a control level. Moreover, monitoring the visual pathways
will provide a much more accurate measurement of awareness than
does generic cerebral cortex activity, because the cortex controls
a number of different functions which may or may not be affected by
the anesthesia depending on the patient whereas visual function is
fairly uniformly impacted by loss of consciousness.
[0181] In summary, using the monitor of the current invention
awareness under anesthesia can be monitored in real-time, and an
alert signaled should the awareness of the patient change thereby
allowing the anesthesiologist the opportunity to make adjustments
to the concentration of anesthesia being administered.
Example 3
VEP Curve Analysis
[0182] In another embodiment of the invention, a more sophisticated
measurement of optic nerve function is proposed. In this
embodiment, not only the peaks, but the entire waveform of the VEP
of the patient is analyzed in accordance with novel techniques to
determine subtle shifts in the function of the optic nerve, and by
proxy the awareness level or risk of POVL of the patient. This
technique will be discussed in reference to FIG. 12, which provides
a plot of a normal flash VEP.
[0183] In prior art studies that have used VEPs to examine the
effects of anesthesia on a patient only the location and size of
peaks has been examined. (See, e.g., Freye, E., Cerebral Monitoring
In The Operating Room And The Intensive Care Unit, reprinted from
J. Clinical Monitoring and Computing, 9:1-2 (2005), the disclosure
of which is incorporated herein by reference.) However, as shown in
FIG. 12, a VEP curve can be broken into many different parts, all
of which are defined below. [0184] Latency 1 (TL1): Is defined
herein as the temporal interval in milliseconds (ms) between the
onset of stimulation (t.sub.0) and the absolute manitude of the
second evoked potential (EVP2) P2 (P2, .mu.V) given as t.sub.1
(ms). [0185] Evoked Potential 2 (EVP2): Is defined herein as the
second and largest maximum visual evoked potential after photopic
stimulation at t.sub.0. [0186] P2: Is defined herein as the
vertical distance between the maximum value of the upslope of EVP2,
to a point corresponding in microvolts (.mu.V) to the nadir (N3) of
EVP2, the measurement of which is P2 (.mu.V) minus N3 (.mu.V),
i.e., P2-N3 in .mu.N. [0187] N3: Is defined as the nadir of the
downslope of EVP2 (.mu.V). [0188] Peak Forward Upslope Of EVP2
(.delta.(EVP2)/.delta.t.sub.max): Is defined herein as the maximum
upslope, or peak first time-derivative (.delta./.delta.t) of EVP2,
is found by extrapolating a line 15% above the baseline on the
upslope at temporal interval t.sub.2 (ms) to a pont 10% below P2 on
said upslope at temporal interval t.sub.3 (ms) and dividing the
magnitude in .mu.V between the 15% and 10% points by the temporal
interval (t.sub.3 minus t.sub.2) separating the said landmarks in
ms, in accordance with the equation below.
[0188] .delta.(EVP2)/.delta.t.sub.max=.mu.V/ms (EQ. 1) [0189] Mean
Slope of EVP2 (.delta.(EVP2)/.delta.t.sub.mean): Is defined herein
as the quotient of P2 and the temporal interval occurring between
the onset of the upslope of EVP2 and P2 (t.sub.4), said interval
occurring after N2, namely, the temporal point at onset of EVP2
being t.sub.4, said temporal interval being TL1 (ms) minus t.sub.4
(ms) (i.e., TL1-t.sub.4), or, alternatively, the temporal interval
of t.sub.1 minus t.sub.4 (t.sub.1-t.sub.4), this being .DELTA.t,
said interval being the time to peak (TTP) or rise time from
t.sub.4 to t.sub.1, the mean slope thus being P2 divided by TTP
(i.e., P2/TTP), or, alternatively P2/.DELTA.t, given as .mu.V/ms.
[0190] Awareness Index (AI): Is defined herein as a dimensional or
dimensionless linear or non-linear function which approximates the
level of cortical occipital lobe electrical activity and optic
nerve conduction of VEPs. The AI may be used to determine the depth
of general anesthesia, awareness under anesthesia and prevention of
optic nerve dysfunction and blindness, that is, blindness caused by
posterior ischemic optic neuropathy (PION).
[0191] By observing the change in the shape of the curve over time,
it is possible to obtain information about the function of the
optic nerve and in turn the effect anesthesia is having on the
patient. It has been discovered that by monitoring specific
features and combinations of features of VEP curve profiles it is
possible to obtain much more nuanced information about the level of
function of the optic nerve. The current invention proposes a
number of different mathematical methodologies for analyzing these
curves: [0192] In a first embodiment (AI-1), the VEP curve is
analyzed in accordance with the following equation:
[0192] AI-1=P2/TL1 in(.mu.V/ms) (EQ. 2) [0193] In a second
embodiment (AI-2), the VEP curve is analyzed in accordance with the
following equation:
[0193] AI-2=(AI-1).sup.n in(.mu.V/ms) (EQ. 3) [0194] where n is an
exponent between 0.333 and 3, and preferably is between 0.5 and 2.
[0195] In a third embodiment (AI-3), the VEP curve is analyzed in
accordance with the following equation:
[0195] AI-3=(P2).sup.x/(TL1).sup.y in(.mu.V/ms) (EQ. 4) [0196]
where x and y are exponents between 0.333 and 3 and preferably
between 0.5 and 2. [0197] In a fourth embodiment (AI-4), the VEP
curve is analyzed in accordance with the following equation:
[0197] AI-4=(AI-3).sup.n in(.mu.V/ms) (EQ. 5) [0198] where n is an
exponent between 0.333 and 3, and preferably between 0.5 and 2.
[0199] In a fifth embodiment (AI-5), the VEP curve is analyzed in
accordance with the following equation:
[0199] AI-5=(.delta.(EVP2)/.delta.t.sub.max)/TL1 in(.mu.V/ms) (EQ.
6) [0200] In a sixth embodiment (AI-6), the VEP curve is analyzed
in accordance with the following equation:
[0200] AI-6=(.delta.(EVP2)/.delta.t.sub.max).sup.x/(TL1).sup.y
in(.mu.V/ms) (EQ. 7) [0201] where x and y are exponents between
0.333 and 3, and preferably between 0.5 and 2. [0202] In a seventh
embodiment (AI-7), the VEP curve is analyzed in accordance with the
following equation:
[0202] AI-7=AI-6.sup.n in(.mu.V/ms) (EQ. 8) [0203] where n is an
exponent between 0.333 and 3 and preferably between 0.5 and 2.
[0204] In an eight embodiment (AI-8), the VEP curve is analyzed in
accordance with the following equation:
[0204] AI-8=(.delta.(EVP2)/.delta.t.sub.mean)/TL1 in(.mu.V/ms) (EQ.
9) [0205] In a ninth embodiment (AI-9), the VEP curve is analyzed
in accordance with the following equation:
[0205] AI-9=(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(TL1).sup.y
in(.mu.V/ms) (EQ. 10) [0206] where x and y are exponents between
0.333 and 3, and preferably between 0.5 and 2. [0207] In a tenth
embodiment (AI-10), the VEP curve is analyzed in accordance with
the following equation:
[0207]
AI-10=(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.s-
up.z).sup.m in(.mu.V/ms) (EQ. 11) [0208] where x, y, z and m are
exponents between 0.333 and 3, and preferably between 0.5 and 2.
[0209] In an eleventh embodiment (AI-11), the VEP curve is analyzed
in accordance with the following equation:
[0209] AI-11=AI-10.sup.n in(.mu.V/ms) (EQ. 12) [0210] where n is an
exponent between 0.333 and 3, and preferably between 0.5 and 2.
[0211] In a twelfth embodiment (AI-12), the VEP curve is analyzed
in accordance with the following equation:
[0211] AI-12=.delta.(EVP2)/.delta.t.sub.max/t.sub.1/P2
in(.mu.V.sup.2/ms.sup.2) (EQ. 13) [0212] In a thirteenth embodiment
(AI-13), the VEP curve is analyzed in accordance with the following
equation:
[0212]
AI-13=(.delta.(EVP2)/.delta.t.sub.max).sup.x/t.sub.1.sup.y/P2.sup-
.z in(.mu.V.sup.2/ms.sup.2) (EQ. 14) [0213] where x, y and z are
exponents between 0.333 and 3, and preferably between 0.5 and 2.
[0214] In a fourteenth embodiment (AI-14), the VEP curve is
analyzed in accordance with the following equation:
[0214]
AI-14=(.delta.(EVP2)/.delta.t.sub.mean).sup.x/(t.sub.1.sup.y/P2.s-
up.z).sup.m in(.mu.V.sup.2/ms.sup.2) (EQ. 15) [0215] where x, y, z
and m are exponents between 0.333 and 3, and preferably between 0.5
and 2. [0216] In a fifteenth embodiment (AI-15), the VEP curve is
analyzed in accordance with the following equation:
[0216] AI-15=AI-14.sup.n in(.mu.V/ms) (EQ. 16) [0217] where n is an
exponent between 0.333 and 3, and preferably between 0.5 and 2.
[0218] In a sixteenth embodiment (AI-16), the VEP curve is analyzed
in accordance with the following equation:
[0218]
AI-16=(.delta.(EVP2)/.delta.t.sub.max).sup.x/(t.sub.1.sup.y/P2.su-
p.z).sup.m in(.mu.V.sup.2/ms.sup.2) (EQ. 17) [0219] where x, y, z
and m are exponents between 0.333 and 3, and preferably between 0.5
and 2. [0220] In a seventeenth embodiment (AI-17), the VEP curve is
analyzed in accordance with the following equation:
[0220] AI-17=AI-16.sup.n in(.mu.V/ms) (EQ. 18) [0221] where n is an
exponent between 0.333 and 3, and preferably between 0.5 and 2.
[0222] In a eighteenth embodiment AI-18, each equation, i.e.
dynamic equations
[0223] AI-1 through AI-17, measured during the course of anesthesia
and surgery, can be divided by a static control value CV, defined
as each of the respective equations, 1 through 17, measured at the
time of the onset of the study and before induction of anesthesia,
the units of said quotient being a dimensionless index (AI-D).
Therefore, the VEP curve is analyzed by the following equation
(s):
AI-D=((AI-1)(AI-17))/(CV(AI-1)CV(AI-17)) (EQ. 19) [0224] where AI-D
is dimensionless, wherein the respective AI-Ds constitute the
preferred embodiment(s) of the method.
[0225] While under anesthesia the VEP curves of a patient are
monitored and analyzed in accordance using one of the above
methodologies. First, the curve is calibrated. To calibrate the
absolute value of P2 (.mu.V) may be implemented as measured prior
to anesthesia, or, alternatively, a calibrated value of P2 can be
made to equal P2 at a pre-determined age. In summary, by monitoring
the values produced by the equations AI-1 through AI-18 it is
possible to determine the level of anesthesia awareness or optic
nerve injury, especially to the posterior portion of the optic
nerve, which is the portion of the optic nerve that is most
vulnerable in the prone (face down) or sitting positions.
CONCLUSION
[0226] In summary, the current invention is directed to a method
and apparatus for monitoring optic function. The two basic
principles are: (1) monitoring VEPs for neural function; and (2)
monitoring at least one additional parameter of optic function such
as intraocular pressure, blood flow or location of the eye to
provide a multi-variable optic function monitor. The invention is
proposed for use in particular to diagnose and potentially prevent
the incidence of POVL and anaesthesia awareness in patients during
medical procedures.
[0227] While the above description contains many specific
embodiments of the invention, these should not be construed as
limitations on the scope of the invention, but rather as an example
of one embodiment thereof. Accordingly, the scope of the invention
should be determined not by the embodiments illustrated, but by the
appended claims and their equivalents.
* * * * *