Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.[1] The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
It's an indepth presentation by Dr. Shah-Noor Hassan.
2. Definition
The presence of
extravasated blood
within the space
outlined by the
1) internal limiting
membrane .
2) nonpigmented
epithelium of the
ciliary body laterally
and the lens zonular
fibers .
3) posterior lens capsule
7. Common causes
Proliferative Retinopathy Non proliferatve Retinopathy
Proliferative diabetic
retinopathy
Vasculitis
Post venous occlusions
Proliferative sickle cell
retinopathy
PVD associated
Trauma
Vasculitis
Terson’s syndrome
Age related macular
degeneration
Retinal macroaneurysm
Valsalva retinopathy
8. Age
Children Young adults Aged>40 yrs
Trauma Eales vasculitis Posterior vitreous
detachment with or
without retinal tear
Pars planitis Trauma Diabetic retinopathy
Tearson’s
syndrome,Shaken baby
syndrome
Secondary vasculitis Vascular occlusions
Retinopathy of
prematurity
Spontaneous Break through bleed in
wet ARMD
After vaginal delivery in
infants
Proliferative DR Others like
IPCV,melanoma,systemic
anticoagulpathies
X Linked
retinoschisis,FEVR,toxoca
riasis
Coagulopathies Trauma
Others like
retinoblastoma,leukemias
, coagulopathies
10. Pathophysiology of Blood Catabolism in Vitreous
Hemorrhage
PMN
Fibrin
dissolution
Macrophages initiate
phagocytosis
Granulation tisssue resorbs
hemorrhage
2 days
2 weeks
Lack of
early
PMN
response
Slow lysis
of fibrin
Extracellul
ar lysis of
RBC
Rapid clot
formation
11. Natural history and prognosis
Depends on the underlying disease.
Non proliferative diseases have better prognosis than
proliferatve retinopathies
Clearance of blood from the vitreous is a slow process,
with a time constant in the order of 1% per day.
Subhyaloid hemorrhage resorbs earlier than vitreous
hemorrhage
12. Complications
A. Visual disablity
B. Proliferative Retinopathy
C. Glaucoma Related To Vitreous Hemorrhage.
Ghost cell glaucoma
Hemolytic glaucoma
Hemosiderotic glaucoma
D. Myopic shift in refraction after vitreous hemorrhage
in infants.
E.Hemosiderosis Bulbi And Retinal Damage
15. Evaluation of a history with
Vitreous Haemorrhage
Present history of
Flashes
Trauma,surgery
Duration
Past history of- Recurrence
Systemic history
Diabetes mellitus
Hypertension
Other systemic illness
23. Vitreous Hemorrhage Density
Grading Scale
Grade 0 - view of the retina/easily treatable
Grade 1 - retinal detail visible, some hemorrhage present but laser
photocoagulation would still be possible
Grade 2 - large retinal vessels visible, central retinal detail is not visible
enough to adequately place panretinal photocoagulation posterior to the
equator
Grade 3 - red reflex is visible but no retinal detail is seen posterior to the
equator
Grade 4 - no red reflex
24. Fundus visible on Indirect ophthalmoscopy
Cause? PVD induced
Repeat I /O with indentation
USG to r/o RD,PVD
Break +
cryo/ LIO
Screen other
eye
F/U after
1-2 weeeks
Cause ?Proliferative,
others
See for signs of
proliferaton,vasulitis,
AMD in B/E
FFA
Laser
No cause
F/U 2 wk
Repeat as above
25. If fundus is not visible
Ultrasound eye(A and B scan).
1. Vitreous cavity.
2. Vitreoretinal interface.
3. Retinochoroidal layer.
30. Technique PVD RD Choroidal
detachment
Topographic Smooth,open
funnel with or
without disc or
fundus
insertion;inserts at
ora or ciliary body
Smooth or
folded,open or
closed funnel with
disc
insertion;inserts at
ora
Smooth,dome or
flat;no disc
insertion;inserts at
ora or ciliary body
Quantitaive Spikes of variable
amplitude;<100%
amplitude at sup
ora
Steeply
rising;100%
amplitude
including at sup
ora
Steeply
rising;thick double
peaked
spike;100%amplitu
de
Kinectic
(aftermovement)
Marked to
moderate
Moderate to none Mild to none
32. Management
1) Observation
2) Laser photcoagulation
3) Pars plana vitrectomy
Others Cryotherapy
Phamacological vitreolysis
Posterior hyaloidotomy
Medical management of IOP
33. Observation
Fresh Vitreous haemorrhage with
1)Unknown aetiology and attached retina on USG-
reevaluate after 1-2 weeks
2) Known cause and attached retina, no PVD
reevaluation at 3-4 weeks.
a. Post laser or post-vitrectomy,
b. Tersons’ syndrome.
c. Bleeding diathesis.
34. Vitrectomy
Retinal detachment and vitreous haemorrhage.
TRD involving or threatening macula
Attached retina, total PVD and non-clearing
vitreous haemorrhage over 1- 2 months.
Advanced proliferative retinopathy where the
vitreous haemorrhage does not clear in 4-6 weeks
after adequate laser therapy .
Ghost cell glaucoma
NVI
35. Factors determining approach
Etiology Proliferative
NVI
Early PPV
(4-6 wk)
Non proliferative Observe 2-3
mnths
Age Children Early PPV
Adults Wait for PVD
Tramatic Frequent follow up &early intervention
Duration >4-6wk PPV
<4-6wk Observe
Recent BCVA Poor recent BCVA-poorer prognosis ?CNVM, macula
ischemia
Other eye O/E- early intervention
NVI Early intervention
36. Laser photocoagulation
Of both involved and fellow eye
1.Proliferative retinopathy
2.Tears and holes
Panretinal photocoagulation
Laser barrage of tear
38. Intravitreal bevacizumab as an adjunctive therapy before
vitrectomy
Dose 1.25mg in 0.05ml ,5 to 7 days before
surgery after r/o RRD or TRD involving
macula
Advantages-Reduction in
1. Fibrovascular proliferation.
2. Intraoperative bleeding
3. Easier dissection of membranes.
4. Recurrence of bleeding in the early
postoperative period.
5. Time of surgery .
6. Frequency of using silicone oil,PFCL use
and relaxing retinotomies with
subsequent reduction of second surgery.
40. Transconjuctival sutureless 23PPV
Specifications pros cons
25 G 0.55mm
Inner dia-0.57mm
Outer dia-0.62mm
Sutureless
Less inflammation
Faster recovery
Less surgical time
Less iatrogenic breaks
Risk of
endoph,hypotony
Difficult vitreous base
excision
23G 0.72mm
Inner dia-0.65mm
Outer dia-0.75mm
Sutureless
Less inflammation
Faster recovery
Less surgical time
Less iatrogenic breaks
Hypotony
endopthalmitis
20G 1.12mm
Requires suture
No hypotony
Less endopthalmitis
Known rates of RD
Requires suture
Delayed recovery
More inflammation
41. Because the port on the 23-g cutter is closer to the tip, you can
cut tissue better, and fluidics offer more stability/control
42. 23G PPV Greater instrument stiffness in 23G allows for more
complete anterior vitrectomy and manipulation of the
globe.
Robust fluidics allow for greater aspiration rates to
generate vitreous detachment and more efficient core
vitrectomy.
These factors improve both the surgical performance and
safety profile of the vitrectomy system.
In sum, 23-g vitrectomy systems enjoy the best of both 20-
and 25-g worlds.
44. DRVS
616 eyes with recent severe diabetic vitreous
hemorrhage reducing visual acuity to 5/200 or less for
at least one month
VA≥5/200 Type 1
( VA≥10/20)
Type 2
( VA≥10/20)
Early PPV 25% 36% 16%
Deferral 15% 12% 18%
45. DRVS
The eyes most suitable for early vitrectomy are
1. Fibrous proliferations and at least moderately severe
new vessels are present.
2. Extensive scatter photocoagulation has already been
carried out or is precluded by vitreous hemorrhage
52. Methods to decrease intraoperative and
postoperative vitreous hemorrhage
Thrombin
Epsilon-amino-caproic acid
Fluid- air exchange
Recombinant tissue plasminogen activator.
53. Terson’s syndrome
Sudden intracranial hypertension
Effusion of clear or bloody CSF into the optic nerve sheath
Optic nerve sheath dilates and compresses and obstructs
retinochoroidal anastomoses
Marked reduction in venous drainage of the eye
Subsequent retinal venous hypertension and hemorrhage.
54. Pathophysiology of Blood
Catabolism in vitreous
Vitreous hemorrhage differs from hemorrhage into other
tissues outside of the eye through the following
characteristics:
1.Rapid clot formation with sharp borders.
Vitreous collagen
Facilitates platelet aggregation.
Inhibits passive diffusion of red cells and fibrin.
55. 2.Slow lysis of fibrin.-
Low level of vitreal tissue fibrinolytic activity (tissue
plasminogen activator).
Lack of a PMN response.
56.
57. Fundus not visible on indirect ophthalmoscopy
USG
Indications of PPV PVD status
Abnormal adhesion
TRD/RRD
Mass lesion
IOFB if trauma
Observation for 4
to 6 wks
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