Request for Question Clarification by
31 May 2006 10:41 PDT
Because I can?t find the answer to all your questions, particularly
the statistics, let me share what I did find. I found that cold
decreases the blood supply to the optic nerve, which is undesirable in
increased IOP. I found no direct link to lower lid blepharoplasty and
IOP is the intraocular pressure, that we all have. I?m going to assume
you are referring to increased open-angle intraocular pressure.
?Visual loss following blepharoplasty is well-described in the
literature, but the mechanism has not been completely understood. The
most likely factor is increased orbital pressure and vascular
impairment subsequent to hemorrhage or edema within the orbit induced
by operative manipulation(3-6). Total vascular insufficiency for
60-120 minutes produces permanent loss of vision(7). Increased
intraorbital pressure can produce a central retinal artery(8) or
vein(3) occlusion with ischemia of the anterior optic nerve or
angle-closure glaucoma in susceptible individuals(6)?
?Draining the Fluid and Intraocular Pressure. The aqueous fluid is
continuously produced within the front of the eye, causing pressure
known as intraocular pressure (IOP). To offset the in-flowing fluid
and to maintain normal IOP, the fluid drains out between the iris and
cornea (an area known as the drainage angle). It does so through two
channels within this angle:
?The trabecular meshwork, a sponge-like, porous network, and its
connecting passageways are referred to as the "conventional" outflow
pathway. Most of the eye fluid outflow occurs in this region and flows
from the trabecular meshwork to a group of vessels encircling the
anterior chamber, called Schlemm's canal. From here, the fluid enters
collection chambers and then flows out into the general blood
circulatory system of the body.
?The uveoscleral pathway is located behind the trabecular meshwork and
is called the "unconventional" pathway. Up to 30% of the fluid flows
out through this channel.?
In glaucoma: ?Most people with glaucoma have the form called
primary-open-angle glaucoma (also called chronic open-angle glaucoma).
Open-angle glaucoma is essentially a plumbing problem.
The disease process may occur as follows:
?The drainage angle remains open, but tiny drainage channels in the
trabecular meshwork pathway become clogged. This pathway is
responsible for most aqueous humor fluid outflow. An imbalance then
occurs as fluid continues to be produced but does not drain out
efficiently. Experts have still not definitely determined the precise
area in the pathway where the blockage is most likely to occur. (In
rare instances the pressure is high because the eye produces too much
?The fluid in the eyes anterior chamber builds up and increases
pressure within the eye. This is called intraocular pressure (IOP).
?The intraocular pressure exerts force on the optic nerve at the back of the eye.
?Over time, the persistent pressure or other factors irreversibly
damages the delicate long fibers of the optic nerve, called axons,
which convey images to the brain.
?As these axons die, the small cup-like head of the optic nerve may
eventually collapse into an enlarged irregular shape.
Optic nerve damage is the basic glaucoma condition. If it is
untreated, eventually the nerve deteriorates until a person loses
sight, first in the peripheral vision (the vision in the "corner of
the eyes"). If it becomes severe, the person loses central vision (in
the middle of the eyes), and may eventually become blind. (Blindness
is fortunately nearly always preventable with early treatment.)
Primary open-angle glaucoma tends to start in one eye but eventually
involves both. In about half of patients the damage in the eye is
diffuse, that is the nerve damage is generalized. In the other half
the disease is localized, causing wedge-shaped abnormalities in the
nerve fiber layers of the retina.?
?The intraocular pressures were 14 mmHg RE and 22 mmHg LE.?
?Normal intraocular pressure (IOP) ranges between 11 and 21 mm Hg:
however, this level may not necessarily be healthy for all people."?
?"Aqueous humor, which helps in lens metabolism and nourishes the lens
and cornea, maintains normal intraocular pressure (ie, normal IOP is
10 to 22 mm Hg) by the rate of its secretion and the resistance to
outflow by the trabecular meshwork."?
?The human eye is a delicate system which consists of a few components
that must be maintained at an optimum to ensure a production of an
undistorted image. These components are transparency, constancy of
form and smoothness of surface. The constancy of form of the ocular
bulb is maintained by the sclera and the IOP (Intraocular pressure).
This pressure is higher than that of the environment and is produced
by the flow of the aqueous humor.
The aqueous humor is a fluid produced by the active transport of
electrolytes. It flows through the anterior chamber and is drained
away every hour by the venous blood flow. If the drainage of the
aqueous fluid front he eye is sufficiently prevented by a physical
obstacle or production exceeds the outflow, then IOP builds up and a
condition known as glaucoma is developed.?
??researchers have determined: 1) that aqueous humor flows and serves
as a nutrient delivery system for the avascular cells in the cornea;
2) that the aqueous humor is pumped into the eye and eventually drains
into a vein; and 3) that the resistance of the drainage system leads
to an increased intra-ocular pressure (IOP), typically 15 mm Hg gauge
(2000 Pa). Higher IOP is necessary to maintain the curvature of the
cornea and thus proper eye function, but increased IOP can lead to
damage to the optic nerve.
?In recent years, emphasis has been given to adding lateral canthal
support as an important adjunct to lower lid blepharoplasty. Lower lid
malposition and ectropion are among the most feared complications
following lower lid blepharoplasty. Lateral canthoplasty and lateral
tarsal strip procedures were initially used to correct established lid
malposition; however, more recently, it has become an accepted and
useful prophylactic measure against lid malposition in cosmetic
blepharoplasty (Glat, 1997; Jelks, 1997; Fagien 1999).?
This site mentions increased orbital pressure ? ?Postoperatively,
orbital hemorrhage is recognized by patient reports of pain, swelling,
and proptosis. Associated changes in light perception may also be
present. This condition is a true emergency that requires an emergency
evaluation by an ophthalmologist. Open the incision, evacuate clots,
and control bleeding. Usually, no one bleeding point is defined. If
increased orbital pressure is suspected, perform a lateral canthotomy
with lateral cantholysis. Control hypertension and consider osmotic
?Pulling fat forward may result in still-bleeding capsule vessels
slipping back into the orbit, and may be a principal cause of raising
the intraorbital pressure postoperatively. Because of this risk,
muscle-septal splitting openings into the orbit should never be
sutured?and need not be, as they will close on their own once the
excess fat is removed.?
?The exact mechanism of the blindness is not clear (2): it may be due
to a build-up of pressure anywhere within the orbit which rapidly
involves the whole orbit and produces proptosis, which in turn leads
to the bulging eye becoming impacted between the tense, swollen lids.
This further raises the pressure both intraorbitally and intraocularly
until the retinal circulation is obliterated and sight is lost.
Increase in pressure may very rarely be due to a retrobulbar
hemorrhage, which is more likely to arise following accident trauma,
intraorbital injection, or manipulation of orbital fractures. It is
possible that unheralded loss of sight may be caused by spasm of the
retinal arteries, by optic nerve ischemia caused by preoperative
drug-induced hypotension, or by undue and prolonged pressure on the
eye during surgery.?
3. ?Why does a small linear increase in intraocular pressure occur
with age in the normal population, as shown in Image 1?
4. Why does a parasympathomimetic medication, such as pilocarpine,
produce a dramatic decrease in intraocular pressure in patients with
ocular hypertension and POAG but only produce a minimal decrease in
intraocular pressure in healthy patients?
Increased aqueous inflow is not the cause of ocular hypertension or
POAG. Ocular hypertension and POAG are caused by a decrease in aqueous
outflow. Aqueous outflow is controlled predominantly by trabecular
meshwork pore size. Davanger examined the relationship of pore size to
intraocular pressure using a hydrodynamic model. He found that as pore
size decreases, intraocular pressure increases according to a
hyperbolic function, as shown in Image 2.?
?Because of the hyperbolic relationship of intraocular pressure to
pore size, the healthy patient experiences only a small increase in
intraocular pressure with age as the diameter of the trabecular pore
size decreases because of the age-related decrease in baseline tension
of the ciliary muscle (see Image 4). On the other hand, patients with
ocular hypertension or POAG have inherited small pores or a protein
that effectively makes the pore diameter smaller. Therefore, although
patients with ocular hypertension and POAG experience the same change
in pore size with age as healthy patients, because of the reduction in
baseline ciliary muscle tension, they are starting near the bend of
the hyperbola (see Image 4). The same age-related change in pore size
produces a dramatic increase in intraocular pressure in those patients
who have inherited smaller pores and results in ocular hypertension
?The two main types of glaucoma are primary open angle glaucoma
(POAG), and angle closure glaucoma. These are marked by an increase of
intraocular pressure (IOP), or pressure inside the eye. When optic
nerve damage has occurred despite a normal IOP, this is called normal
?Some people with normal pressure may experience vision loss from
glaucoma, and many people with high IOP (sometimes called ocular
hypertension) do not develop glaucoma. However, the higher the IOP,
the more likely optic nerve damage will occur.?
?Primary open-angle glaucoma
Primary open-angle glaucoma accounts for 60-70% of glaucoma cases in
the United States. In open-angle glaucoma, the aqueous humor is unable
to drain out of the eye. For unknown reasons, the trabecular meshwork
(i.e., eyes filtration area) does not function normally, the pressure
in the eye increases, and the optic nerve is damaged.
Most people do not experience symptoms until their vision is
compromised and extensive damage to the optic nerve has been done.
Peripheral vision is affected before central vision.?
?There is evidence that altered optic nerve head (ONH) blood flow may
play a role in the development and progression of glaucoma. In the
present study, investigators examined the baseline characteristics in
a population participating in a clinical trial in which the ocular
hemodynamic effects of timolol and dorzolamide were compared. The
trial included 140 patients with primary open-angle glaucoma (POAG) or
ocular hypertension (OHT); their baseline parameters were compared
with those of a group of 102 age-matched control subjects. Researchers
used scanning laser Doppler flowmetry to measure blood flow in the
temporal neuroretinal rim and the cup of the ONH. They assessed
pulsatile choroidal blood flow by laser interferometric measurement of
fundus pulsation amplitude. They also calculated hemodynamic
parameters and mean arterial pressure in both groups.
All ocular hemodynamic parameters were significantly lower in the
POAG/OHT group compared with the control group. In addition, results
showed a significant positive correlation between laser Doppler
flowmetry readings and mean arterial pressure in patients with
glaucoma but not in healthy control subjects. Likewise, the
correlation coefficient between fundus pulsation amplitude and mean
arterial pressure was higher in patients with glaucoma than in healthy
This study indicates reduced ONH and choroidal blood flow and an
abnormal association between blood pressure and ocular perfusion in
patients with POAG or OHT, independent of topical antiglaucoma
medication. Hence, vascular dysregulation appears to be an early
manifestation in glaucoma that is not caused by pharmacologic
?The effects of exercise and water replacement on intraocular pressure
(IOP) have not been well established. Furthermore, it is not known
whether the temperature of the fluid ingested influences the IOP
response. In the present study we determined the effect of water
ingestion at three temperatures (10, 24 and 38ºC; 600 ml 15 min before
and 240 ml 15, 30 and 45 min after the beginning of each experimental
session) on the IOP of six healthy male volunteers (age = 24.0 ± 3.5
years, weight = 67.0 ± 4.8 kg, peak oxygen uptake (VO2peak) = 47.8 ±
9.1 ml kg-1 min-1).?
The effects of physical exercise on IOP have received some attention
since the beginning of the 20th century (2) and there have been
reports suggesting that IOP decreases during exercise (2-9). However,
these studies often failed to control for variables such as the type,
intensity and duration of exercise, or subject age and level of
fitness and possible tonometric errors (10). Thus, definite
conclusions concerning IOP changes due to exercise cannot be reached.
The metabolic muscular heat produced during exercise increases body
temperature and activates thermoregulatory mechanisms to dissipate
excess heat. In hot environments, sweat is the main mechanism for heat
loss during exercise, leading to weight loss. Sweat contains small
amounts of minerals such as sodium and potassium (1). Profuse sweating
may lead to changes in plasma osmolarity, which could affect IOP.
Under certain conditions, hyperthermia induced by physical exercise
may be hazardous to health and physical performance. To counteract the
effects of dehydration, sweat losses during exercise must be replaced
with adequate amounts of water (1).
In experimental studies on rabbits, severe hypothermia caused a
decrease in IOP, while hyperthermia caused an increase in IOP (10) and
a decrease in IOP was reported after exposing the cornea to cold air.
The literature shows that water ingestion affects IOP in humans. It
was observed that 78% of healthy volunteers showed an increase of 2.7
mmHg in IOP 10 min after drinking 1000 ml of water and progressive
increases in IOP during a period of 30 min, and a return to basal
levels within the next 30 min (11).
The water temperatures were selected to produce physical cooling
(10ºC), to simulate body temperature (38ºC) and to reach an
intermediate point (24ºC).
IOP was measured by the applanation tonometry method using a
Haag-Streit Goldmann tonometer, model R 900, prior to the intake of
600 ml of water, 10 min after the intake of 600 ml of water, just
after the end of each experimental session (exercising or resting),
and 15, 30 and 45 min after the end of each session.
There was a 3-day interval between the different experimental
conditions and each volunteer performed the sequence of experiments at
the same time of day.
The results were similar when the right eye and the left eye were
compared. A statistically significant increase in IOP was observed
between the first and the second, the first and the third, and the
first and the fourth measurements of IOP, in both exercising and
resting sessions. There were no significant differences in IOP between
the resting and exercising conditions
Certain inverse relationships have been found between osmolarity and
IOP (5.8) and these changes in IOP have been attributed to serum
lactate or blood pH by some authors (5,6,8).
The loss of water and electrolytes that occurs during exercise may
affect plasma osmolarity and volume, which could cause changes in IOP.
In the present study, heart rate, blood lactate, mean skin
temperature, oxygen consumption, carbonic gas extraction, and
hydration status were consistently different between rest and
exercise, but no significant differences in IOP were found between
exercising and resting conditions. Furthermore, the temperature of the
water ingested by the volunteers during the different experimental
treatments did not influence the IOP results.
The variations in IOP - an initial increase followed by a return to
basal values (Figure 1) - were similar during exercise and rest and
were probably due to the ingestion of water, a result previously
reported in the literature (11).
We may conclude that metabolic changes induced by exercise under
conditions of water ingestion or the temperature of the ingested water
had no significant effects on IOP. In fact, only a transient increase
in IOP was observed, related to the ingestion of water.?
© 2006 Brazilian Journal of Medical and Biological Research
Av. Bandeirantes, 3900
14049-900 Ribeirão Preto SP Brazil
Tel. / Fax: +55 16 3633-3825
The above are only snippets of the entire article.(Copyrighted) You
may be able to access the entire article through your public library?s
First Search subscription.
Braz J Med Biol Res, January 2002, Volume 35(1) 121-125 (Short Communication)
Effects of submaximal exercise with water ingestion on intraocular
pressure in healthy human males
M.A. Moura1, L.O.C. Rodrigues2, Y. Waisberg1, H.G. de Almeida1 and E.
I found the article above without need for a library!
?Glaucoma is often associated with an increase in the intraocular
pressure (IOP) . The regulation and increase of IOP is not fully
understood but it has been suggested that the trabecular meshwork (TM)
cells are important. One gene proposed as a candidate gene for
glaucoma is the Oculomedin (OCLM) or Trabecular meshwork-Inducible
Stretch Response gene (TISR). The function of the gene is unknown, but
it is induced by cyclic stretching in TM cells. The TM is located in
the iridocorneal angle which is the principal site of aqueous outflow
from the eye. It is proposed that the trabecular cells sense the
intraocular pressure and regulate the aqueous outflow. The gene is
expressed in the TM and retina, but not in other tissues. Oculomedin
translates into a small protein containing 44 amino acids. The gene
has homology to neuromedin K and an ALU repeat in the 5' UTR . It
is a valid candidate for glaucoma by the analogy to the TIGR/MYOC
?The increased IOP could lead to the tissues, and thereby the cells,
in the eye undergoing stress in the form of mechanical stretching. The
discovery of a gene product induced by cyclic stretching in the tissue
involved in regulation of intraocular pressure was interesting, since
mutations in such a gene could very well give a phenotype that
involves elevated pressure in the eye?
In rabbits:?Circadian rhythms of IOP and body temperature were present
under the regular light-dark cycle and in constant dark. As did
pupillary enlargement, IOP rose sharply at the beginning of the
subjective dark phase and peaked shortly thereafter. Body temperature,
however, increased gradually and peaked in the late subjective dark
phase. In rabbits with unilaterally decentralized ocular sympathetic
nerves, the circadian rhythm of pupil size was present only in the
intact eye. In addition, the circadian IOP elevation in the
decentralized eye was reduced significantly. CONCLUSIONS: In
light-dark entrained rabbits, basal pupil size changes in a circadian
pattern and peaks at the beginning of the dark phase. The circadian
pupillary rhythm disappears after ocular sympathetic decentralization.
There are similar characteristics in the circadian rhythm of IOP. The
increase of basal pupil size in the early dark phase is not related to
the nocturnal increase of body temperature.?
This article is not copy-able, but pp. 12-13 have some information on
IOP and glaucoma.
This is interesting, but please discuss any supplements you would
consider using, with your ophthalmologist first.
Q; Are there any natural alternatives to aid in the treatment of glaucoma?
A: Yes, the key with glaucoma treatment is to increase circulation in
and around the eye. Ginkgo biloba 120 mg twice a day should help
increase overall circulation and Magnesium 500 mg, which I recommend
taking at bedtime when the eye is in repair and the IOP is highest.
Also recommended is the trifola formula made by my colleague, Alan
Tillotson, Ph.D. (302-994-0565, firstname.lastname@example.org) which works in
numerous ways to support eye health and reduce your stress in general.
The B vitamins, especially B 12, DHA, Vitamin E and alpha lipoic acid
all support nerve and photo receptor cell function.?
?Patients with glaucoma who had evidence of acral vasospasm, however,
were more likely to show deterioration in visual fields after cooling
than patients without acral vasospasm (P = 0.007). CONCLUSIONS:
Patients with glaucoma have an abnormal increase in plasma ET-1 after
the body cools. It is possible that at least in some patients,
increased levels of ET-1 in response to vasospastic stimuli may be
involved in the pathogenesis of glaucomatous damage.?
?The mechanisms that lead to the development of glaucomatous optic
neuropathy are still not completely understood. In at least some
patients, factors besides increased intraocular pressure (IOP)
probably play a role in the pathogenesis of the disease. Among these
other factors, vasospasm has been suggested to be causative by several
investigators, leading to decreased blood flow or a diminished
capacity to autoregulate blood flow to the optic nerve head.1?
Please visit each web site for complete information.
temperature + increased IOP
postoperative complications + lower lid blepharoplasty
increased iop + lower lid blepharoplasty
Increased IOP + trabecular meshwork
ocular hypertension + lower lid blepharoplasty
trabecular damage + lower lid blepharoplasty
cold weather + increased IOP
cold + effect + increased IOP
cold + effect + IOP
cold + effect + glaucoma