Primary Open Angle Glaucoma

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Slide 1:

Primary Open Angle Glaucoma BY Hala Fathi Hannot

Slide 2:

بسم الله الرحمن الرحيم قالو سبحانك لاعلم لنا الا ما علمتنا انك انت العليم الحكيم صدق الله العظيم الآية (32) سورة البقرة


POAG Investigation gonioscopy Tonometry Examination History Treatment Summary

Important N.B:

Important N.B Primary open angle glaucoma is age relaed trabecular sclerosis Primary open angle glaucoma is diagnosis of exclusion Primary glaucoma is a bilateral disease which is asymmetrical and progressive

History (to detect risk factors):

History (to detect risk factors) 1. Age - most cases present after age 65 years 2. Race - 3. Family history Risk is increased by x2 if parent has POAG Risk is increased x4 if sibling has POAG 6. Myopia more common, earlier onset and more severe in blacks 4. Diabetes mellitus – cardiac-hypo & hypertension- Drugs( anticholinerguc , antihistaminic, antipsychotics 7. CRVO 5 . steroid

Examination :

Examination (To confirm diagnosis): to detect risk factors, exclude 2ndry causes:

Tonometry & IOP phasing :

Raised IOP (we can’t diagnose glaucoma by measuring IOP alone ,there is low and normal tension glaucoma, also there are 2% of population over age of 40 have IOP more than 24 mmHg Diurnal fluctuations in IOP more than 5 mmHg Asymmetry in IOP measurement between the 2 eyes of 5 mmHg or more Tonometry & IOP phasing


Angle examination is important to exclude other causes of 2ndry glaucoma(PDS-PXE-angle recession-chronic type of angle closure glaucoma- neovascularization detection) Gonioscopy

Fundus examination:

Fundus examination

Optic Disc: normal variation The ISNT Rule:

Optic Disc: normal variation The ISNT Rule

Early signs of glaucomatous damage:

Early signs of glaucomatous damage Retinal nerve fibre layer Nerve fiber layer dropout Optic nerve head Focal notching of neuroretinal rim - Thining of infero -temporal Rim (ISNT rule is not preserved) Vertical elongation of cup Asymmetry of cupping between 2 eyes Non specific signs of glaucomatous damage Baring of circumlinear blood vessels Splinter haemorrhages

Late signs of glaucomatous damage:

Late signs of glaucomatous damage Optic nerve head Generalized enlargement of cup Vertical elongation of cup Asymmetry of cupping between 2 eyes Peripapillary changes Non specific signs of glaucomatous damage Exposure of lamina cribrosa Bayoneting (double angulation of blood vessel)

Optic Disc: glaucoma Rim loss: focal:

Optic Disc: glaucoma Rim loss: focal

Optic Disc: glaucoma Rim loss: diffuse:

Optic Disc: glaucoma Rim loss: diffuse

Optic Disc: glaucoma Rim loss: combined:

Optic Disc: glaucoma Rim loss: combined

Optic Disc: glaucoma Baring of circumlinear vessel:

Optic Disc: glaucoma Baring of circumlinear vessel

Optic Disc: glaucoma Haemorrhage:

Optic Disc: glaucoma Haemorrhage

Red Flag signs (not glaucoma):

Red Flag signs (not glaucoma) When Visual acuity is out of proportion to cupping When colour vision is lost especially red and green When optic nerve pallor is out of proportion to degree of cupping When there is fundus abnormalities like optic nerve pit, drusen , tiltes disc,..


Investigations Perimetry Focal visual field defects respecting the horizonal meridian including Nasal step- Baring of blind spot- Paracentral scotoms - Arcuate defects- Altitudinal defects Generalized depression Red Flag signs (not glaucoma ) Visual field defects greater than expected Visual field patterns not typical to glaucoma e.g defects respect vertical midline- hemianopic defects-enlarged blind spot Functional assessment SWAP- frequency doubling perimetry - humphery

Optic Disc imaging :

Optic Disc imaging Subjective Photography Steroscopy Objective OCT (Optical coherence tomography) GDx ( scanning laser polarimetry ) Heidelberg Retina Tomograph (HRT, Heidelberg Eng.) RTA (Retinal thickness analyizer ) structural assessment

Slide 21:

Neural retinal rim Cup area Normal Glaucoma ONH parameters & RNFL thickness map s RNFL TSNIT graph RNFL Thickness Map Imaging of the ONH 3-D , true optic nerve topography OCT

It provides more information than other advanced imaging technologies :

It provides more information than other advanced imaging technologies only surface topography

Differential diagnosis of POAG :

Differential diagnosis of POAG Other causes of increased IOP Ocular hypertension 2ndry open angle glaucoma Chronic angle closure glaucoma Other causes of cupping and field defects Physiological cupping Optic nerve drusen Congenital optic nerve defects Optic arophy

Treatment of POAG :

Treatment of POAG T arget IOP Aim of TTT: to enhance or at least maintain patient’s health.

Slide 25:

Definition of target IOP : The mean IOP obtained with treatment that prevents further glaucomatous damage . Choice of target IOP: It is usually 20% reduction of basal IOP but it should be individualized for each patient based on initial intraocular pressure Degree of existing damage .(Optic nerve cupping, visual field loss and nerve fiber layer thickness) Patient condition: Age (life expectancy), other risk factors (Family history of glaucoma, diabetes and arteriosclerotic vascular diseases)

Slide 26:

Short (old age) Mild Low Initial IOP when damage occurred Advanced High Long (young) Life expectancy Damage High Target e.g 18 Target IOP LOW e.g 11 Target IOP European Glaucoma society guidelines

Slide 27:

How will I achieve target IOP medical therapy (will be discussed later) Laser Argon laser trabeculoplasty (ALT) : may be the 1 st line of treatment especially in noncompliant patients Selective laser trabeculoplasty (SLT) : repeatable (twice per a year) more effective Surgery ( Trabeculectomy ) Indications: failed medical therapy and laser As primary therapy in advanced disease Early Aggressive Therapy Combined drugs – ALT - Surgery : if High IOP Advanced glaucoma in young age Rapid rate of progression Central vision loss is expected within pt’s lifetime ”long life expectancy” Advanced glaucoma in other eye

Slide 28:

M edical therapy

Slide 29:

Starting the treatment in one eye to determine the drug efficacy then recheck after 3:6 weeks The patients should be treated with the lowest concentration(s), the smallest number of medicines and the fewest number of administrations per day that have the desired effect.

Slide 30:

Choosing initial and combination medical therapy for glaucoma:

Mechanism of action of anti-glaucomatous drugs:

Mechanism of action of anti-glaucomatous drugs

Slide 32:

Follow-up and resetting target IOP ( Target IOP is a dynamic value ) The initial efficacy of therapy is determined by its effect on IOP , but long-term efficacy must be determined by the analysis of damage ( visual field , the optic nerve head , retinal nerve fiber thickness ). Deterioration in any of these parameters is a sign to consider more aggressive therapy (i.e. to re-set the target intraocular pressure at a lower level ) taking into consideration the other risk factors

To summarize treatment:

To summarize treatment Choice of target IOP should be individualized for each patient. We will start with medical treatment as monotherapy  if not good  change it  if not good add adjunctive. We can start by aggressive treatment in some cases follow-up (assessing RNFL- optic nerve) and resetting target IOP to lower level if there is deterioration by current treatment( adding another drug) Follow up more frequently till we assure that we reached the target IOP ( no damage with current treatment)-> if cant be achieved by medical treatment  laser or surgery.

Slide 34:

Thank you