Papilloedema.pptx

This PPT is very beneficial for undergraduate Medical Students

1. Papilloedema Dr. Atul K umar Anand Senior Resident AIIMS Patna

2. Optic disc Optic cup Vein Arterioles Fovea Normal Ocular Fundus

3. Definition Passive hydrostatic, non inflammatory, swelling of optic nerve head secondary to raised intracranial pressure. Almost bilateral ;( although it may be asymmetrical ) may also be unilateral sometimes Optic disc swelling in the absence of raised intracranial pressure is referred to as optic disc edema.

4. PSEUDOPAPILLEDEMA More correctly, pseudodisc edema- abnormalities that produce elevation and irregularities of the optic nerve head that mimic disc edema. Hyaline bodies (optic disc drusen ) Tilted discs optic disc in hypermetropic eyes

5. Normal disc

6. Disc edema

7. Normal disc swollen disc

8. Pseudo disc edema

9. Papilloedema Passive bilateral disc swelling associated with increased intracranial pressure (ICP) Develops over days 2-3 month resolution time after restoration of normal ICP Associated with Headache Vomiting Diplopia from abducens palsy

10. Pathophysiology Disturbance in axoplasmic flow causing stasis swelling of axons and leakage. Increased intracranial pressure(ICT) is transmitted along subarachnoid space with optic nerve sheath acting as a tourniquet. Increased ICT leads to increased optic nerve tissue pressure which alters pressure gradient resulting in stasis.

11. Pathophysiology Mechanical/vascular causes combine to produce B lockage of optic nerve - axoplasmic flow Disturbance of pressure gradient across the lamina cribrosa Disc edema ( Involves only that part of optic nerve anterior to lamina cribosa )

12. Causes(Bilateral) Space occupying lesions.(ICSOL) Blockage of CSF flow. Reduction in CSF resorption . Increased CSF production .

13. Idiopathic Intracranial Hypertension (pseudo- tumor cerebri ) Focal or diffuse cerebral edema . Vitamin A toxicity.

14. Causes(Unilateral) Foster kennedy syndrome Previous unilateral optic atrophy .

15. Foster-Kennedy Syndrome:-unilateral papilloedema with primary optic atrophy on the other side suggest a tumour of the opposite o lfactory lobe or orbital surface of front lobe.

16. Symptoms(General) Symptoms of increased intracranial pressure include: Headache- - severe or associated with nausea and vomiting or a sense of pressure around the ears. worse in a recumbent position, or in the early morning, when the patient wakes up, but improves during the day. Projectile vomiting. Loss of consciousness Diplopia

17. Symptoms Transient obscurations of vision monocular or binocular blackouts, that last 3-4 seconds occur as the patient arises from the recumbent position to sitting or standing. visual blurring is because of enlargement of blind spot and adjacent retinal folds or edema (reversible) injury to optic nerve- associated with secondary optic atrophy(permanent) which results in constricted visual fields and poor color vision.

18. Signs(Mechanical) Elevation of the optic disc.(3D=1mm elevation Blurring of the optic disc margin . Filling in of the physiological cup. Edema of the peripapillary nerve fiber layer . Retinal or choroidal folds(Paton’s lines ) Macular fan .

19. Signs of optic disc edema Vascular signs 1. Hyperemia of the optic disc ( Kestenbaum's number may be greater than 12) 2. Venous congestion (venous dilatation and tortuosity ) 3. Peripapillary hemorrhages 4. Exudates in the disc or peripapillary area 5. Nerve fiber layer INFARCTS

20. Classification of papilloedema (according to severity and its chronicity ) Early Established (acute) Longstanding (chronic) Atrophic (secondary optic atrophy)

21. Early papilloedema VA - normal Mild disc hyperemia Indistinct disc margins - initially nasal Mild venous engorgement Normal optic cup Spontaneous venous pulsation - absent (also absent in 20% of normals )

22. Established papilloedema (acute) VA - usually normal Severe disc elevation and hyperemia Very indistinct disc margins Obscuration of small vessels on disc Marked venous engorgement Reduced or absent optic cup Haemorrhages + cotton-wool spots Macular star

23. Longstanding papilloedema (chronic) VA - variable Marked disc elevation but less hyperaemia Disc margins - indistinct Variable venous engorgement Absent optic cup

24. Atrophic papilloedema (secondary optic atrophy) VA - severely decreased Mild disc elevation Indistinct disc margins Disc pallor with few crossing vessels Absent optic cup

25. Histopathological Findings Acute disc edema Accumulation of extracellular fluid in and anterior to retinal lamina cribrosa , with enlargement of subarachnoid space with stretching . Engorgement of axons occurs in prelaminar portion.

26. Chronic disc edema Degenerative and fibrotic changes in both anterograde and retrograde manner. (hence atropy may occur anywhere from retinal nerve fiber layer to optic nerve)

27. Visual field changes

28. Enlargment of blind spot. Earliest loss of visual field commonly involves inferior nasal quadrent . Peripheral concentric constriction.

29. Relative scotoma (first to green and red ). Complete blindness. In all cases visual field changes should be monitored carefully and decompression to be done before peripheral constriction sets in .

30. Differential diagnosis of Papilledema Papillitis . Pseudopapilledema . - Drusen of optic disc. - High Hypermetropia (c rowded nerve fibers at disc). - AION. Optic neuritits . Tilted optic disc. Myelinated nerve fibers .

31. Papillitis

32. Pseudopapilledema - Drusen of Optic disc

33. Pseudopapilledema - Hyperopic disc

34. Tilted optic disc

35. Myelinated nerve fibers

36. Papillitis papilloedema Unilateral Sudden diminished of vision Sustained pupillary reaction marcus gunn pupil Media might be hazy due to exudation into vitreous Disc swelling rarely more than 2-3D Field defect central or centrocaecal scotoma between the fixation and blind spot especially for red and green x-ray skull : normal condition temporary and recovers in a few weeks Bilateral For long central vision is unalter Pupil round and reacts briskly to light Media clear May be as high as 6D Enlarged blind spot later contraction of the peripheral field Shows silver beaten appearance erosion of posterior clinoid process and dorsum sellae Condition progressively deteriorates and ends in blindness unless treated in time

37.   History and physical examination including blood pressure measurement . Ophthalmic examination - In addition to fundus examination, assessment of visual acuity, pupillary examination, ocular motility & alignment, and visual fields. MRI with or without contrast is the best investigation of choice. Investigations

38. CT S can To rule out - Intracranial lesions. - Obstructive hydrocephalus. Can detect - Subarachnoid , epidural & subdural hemorrhages . - Acute infarctions. - Cerebral edema . Contraindication for MRI .

39. Lumbar puncture   Diagnostic - Recording opening pressure. CSF for microbial and infectious studies . Therapeutic procedure - Pseudotumor cerebri

40. Fundus Fluoroscence Angiography(FFA ) Early Phase disc capillary dilation Dye leakage spots Microaneurysm over the disc Late Phase Leakage of dye beyond disc margin Pooling of dye around the disc

41. Treatment directed at underlying cause. Timely intervention has a remarkable effect on prognosis. (unless nerve is irreversibly damaged) Vision recovery is faster than subsidence of fundus features . Treatment

42. Brain Tumor - Craniotomy to remove tumor . Resolution of papilledema within 6-8weeks.

43. Pseudotumor C erebri Surgical Repeated Lumbar puncture Decompression Shunting procedure Resolution of papilledema within 2-3weeks of shunt procedure. - Medical Acetazolamide Oral Glycerol Corticosteroids Weight reduction

44. Papilledema in PIH General – bed rest. Control of BP. Control of edema – Diuretic, Hypertonic glucose. Non responders – Termination of pregnancy.

45. Surgical Decompression Indications Failure of Medical treatment - Marked disc swelling(>5D) - Engorged veins - Extensive hemorrhages - Early exudate spots - Progressive headache Progressive optic neuropathy (early field constriction) Direct Fenestration of optic nerve sheath.

46. Therapeutic success Relief of headache. Transient visual obscuration decreased. Stability/ improvement of field defects.