Loading....
Coupon Accepted Successfully!

 

Developmental Glaucoma

 

Sporadic 90%, AR 10% =GLC 3A(CHR 2P) AND 3B(CHR 1P)

  1. Primary congenital Glaucoma (most common form of Congenital Glaucoma),     

 

Buphthalmos -

(As the eyeball enlarges)

 

Pathogenesis - Developmental anomaly of angle of anterior chamber - Trabeculodysgenesis

  1.  Clinical feature-
    1. Triad of
      i. Photophobia    
      ii. blepharospasm        
      iii. lacrimation
       
      Eye-rubbing is there.
    2. Corneal signs -
      1. Corneal edema
      2. Corneal enlargement - (>13 mm)
        >11m at birth,>12mm at 1yr of age or between 1to 2,>13mm after any age
        C/F of glaucoma
        Haab's Striae - break in DM (Horizontal) vs Vogt’s striae in Keratoconus(Vertical)
    3. Buphthalmos     
      1. Blue and thin sclera, stretched limbus.
      2. Iridodonesis
      3. Deep AC  
    4. Glaucomatous cupping -   Reversible mcq
    5. IOP - Raised, but neither marked nor acute.
  2. D/D :
    1. Cloudy Cornea
      1. Birth trauma                    
      2. Intrauterine rubella
      3. Metabolic disorders - mucopolysaccharidosis, lipidosis and cystinosis
    2.  Large Cornea :
      1. Megalocornea                  
      2. Myopia
    3. Lacrimation - Non-patent NLD.
    4. Secondary Glaucoma
      1. Retinoblastoma                        
      2. Juvenile Xantho granuloma      
      3. Persistent hyperplastic primary vitreous   
      4. ROP
  3. Tt :  
    1. Goniotomy                               
    2. Trabeculotomy         
    3. Combined trabeculotomy &  Trabeculectomy ± MMC (Mitomycin)

Extra Edge:
Now a days Best modality is Trabeculectomy combined with trabeculectomy +/- MMC

  1. Glaucoma associated with congenital anomalies
  1. With irido-corneal dysgenesis

                        i.    Axenfeld's anomaly=AR   

                       ii.    Riegers anomaly      

                     iii.    Reigers syndrome    

                     iv.    Peter's anomaly=SPORADIC

 

Extra Edge
  Post embryotoxon +ant iris strands= Axenfeld
  Axenfeld + iris hypoplasia = Rieger’s anomaly
  Anomaly + Systemic = Syndrome

  1. With Aniridia IN 75%
    1. Associated with WAGR
    2. 2/3RD AD,1/3RD SPORADIC AR RARE
  2. Associated with ectopia-lentis syndromes –
    1. Marfan syndrome,
    2.  Weil-Marchesani syndrome
    3. homocystinuria
  3. Phacomatosis
    1. Sturge - Weber syndrome        
    2. Von-Recklinghausen's Disease
  1. POAG
    1. Etiopathogenesis
      1. Heredity (Multifactorial)                                  
      2. Age - common in elderly        
      3. Myopes - more common        
      4. Diabetics - more common                      
      5. Hypertension - more common                
      6. Sex-Male>female
      7. Rise in IOP - due to decreased outflow - Due to thickening and sclerosis of trabeculae

C/F-

  1. Mild headache / Eye ache
  2. Difficulty in reading and close work.
  3. Frequent change of presbyopic glasses. (Most important features)
  4. Delayed dark adaptation.

 

Signs

 

Iop Changes:

  1. Exaggeration of normal diurnal variation (>8 mmHg.)
  2. Increase in IOP.
  1. Normal Tension Glaucomamcq   
    1. Females > Males
    2. Normal IOP (10-21mm Hg), but with Disc changes and field defects
    3. Common In Japanese, Females
Clinical Features
  1. Visual Field Defect closer to fixation, deeper, steeper and more localized
  2. Raynaud’s phenomenon (Peripheral vascular spasm on cooling) is seen
  3. Nocturnal Systemic Hypotension
  4. Reduced blood flow velocity in the ophthalmic artery
  5. Wider diurnal fluctuation

Disc Pattern

  1. Neuro-retinal rim thinning / notching.         
  2. Deepening of the Cup-Laminar-dot-sign (advanced stage)
  3. C: D > 0.3                                   
  4. C: D asymmetry > 0.1 - 0.2 between 2 eyes (vertical)
  5.  Vascular Signs-
  • Optic disc haemorrhage - Flame-shaped (splinter haemorrhages)
  • Nasal shifting of vessels          
  • Bayonetting sign              
  • Over pass sign
  1. Peripapillary Changes
  1. Visual Field Defects
    1. Early Defects
      •  Scotoma at Bjerrum’s area.         
      • Seidel Scotoma - joins with blind spot.
      • Baring of blind spot.                     
      • Isolated paracentral scotoma (Usually earliest)
      • Nasal (Roenne) step.   

Nasal field defects first to appear mcq          Temporal field defects last to appear

  1. Late Defects
    • Arcuate Scotoma.
    • Double arcuate or ring scotoma.
    • Full loss except Small Island of central and temporal vision.
  1. PACG
    1. Predisposing Risk Factors

      1. Hypermetropic eyes with shallow anterior chamber                  
      2. Iris - Lens diaphragm placed anteriorly.
      3. Narrow angle of anterior chamber.                           
      4. Age - more common after 5th decade.                         
      5. Sex - Females are more prone.                        
      6. Family history - Positive.
    2. Stages of Pacg

 

  1. Secondary glaucomas
    1. Lens - Induced Glaucoma
      1. Phacomorphic glaucoma
         
        Phacomorphic glaucoma is secondary angle-closure glaucoma due to lens intumescence. SHALLOW AC
      2. Phacolytic glaucoma

          

d. Phacotopic glaucoma due to lens subluxation or dislocation

 

2. Pigmentary glaucoma -
 

 

Treatment – On the lines of POAG.

 

Features

  1. Pigmented Trabecular Meshwork
  2. Transillumination defectmcq (Radial Slit like)
  3. Krukenberg spindleMCQ (on corneal endothelium and inferiorly due to convention current)
  1. Pseudo-exfoliative glaucoma - (Glaucoma Capsulare)
    1. Due to deposition of, grey dandruff-like material in the trabecular meshwork.
    2. More common in Scandinavian countries
    3. Tt - On the lines of POAG.
  2. NVG - neovascular glaucoma

Associated with neovascularisation of iris (Rubeosis iridis)


Causes :             

  • DR            
  • CRVO
  • Eales Ds      

Tt - Panretinal photocoagulation with Artificial shunt operation.

  1. Steroid - induced glaucoma
     
    Due to deposition of muco polysaccharides, in the trabecular meshwork.
  2. Traumatic glaucoma
    1. Blunt injury - Angle - Recession (cleavage) Glaucomamcq
      1.  Comes late after few months mcq  of trauma
      2. Gonioscopy-Irregular widening of Ciliary body band
    2. Inflammatory glaucoma
      1. Due to Intra-ocular haemorrhage
      2. Lens - induced glaucoma
  3. Ciliary - block - glaucoma - (Malignant-Glaucoma)
    1. Increased IOP with shallow anterior chamber
    2. Treatment =      
      1. dilate with atropine-impt glaucoma requiring dilatation
      2. Yag laser post capsulotomy or ant. Hyaloidotomy
  4. With intraocular haemorrhage-
    1. Red cell Glaucoma -  Due to RBCs blocking the trabecular meshwork
    2. Haemolytic Glaucoma-  Due to macrophages laden with RBCs, causing blockage
    3. Ghost cell Glaucomamcq seen in vitreous hemorrhage
    4. Hemosiderotic Glaucoma -  Due to iron from phagocytosed haemoglobin.
  5. With Irido-corneal Endothelial Syndromes -
    1. Progressive Iris Atrophy              
    2. Chandler's Syndrome        
    3. Cogan-Reese Syndrome





Test Your Skills Now!
Take a Quiz now
Reviewer Name