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Tony.Ching.AAO (talk) 09:38, May 31, 2022 (PDT)
Topic draft from User:Gayathrisreekanth1974
Causes and management of sudden Painless loss of vision
Dr.Gayathri Sreekanth, DO;FRCS;FRCOphth
Sudden loss of vision (SLOV) can be devastating to a patient as it happens when they least expect it. SLOV can be painless or painful.
Painless loss of vision, if not diagnosed and treated promptly and appropriately, can result in painful blind eyes. Usually, unilateral loss of vision indicates a localized pathology while bilateral can be intracranial or vascular.
The general consensus is, if the eye is white and looks normal, there is a high chance of blindness
Table of contents
1.History
2.Examination
3.Cause
a. Vitreous Hemorrhage ICD-9 379.23; ICD-10 H43.1
b. Retinal Detachment
c. Retinal artery occlusion ICD-10 H34.0,H34.1,H34.2
d. Retinal venous occlusion ICD-10 H34.8
e. Choroidal Neovascularization
f. Amaurosis Fugax ICD-10 (1) 45.3[
g. Spontaneous Hyphema ICD-9 CM : 364.41, ICD-10 CM H21.0
h. Functional visual Loss
I. Purtscher's like retinopathy ICD-1034.9
History
Irrespective of painless of painful loss of vision, History must be thorough, detailed and must be carefully documented.
Initial History is crucial for diagnosis, further management and also for medico legal purposes.
1. Verify name and age of patient with DOB and Hospital number
2 Time of onset and duration- sudden or gradual; seconds, minutes, hours, days. Weeks or months
3.Laterality: Unilateral or Bilateral
4.Description of vision loss- Scotoma, metamorphopsia, curtain/veil like vision loss, accompanied with aura, total loss with no recovery
5.Fluctuation of vision: pattern change and pain variation with change in posture
6.Type of pain: Use subjective pain scale measure from 1-10 to understand the severity. Nature of pain:(throbbing, pulsating, shearing, retro orbital and with eye movements- Direction) If they are accompanied by photophobia, headache, jaw claudication, myalgia, mastication, fever.
6.Previous similar history and mechanism of loss of vision and treatment; stroke, migraine, amaurosis, ocular inflammation
7. History of trauma- Blunt, penetrating, perforating, mechanism of trauma.
8. Previous ocular surgeries or interventions like intravitreal injections or use of steroid implants or laser (YAG, Argon, SLT) in the eyes; Use of eye drops- indications, frequency and duration.
9.General medical history: Diabetes, Hypertension, cholesterol, thyroid status, cardiovascular, neurological, neurosurgical, vascular, endocrine, connective tissue, cancer, chemotherapy and radiotherapy
10.Social history: Smoking, Alcohol, Substance abuse, Sexual history
11.Drug history: Many drugs are known to directly impair vision. All the current medications and dosage must be documented: (Example: if there is a history of use of Warfarin, check for INR status, duration of warfarin and the dosage.)
12. Allergy history- Severity of reaction to the allergic drug
Examination :
Systematic and meticulous examination will help in clinching the diagnosis
Observe: Behavior, Habitus, facial symmetry, Globe position
Record: Best corrected visual acuity for each eye- with glasses, with pinhole, distance and near
Note and document: Obvious facial or ocular anomalies, Ptosis, proptosis, lid position, swelling or hyperemia, symmetry, lacerations or lagophthalmos,
Color vision – with pseudo-Ishihara chart for quick screening, especially if neurological cause is suspected. If poor vision of involved eye, record color vision for the ‘good’ eye.
Confrontational visual field check: Useful in office set up to understand the pattern, field involved and the extent of peripheral or central visual loss.
Pupil; check for Size, Shape and Symmetry. Look for sluggish reaction to light, Anisocoria or RAPD
Conjunctival and corneal sensation: Useful to also check for supra and infra orbital sensations
Extra ocular eye movements- Painful or Painless; if pain in which direction and if consistent. Question on Increase in pain after exercise or hot shower. Use Subjective pain scale.
Check for saccades, pursuits, accommodation and Bell’s phenomenon in selective cases
Slit lamp examination: Examination of anterior and posterior segment slit lamp examination arrows down the diagnosis and This must include a quick adnexal examination, Hyperemia and swelling and ecchymosis of eyelids, hyperemia and swelling of the conjunctiva, episcleral or scleral vessels- (If scleral- document as sectoral or diffuse, necrotizing or non-necrotizing. Check for features of Thinning, melting, perforation and uveal tissue prolapse status; if any of the above seen, record the number of clock hours involved; presence of cork screw vessels) Note of symblepharon, discharge, membranes/pseudo membrane in relevant cases
Limbus: Assessment of limbal inflammation, scarcity of limbal cells, ischemia- number of clock hours involved, signs of trauma, chemical injury
Cornea: Examination without and later with fluorescein stain for foreign body, corneal abrasion, depth of corneal involvement, presence of ulcer, corneal haze, corneal thinning, extent and measurement of infiltrate or ulcer, opacity, scarring, pigmentation and vascularization. Check for Siedel’s. Photo document is preferred practice for objective measurement of lesion if cornea is involved.
Anterior chamber: Look carefully for presence of cells, flare, fibrin, pigments, hypopyon, Hyphemia, foreign body, tumors Van-Herricks grading of chamber, Anterior chamber depth assessment with Smith technique
Iris: Iris stromal features, anterior segment tumors, neovascularization, iris atrophy, Iris bombe, Transillumination, atrophy and
Pupil: Anisocoria, RAPD, presence of synechiae, pseudo exfoliation material, pupil shape, symmetry and size in dim and ambient light. The source of light must be adequately bright and the check must be done both in ambient and dim light.
Lens: subluxation, dislocation, lens capsule and the zonule status, cataract- lens opacity can be quantified by LOC III grading
Retrolental: cells, flare, bleed. One must take advantage of slit lamp tilt to view the vitreous better
Posterior segment: Check for media clarity, vitreous status, presence of Weiss ring, posterior pole for optic nerve, spontaneous venous pulsation, Papillo macular bundle, macula, retina, arteries, veins, peripheral and equatorial retina with 90D/78D. Assess the choroidal status. Three mirror lens assessment and Indirect ophthalmoscope with indentation will add value.
Optic nerve: size, shape, margins, contour, neuro retinal rim health, peripapillary atrophy, CD ratio, venous pulsation, nerve bleed, hyperemia, swelling and pallor to be checked and documented
Systemic examination based on the cause- to include Central nervous system, cranial nerve examination, respiratory system, cardiovascular system, endocrinological, radiological and vascular system examination as part of multi-disciplinary examination
If functional vision loss suspected – VA, color check, mirror test, prism bar test, Visual field examination, EDT
Causes:
Sudden loss of vision can be painful/painless
Painless cause of vision loss
1.Vitreous hemorrhage:
Rule out Trauma
Common painless cause of VH is
Proliferative Diabetic retinopathy
Retinal vein Occlusion (CRVO, BRVO, HRVO)
Retinal detachment with traction
Retinal tears (especially Horse shoe tear with vessel traction)
Choroidal neovascularization
Hemorrhagic Posterior vitreous detachment
Proliferative vitreo-retinopathy
Other causes, not as common are
Hypertensive retinopathy – most commonly retinal artery macro aneurysm, in the first vascular arcade.
Eales disease
ROP/FEVR
Macular or retinal telangiectasia
Localized causes- like uveitis (can be painless or painful: Bechet's, PAN, Sarcoidosis, syphilis, POHS, toxoplasmosis, MFC, etc.;), Retinitis (Sheathing, exudates, vascular leakage)
Blood dyscrasia and hemoglobinopathies
Valsalva retinopathy
Painful causes of vitreous hemorrhage can be secondary to trauma, chemical injury, Ocular ischemic syndrome, Terson’s syndrome, Sickle cell hemoglobinopathy, GCA, later stage of RVO’s, posterior uveitis and angle closure NVG
History:
Presentation in adults, irrespective of cause of vitreous hemorrhage is one or more of the following histories:
Flashes
sudden onset of multiple floaters
cobwebs in the vision
painless severe loss of vision (if macula involved); if macula not involved, reduced VA
Photophobia or glare
H/o cough, weight lifting, heavy nose blowing and constipation – if Valsalva retinopathy suspected.
History of diabetes- duration, HBA1C status, treatment compliance, association of neuropathy and nephropathy. Ask for recent history of Intravitreal injections, lasers, steroid retinal implant.
H/o previous ocular surgeries- failed RD surgery, trabeculectomy, multiple ocular surgery- clue to PVR
Blood pressure (how long, how well controlled, treatment, previous history of stroke, CVS and vascular status)
Cholesterol, sickle cell, hemoglobinopathy status, Terson’s.
Use of Blood thinners- anti thrombotic, anti-coagulants; Connective tissue disorders
The history will be different for painful VH such as- Trauma, sickle, OIS, shaken baby syndrome, NVG, sickle cell retinopathy or inflammatory cause.
Examination:
Check for Visual acuity,
R/o Signs of trauma (Blunt injury, perforating injury and penetrating injury)
Assess pupil for RAPD
Look for corneal clarity, NVI, AC hyphema, NVA, Shaffer’s sign, cataract
Fundus: Indirect ophthalmoscope examination with indentation is invaluable. look for presence of Weiss ring, partial PVD, retinal hole, retinal tear- which quadrant, clock hours involved, with or without SRF and extent of SRF, presence of traction, other peripheral retinal degeneration, if vitreous bleed, levels of bleed and the colors (old bleed- white; new bleed- red)
Retinal bleed (BRVO, CRVO, OIS – extent and number of quadrants of bleed, disc involvement, macular status) Macular bleed, retinal microaneurysm, proliferative vitreo-retinopathy, (extent and grade of involvement, associated retinal detachment),
Retinal folds, gliosis, rigidity, pigment disturbances-PVR
uveitis- (sarcoidosis, Bechet's, Vaso occlusive, inflammatory causes) retinitis, vasculitis (tortuosity of retinal vessels, sheathing, exudation, non-perfusion and bleed) choroiditis, association with choroidal effusion or hemorrhage.
Check for IOP.
Investigations:
Ocular
ultra sound B scan with A scan overlay- gives a clue to aid in diagnosis
low reflectivity on A scan suggests PVD; attachment of vitreous to the posterior pole, - partial PVD
High reflectivity – Retinal detachment – if with tenting into vitreous- tractional detachment, smooth and convex- Rhegmatogenous detachment, Dome shaped- choroidal or exudative retinal detachment;
Elevated posterior vitreous phase with delay in movement with ocular motility- sub retinal hemorrhage
AS-OCT- if angle or AC involved secondary to VH
Gonioscopy
Fundus fluorescein angiogram,
OCT/OCT-Angio- optic nerve head and macula- if media is clear
Fundus photograph
Brain and orbit imaging- in trauma, foreign body, tumors
Systemic: Blood sugar, CBC, bleeding time, clotting time, Sicke cell status, hemoglobinopathy assessment, INR check, uveitis work-up (if cause), ECG, carotid doppler scan, Chest X ray and Echocardiogram.
Treatment:
Conservative: One or more of the following, depending on the cause of vitreous bleed.
Ocular: Observation with follow up if minimal hemorrhage with no surgical cause. Bed rest, head end elevation, avoid NSAIDs, blood thinners, if possible
Intravitreal injections with anti VEGF or steroid implants.
Argon laser –focal or sectoral or pan retinal photocoagulation
Surgical: PPV with vitreous lavage +/- gas or silicone oil tamponade and +/- Endo laser +/- Cryotherapy
Anti-Glaucoma medication in relevant cases
General management: Glycemic control, Blood pressure control, cholesterol optimization, review of systems.
Prognosis: Depends on the cause.
2. Retinal detachment and retinal tear: Retinal tear and rhegmatogenous retinal detachment are symptomatic.
If macula is involved or if there is combined RRD/TRD or with vitreous hemorrhage, there may be sudden loss of VA, mostly painless.
History
Reduced visual acuity-central, if macula is involved. Peripheral loss of vision, otherwise.
Photopsia, flashes, floaters, veil like vision- Ask for duration and frequency
Visual field defect (usually on the side that is opposite to the tear or detachment)
Refractive history: Myopia, previous laser treatment for refractive surgery
Recent complicated ocular surgery- like cataract trabeculectomy, retinal detachment or strabismus, laser treatment- its indications and intra operative complications and follow-up plan
Strong family history of retinal detachments, Connective tissue disorders.
Recent intra ocular injections or implants;
Trauma
Previous Ocular co-morbidity- Like Glaucoma, Uveitis and the treatment for the condition
Examination:
VA- distance, near with pinhole and with glasses.
Pupil- RAPD, dilatation status, alpha blocker intake (for eventual laser/surgery),
A/C involvement: cells, flare, posterior synechia.
Lens: cataract; Vitreous hemorrhage, Shaffer's.
IOP is often reduced compared to the fellow eye
Fundus: (indirect ophthalmoscope examination with indentation is mandatory): Extent and type of detachment, number of clock hours involved, presence of bleed, sub retinal fluid, macular involvement, retinal folds, gliosis, traction, pigment disturbance, stiffness, cysts, demarcation lines, tears, breaks or holes (numbers and position), peripheral retinal degenerative changes
Diagnosis of detachment is based on the clinical findings:
Rhegmatogenous retinal detachment: Assess PVD; Be aware that low or moderate myopes with previous recent eye surgery; RRD in another eye are high risk
Other uncommon causes: connective tissue anomalies like Stickler syndrome, Marfan’s, Ehler-Danlo's syndrome vitreo-retinopathies like Wagners and Jansen's syndrome, homocystinuria, acute retinal necrosis syndrome; Pars-planitis and ocular toxoplasmosis,
Fundus: SRF that is dome shaped, freely mobile retina that is convex and corrugated associated with breaks or tears and the fluid following Lincoffs' rule. Most common site is superior temporal quadrant. There may be more than one break if carefully examined. The field defect is relative with no laser uptake (contrary to retinoschisis), if chronic associated with pigment demarcation lines.
Exudative retinal detachment:
The cause of this detachment is subretinal. Central vision is spared until late. Peripheral visual field defect and if associated with inflammation, Pain is the common presenting symptom.
The features are that of spontaneous detachment Clinically on examination, retina is dome shaped, smooth and convex with no associated tears or breaks associated with shifting and position dependent sub retinal fluid.
Examine to check for Nonophthalmic eyes, UES, FEVR, Coat’s, CSR, Retinoblastoma, hypertensive retinopathy, choroidal colobomas, choroidal tumors, lymphoma, secondaries, look for excessive cryotherapy or recent pan retinal photocoagulation scars, Examine sclera for scleral buckle, check for connective tissue disorders, Chronic renal disease, DIC. (ERD may be painful in: IOID, posterior scleritis, active inflammatory uveitis like sarcoidosis, post operative inflammation, Lyme, syphilis, CMV, Toxoplasmosis, ).
Tractional Retinal detachment:
Unlike rhegmatogenous and exudative retinal detachment, traction detachment is concave with shallow SRF distribution. The retina is rigid, stretched ischemic and may be associated with fibrovascular gliosis. There may be significant pigment disturbance
Causes are: proliferative diabetic retinopathy, Burnt out and overly treated PDR, Coats disease, ROP, PVR,long standing or untreated RVO’s, Sickle cell retinopathy, FEVR, VMT, retinal dysplasia and retinal X syndrome
Management of Retinal detachment:
systemic examination.
BP check, Blood sugar, CBC, U&E, urinalysis, referral to medical team as part of systemic work up and relevant blood tests, gene tests and specialty specific examinations. Multidisciplinary approach for non RRD conditions
Management:
Conservative for Exudative retinal detachment:
infection: broad spectrum antibiotics; Inflammation: ocular or systemic steroids and/ or immunosuppressants. If associated with exudates or neovascularization: anti-VEGF; If Tumor: chemotherapy, radiosurgery or selective surgery if localized.
Surgery RRD/ERD: PPV with one of the following options, scleral buckle, pneumo-retinopexy, gas or silicone oil or Densiron tamponade, SRF drainage, delamination, membrane dissection, relaxing retinectomy or segmentation with or without anti-VEGF injections.
If PVR – Offer poor prognosis
Central retinal artery occlusion/Branch retinal artery occlusion
H/o Sudden, painless loss of vision
Causes: Carotid artery and CVS causes
Carotid emboli; Cholesterol emboli (Hollenhorst retinal arteriolar plaques); Fibrin platelet emboli (can cause amaurosis fugax) ;Calcific emboli; Cardiac emboli (younger patients);Thrombi -from myocardial infarct or mitral or aortic valve stenosis; Vegetative thrombi from bacterial endocarditis; Myxomatous thrombi from atrial myxoma
Vascular
Systemic lupus, polyarteritis nodosa, Protein C deficiency, protein S deficiencies, antithrombin-III deficiency, anti-phospholipid syndrome, Hyperhomocystenemia,
Ocular
Rule out Painful causes of CRAO: ↑ IOP of more than 60mmHg, GCA, retrobulbar hemorrhage, intra Orbital compressive tumor, IOID, RD surgery especially with scleral buckle or large volume of gas in eyes, Sickling haemoglobinopathies, Vasospasm (migraine) and Susac syndrome
Examination: Check for VA, presence of RAPD (almost always seen); Check for thrombi/emboli/plaques in the artery especially at the bifurcation, cattle track sign with blood sludging in the arteries, arterial attenuation, pale edematous fundus (ground glass retina) and cherry-red spot in the macula.
Poor or nil visual prognosis with only one-thirds of patients showing some improvement in visual acuity It is important to rule out GCA, (ESR, CRP, platelets, CBC, ultrasound or biopsy of temporal artery, urgent referral to the stroke team), OIS, rubeotic glaucoma
Ocular associations with CRAO are; Optic nerve head drusen, retinal migraine.
Management:
Urgent stroke team referral and vascular specialist referral; Start anticoagulants if atrial fibrillation is the cause,
Approach for CRAO must be multi-disciplinary.
Look for systemic causes of CRAO like Hypertension, CVS disease – check for pulse rate- Atrial fibrillation, Carotid artery disease- check of carotid bruits;
fever- suspect infective endocarditis-Blood culture
Auscultate for murmurs,
Blood tests for anti-phospholipid antibody syndrome, HyperHomocystinaemia, leukemia, lymphoma.
in all such cases, consider PTT, APTT, Thrombophilia Screening-Protein S Protein C, Protein V, anti-phospholipids screening,
RF, anticardiolipin antibody, antinuclear antibody, anti-double stranded DNA antibodies, - PAN/ SLE/small and medium vessel inflammatory disease
VDRL/THPA- syphilis
Plasma protein electrophoresis- multiple myeloma,
ECG, ECHO- if endocarditis, septal defects, substance abuse suspected,
Carotid doppler: to assess the carotid blood flow and check for stenosis
Treatment
Treatment is difficult and challenging. Some improvement if managed within 2 hours.
Supine posture to improve perfusion
Gonio massage with 3 mirror lenses to displace the thrombi or emboli
AC paracentesis with 27 Guage needle under aseptic conditions for sudden eye decompression to dislodge clots or emboli.
IV 500 mg of acetazolamide along with topical timolol 0.5% or apraclonidine 1% drops for sustained ocular hypotension
Thrombolysis, hyperbaric oxygen, Argon laser clot lysis and arterial catheterization are not of benefit and therefore not commonly practiced anymore;
If GCA- consider systemic steroids as prophylaxis for another eye
Central retinal vein occlusion/Branch retinal vein occlusion/Hemi-retinal vein occlusion
Presentation can be painless which can become painful blind eye that can lead to painful phthisis if not managed appropriately at early stages
Risk factors:
Age>65 years,
Hypertension,
diabetes,
hypercholesterolemia,
atherosclerosis,
obesity,
Smoking
OCP
Glaucoma
Uncommon causes
Dehydration, Myeloproliferative disorders (Myeloma, polycythemia, sickle cell disease), hyperhomocystenemia, protein S, protein C, anti-thrombin deficiency, factor V Leiden mutation, Walden Strom's macroglobulinemia, anti-phospholipid antibodies, inflammatory causes – secondary RVO due to occlusive Vaso phlebitis- SLE, PAN, Bechet's GPA, Sarcoidosis, Good pastures, Chronic renal failure
Examination
Sudden loss of vision is usually because of ischemic RVO. Features are severe drop of VA to blindness (can be painful if with NVG not detected early).
Metamorphopsia and central scotoma
Anterior segment: look for features of corneal edema, RAPD, NVI, NVA, ↑ IOP, flare
Fundus: Dilated tortuous vessels with deeper, darker retinal bleed in one quadrant (BRVO), hemi quadrant (HRVO) and all four quadrants (CRVO), flame shaped hemorrhages, cotton wool spots, vitreous hemorrhage, collateral formation, tractional retinal detachment, NVD and NVE , optic disc hyperemia Recurrent vitreous hemorrhage, CMO (acute, chronic or non-responsive) in the macula with intra retinal cysts or subretinal fluid., pigment disturbances in the retina.
Assessment must be multi-disciplinary:
Investigations:
Ocular: FFA: collateral confirmation, non-perfusion and delayed filling in ischemia, macular edema, leakage at neovascularization sites,
OCT: Macular edema, macular thickening, Intra retinal fluid, cystoid edema, sub retinal fluid, Epiretinal membrane in chronic cases.
Systemic
BP, FBC, ESR, blood sugar, U&E and lipids for all patients.
There is no need for an extensive investigation unless warranted and they include CRP (if GCA, inflammation), ANA, RF, ANCA, serum ACE, thrombophilia screening (protein S, protein C, factor V, anti-thrombin) anti-DNA, CXR, anti-cardiolipin, syphilis /Lyme screening, routine and exhaustive blood check offers limited yield and therefore not required.
Treatment:
Ischemic without NV: close monitoring and 3 monthly follow up for up to years, then consider discharge- beware of ‘100-day glaucoma’
With NV: PRP +/- intravitreal injections; Steroid implants in the eye. Micro pulse laser not much in use but can be tried in non-responsive patients.
Adjunct treatment: Cycloplegic drops; Lubricants for compromised epithelium, steroid eye drops if eye inflamed, ↓ IOP with anti-glaucoma drops.
if no response to anti Glaucoma drops- consider cryoablation/valve surgery if no response;
painful blind eye with nil visual potential- retrobulbar alcohol, evisceration/enucleation.
Amaurosis fugax
The Amaurosis Fugax Study Group classification for cause of TIA
Embolic- most common cause of TIA
Hemodynamic
Ocular
Neurologic
Idiopathic
Causes
Carotid artery atherosclerosis,
Carotid artery emboli
Cardiac causes of emboli
Vasculitis
Coagulation disorders
Gaze evoked amaurosis
Optic nerve drusen
Papilledema
Painful amaurosis (Amaurosis Fugax, by definition is strictly painless, however there are causes that can mimic TIA warranting urgent stroke team referral and emergency management)
GCA
Migraine
Anterior ischemic optic neuropathy
Raised IOP
H/O curtain like loss of vision – usually lasting seconds to minutes but rarely hours. The loss of vision can happen multiple times in a day. Recovery is of the same pattern as the vision loss but it is usually slower. Vision loss can be generalized (systemic) or gaze evoked (localized cause- orbit or retro orbital lesion). While commonly uniocular, binocular causes have been documented. Commonly known as ‘mini stroke ‘in the eyes,
The diagnosis is MDT. Common cause is optic nerve transient hypoperfusion-
Check for Hypotension, Thrombus, embolus, arteritis, or vasospasm.
History should include migraines, CVS pathologies (CAD, atherosclerosis, atrial fibrillation, hypertension, diabetes, hyperlipidemia, hypercoagulable state, and myeloproliferative disorders.).
Look for emboli or plaques in the retinal blood vessels.
Investigation: CBC, ESR, CRP (if GCA suspected) , echo cardiogram, cardiac ultrasound, carotid doppler, CTA/MRA if CNS involvement suspected. If Bilateral, suspect Seizures and sought neurology opinion.
, Arrange for urgent stroke team referral to start on high dose anti platelet, anti-coagulants. If plaques suspected from carotid, urgent Vascular surgeon opinion
CNV with large macular bleed:
There are multiple causes for macular bleed but age-related macular degeneration bleed is the most common
History
sudden painless loss of vision with gray scotoma or ‘blind spot’ in the central field of vision, metamorphopsia.
Ask for age (wet AMD), Refractive status (myopic CNVM, Polypoidal choroidal vasculopathy), connective tissue disorder ( Angioid streaks); ocular tumors (hemangioma, melanoma), post pan retinal photocoagulation.
Painful or symptomatic: Trauma (choroidal rupture), Inflammatory causes (Bechet's, sarcoidosis, VHK, MFC, Serpiginous choroiditis)
family history,
smoking,
CVS status,
use of blood thinners/ AMD supplements.
Anterior segment usually is not involved unless tumor or inflammation.
Macula: Edema, SRF, bleed (sub retinal- gray; retinal- red), + choroidal/break-through retinal, vitreous bleed, exudates, pigment epithelial detachments (serous, drusenoid, fibrous), Drusen's, CMO, RPE tears or retinal rips, right angled vessels and discoloration (mac.Tel) , features of RAP, residual pigment mottling, chronic lipid deposition and chorio-retinal atrophy.
Investigations:
FFA (to define classic, occult, mixed, RAP lesions, RPE atrophy, Demonstrates leakage to indicate activity for treatment),
ICG (if PCV suspected),
OCT, OCT-A- for IRF/SRF/NV and in cases where FFA is contra indicated (like allergy/ renal failure, cardiac compromise etc.
Fundus auto fluorescence
Treatment:
Anti-VEGF's, PDT- if sub foveal/PCV with variable outcomes)
Surgical: pneumatic displacement of sub macular bleed with perfluorocarbon +/- recombinant tissue plasminogen activator with good success.
Prognosis:
Depends on the cause and response to treatment.
Papilledema
The term papilledema is specific to optic nerve swelling secondary to space occupying lesion in the brain.
Symptoms are
Asymptomatic: initial phase of papilledema. Patients almost always have no symptoms
Headaches: Is due to ↑ ICP stretching the tentorium and meninges. The headaches can be Progressive and they gradually worsen. Typically, early morning and increases in intensity with posture changes like lying down, sudden head movement, bending or coughing.
Nausea associated projectile vomiting
Pulsatile tinnitus
Sensori-Neural deafness
Facial weakness
Peripheral and limb weakness; Bladder and bowel incontinence,
Fever, rashes, Neck rigidity- features of meningitis, encephalitis
Deterioration or loss of consciousness
Transient visual obscurations lasting up to 30 seconds in one or both eyes –gaze or position evoked - bending, coughing or the Valsalva maneuver;
Horizontal diplopia - false localizing sign if VI nerve involved.
Vision is initially normal but can severely reduce because of secondary optic atrophy.
Refraction: hypermetropic shift
Visual field defect: Enlarged blind spot
Check for: color vision, red desaturation, saccades, pursuits, accommodation, corneal sensation, bells phenomenon, nystagmus, RAPD, gaze evoked amaurosis, IOP check, look for proptosis (axial, Non-axial) ) and ptosis
Stereo disc evaluation shows bilateral disc swelling (use Friesen scale grading for staging), loss of spontaneous venous pulsation, peripapillary hemorrhages, retino-choroidal folds, collaterals, shunt vessels and optic atrophy.
Investigate: Cardiac status, previous history of Intra cranial bleed or tumors, hyper coagulation or bleeding/coagulation abnormalities,
Check for BMI.
MRI with contrast,MRV (for sinus thrombosis, venous pathology), LP after MRI
Ocular: FFA,,OCT of the optic nerve, stereo photo for optic nerve, Humfreys visual fields
Treatment: Shared care- Neurologist, neurosurgeons, endocrinologist, radiologists, ENT and ophthalmologists play a role as part of multi-disciplinary team work up
Spontaneous hyphemia-Painless:
Rule out sickle cell disease, OIS and trauma
Chronic glaucoma-NVG (painful in later stages)
tumors of the eye- Retinoblastoma, Iris melanoma
Long standing anterior uveitis ( patient will have Photophobia)
vascular anomalies –juvenile Xanthogranuloma
Neovascularization of iris- due to any cause
Myotonic dystrophy
Lympho-proliferative or myelo-proliferative disorders: lymphoma, Leukemia, Hemophilia, Von Willibrand disease
Drugs; Warfarin, Aspirin
UGH syndrome
Examination: Assess the size of hyphema ( one quarter, quarter, half or complete),Look for the cause of bleed in spontaneous hyphema. Be aware that bleed can happen again after five days or during clot lysis. Check for
Corneal edema or haze
Corneal blood staining – May cause hemosiderosis
Risk of amblyopia in children if more than 50% anterior chamber involved for more than 5 days
↑ IOP- Secondary Glaucoma
Assess fundus if view is clear or perform ultrasound B-scan to check for posterior segment bleed or tumor.
Management
Conservative:
Admit
Bed rest,
Head elevation
Topical steroids and cycloplegic agents
Topical glaucoma medication
Consider using Aminocaproic acid • Tranexamic acid
Avoid aspirin,NSAIDS and warfarin after cardiology opinion
Surgery:
AC paracentesis and washout
Clot expression and AC wash-out
If IOP still high, trabeculectomy
Functional vision loss:
History of sudden severe loss of bilateral vision – but no correlation to history of examination. Patient navigates easily around the room when no one around to observe. Recent stressful event-psychosomatic conversion.
Assessment: Normal anterior and posterior segments, normal pupil, normal neurological examination. normal EDT and neuroimaging. Diagnosis must be made only after excluding organic causes.
Tests to confirm: OKN: shows normal corrective saccades, prism tests: normal breaking of fusion; Goldman perimetry: spiraling or significant peripheral constriction of visual fields, Ishihara: Inconsistent response. Crossed cylinder technique, and fogging technique to reinforce functional loss objectively
Management: Counselling, reassurance, encouragement. Referral to a specialist with experience in handling patients with functional visual loss
Purtscher's like retinopathy:
While putschers retinopathy is common in head injury, putschers like retinopathy is a term used for non-traumatic conditions like acute pancreatitis, fat embolism, post-partum, long bone fractures, severe generalized vasospasm, Hemolytic uremia syndrome, Renal failure or thoracic and abdominal crush injury resulting in sudden severe loss of painless vision, retinal whitening (usually at the junctions between artery and vein), cotton wool spots, retinal hemorrhage, retinal vascular sheathing, vessel attenuation, RPE changes and eventually optic nerve pallor.
Investigation: MDT approach based on cause Ocular examinations include FFA, Fundus photo, OCT and ERG ( reduced A and B waves). No treatment options available. IV steroids have little or limited evidence in treatment
References:
American Academy of Ophthalmology. Retinal detachment. July 26, 2019.
Haimann MH, Burton TC, Brown CK. Epidemiology of retinal detachment. Arch Ophthalmol. Feb 1982; 100(2):289-92.
Witmer MT, Cohen SM. Oral anticoagulation and the risk of vitreous hemorrhage and retinal tears in eyes with acute posterior vitreous detachment. Retina. 2013 Mar;33(3):621-6.
Early Treatment Diabetic Retinopathy Study design and baseline patient characteristics. ETDRS report number 7. Ophthalmology. 1991 May;98(5Suppl):741-56
https://www.aao.org/preferred-practice-pattern/retinal-ophthalmic-artery-occlusions-ppp-2016
Cugati S, Varma DD, Chen CS, Lee AW. Treatment Options for Central Retinal Artery Occlusion. Neurol. 2013 Feb;15(1):63–77.
he Eye Disease Case-Control Study Group. Risk Factors for branch retinal vein occlusion. American Journal of Ophthalmology. 116(3):286-96,1993.
Thompson HS. Functional Visual Loss. Amer J Ophthalmol. 1985;100:209-13.
Ocular Pathology Atlas. American Academy of Ophthalmology Web site.
P Vijayalakshmi, et al. Bilateral spontaneous hyphaema in juvenile xanthogranuloma. Indian Journal of Ophthalmology. 2006. Vol 56 (1): 45-46.
American Academy of Ophthalmology. Retinal detachment
Leaver PK. Proliferative vitreoretinopathy. Br J Ophthalmol. 1995 October; 79(10): 871–872.
Carrera CRL, Pierre LM, Medina FMC, Pierre-Filho PDTP. Purtscher-like retinopathy associated with acute pancreatitis. Sao Paulo Med J. 2005;123(6):289–91. doi:/S1516-31802005000600008.
Tabandeh H, Rosenfeld PJ, Alexandrakis G, Kronish JP CN. Purtscher-like retinopathy associated with pancreatic adenocarcinoma. Am J Ophthalmol. 1999;128:650–2.
Stoumbos VD, Klein ML GS. Purtscher-like retinopathy in chronic renal failure. Ophthalmology. 1992;99:1833–9.
Basic Clinical and Science Course. Retina and Vitreous. 2013-14. Section 12 pg 85-86
Coleman HR, Chan CC, Ferris FL III, Chew EY. Age-related macular degeneration 2008. Lancet 372(9652):1835-1845
Oxford handbook of ophthalmology-4th edition
