AqueoUS HUMOUR DYNAMICS

1. SIVATEJA CHALLA
SSSIHMS

2. • Is a clear, colourless, watery solution
• Flows from posterior to anterior chamber
• In healthy eye flow against resistance
generates 15 mm hg

3. • Aqueous formation (F), facility of outflow (C),
and episcleral venous pressure (P0) are the
major intraocular determinants of IOP. These
factors are related to one another by the
Goldmann equation:
F = C (Po - Pv)
P0 is IOP in undisturbed eye
With the discovery of pressure independent
mech the equation is modified
F = C (Po - Pv)+U
U is the sum of pr independent pathways

5. • Nutrition to lens cornea and iris
• Removes metabolically toxic products
• Refractive index 1.33
• Inflates globe and maintains IOP
• Ascorbate-anti oxidant-uv protection
• Facilitates cellular and humoral response
of eye to inflammation And infection

6. • Anatomy of aqueous formation and
drainage structures
• Aqueous humor formation
• Aqueous humor outflow

7. • Primary ocular structures involved are
1.Ciliary body
2.Posterior chamber
3.Anterior chamber
4.Angle of anterior chamber
5.Aqueous outflow system

8. 1.CILIARY BODY

9. • CILIARY PROCESS
-70-80
-2 mm length and 5mm
width
• Network of capillaries
• Stroma
• Inner pigmented
epithelium
• Outer non pigmented
epithelium

11. 2.POSTERIOR CHAMBER 0.06ml

12. 3.ANTERIOR CHAMBER-0.25ml

13. 4.ANGLE OF ANTERIOR CHAMBER

14. • Complex pathway
• Ciliary processes are site of aqueous humour
formation
• Mainly by three machanisms
1.Ultra filtration 20%
2.Active transfer 70%
3.Diffusion 10%

15. 1.ULTRAFILTRATION
Process thru which fluids and solutes cross
through semi permeable memb
Capillary blood flow 150ml/min
4%filters thru fenestrations
Favoured by hydrostatic pressure diff b/w
capillary and interstitial pr.
Enough to move fluid to stroma but further req
active transport
Leads to formation of stromal pool

16. 2.ACTIVE TRANSPORT
Energy dependent
Majority production by active secretion
Uses ATP
AA:Decreased by hypoxia, hypothermia and
inhibitors of active metabolism.
Majority of investigators proposed that active
transport of sodium is key in aq humor
formation

17. • Sodium-70% is actively transported by specific
secretary pump. Rest by diffusion, ultrafiltration.
• Chloride-dependent on sodium
• Ascorbic acid- secreted against large
concentration gradient.
• Amino acids-By 3 carriers.
• Bicarbonate-by carbonic anhydrase mediated
reaction.

19. 3.DIFFUSION
Active Transport of substances described above
lead to osmotic and electrical gradient
To maintain the balance small partices like water
and small plasma constituents move in to post
chamber by diffusion

20. • Consists of two
pathways
1.Trabecular or
conventional outflow
2.Uveoscleral or
unconventional outflow

21. UVEOSCLERAL OUTFLOW
 Pressure independent,10-25%
 0.3microl/min and independent of IOP
CILIARY BODY
SUPRA CHOROIDAL SPACE
CILIARY BODY VENOUS CIRCULATION
CHOROID
SCLERA
ORBITAL TISSUE

22. INCREASE
• Prostaglandins-one of most potent IOP
reducing agents
• Cycloplegics
• Alpha agonists-
epinephrine,brimonidine,apraclonidine
• Atropine
DECREASE
• Pilocarpine

23. TRABECULAR OUTFLOW
• Pressure dependent,90%
TRABECULAR MESHWORK
SCHEMMS CANAL
INTRASCLERAL CHANNELS
EPISCLERAL AND CONJUNCTIVAL VEINS
CAVERNOUS SINUS

25. TRABECULAR MESHWORK

27. • VACUOLATION THEORY:- vesicles and vacuoles in endothelium open and
close intermittently to transport aqueous from TM cells to Schlemm’s canal
Non
Vacuolat
ed state
Early stage
of basal
infolding
Macrov
acuole
formati
on
Vacuolar
transecell
ular
channel
formation
Oclusion
of basal
infolding

28. SCHLEMMS CANAL
• Endothelial lined oval channel present
circumferentially in Scleral sulcus.
• Cells irregular spindle shaped & contain
giant vacuoles.
• Outer wall contains openings of collector
channels.
• Torus or lip like thickenings near collector
channel help to keep canal open.
• AA: Gaint vacuoles are lost with increasing
age and this is implicated in POAG.

30. COLLECTOR CHANNELS
• 25-30 intrascleral aqueous vessels
• Valveless,wide at origin
• Direct system
• Indirect system
EPISCLERAL VEINS
• drain ultimately in to cavernous sinus via
ant ciliary and sup ophthalmic veins

31. • POAG - loss of trabecular endothelial cells.
- collapse of schlemms canal.
- obstruction of collector channels.
• Infantile glaucoma – outflow structures not
developed properly (Trabeculodysgenesis).
• Angle closure glaucoma – peripheral iris
pushed against meshwork.
• Secondary open angle – obstruction by RBCs,
WBCs, tumor cells , pigment & lens particles.

32. • Rate: 2.4+/-0.6 microL/min
• Volume: 0.31ml( 0.25ml AC, 0.06ml PC)
• Refractive index: 1.336
• Viscosity:1.025-1.040
• Osmotic pressure: 3-5mosm/L
• pH:Acidic,7.2
• Turnover: 1.5-2hrs

33. • Water -99.9%.
• IgM & IgG ,but no IgA and IgD.
• Plasminogen and its activators but no other
clotting factors.
• Most important- low protein content (200 times
less) and high ascorbate (20 times).ascorbate
acts as anti oxidant and protects ocular
structures from uv light induced oxidative
damage
• Comparision b/w PC and AC aqueous
bicorb and ascorbate pc>Ac
chloride ac>pc

34. Component (mmol/kg h2o) Plasma conc Aq humor conc
Sodium 146 163
chloride 109 134
Bicarbonate 28 20
Ascorbate 0.04 1.06
Glucose 6 3
Urea 9 7
lactate 4.3 7.4

35. • The tight junctions
connecting the apical
portions of adjacent non
pigmented epithelial cells
forms the blood aqueous
barrier.
• Responsible for maintaining
the difference in chemical
composition b/w aq and
plasma

37. Break down
• Proteins appear in aqueous humor:
Plasmoid (Secondary )aqueous
On SLE-Pronounced Tyndall beam
>20mg / 100 ml ,phenomenon of FLARE.
• Fibrinogen enters- clotting of aqueous.
• INFECTIONS-brings mediators of cellular and
humoral immunity
• UVEITIS AND TRAUMA-dev of cataract and
synechiae formation
AA: Rate of penetration of PAH, fluorescein,
Evan’s blue increases-Diagnostic indicator.

38. • Avg is 2.6-2.8 micro lit/min
• Diurnal variation : maximum in morning hours &
min late at night, due to decreased stimulation
of ciliary epithelium by catecholamines during
sleep.
• Age and sex: similar in males & females , reduces
with age.
• Ocular inflammation ,hypothermia ,systemic
acidosis & anesthetics like halothane ,
barbiturates & ketamine decrease formation.

39. • Blood flow to ciliary body: profound
vasoconstriction decreases formation.
• Sympathetic system: stimulation by β2 &
inhibition via α2 receptors.
• Parasympathetic system: decreases via M3
receptors.
• Intracelluar regulators: cyclic AMP
increases aqueous formation.

40. PHYSICAL METHODS-pressure dependent
• -When fluid is introduced in to a closed system
there is intermediate increase in pressure in the
system
• Can be calc using goldmans equation
F = C (Po - Pv)
F- Rate of aqueous outflow (mmHg)
C- Coefficient of outflow facility
(microL/min/mmHg)
Po -Baseline IOP (mmHg)
Pv- Episcleral venous pressure (mmHg)

41. By
1.Tonography
2.Suction cup
3.Perfusion
tonography
• Non-invasive technique
• Schiotz tonometer placed on eye for 4min ,
raises IOP.
• Rate of flow calculated based on rate of rise
of IOP.
• Normal: 0.28microl/min/mmHg
• Most glaucoma patients have values less than
0.17microl/min/mmHg.

42. TRACER METHODS
• Measures rate of appearance or
dissappearance of various tracers in ac
• Any aq passing posteriorly to vitreous and
retina cannot be detected
-Photogrammetric estimation
-Radiolabelled isotopes
-Fluorescein technique
-PAH technique

43. • CLINICAL CONDITIONS
-hypothemia and systemic acidosis
decreases aq production and vice versa
-IDDM decrease aqueous outflow

44. • PHARMACOLOGICAL AGENTS
INCREASE PRODUCTION
-beta adrenergic agents
-hydrocortisone adm systemically
-intracameral ANP
DECREASED PRODUCTION
-CA inhibitors
-Beta blockers
_ouabain
-cyclodestructive procedures