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D R .
D R . ZI K R U L L A H
M A L L I C K
PHYSIOLOGY OF INTRAOCULAR
PRESSURE AND THE EFFECTS OF
ANAESTHETIC DRUGS ON
INTRAOCULAR PRESSURE
PHYSIOLOGY OF INTRAOCULAR
PRESSURE
 Intraocular pressure is the pressure exerted by fluids
inside the eye ball
 It is regulated by the resistance to the outward flow
of aqueous humour.
 The normal value of intraocular pressure is 10-
20mm Hg.
 Value in excess of 25 mm Hg is considered
pathological.
 The intraocular pressure should be maintainted
within this normal range to ensure-
 constant corneal curvature
 a proper refracting index of the eye.
 The orbit globe is essentially a non compliant
sphere within a rigid box.
 Intraocular pressure can be influenced by a change
in volume of the orbit or by external pressure.
INTRAOCULAR PRESSURE
REGULATION
 Normal regulation of intraocular pressure occurs
chiefly through the regulation of volume of aqueous
humour in the anterior chamber of the eye.
 The vitreous humour in the posterior chamber has a
relatively fixed volume and is not involved in
intraocular pressure regulation.
AQUEOUS HUMOUR DYNAMICS
 Aqueous humour is produced in the ciliary bodies to
supply oxygen and glucose to the avascular lens and
cornea.
 Production of aqueous is predominantly by
 active secretion mechanisms (80%); the Na K+
ATPase enzyme creating an osmotic gradient for
passage of water into posterior chamber.
 More minor pathway for aqueous humour
production is (20%) is through ultrafiltration of
plasma.
 Filtration: the rate of filtration is influenced by
blood pressure in the ciliary body capillaries,
plasma oncotic pressure and inta ocular pressure.
 The aqueous produced in the posterior chamber
circulates through the pupil,enters the anterior
chamber, bathes the lens and cornea and exits via
the trabecular meshwork in the angle of the
anterior chamber between the peripheral cornea
and iris.
REABSORPTION
 Aqueous is reabsorbed two mechanisms
 1) Trabecular outflow
 2)Uveoscleral outflow
 The bulk of reabsorption occurs through the
trabecular network and canal of schelmm in the angle
between the cornea and the iris.
 Having passed through Fontana's trabecular spaces,
the aqueous enters the venous system following its
passage through the canal of Schlemm.
.
 The fluid enters the aqueous veins in the episcleral
tissue and drains into the orbital venous system and
eventually reaches the cavernous sinus via the
superior and inferior ophthalmic veins
 As the canal communicates directly with the
episcleral veins,absorption through this route is thus
dependant upon the gradient of intraocular pressure
to episcleral venous pressure
 Around 20% reabsorption occurs through the
uveoscleral route which is reverse of ultrafiltration,
relying on the pressure gradient from the anterior
chamber (intraocular pressure) to the interstitium
of the sclera.
Schematic diagram of the aqueous humor cycle.
Llobet A et al. Physiology 2003;18:205-209
©2003 by American Physiological Society
 Interference with aqueous drainage through
trabecular spaces has a major impact on
intraocular pressure.
 When the space narrows the resistance to flow
increases and a marked rise in intraocular pressure
follows.
Implications of the above are
14
 A rise in the intraocular
pressure will be compensated to
some degree by an increased
rate of aqueous drainage.
 Aqueous humour production is
largely constant. When the
capacity of the trabecular
drainage system is reduced
(e.g.glaucoma) or the episcleral
venous pressure is raised (e.g. a
rise in central venous pressure),
IOP will rise.
Factors affecting Intraocular Pressure
EFFECT OF ANAESTHETIC DRUGS ON
INTRAOCULAR PRESSURE
Drugs administered to patients during anaesthesia
may affect intraocular pressure directly through
 action on the central dieneephalic control centres
 through facilitation or inhibition of aqueous
production and drainage
 through relaxation or contraction of extraocular
and orbicularis oculi muscles or
 indirectly through their effects on the
cardiovascular or respiratory systems.
Induction agents
 Central nervous system depressants in general lower
intraocular pressure.
 All induction agents lower the intraocular pressure
exept ketamine.
 Sedative doses of barbiturates lower intraocular
pressure and thiopentone has been shown to lower
intraocular pressure in both normal and
glaucomatous eyes.
 In earlier studies, when given IV or IM to children,
ketamine increased intraocular pressure.
 In more recent studies, ketamine when given
following diazepam-meperidine premedication
produced no change in intraocular pressure in adult
patients and a 25 per cent reduction in intraocular
pressure administered IM to children.
Inhaled anesthetics
 All Inhalational anesthetics decrease intraocular
pressure in proportion the depth of anesthesia.
 The decrease has multiple causes:
1. A drop in blood pressure reduces choroidal voume
2. relaxation of the extraocular muscles lowers wall
tension
3. pupillary constriction facilitates aqueous outflow.
Muscle relaxants
 Succinylcholine increases intraocular pressure by
5-10 mm Hg for 5-10 minutes principally through
prolonged contracture of the extraocular muscles.
 A rise in intraocular pressure may cause extrusion
of ocular contents through an open surgical or
traumatic wound.
 Non depolarising muscle relaxants do not increase
intraocular pressure.
 Opiods have no direct effect on intraocular pressure
but they attenuate the elevation of pressure due to
intubation.
The effect of anesthetic agents on intraocular pressure
(lOP).
INTRAOCULAR PRESSURE
MANAGEMENT IN
OPTHALMIC SURGERY
Opthalmic surgeies can be simply classified as
 Extraocular
Closed e.g. Strabismus
Intraocular
Closed e.g. Vitrectomy
Open e.g. Intracapsular cataract extraction -
intraocular lens
Glaucoma surgery
 Mixed e.g. Extracapsular cataract extraction ~
intraocular lens
Drainage subretinal fluid -+ gas tamponade
Penetarting injury
 For a purely extraocular procedure such as
strabismus correction intraocular pressure has no
impact on conduct of surgery.
 Control of intraocular pressure is crucial for open
ophthalmic procedures such as-
 traditional intracapsular cataract extraction
 drainage operations for glaucoma.
 These procedures, and repair of penetrating eye
injuries, present special challenges to the
anaesthetist and proper anaesthetic management
contributes significantly to a successful surgical
outcome.
 Most important factor in determining intraocular
pressure acutely is the episcleral venous pressure
which is determined by central venous pressure.
 A raised episcleral venous pressure will lead to
vitreous chamber venous engorgement and a
reduction in aqueous humour drainage, both of
which will raise intraocular pressure.
Anaesthesia for a patient with open eye
should include consideration of following
factors:
 Smooth induction with muscle relaxation
 Intubation or LMA placement with care to avoid
coughing and hypertensive response to intubation.
 Use of reverse trendelenberg position and
avoidance of venous congestion caused by neck
positioning are important factors in controlling
intraocular pressure.
 Laryngoscopy and intubation can lead to rise of 10-
20 mm Hg and this may be prevented by avoiding
hypertensive response to intubation by-
 using a laryngeal mask ,
 using indution agent like propofol,
 covering intubation with lidocaine, clonidine or
beta blockers.
 Meticulous avoidance of post operative nausea and
vomitting.

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anesthetic effect in IOP surgery and its drugs action

  • 1. D R . D R . ZI K R U L L A H M A L L I C K PHYSIOLOGY OF INTRAOCULAR PRESSURE AND THE EFFECTS OF ANAESTHETIC DRUGS ON INTRAOCULAR PRESSURE
  • 2. PHYSIOLOGY OF INTRAOCULAR PRESSURE  Intraocular pressure is the pressure exerted by fluids inside the eye ball  It is regulated by the resistance to the outward flow of aqueous humour.  The normal value of intraocular pressure is 10- 20mm Hg.  Value in excess of 25 mm Hg is considered pathological.
  • 3.  The intraocular pressure should be maintainted within this normal range to ensure-  constant corneal curvature  a proper refracting index of the eye.  The orbit globe is essentially a non compliant sphere within a rigid box.  Intraocular pressure can be influenced by a change in volume of the orbit or by external pressure.
  • 4.
  • 5. INTRAOCULAR PRESSURE REGULATION  Normal regulation of intraocular pressure occurs chiefly through the regulation of volume of aqueous humour in the anterior chamber of the eye.  The vitreous humour in the posterior chamber has a relatively fixed volume and is not involved in intraocular pressure regulation.
  • 6. AQUEOUS HUMOUR DYNAMICS  Aqueous humour is produced in the ciliary bodies to supply oxygen and glucose to the avascular lens and cornea.  Production of aqueous is predominantly by  active secretion mechanisms (80%); the Na K+ ATPase enzyme creating an osmotic gradient for passage of water into posterior chamber.  More minor pathway for aqueous humour production is (20%) is through ultrafiltration of plasma.
  • 7.  Filtration: the rate of filtration is influenced by blood pressure in the ciliary body capillaries, plasma oncotic pressure and inta ocular pressure.  The aqueous produced in the posterior chamber circulates through the pupil,enters the anterior chamber, bathes the lens and cornea and exits via the trabecular meshwork in the angle of the anterior chamber between the peripheral cornea and iris.
  • 8. REABSORPTION  Aqueous is reabsorbed two mechanisms  1) Trabecular outflow  2)Uveoscleral outflow  The bulk of reabsorption occurs through the trabecular network and canal of schelmm in the angle between the cornea and the iris.  Having passed through Fontana's trabecular spaces, the aqueous enters the venous system following its passage through the canal of Schlemm. .
  • 9.  The fluid enters the aqueous veins in the episcleral tissue and drains into the orbital venous system and eventually reaches the cavernous sinus via the superior and inferior ophthalmic veins  As the canal communicates directly with the episcleral veins,absorption through this route is thus dependant upon the gradient of intraocular pressure to episcleral venous pressure
  • 10.  Around 20% reabsorption occurs through the uveoscleral route which is reverse of ultrafiltration, relying on the pressure gradient from the anterior chamber (intraocular pressure) to the interstitium of the sclera.
  • 11. Schematic diagram of the aqueous humor cycle. Llobet A et al. Physiology 2003;18:205-209 ©2003 by American Physiological Society
  • 12.
  • 13.  Interference with aqueous drainage through trabecular spaces has a major impact on intraocular pressure.  When the space narrows the resistance to flow increases and a marked rise in intraocular pressure follows.
  • 14. Implications of the above are 14  A rise in the intraocular pressure will be compensated to some degree by an increased rate of aqueous drainage.  Aqueous humour production is largely constant. When the capacity of the trabecular drainage system is reduced (e.g.glaucoma) or the episcleral venous pressure is raised (e.g. a rise in central venous pressure), IOP will rise.
  • 16. EFFECT OF ANAESTHETIC DRUGS ON INTRAOCULAR PRESSURE Drugs administered to patients during anaesthesia may affect intraocular pressure directly through  action on the central dieneephalic control centres  through facilitation or inhibition of aqueous production and drainage  through relaxation or contraction of extraocular and orbicularis oculi muscles or  indirectly through their effects on the cardiovascular or respiratory systems.
  • 17. Induction agents  Central nervous system depressants in general lower intraocular pressure.  All induction agents lower the intraocular pressure exept ketamine.  Sedative doses of barbiturates lower intraocular pressure and thiopentone has been shown to lower intraocular pressure in both normal and glaucomatous eyes.
  • 18.  In earlier studies, when given IV or IM to children, ketamine increased intraocular pressure.  In more recent studies, ketamine when given following diazepam-meperidine premedication produced no change in intraocular pressure in adult patients and a 25 per cent reduction in intraocular pressure administered IM to children.
  • 19. Inhaled anesthetics  All Inhalational anesthetics decrease intraocular pressure in proportion the depth of anesthesia.  The decrease has multiple causes: 1. A drop in blood pressure reduces choroidal voume 2. relaxation of the extraocular muscles lowers wall tension 3. pupillary constriction facilitates aqueous outflow.
  • 20. Muscle relaxants  Succinylcholine increases intraocular pressure by 5-10 mm Hg for 5-10 minutes principally through prolonged contracture of the extraocular muscles.  A rise in intraocular pressure may cause extrusion of ocular contents through an open surgical or traumatic wound.  Non depolarising muscle relaxants do not increase intraocular pressure.
  • 21.  Opiods have no direct effect on intraocular pressure but they attenuate the elevation of pressure due to intubation.
  • 22. The effect of anesthetic agents on intraocular pressure (lOP).
  • 24. Opthalmic surgeies can be simply classified as  Extraocular Closed e.g. Strabismus Intraocular Closed e.g. Vitrectomy Open e.g. Intracapsular cataract extraction - intraocular lens Glaucoma surgery  Mixed e.g. Extracapsular cataract extraction ~ intraocular lens Drainage subretinal fluid -+ gas tamponade Penetarting injury
  • 25.  For a purely extraocular procedure such as strabismus correction intraocular pressure has no impact on conduct of surgery.  Control of intraocular pressure is crucial for open ophthalmic procedures such as-  traditional intracapsular cataract extraction  drainage operations for glaucoma.
  • 26.  These procedures, and repair of penetrating eye injuries, present special challenges to the anaesthetist and proper anaesthetic management contributes significantly to a successful surgical outcome.
  • 27.  Most important factor in determining intraocular pressure acutely is the episcleral venous pressure which is determined by central venous pressure.  A raised episcleral venous pressure will lead to vitreous chamber venous engorgement and a reduction in aqueous humour drainage, both of which will raise intraocular pressure.
  • 28. Anaesthesia for a patient with open eye should include consideration of following factors:  Smooth induction with muscle relaxation  Intubation or LMA placement with care to avoid coughing and hypertensive response to intubation.  Use of reverse trendelenberg position and avoidance of venous congestion caused by neck positioning are important factors in controlling intraocular pressure.
  • 29.  Laryngoscopy and intubation can lead to rise of 10- 20 mm Hg and this may be prevented by avoiding hypertensive response to intubation by-  using a laryngeal mask ,  using indution agent like propofol,  covering intubation with lidocaine, clonidine or beta blockers.  Meticulous avoidance of post operative nausea and vomitting.