Traumatic and Metabolic cataract

Traumatic & Metabolic Cataract
By
Prof. Naimatullah Khan Kundi
Head, Department of Ophthalmology
Khyber Teaching Hospital
Peshawar
Metalosis
Siderosis Bulbi
Chalcosis
Metalosis
Siderosis Bulbi
Retained iron IOFB can result in siderosis bulbi
Fe Molecules Deposit in the:
Trabecular Meshwork
Lens epithelium
Iris
Retina
Lens: Yellowish tinge to lens epithelium and cortical fibers ® rusty brown discoloration
Cortical cataract (complete) – lens involvement early if FB is close to the lens
Metalosis
Chalcosis
Condition resulting from retained copper IOFB
Copper deposited in:
Deseemt’s membrane
Lens capsule and
Other intraocular basement membranes
Sunflower cataract:
Petal-shaped deposition of yellow/brown pigmentation in the lens capsule, radiating from the anterior axial pole of the lens to its equator
Usually causes no significant loss of VA
Pure copper (> 90%) IOFB causes a severe inflammatory reaction and intraocular neerosis
Electrical Injury
Electrical shock can cause protein coagulation and cataract formation
Lens manifestations more likely when transmission of current involves the patient’s head
Initially vacuoles in the anterior midperiphery of the lens, followed by linear opacities in the anterior subcapsular cortex
Cataract:
Stationary
Mature to complete cataract over months/yrs
Metabolic Cataracts
Diabetic cataract
Galactosemia cataract
Hypocalcemic (Tetanic) cataract
Metabolic cataract
Diabetic cataract
Diabetes mellitus can affect
Lens clearity
Refractive index
Accommodative amplitude
­ blood glucose ® ­ glucose in aqueous humor ® diffusion into lens ® ­ glucose content of the lens
Some of the glucose – is converted by enzyme aldose reductase to ® sorbital, which is not metabolized but remains in the lens
Metabolic cataract
Diabetic cataract (cont’d)
Sorbitol causes water influx into the lens (lenticular hydration)
Lens swelling effects refractive power of the lens:
Transient myopic refractive change
Hyperopic occasionally
Diabetic patients exhibit ¯ amplitude of accommodation compared to the age matched control
Presbyopia: At a younger age in diabetic patients than in non-diabetic patients
Cataract two types:
True diabetic (snowflake)
Senescent
Metabolic cataract
Diabetic Cataract (Cont’d)
True diabetic cataract"
BL, Subcapsular lens opacities of abrupt onset and acute progression, typically in young people with uncontrolled diabetes mellitus
Initially multiple gray-white subcapsular opacities in the superficial anterior and posterior cortex
Vacuoles and clefts form in the subscpsular cortex
Metabolic cataract
Diabetic Cataract (Cont’d)
True diabetic cataract"
The punctate white subcapsular opacities have "snow flake" appearance
Progression: Intumescence and maturity of the cortex
True diabetic cataract is rare seen in clinical practice today, any rapidly maturing BL cortical cataracts in a child/young adults should alert the clinician to the possibility of diabetes mellitus
Metabolic cataract
Diabetic Cataract (Cont’d)
Senescent cataract:
Frequently observed in diabetic patients
Diabetic patients have ­ risk of age-related lens changes
These tend to occur at a younger age than in patients without diabetes mellitus
The risk of ages related cataracts in diabetic patients may be due to:
Sorbital accumulation
Hydration changes
­ Glycosylation of proteins
Galactosemia cataract (cont’d)
Galactosemia can result from defect in one of three enzymes involved in Galactose Metabolism
Galactose-1-Phosphate uridyl transferase (cause classic galactosemia)
Galactokinase
UDP-Galactose-4-Epimerase
Transferase most commonly defective enzyme
Galactosemia autosomal recessive inherited inability to convert galactose into glucose
Galactosemia cataract (cont’d)
Excessive galactose ® galactitol (dulcitol)
Classic galactosemia: – Symptoms appear within first few weeks of life
Symptoms of malnutrition
Hepatomegaly
Jaundice
Mental dificiency
The disease is fatal if undiagnosed and left untreated
Diagnosis: - Non – glucose – reducing substance galactose in urine
Galactosemia cataract (cont’d)
Cataract:
75% develop within first few weeks after birth
­ galactose and galactitol in the lens:
­ intracellular osmotic pressure
­ fluid influx
Typically nucleus and deep cortex opacified causing "oil droplet" appearance on retroillumination
Early cataract may be reversed by timely diagnosis and dietry intervention

Galactosemia cataract (cont’d)
Cataract:
Untreated disease:
cataract progress to total opacification of the lens
Cataract in galactosemia due to epimerase and galactokinase deficiency may also be seen but tend to present later in life than in classic galactosemia
Treatment: Elimination of milk and milk product from diet
Hypocalcemia (tetanic) cataract
Cataract may develop with any condition that results in hypocalcemia
Hypocalcemia:
Idiopathic
Destruction of parathyroid glands during thyroid surgery
BL, punctate iridescent opacities in the anterior and posterior cortex beneath the lens capsule and usually separated by a zone of clear lens
Opacities:
Stable
Mature into complete cortical
Wilson disease (hepato-lenticular degeneration)
Autosomal recessive inherited disorder or copper metabolism
Kayser – Fleischer ring:
Characteristic ocular manifestation
Golden-brown discoloration of descement’s membrane around the periphery of the cornea
Wilson disease (hepato-lenticular degeneration) (cont’d)
Sunflower cataract:
Another characteristic feature
Reddish-brown pigment (cuprous oxide) deposited in the anterior lens capsule and subcapsular cortex in a stellate shaped that resembles the petals of a sunflower
In most cases the sunflower cataract does not produce serious visual impairment
Myotonic Dystrophy
Autosomal dominant inherited disorder
Clinical features:
Delayed relaxation of contracted muscles
Ptosis
Weakness of facial muscles
Cardiac conduction defects
Prominent forntal balding in affected male patietns
Lens:
Polychromatic iridescent crystals in the lens cortex
PSC progressing to complete cortical opacification

Nutritional Diseases
Nutritional deficiencies cause cataracts in animal models
This causation has been difficult to confirm in humans
­ plasma level of riboflavin, vit. C, vit. E and carotene are associated with ¯ risk of nuclear and cortical cataract formation (epidemiologic studies)
Severe episodes of Dirrhoea with attendant risk of malabsorption and electrolyte disturbance may be associated with ­ risk of cataract formation
Cigarette smoking: ­ Risk of PSC and nuclear sclerosis (Prospective studies)
Cataract associated with Uveitis
Chronic uveitis:
PSC
Anterior lens changes
Posterior synechiae associated with thickening of anterior capsule and fibrovascular membrane across the pupil (pupillary membrane)
Lens changes secondary to uveitis may progress to mature cataract
Cataract associated with Uveitis (cont’d)
Ca++ deposits may be observed:
On the anterior capsule
Within the lens substance
Fuchs heterochromic uveitis:
Cataract 70%
Cataract may be iatrogenic (steroid use)
Exfoliation syndromes
True exfoliation
Pseudoexfoliation
True exfoliation
True exfoliation of lens capsule rare
Observed in glassblowers and blast furnace operators
Exposure to IR radiation and heat presumably cause superficial lens capsule to delaminate and peel off in scrolls
Exfoliation syndromes (cont’d)
Pseudo-exfoliation
In exfoliation syndrome basement like fibrillo-granular white material is deposited on:
Lens
Cornea
Iris
Anterior hyaloid face
Ciliary processes
Zonular fibers
Trabecular meshwork etc.
Exfoliation syndromes (cont’d)
Pseudo-exfoliation (cont’d)
These deposits believed to arise from basement membranes within eye
Appear as grayish white flecks
Prominent at pupillary margin and lens capsule
Associated changes:
Iris atrophy at pupillary margin
Deposition of pigments on anterior iris surface
­ Pigmentation of trabecular meshwork
Open angle glaucoma
Subluxation of lens
Exfoliation syndromes (cont’d)
Pseudo-exfoliation (cont’d)
UL / BL
Onset: -- 6th to 7th decade
­ prevalence of senile cataract (some studies)/coincidental
Zonular fibers weakness:
Spontaneous lens subluxattion
Phacodonesis
Poor zonular integrity may affect cataract surgery technique and IOL implantation
Cataract and skin diseases
Atopic dermatitis
Chronic, itching, erythematous dermatitis
­ level of IgE
History of multiple allergies / asthma
Cataract:
25%
BL
Onset 2nd to 3rd decade
Anterior subcapsular opacities (Shield like plaques)
Lens induced uveitis phacoantigenic (phaco-anaphylactic uveitis)
Normally the eye appears to have immunologic tolerance to the small amount of lens protein (antigen) leakage through the lens capsule
Liberation of a large amount of lens protein into
anterior chamber disrupts the immunologic
tolerance and may tigger a sever inflammatory reaction
Lens induced uveitis phacoantigenic (phaco-anaphylactic uveitis) (cont’d)
Phacoantigenic uveitis is an immune-mediated granulomatous inflammation initiated by lens proteins leak through ruptured lens capsule (traumatic cataract/surgery)
Onset: days to weeks after injury / surgery
Lens Induced Glaucoma
Phacolytic Glaucoma
Phacomorphic Glaucoma
Lens Protein Glaucoma
Lens induced glaucoma
Phacolytic Glaucoma
It is a complication of
Mature
Hypermature cataract
Denatured liquefied high-molecular-wt lens proteins leak through an intact but permeable lens capsule
An immune response is not elicited,
macrophages ingest theses lens proteins
Lens induced glaucoma (cont’d)
Phacolytic Glaucoma (cont’d)
Clinical presentation
Pain abrupt onset
Redness
Cataractous eye that had poor vision for sometime
Cornea oedema
Significant flare reaction in A/C
White floculent material appears in a A/C and often adherent to lens capsule as well
IOP markedly elevated
A/C angle open, may show precipitate of white floculent material
Lens induced glaucoma (cont’d)
Phacolytic Glaucoma (cont’d)
Treatment:
Initial control of IOP with anti-glaucoma
Inflammation with steroids
Surgical removal of lens definitive treatment
Lens induced glaucoma (cont’d)
Phacomorphic Glaucoma
Intumescent cataractous lens causes:
Forward displacement of the iris
Shallowing of A/C
Leading to pupillary block and 2ndary ACG
Lens induced glaucoma (cont’d)
Phacomorphic Glaucoma (cont’d)
Presentation:
Redness
Pain
Cornea Oedmatous
A/C shallow
Gonioscopy closed A/C angle
History of ¯ VA as result of cataract formation prior to the acute onset
Lens induced glaucoma (cont’d)
Phacomorphic Glaucoma (cont’d)
Treatment:
Initial medical to ¯ IOP
Laser iridotomy
Cataract extraction definitive therapy
Lens induced glaucoma (cont’d)
Lens Particle (protein) Glaucoma
Lens cortex liberated into A/C after:
Penetrating lens injury
ECCE with retained cortical material
Nd: YAG laser capsulotomy (Uncommon)
Lens induced glaucoma (cont’d)
Lens Particle (protein) Glaucoma (cont’d)
Cortical material causes obstruction of aqueous outflow through the trabecular-meshwork causing ­ IOP
Onset of glaucoma delayed for days/weeks after surgical event/ lens injury
Examination reveals white, fluffy, cortical lens material in A/C and along trabecular-meshwork (gonioscopy)
Associated A/C inflammation may be seen
Lens induced glaucoma (cont’d)
Lens Particle (protein) Glaucoma (cont’d)
Treatment:
Medical therapy to:
¯ IOP with anti-glaucoma therapy
Inflammation with steroids
Surgical removal of retained lens material