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Kuliah Program S1 Keperawatan Wira Medika PPNI Bali 22 Maret 2016

PATOFISIOLOGI SISTEM SENSORI

GANGGUAN
KELOPAK MATA

ni made ari suryathi


0852 5365 1928
ANATOMI KELOPAK MATA
1. Rongga mata ( Cavum orbita )
2. Kelopak mata ( Palpebra )
3. Alis mata ( Supersilium )
4. Bulu mata ( Siliae )
5. Otot mata ( musculus okuli )
RONGGA MATA (CAVUM ORBITA)
1. Rongga Mata (Cavum Orbita)
ORBITAL FLOOR FRACTURES

Pathogenesis of blowout fractures:


The striking object causes a compressive force at the
inferior rim, which leads directly to buckling of the orbital
floor. The degree of increased orbital pressure determines
whether or not orbital tissues are pushed down through
the fracture into the maxillary antrum
Diagnosis of orbital blowout fracture
History of the orbital entrance being stuck by an object
usually larger than the diameter of the orbital opening.

Orbital blowout fracture should be suspected in any


patient who has received a periorbital blow of
sufficient force to cause ecchymosis
Typical findings of the physical examination
Eyelid signs: Ecchymosis and edema
Diplopia with limitation on upgaze and/or downgaze
Enophthalmos and ptosis of the globe
Hypoesthesia in the distribution of the infraorbital
nerve
Emphysema of the orbit and eyelids

CT scans with coronal or sagittal views to evaluate


extra-ocular muscle entrapment and fracture size to
predict anticipated enophthalmos
Le Fort Fracture
Complications:
Loss of vision, orbital hemorrhage, globe injuries

Management
1. Most orbital floor fractures do not require surgical
intervention
Usually observed for 7-10 days to allow swelling
and orbital hemorrhage to subside. Oral steroid (1
mg/kg/day for the first 7 days) will decrease edema
and may limit the risk of long-term diplopia from
inferior rectus contracture and fibrosis
Exception Children with profoundly limited vertical
excursions and frank extraocular muscle entrapment on
CT scan oculocardiac reflex

2. Surgical intervention
Preferable to proceed with the repair within 2 weeks
after the initial trauma
KELOPAK MATA (EYELID / PALPEBRA)
DIFFUSE EYELID DISEASE
1. Allergic
Acute oedema
Contact dermatitis
Atopic dermatitis

2. Infections
Preseptal cellulitis
Herpes simplex
Herpes zoster ophthalmicus
Impetigo

3. Others
Fat herniation
Systemic causes
Acute allergic oedema

Causes - insect bites, urticaria and angioedema


Unilateral or bilateral
Painless, red, pitting oedema
Chemosis may be present
Self-limiting
Contact dermatitis

Sensitivity to topical medication


Unilateral or bilateral
Painless oedema and erythema
Vesiculation and crusting
Thickening if chronic
Atopic dermatitis
Associated with asthma and hay fever
Chronic itching and scratching

Facial - in young children Flexural - knees, elbows, wrists and ankles


Ocular associations of atopic dermatitis

Thickening, crusting and Staph. blepharitis


fissuring

Angular blepharitis Vernal disease in children


Preseptal cellulitis
Causes
Skin trauma or insect
bites of lids or eyebrows
Spread from local
infection
Upper respiratory
or ear infection
Signs
Usually unilateral
Tender and red
Periorbital oedema
Treatment - systemic
antibiotics
Herpes simplex

Signs
Crops of small vesicles
Rupture and crust
Heal without scarring
after 7 days

Complications
Follicular conjunctivitis
Keratitis

Treatment - topical
antivirals
Herpes zoster ophthalmicus

Painful vesicles and pustules Crusting ulceration


Periorbital oedema - may be Treatment - oral antivirals
bilateral
Impetigo

Infection with Staph.


or Strep.

Initially small vesicles


and bullae

Later golden-yellow crusting

Treatment - topical and


systemic antibiotics
Fat herniation

Age-related,
usually bilateral

Pockets of fat
herniating into
upper lids, especially
medially

Treatment
- blepharoplasty
Systemic causes of lid oedema

Myxoedema

Renal disease

Congestive
heart failure

Obstruction of
superior vena
cava

Fabry disease
ENTEROPION
EKTEROPION
ECTROPION AND ENTROPION
1. Ectropion
Involutional
Cicatricial
Paralytic
Mechanical

2. Entropion
Involutional
Cicatricial
Congenital
Epiblepharon
Involutional

Affects lower lid of elderly patients

May cause chronic conjunctival inflammation


and thickening
Causes of cicatricial ectropion
Contracture of skin pulling lid away from globe
Unilateral or bilateral, depending on cause

Unilateral ectropion due to Bilateral ectropion due to severe


traumatic scarring dermatitis
Paralytic ectropion
Caused by facial nerve palsy which,
if severe, may give rise to the following:

Exposure keratopathy caused byEpiphora caused by combination of:


lagophthalmos Failure of lacrimal pump
mechanism
Increase in tear production
resulting from corneal exposure
Mechanical ectropion
Mechanical lid eversion by tumour

Treatment
Removal of the cause, if possible
Correction of significant horizontal lid laxity
Treatment Options for Ectropion
1. Temporary treatment
Lubrication with tear substitutes in mild cases
Botulinum toxin injection into levator muscle for corne
exposure
Temporary tarsorrhaphy in patients with poor
Bells phenomenon
2. Permanent treatment
Medial canthoplasty if medial canthal tendon is intact
Medial wedge resection to correct medial ectropion
associated with medial canthal laxity
Lateral canthal sling to correct residual ectropion
and raise lateral canthus
Treatment of ectropion
Method depends on severity

Mild localized cases are treated Severe cases require transposition flaps
by excision of scar tissue or free skin grafts
combined with Z-plasty
ENTEROPION
Involutional entropion

Affects lower lid because upper lid If longstanding may result in corneal
has wider tarsus and is more stable ulceration
Pathogenesis of involutional entropion

Horizontal lid laxity Overriding of preseptal over


pretarsal orbicularis during lid
Canthal tendon laxity closure
Weakness of lower lid retractors
Cicatricial entropion

Severe scarring of palpebral conjunctiva


which pulls lid margin towards globe
May affect lower or upper eyelid
Causes include cicatrizing conjunctivitis,
trachoma and chemical burns
Congenital entropion

Very rare - not to be confused with epiblepharon


Inturning of entire lower eyelid and lashes
Absence of lower lid crease
When skin is pulled down lid also pulls away from
Does not resolve spontaneously
globe
Treatment options for entropion

Transverse everting Weis procedure Jones procedure


sutures (temporary) (permanent) (for recurrences)
BENIGN EYELID LESIONS
1. Nodules
Chalazion
Acute hordeolum

Xanthelasm
a
2. Cysts
Cyst of Moll
Cyst of Zeiss
Sebaceous cyst
Hidrocystoma
3. Tumours
Viral wart
Keratoacanthoma

Capillary haemangioma
Signs of chalazion (meibomian cyst)

Painless, roundish, firm lesion May rupture through conjunctiva


within tarsal plate and cause granuloma
Treatment of chalazion

Injection of local anaesthetic Insertion of clamp Incision and curettage


Acute hordeolum
Internal hordeolum External hordeolum (stye)
( acute chalazion )

Staph. abscess of meibomian Staph. abscess of lash follicle and


glands associated gland of Zeis or Moll
Tender swelling at lid margin
Tender swelling within tarsal plate
May discharge through skin May discharge through skin
or conjunctiva
Xanthelasma

Common in elderly or those with


hypercholesterolaemia
Yellowish, subcutaneous plaques
containing cholesterol and lipid
Usually bilateral and located medially
Eyelid cysts
Eccrine sweat gland
Cyst of Moll hidrocystoma

Translucent Similar to cyst of Moll


On anterior lid Not confined to lid
margin margin
Cyst of Zeis Sebaceous cyst

Opaque Cheesy contents


On anterior lid Frequently at
margin inner canthus
Viral wart (squamous cell papilloma)
Most common benign lid tumour
Raspberry-like surface

Pedunculate Sessil
d e
Keratoses
Seborrhoeic Actinic

Common in elderly Affects elderly, fair-skinned individuals


Discrete, greasy, brown lesion Most common pre-malignant skin lesion
Friable verrucous surface Rare on eyelids
Flat stuck-on appearance Flat, scaly, hyperkeratotic lesion
Capillary haemangioma

Rare tumour which presents soon after birth May be associated with intraorbital
extension
Starts as small, red lesion, most frequently
on upper lid Grows quickly during first year

Begins to involute spontaneously


Blanches with pressure and swells on crying during second year
SCC
BCC
basal cell carcinoma

Lower lid - 70% Medial canthus - 15%

Upper lid - 10% Lateral canthus - 5%


Squamous cell carcinoma
Less common but more aggressive than BCC

May arise de novo or from actinic keratosis


Predilection for lower lid

Nodula Ulcerative
r

Hard, hyperkeratotic nodule Red base


May develop crusting Borders sharply defined, indurated
fissures
No surface vascularization and elevated
PTOSIS
CLASSIFICATION OF PTOSIS
1. Neurogenic
Third nerve palsy
Third nerve misdirection
Horner syndrome
Marcus Gunn jaw-winking syndrome
2. Myogenic
Myasthenia gravis
Myotonic dystrophy
Ocular myopathies
Simple congenital
Blepharophimosis syndrome
3. Aponeurotic
4. Mechanical
PTOSIS
1. Evaluation
Pseudoptosis
True ptosis
2. Classification
Neurogenic ptosis
Myogenic ptosis
Aponeurotic ptosis
Mechanical ptosis

3. Treatment options
Aponeurotic ptosis
Weakness of levator aponeurosis
Causes - involutional, postoperative and blepharochalasis
Mild

High upper lid crease Good levator function


Severe

Absent upper lid crease Deep sulcus


Mechanical ptosis
Causes

Dermatochalasis Large tumours

Severe lid oedema Anterior orbital lesions


Fasanella-Servat procedure
Indicated for mild ptosis with good levator function

..
Excision of upper border of tarsus, lower border of Muller muscle
and overlying conjunctiva
Levator resection
Indicated for any ptosis provided levator function is at least 5 mm

Shortening of levator complex Amount determined by levator


function and severity of ptosis
Frontalis brow suspension
Main indications
Severe ptosis with poor levator function ( 4 mm or less )
Marcus Gunn jaw-winking syndrome

Attachment of tarsus to frontalis muscle with


sling
EYELASHES
2. Bulu mata
DISORDERS OF LASHES
1. Trichiasis

2. Distichiasis

3. Phthiriasis palpebrarum

4. Madarosis

5. Poliosis

6. Bleparitis
1. Trichiasis
Signs Complications

Posterior misdirection of normal lashes Inferior punctate epitheliopathy


Most frequently affects lower lid Corneal ulceration and pannus
Treatment Options for Trichiasis

1. Epilation - but recurrences within few weeks

2. Electrolysis - but frequently repeated treatments requir

3. Cryotherapy - for many lashes

4. Laser ablation - for few scattered lashes

5. Surgery - for localized crop resistant to other methods


2. Distichiasis
Signs Treatment

Second row of lashes arising Division into anterior and posterior


from meibomian gland orifices lamellae
Congenital Cryotherapy to posterior lamella
Occasionally dominantly inherited Reapposition of lamellae
3. Phthiriasis palpebrarum
Infestation of lashes by pubic crab louse and its ova (nits)
Typically affects children in poor hygenic conditions

Lice gripping base of lashes Nits and empty shells adhere to base of lashes
Treatment - removal, destruction and delousing
4. Madarosis
Decrease in number or complete loss of lashes
Local causes
Chronic anterior
lid margin disease
Infiltrating tumours
Burns, radiotherapy
or cryotherapy
Systemic causes
Generalized alopecia
Myxoedema
SLE
Syphilis
Leprosy
Following removal
5. Poliosis
Premature localized whitening of hair

Ocular associations

Chronic anterior blepharitis

Sympathetic ophthalmitis

Systemic associations

Vogt-Koyanagi-Harada
syndrome

Waardenburg syndrome
6. BLEPHARITIS
1. Anterior
Staphylococcal
Seborrhoeic

2. Posterior
Meibomianitis
Meibomian seborrhoea
6.1. Staphylococcal blepharitis

Chronic irritation worse in mornings Hyperaemia and telangiectasia of anterior


lid margin
Scales around base of lashes
(collarettes) Scarring and hypertrophy if longstanding
Complications of staphylococcal blepharit

Trichiasis, madarosis poliosis Recurrent styes


,

Marginal keratitis Tear film instability


6.1.Seborrhoeic blepharitis

Shiny anterior lid margin Greasy scales


Hyperaemia of lid margin Lashes stuck together
6.2.Meibomianitis

Inflamed and blocked meibomian Toothpaste-like plaques from meibomian


gland orifices glands

Thickened posterior lid margin Meibomian cyst formation


Meibomian seborrhoea

Oil globules over meibomian gland orifices Oily and foamy tear film
Treatment of Blepharitis

1. Lid hygiene - with 25% baby shampoo

2. Tear substitutes - for associated tear film instability

3. Systemic tetracyclines - for severe posterior blepharitis

4. Warm compresses - to melt solidified sebum


in posterior blepharitis
Alis
Madarosis
Decrease in number or complete loss of lashes
Local causes
Chronic anterior
lid margin disease
Infiltrating tumours
Burns, radiotherapy
or cryotherapy
Systemic causes
Generalized alopecia
Myxoedema
SLE
Syphilis
Leprosy
Following removal
Poliosis
Premature localized whitening of hair

Ocular associations

Chronic anterior blepharitis

Sympathetic ophthalmitis

Systemic associations

Vogt-Koyanagi-Harada
syndrome

Waardenburg syndrome
OTOT MATA
ESOTROPIA EXOTROPIA
Initially intermittent
Normal AC/A ratio
Excessive hypermetropia

Fully accommodative Partially accommodative

Esotropia greater for near Straight for distance

Straight for distance and near Esotropia for near


PATCHING
Refraction - prescribe full cycloplegic refraction under age 6 years

Treatment of amblyopia

Surgery - if spectacles do not fully


correct deviation

Recession Resection
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Matur Suksma

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