Glucoma Flashcards
Definition: ACUTE GLAUCOMA
> IOP–> optic atrophy.
Definition:CHRONIC GLAUCOMA
optic atrophy –> > IOP/ normal IOP if caused by vascular insufficiency of the optic disc.
Classification
1. Acute: Acute angle closure glaucoma 2. Chronic: Developmental glaucoma Chronic open angle glaucoma
Cause
- Idiopathic
2. Secondary ocular abnormality
PRIMARY ACUTE ANGLE CLOSURE GLAUCMA
Epidemiology Pathophysiology Diagnosis Presentation Treatment
EPIDEMIOLOGY
Much less common than primary open angle glaucoma.
More common in older people.
There is a familial tendency.
PATHOPHYSIOLOGY
- PHYSIOLOGICAL RELATIVE PUPIL BLOCK
- Close proximity of the posterior surface of the iris and the anterior lens capsule at the pupillary border causes a slight resistance to flow of aqueous from the posterior chamber through the pupil, known as physiological relative pupil block.
- It may become > as a result of normal anatomical and physiological variation and change:
- Anatomical: A relatively shallow anterior chamber. Age-related enlargement of the lens.
- Physiological: Size of the pupil and tension in the iris diaphragm. Iris-lens contact is usually the greatest when the pupil is middilated. Consequently all factors that influence the size of the pupil play a rôle: lighting, emotion, accommodation, sleep. - CLOSURE OF THE DRAINAGE ANGLE
- abnormal degree of relative pupil block.
- accumulation of aqueous in the posterior chamber
- anterior bulging of the peripheral iris diaphragm which may be sufficient to cover the trabecular meshwork and so occlude the drainage angle.
- Angle closes: no tendency to spontaneous resolution, and continuous secretion of aqueous causes a sharp increase in intraocular pressure to very high levels: 60 - 100 mmHg.
- The corneal endothelial pump: unable to pump sufficient fluid out of the corneal stroma into the anterior chamber against the resultant pressure gradient, and corneal oedema develops.
- > IOP approaches and then exceeds pressure in bv that supply the eye, ocular ischaemia occurs–> The net effect is the dramatic onset of severe symptoms and signs.
DIAGNOSIS
Clinical:Pain, A fixed middilated pupil and corneal oedema are cardinal signs, without which the diagnosis cannot be made.
SYMPTOMS
1. Acute onset of deep-seated, intense, unilateral eye pain radiating into the entire ipsilateral hemicranium, and often sufficiently severe to cause prostration, nausea and vomiting. The pain is caused by ocular ischaemia.
2. Red eye.
3. Dramatic decrease in visual acuity due to corneal oedema and ocular ischaemia.
4. Coloured halos around lights due to corneal oedema.
5. Reflex tearing due to trigeminal irritation.
6. Photophobia may occur but is not a prominent symptom.
SIGNS
1. < VA: Vision may be reduced to hand movements within hours of the onset.
2. Fixed, middilated pupil due to ischaemic paralysis of both sphincter and dilator pupillae.
3. Ciliary injection. The eye is often so red that the ciliary pattern is not obvious.
4. Corneal haze due to corneal oedema.
5. Shallow anterior chamber due to anterior bowing of the iris: the eclipse test is positive.
6. The fundus cannot be seen due to the corneal haze.
7. Markedly raised intraocular pressure: the eye feels hard on palpation.
EMERGENCY TREATMENT: Only < IOP and better symptoms
Treatment is urgent as irreversible blindness may occur within hours.
1. ACETAZOLAMIDE (Diamox®): carbonic anhydrase inhibitor reduces aqueous secretion. Dose: 500mg stat, preferably IV or IM, otherwise orally.
2. GLYCEROL: osmotic diuretic effect draws water out of the eye. Dose: 1ml/kg stat PO.
3. TOPICAL β-BLOCKER: reduces aqueous secretion. Preferably cardioselective eg Betaxolol (Betoptic®) Otherwise nonselective eg Levobunolol (Betagan®) Dose: 1 drop 1⁄2 hourly for not more than 2 hours. Monitor respiratory and cardiovascular systems for side effects.
4. PILOCARPINE: cholinergic agonist stimulates the iris sphincter. As the intraocular pressure falls, the iris sphincter becomes reperfused, it’s function is restored, and it
pulls the peripheral iris out of the angle. Dose: 1 drop 1% 1⁄4 hourly for 2 hours.
5 SYSTEMIC ANALGESIC ANTIEMETIC As required.
DEFINITIVE TREATMENT
- Prophylactic surgical peripheral iridectomy on the affected eye –> Aqueous cant accumulate behind iris because as it flows through the peripheral iridectomy into the anterior chamber.
- prophylactic surgical iridectomy or laser iridotomy is also performed on the unaffected eye.
SECONDARY ACUTE ANGLE CLOSURE GLAUCOMA
Cause
Treatment
CAUSES
Ocular abnormalities which cause an increase in pupil block:
1 Posterior synechiae in anterior uveitis.
2 Lens swelling in an advanced cataract.
3 Lens displacement in lens subluxation and dislocation.
4 Drugs: miotics and mydriatics.
TREATMENT
- pressure must be reduced urgently medically –> Pilocarpine contraindicated
- Further medical and surgical management by the ophthalmologist is dependent upon the cause.
PRIMARY OPEN ANGLE GLAUCOMA
Epidemiology Pathophysiology Presentation Diagnosis Treatment
EPIDEMIOLOGY High risks groups: 1. Genetic factors: (a) Family history (b) Black African ancestry 2. Older patients: occurs in approximately 2% of Caucasians and 4% of Black Africans over 50 years of age.
PATHOPHYSIOLOGY
- Although the angle is anatomically open, its function is impaired.
- Aqueous secretion > drainage and the intraocular pressure rises until a new equilibrium is reached at a slightly higher pressure.
The mild to moderate intraocular pressure elevation over a long period of time causes gradual and progressive optic nerve damage.
SYMPTOMS
1. The condition is nearly always asymptomatic until it is terminal.
2. The patient does not notice the characteristic field loss and visual acuity remains normal until shortly before all useful vision is lost.
SIGNS
1. Decrease in visual acuity only when terminal.
2. Loss of visual field is characteristic and automated visual field testing is essential to evaluate disc
damage and progression of the disease. Note that only advanced visual field loss can usually be demonstrated with confrontation.
3. Disc changes:
(a) Colour: neuroretinal rim pallor
(b) Cup:
large: C/D > 0,6 is very suspicious
deep: laminar dots undermined edge vertically oval asymmetrical between the eyes
(c) Vessels: nasal displacement.
(d) Border: a nerve fibre layer haemorrhage on the disc margin is seldom seen but is highly suggestive of a fresh infarction.
4. An increase in intraocular pressure can usually be demonstrated.
DIAGNOSIS
- GP screen > risk group–> optic disc examination.
- Refer ophthalmologist.
MANAGEMENT
MEDICAL
1. TOPICAL β-BLOCKERS: reduce aqueous secretion. Important side effects: cardiovascular and respiratory. Patients prone to asthma should not be placed on a nonselective β-blocker.
2. TOPICAL PROSTAGLANDIN ANALOGUES: increase aqueous outflow. Well tolerated, but may cause a permanent increase in iris pigmentation.
3. TOPICAL ADRENALINE PREP ARA TIONS: increase aqueous outflow. Important side effects: cardiovascular.
4. TOPICAL PILOCARPINE: increases aqueous outflow. Cholinergic agonist stimulates the ciliary muscle to put traction on and so open the trabecular meshwork. Important side effects: discomfort, miosis.
SURGICAL
1. Trabeculectomy: canal made through trabeculum and sclera to > the aqueous drainage into the subconjunctival tissue.
SECONDARY OPEN ANGLE GLAUCOMA
Causes
Treatment
CAUSES
- Clogging of the trabeculum: eg white cells in uveitis, red cells in hyphaema.
- Trabeculitis: mechanical trauma, keratitis, uveitis, alkali burns.
- Trabecular scarring: occurs late after trabeculitis.
- Drugs: steroids.
Note that an increase in intraocular pressure is not regarded as glaucoma until it leads to optic disc damage.
TREATMENT
Medical and surgical management by the ophthalmologist depends on the cause.
DEVELOPMENTAL GLAUCOMA
Pathophysiology
Presentation
Diagnosis
Treatment
Caused by abnormal development of the drainage angle known as trabeculodysgenesis.
Trabeculodysgenesis is usually caused by sporadic mutation, but may be secondary to inflammation of the developing trabeculum, as in congenital ocular rubella.
The drainage angle is thus anatomically abnormal from birth. Despite the abnormal angle, aqueous outflow may frequently initially be sufficient to maintain a relatively normal intraocular pressure for a variable period of time. Later decompensation causes a rise in intraocular pressure, which is eventually sufficient to cause optic disc damage and consequently glaucoma. Because optic disc damage is required to make a diagnosis of chronic glaucoma, the age at which it first occurs determines whether the glaucoma is defined as congenital, infantile or juvenile.
SYMPTOMS 1. Tearing 2. Photophobia 3. Blepharospasm SIGNS 1. Megalocornea and enlarged globe: buphthalmos--> > IOP before or just after birth, stretching the ocular walls irreversibly when they are still soft and elastic. It does not occur in adults. 2. Corneal haze due to corneal oedema. 3. Enlarged optic cup. 4. Small to moderate rise in intraocular pressure.
DIAGNOSIS
- A high index of suspicion in young children with tearing, photophobia and blepharospasm.
- An examination under anaesthesia by an ophthalmologist is necessary to confirm the diagnosis in young children.
TREA TMENT
Treatment is surgical: trabeculotomy or goniotomy: the drainage angle is incised to improve aqueous access and drainage.
Measurement of IOP
NORMAL RANGE
10 – 20 mmHg
METHODS
1 DIGITAL
Palpate tarsal plate
2 SCHIØTZ INDENTATION TONOMETER
The footpiece of the instrument is placed directly on the anaesthetised cornea of the supine patient.
The central cylinder slides through a hole in the centre of the footpiece and indents the cornea.
The degree of corneal indentation is inversely proportional to the intraocular pressure and can be read from the scale on the instrument.
If the indicator reads near the edge of the scale, weights are added to the cylinder until the indicator reads near the centre of the scale.
The supplied table is then used to determine the intraocular pressure from the degree of corneal indentation and the weight of the cylinder.
3 GOLDMANN APPLANATION TONOMETER
tonometer at slit lamp.
Gold standard
Cornea is flattened instead of indented, and pressure is applied horizontally instead of vertically.
4 TONO-PEN
Hand held electronic applanation tonometer
It is accurate
5 NONCONTACT TONOMETERS
“puff” tonometers: Indentation of the cornea by stream of air with linearly > velocity is measured optically.
The higher the intraocular pressure, the longer the period of time before the cornea indents.
The method is accurate and does not involve contact with the eye. It is used primarily by optometrists.
Anatomy:Aqueous humour
Secretion
Circulation
Drainage
Cornea
SECRETION
Active secretion by the epithelium of the ciliary processes into the posterior chamber.
CIRCULATION
Flow is through the posterior chamber and pupil into the anterior chamber.
DRAINAGE
Exit from the anterior chamber is via the trabecular meshwork in the iridocorneal (drainage) angle. The fluid then enters the sinus venosus sclerae (canal of Schlemm), from which it drains into the episcleral veins.
THE CORNEA
The transparency of the cornea is dependent, dehydration. The latter is maintained mainly by an active pump mechanism in the endothelium, which pumps fluid from the corneal stroma into the anterior chamber.
Physiology: Vitreous functions
- Nutrition, transport of waste products, buffering and thermoregulation of the surrounding avascular ocular structures.
- Optical medium for the conduction of light.
- Maintenance of IOP
equilibrium between the rates of secretion and drainage of aqueous.
