The document discusses vitreous hemorrhage, detailing its definition, pathologic mechanisms, common causes, and various types. It outlines the etiology, prognosis, and management strategies, including observation, laser photocoagulation, and vitrectomy. Additionally, it highlights relevant complications, evaluation methods, and advancements in surgical techniques for treating this condition.

1. DR.SHAH-NOOR HASSAN
FCPS,FRCS(Glasgow)

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

3. Vitreous and subhyaloid hemorrhage

4. Pathologic mechanism
New vessels.

5.  Rupture of normal retinal vessels.

6. Extension of hemorrhage through retina from other
sources

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

9. Etiology
PDR (32%)
Retinal tear(30%)
RVO(11%)
PVD(8%)
PSR(2%)
other(13%)
Survey of ophthalmology vol 42

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

13. Differential diagnosis
 Endophthalmitis
 Intermediate uveitis
 Asteroid hyalosis
 Dense PCO
 Grade 4 NS

14. Clinical characteristics
 Symptoms
1. Visual loss sudden ,painless
2.Floaters, cloudiness

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

16. Ocular examination1.Recent visual acuity- Reference
baseline for follow-up
examination.
2.Relative afferent pupillary
defect.
? Retinal detachment
3.Intraocular pressure.
Hypotony
Raised IOP RAPD

17.  Anterior segment
examination
Keratic precipitates, Cells and flare
signs of trauma
 Rubeosis iridis, Angle new
vessels.
 Fundus examination
Involved eye
Fellow eye.

18. Proliferative retinopathy

19. Fellow eye
Peripheral vasculitis eg Eale’s disease

20. Involved eye
Retinal tear with bridging vessels

21. Fellow eye
Lattice degeneration

22. MANAGEMENT
Fundus
VISIBLE Not visible
Indirect
ophthalmoscopuy
USG

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.

26. Subhyaloid hemorrhage

27. Vitreous hemorrhage

28. Vitreous hemorrhage with Total
PVD

29. Vitreous hemorrhage with RD

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

31. Associated TRD

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

37. Cryotherapy
 Post-vitrectomy eyes with recurrent vitreous
haemorrhage from sclerotomy sites or early anterior
hyaloid proliferation.

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.

39. Disadvantages-Risk of
1. Progression of TRD.
2. Endopthalmitis.

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.

43. Pharmacological vitreolysis
 Microplasmin
 Dispase
 Hyaluronidase
 Chondroitinase
 Plasminogen tissue activator, urokinase,streptokinase,
natokinase, collagenase, plasmin

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

46. Visual prognosis
Etiology Visual improvment
PDR 67%
BRVO 88% -100%
CRVO 33%
Terson’s syndrome 93-100%
ARMD,IPCV Poor prognosis
Others like Eale’s ,Behcets,avulsed
retinal vessels,accidental andsurgical
trauma,
Good prognosis
Survey of opthal 97

47. Thank you

50. Uncommon causes
Inflammatory
 Behcet’s disease
 Sarcoid posterior uveitis
 Multiple sclerosis with retinal
vasculitis
 Pars planitis
 Syphilitic retinitis

 Systemic lupus erythematosus
 Toxocara
Vascular
 1. Coat’s disease
 2. Retinal branch artery
malformation
 3. Retinopathy of prematurity
 4. Ocular ischaemic syndrome
 5. Branch retinal artery occlusion
 6. Central retinal artery occlusion
 7. Choroidal vascular aneurysm
 8. Retinal vein rupture
. 9. Hypertensive uveitis
 10. Persistent hyaloid artery

51. Uncommon causes
Complications of surgical
procedures Tumors
 laser photocoagulation
 molteno implant surgery
 Trabeculectomy
 Ocular perforation during retro /
peribulbar injection
 Secondary intraocular lens
implantation
 Iris vessel alteration from a
prolapsed posterior chamber
intraocular lens haptic.
 Cataract wound neovascularisation
 Retinoblastoma.
 Choroidal malignant melanoma
Miscellaneous
 Senile bullous retinoschisis
 Juvenile retinoschisis
 Valsalva retinopathy
 Chest compression
 Newborn after vaginal delivery
Blood disorders

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.

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
?
?