Tuesday 12 May 2015

OCULAR TRAUMA TERMINOLOGY AND CLASSIFICATION

Image result for OCULAR TRAUMA IMAGE


Ocular trauma terminology (proposed by Kuhn and co-workers)
TERM
DEFINITION
Eyewall
Sclera and cornea
Closed globe
Eyewall doesn’t have full thickness wound, may harbor partial thickness laceration.
Open globe
Eyewall has full thickness wound.
Rupture
Full thickness wound caused by blunt object. May or may not be at the impact site.
Laceration
Full thickness wound caused by sharp object occurring at the site of impact.
Penetrating injury
Single, full thickness wound usually caused by sharp object.
Intraocular foreign body injury
Retained foreign body through a single entrance wound.
Perforating injury
Two full thickness wounds of the eyewall caused by a same projectile.
Contusion
Closed globe injury caused by a blunt object. May or may not be at the site of impact.
Lamellar laceration
Closed globe (partial thickness) injury of the eyewall or bulbar conjunctiva caused by a sharp object at the site of impact.
Superficial foreign body
Closed globe injury with  impacted foreign body in the eyewall or conjunctiva not resulting in a full thickness defect in the eyewall.


The Ocular Trauma Classification Group has proposed a standardized system for classification of ocular injuries. It is based on four characteristics: Mechanism of injury, initial visual acuity, pupillary involvement and most posterior location of wound.



OCULAR TRAUMA CLASSIFICATION SCHEME

OPEN GLOBE INJURY
CLOSED GLOBE INJURY
TYPE
A.      Rupture
B.      Penetrating
C.      Intraocular foreign body
D.      Perforating
E.       Mixed
TYPE
A.      Contusion
B.      Lamellar laceration
C.      Superficial foreign body
D.      Mixed
GRADE
Visual acuity
1.       >=20/40
2.       20/50 - 20/100
3.       19/100 – 5/200
4.       4/200 – light perception
5.       No light perception
GRADE
Visual acuity
1.       >=20/40
2.       20/50 – 20/100
3.       19/100 – 5/200
4.       4/200 – light perception
5.       No light perception
PUPIL
Positive - RAPD + in affected eye.
Negative- RAPD – in affected eye.
PUPIL
Positive - RAPD + in affected eye.
Negative – RAPD – in affected eye.
ZONE
I. Isolated to cornea including corneoscleral limbus.
II. Corneoscleral limbus to 5mm posterior into the sclera.
III. Posterior to the anterior 5mm of sclera. 
ZONE
I. External (limited to bulbar conjunctiva, cornea and sclera).
II. Anterior segment involvement upto pars plicata including posterior lens capsule.
III. Posterior segment involvement.


OCULAR HYPERTENSION TREATMENT STUDY


Image result for EYE IMAGES





Eyes with ocular hypertension (OHT) are at increased risk of developing primary open angle glaucoma (POAG). Prompt diagnosis and treatment of OHT may prevent the development of POAG and visual disability. OHT is defined as IOP greater than 21 mmHg without any evidence of optic nerve damage and visual field loss. There should be no ocular and systemic cause for the raised IOP levels.  
Ocular Hypertension Treatment Study (OHTS)1  is a long term, multicenter, randomized clinical trial started in 1994. It has helped in understanding the natural course of OHT, role of ocular hypotensives in its treatment and significant risk factors contributing towards its progression to POAG. OHTS has contributed in better understanding and early identification of high risk individuals thereby, reducing the ocular morbidity due to glaucoma.  
OBJECTIVE-
1.     To determine whether ocular hypotensive agents are helpful in delaying the onset of glaucomatous optic nerve damage and visual field defects in subjects those who are at moderate risk of developing POAG.
2.     To produce natural history data to assist in identifying patients at most risk of developing POAG and whether they are benefited by early treatment or not.
3.     To quantify risk factors for developing POAG among ocular hypertensives. 
STUDY DESIGN-  OHTS is a long term, multicenter, randomized clinical trial started in 1994 with 1636 participants at 22 different clinical centers. The eligible candidates had no evidence of glaucomatous damage, aged between 40 to 80 years with IOP between 24-32 mmHg in one eye and 21-32 mmHg in other eye. The eligible candidates were randomized in equal proportion to either the medication group or observation group.2
Goal in medication group was to decrease IOP by 20% or more from the observed baseline readings and to attain target IOP of 24 mmHg or less. Topical medication was changed and/or added until both of these goals were met or the participant was receiving maximum tolerated topical medical therapy.
RESULTS-  At 60 months, the cumulative probability of medication group of developing POAG was 4.4% as compared to 9.5% in observation group (hazard ratio, 0.40; 95% confidence interval, 0.27-0.59; p<0.0001). There was little evidence of increased systemic/ocular risk associated with ocular hypotensive medication.
CONCLUSION- The OHTS has shown that topical ocular hypotensive medication is effective in reducing the incidence of glaucomatous optic nerve damage and visual field loss in individuals with elevated IOP between 24-32 mmHg.
RISK FACTORS PREDICTED BY OHTS FOR CONVERSION OF OHT TO POAG-
1.     CENTRAL CORNEAL THICKNESS (CCT) – CCT was found to be a powerful predictor for the development of POAG.3 IOP assessed by applanation tonometry may be overestimated or underestimated in thicker and thinner corneas, respectively. CCT less than 555µ were found to be at greater risk than eyes with CCT more than 588µ. The relative risk of POAG increased by 81% for every 40µ decrease in CCT. 
2.     IOP - Studies have revealed the normal IOP range of 10-21 mmHg.4 Although, IOP readings may show considerable variations among glaucoma patients, IOP reading more than 22 mmHg is a positive predictive factor for the development of POAG.3
3.     AGE – Age is an independent risk factor for the development of POAG. Individuals with older age had a greater risk for conversion to glaucoma. OHTS found an increased risk of POAG with age (per decade), of 43% in the univariate analysis and 22% in the multivariate analysis.3
4.     PATTERN STANDARD DEVIATION (PSD) - Although the patients with ocular hypertension may not have visual field defects on Standard Automated Perimetry (SAP), OHTS found that greater PSD on SAP correlated with increased risk of progression to POAG. With 0.2dB increase in PSD, 22% increase in relative risk was found in OHTS.3
5.     OPTIC NERVE – Although OHT patients have no apparent glaucomatous disc changes, increased vertical and horizontal cup-disc ratio is a risk factor for progression to POAG. Increase in cup-disc ratio by 0.1 leads to 32% and 27% increase in relative risk in vertical and horizontal cupping, respectively.3


Monday 23 February 2015

OCRIPLASMIN (JETREA) : THE VITREOLYTIC AGENT


Image result for chemical bonds


OCRIPLASMIN(JETREA) is a recombinant truncated human serine protease plasmin with activity against fibronectin and laminin which are the components of normal vitreo-retinal interface.

  • Phase II trials have shown that upto 3 injections of 125 micrograms of Ocriplasmin at monthly interval can lead to resolution of vitreo-macular traction and closure of macular hole (<400 microns) without serious complications.
  • Less effective in VMTS + ERM or vitreomacular adhesions >1500 microns.
  • Jetrea has not been studied extensively in Macular hole > 400 microns, myopia > 8D, axial length > 28mm, aphakia, history of rhegmatogenous RD, lens-zonule instability, proliferative diabetic retinopathy, ischemic retinopathy, retinal vein occulusions, wet AMD, vitreous hemorrhage. Hence, treatment is not recommended in these patients.
  • No clinical data is available on its concurrent use with anti VEGF agents.
  • Available as 0.5mg/0.2ml vial ,which is diluted in 0.2ml of 0.9% NaCl to get the final concentration of 125 micrograms/0.1ml.
  • Stored at -20+/- 5 degree Clecius.
Adverse effects:

  • Transient rise in IOP upto 60 minutes post injection and reduced optic nerve perfusion pressure.
  • New macular hole formation or enlargement of pre-existing macular hole in strong adhesions.
  • Infection
  • Vitreous floaters
  • Eye pain
  • Photopsia
  • Subconjunctival hemorrhage.

Friday 13 February 2015

MARCUS GUNN PHENOMENON AND ITS VARIANTS

Image result for MARCUS GUNN JAW WINKING PHENOMENON

MARCUS GUNN PHENOMENON:


  • Elevation of ptotic lid with movement of jaw.
  • Due to aberrant connection between 3rd nerve and mandibular division of 5th nerve.
  • More common on left side.
  • May be associated with superior rectus weakness.
  • Grading : 
                          Mild- <2mm elevation of ptotic lid.
                          Moderate- 3-6 mm elevation of ptotic lid.
                          Severe- >= 7 mm elevation of ptotic lid.

INVERSE MARCUS GUNN PHENOMENON:

  • Increase in ptosis on jaw movement.
  • Due to synkinesis between pterygoids (5th nerve) and orbicularis (7th nerve).
  • Also known as ATOIN SYNDROME.
REVERSE MARCUS GUNN PHENOMENON :
  • Lateral displacement of jaw on touching cornea.
  • Due to synkinesis between ophthalmic division (I) and mandibular division (III) of 5th nerve.
  • Seen in supranuclear 5th nerve palsy.

                           

Friday 6 February 2015

DIAGNOSTIC CRIETERIA FOR IDIOPATHIC INTRACRANIAL HYPERTENSION


  1. Signs and symptoms suggestive of raised intracranial tension and papilledema.
  2. High opening pressure on lumbar puncture.
  3. Normal CSF study.
  4. Normal brain MRI. 
  5. No systemic cause including medications.

TEN SIGNS OF OPTIC DISC EDEMA


5 MECHANICAL SIGNS :


  1. Blurring of the optic disc margins.
  2. Full optic disc cup.
  3. Elevated optic disc head (1mm elevation induces 3D of hypermetropia).
  4. Nerve fiber layer edema.
  5. Retinal folds (Paten's striae) or choroidal folds.
5 VASCULAR SIGNS :

  1. Venous congestion.
  2. Papillary and peripapillary hemorrhages.
  3. Cotton wool spots.
  4. Hyperemic optic disc.
  5. Hard exudates over disc.

PHOTOSTRESS RECOVERY TEST




IMPORTANT POINTS:


  • Done in each eye separately.
  • Visual acuity must be 20/80 or better for reliable results.
  • Eye is exposed to bright light for 10 seconds, source is held 2-3 cms from the eye.
  • Ask the patient to read previously read best visual acuity line immediately after withdrawl of light source and the recovery time is noted. 
  • Normal recovery time is 45-60 seconds.
  • Prolonged recovery time upto 180 seconds or more in patients with maculopathy.
  • Normal recovery time in optic neuropathy.