Traumatic chorioretinal pathologies can result from both penetrating and non-penetrating ocular injuries. Males under 40 are most commonly affected. Closed globe injuries may cause commotio retinae, while open globe injuries risk choroidal rupture. Indirect injuries like Valsalva retinopathy or Terson syndrome can also cause intraocular bleeding. Traumatic macular holes and retinal detachments require surgical repair like vitrectomy. Overall ocular trauma remains a major cause of blindness worldwide.

1. TRAUMATIC
CHORIORETINOPATHIES

2. • Ocular trauma is a major cause of worldwide visual impairment
• Approximately 2.4 million ocular injuries annually
• MALES are affected 9 times more than females
• Most victims are BELOW 40 YRS

3. Ocular injuries

5. • Open globe or closed globe
• Closed globe injury-no full thickness tear in cornea or sclera
Pathogenesis - Coup
- counter-coup
- direct compression

6. COMMOTIO RETINAE
• Berlins edema
• Transient opacification of the deep retina
• Opposite the site of impact (a contrecoup injury)
• If the posterior pole is involved, the fovea is often spared, resulting in a pseudo cherry-
red spot.
• Blood retinal barrier relatively intact
• Extracellular edema, intracellular edema (of glial cells), and photoreceptor outer
segment disruption, retinal pigment epithelial cells, nerve fibers, and the outer plexiform
layer axons of photoreceptor cells

8. Grade 1-increase in IS-OS junction reflectivity with the disappearance
of the thin hyporeflective optical space
Grade 2- COST defect only
Grade 3- COST and IS-OS junction defects
Garde 4- COST, IS-OS junction, and ELM defects

9. CHOROIDAL RUPTURE
• Von Graefe
• Usually are single lesions located temporal to the disc in a concentric fashion.
• Direct ruptures are located anteriorly at the site of impact (coup injury) and are
oriented parallel to the ora – Compression necrosis
• Indirect choroidal ruptures occur opposite the site of impact (contrecoup injury) -
appear as the typical curvilinear shaped lesion of the posterior pole, oriented
concentric with the disc margin

10. • Trauma induces compressive forces that rupture the relatively inelastic Bruch’s
membrane and its adherent choriocapillaris (resulting in acute subretinal
hemorrhage), as well as the retinal pigment epithelium (resulting in late pigment
changes).
• Develops a gliotic scar within a few weeks, and hyperpigmentation develops at
the margins of the healed lesions
• CNV from margins, chorioretinal vascular anastomosis

11. Choroidal rupture in the macula with associated
subretinal hemorrhage
Five weeks later, blood has resolved except there is a
small subretinal blood at the fovea. There is also
subretinal fluid at the superior edge of the choroidal
rupture consistent with the development of a choroidal
neovascular membrane.

12. Area of the choroidal rupture as a discontinuity
in Bruch’s membrane. There is subretinal
hyperreflective material consistent with the
subretinal hemorrhage
Subretinal hyperreflective material in the area of the
choroidal rupture and subfoveal hyperreflective material
in the area of the dehemoglobinized hemorrhage.

13. • FFA –early cases-hyperfluroscence
• Healed choroidal ruptures -early hypofluorescence within the rupture because of
the damaged choriocapillaris (the large choroidal vessels usually are intact) and
late hyperfluorescence from diffusion from the surrounding intact choriocapillaris
• T/T Anti VEGF

14. Sclopetaria (Traumatic Chorioretinal Rupture)
• Goldzieher
• Rupture of the choroid and retina after nonpenetrating ocular trauma in which a
high-velocity projectile strikes or passes tangential to the globe.
• Chorioretinitis proliferans, traumatic proliferating choroidoretinitis, retinitis
proliferans, and acute retinal necrosis
• coup injury
eg shotgun injury

15. • High velocity projectiles cause rapid deformation of the globe and a sudden
increase in the tensile stresses in the ocular tissues. These stresses may exceed
the tensile strength of the retina and choroid, but not the relatively elastic
posterior hyaloid or the relatively strong sclera
• Characterized by an area of absent retina, retinal pigment epithelium, Bruch’s
membrane, and choroid in the same quadrant as the projectile injury

16. • Acute cases- Bare sclera may not be visible due to VH
• As VH resolves irregular, scarred, pigmented borders and the posterior hyaloid
usually remains attached
• Complications - retinal detachment, vitreous hemorrhage

17. Sclopetaria. Inferotemporal area of bare sclera, pigment, and hemorrhage in a
19-year-old man after a shotgun injury

18. Traumatic Macular Hole
• Severe ocular contusion may result in cystoid macular edema.
• Rupture of the inner retinal layer occasionally occurs, resulting in a lamellar hole;
rupture of both the inner and outer retinal layers results in a full-thickness
macular hole
• CME to macular hole may take months to years

19. • A sudden separation of the posterior hyaloid from the retina at the macula may
produce a dehiscence of retinal tissue at the fovea
• Close spontaneously tend to be in younger patients and in patients with
smaller holes (less than 1/3 disc diameter) and without a fluid cuff

20. Treatment:
• Vitrectomy+ gas
• Surface tension of gas at the site of the hole provides a seal that prevents re-
accumulation of the intraretinal fluid as the hole closes with time.

21. TRAUMATIC RETINAL DETACHMENT
CAUSE TRAUMATIC RETINAL
DETACHMENT
NON TRAUMATIC RETINAL
DETACHMENT
RETINAL DIALYSIS 53% 5%
GIANT RETINAL TEAR 16% 2%
HORSE SHOE TEAR 11% 45%
LATTICE DEGENERATION 8% 38%

22. Factors suggesting trauma-induced retinal detachment include
• Unilateral vitreoretinal pathology,
• Retinal dialysis or giant retinal tear,
• Age younger than 40 years,
• Interval from trauma to diagnosis of retinal detachment less than 2 years,
• Objective evidence of trauma.

23. VITREOUS BASE AVULSION
• 26% of patients with traumatic retinal detachment.
• Fundus reveals an arcuate band elevated from the peripheral retina.
• When the superior vitreous base is avulsed, it may appear draped over the
superior peripheral retina
• Cryopexy

24. Superior mid-peripheral fundus demonstrating draped
ribbon-like opacity (avulsed vitreous base)

25. RETINAL DIALYSIS
• Discontinuity or separation of the retina from the pars plana at the ora, and it
may result in retinal detachment
• Quadrants IT>SN>ST>IN
• All patients with a history of blunt ocular trauma should undergo scleral
depression to assess for retinal dialysis (after an open globe is ruled out).
• Indirect ophthalmoscopy reveals a slit at the ora that opens with scleral
depression, and serrations within the dialysis are less prominent than normal

26. • RD often is localized and elevated minimally, especially if the dialysis is small or
located inferiorly
• One or more demarcation lines
• Photocoagulation or cryopexy as prophylaxis for retinal detachment.
• When with RD- scleral buckling

27. Inferotemporal retinal dialysis in a 65-year-old woman who suffered
blunt ocular trauma 2 years prior in a motor vehicle accident

28. RETINAL TEARS
• Areas of strong vitreoretinal adhesion
• HST and operculated tears
• Often are located at areas of lattice degeneration or at the edges of chorioretinal
scars.
• Photocoagulation or cryopexy as prophylaxis for retinal detachment.
• RD- scleral buckling/vitrectomy

29. GIANT RETINAL TEAR
• Retinal breaks extending circumferentially more than 3 clock-hours (equal to or
greater than 90°), and they occur in the presence of a posterior vitreous
detachment.
• Oriented circumferentially, and there may be a radial extension posteriorly at one
or both ends.
• GRTs occur at the posterior edge of the vitreous base
• Differ from dialyses in that the anterior edge of a GRT is a strip of attached retina
under the vitreous base

30. • In eyes with GRTs the posterior hyaloid is detached while in eyes with retinal
dialysis the vitreous remains attached.
• In GRTs, retinal detachment often develops because liquid vitreous easily enters
the subretinal space
• GRTs fewer than 4 clock-hours in size without an inverted flap and without
evidence of proliferative vitreoretinopathy –scleral buckling
• Remaining GRT-vitrectomy + FAE+ Silicon oil insertion +/- scleral buckle
• PFCL

31. Optic Nerve Avulsion
• Occurs after nonpenetrating or penetrating ocular trauma, when an object enters
between the globe and the orbital wall and displaces the eye.
• Acute loss of vision(May be no PL)
• Complete or partial

32. Complete avulsion is characterized by
• complete separation of the retina from the optic nerve,
• the lamina cribrosa is retracted from the scleral rim.
Funduscopic findings in complete optic nerve avulsion include
• extensive hemorrhages around the optic nerve
• vitreous hemorrhage
• excavation of the optic nerve
• hemorrhage within the optic nerve
• central retinal artery occlusion

33. The area of the optic nerve head was excavated and filled with hemorrhage (arrows)
with blood emanating into the vitreous. There was also a ring of peripapillary
hemorrhage and central retinal artery occlusion

34. INDIRECT OCULAR INJURY

35. Purtscher Retinopathy
• Purtscher flecken appear in about 50% of the patients following severe head
trauma
• These are polygonal areas of retinal whitening in the inner retina, between retinal
arterioles and venules and have a characteristic zone of normal appearing retina
extending for an average of 50 μm on either side of the vessels.
• Mostly bilateral
• sudden onset, multifocal lesions, otherwise healthy retinal vessels, and the
characteristic distribution of ischemic patches

36. Right eye demonstrating patches of superficial retinal whitening throughout the posterior pole
Left eye shows symmetrical involvement

37. • acute and chronic pancreatitis
• long bone fracture
• chest compression injuries
• air embolization
• amniotic fluid embolization
• connective tissue diseases such as lupus, scleroderma,dermatomyositis
• thrombotic thrombocytopenic purpura.

38. Pathogenesis:
• arteriolar occlusion from air or amniotic fluid or fat embolization
• arteriolar or venous damage resulting from elevated intravascular pressure
• complement-induced granulocyte aggregation. ( Severe trauma can activate the
clotting and complement systems, and acute pancreatitis has been shown to
activate complement.)
• Complement C5A levels are elevated in patients with Purtscher retinopathy from
acute pancreatitis.

39. Terson Syndrome
• Litten
• Subarachnoid haemorrhage with intraocular haemorrhage
• Mostly due to rupture of intracranial aneurysm
• 20% of patients with subarachnoid hemorrhage may develop the condition.
• VH with multiple pre,sub and intra retinal haemorhages
• 63%-ERM later

40. Pathogenesis:
• Intracranial hemorrhage produces an acute elevation of intracranial pressure that
is transmitted within the optic nerve sheath to obstruct the venous drainage from
the eye.
• This acute rise in venous pressure causes distension and rupture of the fine
papillary and retinal capillaries, often resulting in significant hemorrhage.

41. • Gradual resolution
• Vitrectomy- in young immature eye, bilateral tersons syndrome
Terson syndrome with hemorrhages in multiple layers. There is a large sub-internal limiting membrane
hemorrhage, multiple intraretinal white-centered hemorrhages, and a large area of subretinal hemorrhage

42. Valsalva Retinopathy
• Duane
• Rupture of superficial retinal capillaries associated with sudden elevation of
ocular venous pressure. Incompetent or absent valves in the venous system of
the head and neck allow transmission of thoracic or abdominal pressure into the
eye
• Heavy lifting, coughing, vomiting, and straining during bowel movement

43. • Classic dumbbell-shaped red elevation beneath the internal limiting membrane in
or near the central macula; larger round or oval hemorrhages
• Occasionally, the subinternal limiting membrane hemorrhage breaks through to
the subhyaloid space or vitreous cavity

44. sub-internal limiting membrane (ILM)
hemorrhage in the macula.
Vertical optical coherence tomography scan showing the
sub-ILM hemorrhage.

45. Shaken Baby Syndrome
• Caffey
• Approximately 30–40% of physically abused children develop ophthalmic
manifestations.
• Retinal hemorrhages , cotton-wool spots,perimacular retinal folds and vitreous
hemorrhage,
• Retinal detachment, retinal folds,retinoschisis,and peripheral chorioretinal
atrophy may also occur

46. • The head accounts for approximately 10% of the weight of an infant. Because
newborns have poorly developed neck muscles, the shaking maneuver causes
rapid acceleration–deceleration of the infant’s head and may result in whiplash-
induced retinal hemorrhages.
• Hypoxic ischemic brain injury has been shown to account for the cerebral
pathology in shaken baby syndrome

47. Presumed shaken baby syndrome. Multiple white-centered intraretinal hemorrhages
in an 8-month old boy who was found unresponsive with multiple fractures