Ophthalmology

Course No. 3. Pathology of the orbit

Notions of orbit anatomy. :
*The walls of the bone skeleton of the orbit consists of seven bones:
1.Frontal bone (Orbital face)
2. Zygomatic bone (Orbital process of zygomatic bone)
3.Maxillary bone (Orbital surface of the maxillary body)
4.Sphenoid bone (Orbital surface of the large wing of the sphenoid bone)
5. Ethmoid bone (Lamina papiracee)
6. Palatine bone (Orbital process of the palatine bone)
7. Lacrimal bone
* In anatomy, the orbit is the cavity or socket of the skull in which the eye and its appendages are situated. Orbit can refer to the
bony socket, or it can also be used to imply the contents. In the adult human, the volume of the orbit is 30 millilitres , of which the
eye occupies 6.5 ml. 
* The orbital contents comprise the eye, the orbital and retrobulbar fascia, extraocular muscles, cranial nerves II III, IV, V,
and VI, blood vessels, fat, the lacrimal gland with its sac and duct, the eyelids, medial and lateral palpebral ligaments, check
ligaments, the suspensory ligament, septum, ciliary ganglion and short ciliary nerves.

*The orbit shelters and protects the eyeball. It is a bony cavity located in the facial mass, on either side of the nasal pyramid. It has
the shape of a quadrilateral pyramid with 4 walls, an apex, content and apertures.

*Orbit dimensions:
Height: (at the level of the front aperture) - 35 mm
Infero-external oblique diameter - 4o mm
Depth - 40 mm.

*The apex of the orbit is crossed by the optical canal and the sphenoid slit through which the orbit communicates with the middle
floor of the skull. The optic nerve, the artery and the central vein of the retina pass through the optic canal.
*The contents of the orbit are made up of the eyeball, oculomotor muscles, nerves, vessels, tear gland and celluloid tissue. The
scleral portion of the globe is covered by the tenon aponeurotic capsule that separates the eyeball from the retroorbital tissue.
* Through its walls, the orbit is in relation to the sinuses of the face and through its orifices, it communicates directly with the
neurocranium, the nasal cavity and the pterygopalatine fossa, so that the local pathology can affect the neighboring regions and
vice versa.

* The axis of the orbit is oriented postero-medially and makes an angle of 23 degrees with the axis of the eyeball. The axes of the
orbit, extended posteriorly, meet at the level of the upper edge of the Sella turcica.
* The eyeball occupies only 1/5 of the volume of the orbit, and the rest of the space is occupied by the vascular-nervous elements
and the orbital adipose tissue

* The superior wall or roof of the orbit is made up anteriorly of the orbital plate of the frontal bone and posteriorly of the small
wing of the sphenoid. It separates the contents of the orbit from the brain substance in the anterior cranial fossa. At the union of
1/3 internal with 2/3 external, the superior rim has a notch which the supraorbital nerve runs and supplies sensation to the
forehead, also the supraorbitar artera and vein. Antero-laterally, the lacrimal fossa is observed, which hosts the orbital portion
of the lacrimal gland
*The optic canal is located at the root of the small wing of the sphenoid and bordered medially by the body of the sphenoid bone.
The optic nerve and the ophthalmic artery, accompanied by sympathetic nerve fibers, reach the orbital cavity through the optic
canal. A defect in the orbital roof may cause pulsatile proptosis due to transmission of cerebrospinal pulsation to the orbit.

* The medial wall is formed from the lesser wing of the sphenoid, the ethmoid bone, the lacrimal bone, and the frontal process of
the maxilla. The part of the ethmoid is thin and covers the middle and posterior ethmoid cells, thus representing a pathway
through which the infection can spread into orbit. Later, the ethmoid bone articulates with the body of the sphenoid, which will
form the medial wall of the cavity to the apex. The lacrimal bone contains a pit for the lacrimal sac. In the anterior part, this pit is
in communication with the lacrimonial canal. Through this wall, the orbit comes in relation to the nasal fossae, the ethmoidal
sinus and the sphenoid sinus.

* The lateral wall of the orbit is formed posteriorly by the orbital face of the
grater wing of the sphenoid and anteriorly by the frontal process of the zygomatic
bone . The orbital tubercle, on which the lateral palpebral ligament is inserted,
marks approximately the middle of the lateral orbital margin. The lateral wall is
the thickest wall of the orbit, especially to the posterior, where it separates the
orbit from the middle cranial fossa.

* The floor is formed from the sphenoid, the orbital process of the palatine bone,
and the orbital process of the maxillary bone. The floor of the orbit is thin and
largely represents the roof of the maxillary sinus, thus explaining the orbital pain
manifested in the maxillary sinusitis, as well as the possibility of dissemination of
a purulent sinus collection at this level. In the medial part, the lower wall is
traversed by the infraorbital canal, open on the anterior face of the jaw, at the
level of the infraorbital foramen, through which pass the infraorbital nerve and the
infraorbital vessels mentioned above.

* The infraorbital nerve also gives off small dental branches (anterior, superior
alveolar, and middle superior alveolar nerves) before exiting facially. Through the
maxillary bone, the orbit comes in relation to the upper dental arch.
 

Orbit communications
* Optical canal - communicates with the anterior cranial fossa and is crossed by the optic nerve and the ophthalmic artery
* Upper orbital fissure - communicates with the middle cranial fossa and is crossed by the lacrimal, frontal, nasociliary,
trochlear, abducens and oculomotor nerves, as well as the superior ophthalmic vein
* Inferior orbital fissure - communicates with the infratemporal region and allows the passage of infrorbital and zygomatic
nerves, orbital branches of the pterygopalatine ganglion, infraorbital artery and inferior ophthalmic vein.
* Anterior ethmoidal foramen - communicates with the anterior cranial fossa and is crossed by the anterior ethmoidal vascular-
nervous bundle.
*Posterior ethmoidal foramen - communicates with the posterior cranial fossa and is crossed by the posterior ethmoidal
vascular-nervous bundle.
*Nose-tear duct - communicates with the nasal fossa
* Zygomatic orbital foramen - communicates with the zygomatic canal through which the zygomatic nerve passes.
Orbital pathology
Semiology of orbital diseases.

1.Symptoms
- Decreased visual acuity, caused by direct damage to the optic nerve, disruption of ocular blood circulation, damage to the cornea
in lagophthalmia (inability to close the eyelid slit) or compression of the eyeball.
- Diplopia occurs in pathological processes involving one or more extrinsic muscles of the eyeball.
- Spontaneous eye pain or eyeball movements occur mainly in inflammatory processes.

2. Signs:
A. Eye protrusion changes: exophthalmos and enophthalmia.
Exophthalmos - the most common sign. Depending on the degree of protrusion, there are medium exophthalmos between 17-20
mm and large, over 20 mm.  
*There are a variety of exophthalmos: exophthalmos and enophthalmia.
- permanent or intermittent (vascular)
- chronic or acute (traumatic, inflammatory)
- nonpulsatile and pulsatile (carotid-cavernous fistula)
- reducible (endocrine, vascular) and non-reducible (tumor)  
- axial or lateral
- unilateral (local cause) or bilateral (general cause)
* Unilateral exophthalmos can be: traumatic in palpebroorbital emphysema, orbital phlegmon after a perforating wound); acute
or chronic inflammatory: cellulitis, phlegmon or orbital abscess, tumors, carotid cavernous fistula, B Basedow at onset.
* Bilateral exophthalmos may occur in thyroid endocrine diseases, acromegaly, pheochromocytoma, cavernous sinus
thrombophlebitis, leukemia, malignant lymphoma, etc.…
* The differential diagnosis of exophthalmos is made with pseudoexophthalmos from:
- unilateral myopic large eye, congenital eye enophthalmia, congenital glaucoma, retraction of the upper eyelid, orbital facial
asymmetry, corneal deformation.

*Enophtalmos implies recession of the globe within the orbit.

It has three main causes:
1. Structural abnormalities: post-traumatic (orbital floor fractures), microphthalmia, birth defects
2. Atrophy of orbital content after irradiation for malignant tumors, orbital varicose veins.
3. Tractions in orbital metastatic tumors, post-inflammatory scars, after excessive resection of extraocular muscles in strabismus
surgery.

B. Ophthalmoplegia (Limitation of eye movements)

In diseases located at the top of the orbit, the movements are limited in all directions because the pathological process affects the
muscular cone. In processes located in the anterior region of the orbit, movements are limited in the direction of the pathological
process.

C. Eyelid and conjunctival edema occur in rapidly growing inflammatory and tumor processes.

D. Ophthalmoscopic signs
Can occur:
- Papillary pallor
- Papillary edema
- Chorioretinal retinal folds in orbital tumors or in thyroid ophthalmopathy
- Retinal detachment.

Traumatic diseases - include:

- Orbit fractures
- Perforating wounds of the orbit
- Outer bodies of orbit
- Orbitopalpebral emphysema
Orbit fractures can be direct or irradiated.
Direct fractures may affect the upper / lower orbital rim or edge of the orbit.

1.Fractures of the upper rim in the outer third may affect the lacrimal gland and those located in the inner half may affect the
supraorbital nerve (giving neuralgia), frontal sinus or anterior ethmoid cells (epitaxis and orbital emphysema occur), or cause
tearing of the reflected superior oblique tendon. giving diplopia and changes in eye motility.
2. Fractures of the lower rim accompany the opening of the maxillary sinus with epistaxis, orbital emphysema and diplopia by
the hematoma of the inferior oblique muscle.

3. Maxillofacial fractures are the most common. It is manifested by pain at the pressure of the malar bone, and at the objective
examination there is ecchymosis and palpebral and conjunctival edema, epistaxis, epiphoria due to interest in the tear ducts, eyelid
ptosis and limitation of eye movements. After a few days, exophthalmos, diplopia and sensitive disorders appear in the territory of
the suborbital nerve.
he fracture of the orbital floor is accompanied by the fracture of the orbital rim. It typically occurs in orbital contusion with the
tennis ball, which causes a sudden increase in intraocular pressure. It is found:
- periocular edema and ecchymosis,
- enophthalmia with resorption of the edema,
- anesthesia of the lower region (lower eyelid, chin, the respective part of the nose, upper lip and upper teeth) is characteristic,
because such a fracture begins at the medial edge of the infraorbital canal and extends to the nose.
- double diplopia in both upward and downward looking.
- epistaxis due to hemorrhage from the maxillary sinus.

4.Irradiated fractures
- Fractures of the base of the skull are manifested by bruising in glasses that occurs 3-5 days after trauma, chemosis, eyelid
emphysema, rhinorrhea by leaking cerebrospinal fluid.
- The irradiated skull fracture at the top of the orbit affects the optic nerve giving the optic canal syndrome characterized by:
amaurosis, loss of direct photomotor reflex with the preservation of the consensual, FO normal appearance or disc swelling and in
three weeks appears optic atrophia.

Orbital floor blowout fracture Moderate limitation of upgaze & downgaze right eye 

   

5.Thyroid eye disease

TED also know as Graves ophthalmopathy (GO) is a very common orbital disorder, and is the most common cause of
proptosis in an adult. GO is an autoimine disorder representing the commonest and most important extrathyroidal manifestation
of Grave disease, but it may occur in patients without current or prior hyperthyroidism ( euthyroidism or ophthalmic Graves
disease) or in patients who are hypothyroid due to chronic autoimmune( Hashimoto’s) thyroiditis.
Hiperthyroidism is a condition involving excesive secretion of thyroid hormones. Grave disease, the most common form of
hyperthyroidism is an autoimmune disorder in which Ig G antibodies bind to thyroid stimulating hormone (TSH) receptors in the
thyroid gland and stimulat secretion of thyroid hormones.
It is more commun in famales and may be associated with other autoimmune conditions.
The onset is often in the fourth or fifth decades with symptoms including weight loss, increase bowl frequency, sweating, heat
intolerance, nervousness, irritability, palpitations, weakness and fatigue.
Cardiac manifestations may include sinus tachycardia and other arrhythmias.

*Risk factors for ophthalmopathy.

In the Grave disease, the major risk factor for developing TED is smoking and giving up smoking seems to reduce the risc.
Typically GO follows a biphasic course.

* Active phase generally lasts for 18–36 months, followed by a stable or inactive phase. It is therefore essential to differentiate
between the concepts of activity (refers to the inflammatory process) and severity (refers to the quality of life or the risk of vision
loss) 

*Pathogenesis of ophthalmopathy
Thyroid ophthalmopathy involves an organ-specific autoimmune reaction in which an antibody that reacts against thyroid gland
cells and orbital fibroblasts leads to inflammation of extraocular muscles, interstitial tissue, orbital fat and lacrimal glands
characterized by pleomorphic cellular infiltration, associated with increased secretion of glycosaminoglycans and osmotic
imbibition of water. There are an increase in the volume of the orbital contents, particularly the muscles, which can swell to eight
time their normal size.
There may be an elevation of intraorbital pressure and the optic nerve may be compressed. The degeneration of muscular fibers
can lead to fibrosis which exerts a tethering effect on the involved muscle, resulting in restrictive myopathy and diplopia.

   
Clinical features. The two most common signs of GO are upper eyelid retraction (90% of patients) and proptosis.
1. Soft tissue involvements
2. Lid retraction
3. Proptosis
4. Optic neuropathy
5. Restrictive myopathy
A commonly used classification foe severity of TED has been issued by European Group on Graves Orbitopathy( EUGOGO):
I. Sight – threatening due to optic nerve or corneal breakdown
II. Moderate-severe with one of moderate- severe soft tissue involvement, lid retraction of 2 mm or more,
diplopia and proptosis of 3 mm or more
III. Mild, with a minor impact on daily life.
1. Soft tissue involvement.
Symptoms: grittiness, red eye, lacrimations, photophobia, puffy lids and retrobulbar discomfort.
Sings may include:
Epibulbar hyperaemia – a sensitive sign of inflammatory activity
Periorbital swelling is caused by edema and infiltration behind the orbital septum; this may be associated with chemosis and
prolapse of retroseptal fat into the eyelid.
Tear insufficiency is common
Corneal signs can include punctate epithelial erosions, superior limbic keratoconjunctivitis, thinning and scaring.

2. Lid retraction.
Upper eyelid retraction is produced by levator/Müller muscle inflammation and fibrosis or by levator complex overaction
secondary to inferior rectus restriction (pseudo-lid retraction)
Retraction of upper and lower lid occurs in 90% of patients with Graves disease.
Symptoms: patients my complain of staring or bulging –eye appearance, difficulty closing the eye and ocular surface symptoms.

Sings
The upper lid margin normally rests 2 mm below the limbus. Lid retraction is suspected when the margin is either level or above
the superior limbus, allowing sclera to be visible.
The lower lid margin normally rests al the level of inferior limbus. Lid retraction may occur in isolation or in association with
proptosis.
Signs:
- Lid retraction in primary gaze,
- A staring and frightened appearance of the eyes which is particularly marked on attentive fixation
- Retarded descendent of the upper lid on the downgaze.

3. Proptosis
Proptosis is caused by expansion of the orbital fat and/or muscles. Also, the lacrimal gland is frequently involved and enlarged.
It is axial, unilateral or bilateral, symmetrical or asymmetrical, and frequently permanent. Severe proptosis may compromise lid
closure and along with lid retraction and tear disfunction can lead to exposure keratopathy, corneal ulceration and infections.

4. Restrictive myopathy
Up to 50% of patients with TED develop restrictive myopathy and it may be permanent. Ocular motility is restricted initially by
inflammatory edema, later by fibrosis.
Signs
Diplopia especially at near vision, and often discomfort in some position of gaze.
Optic neuropathy
Dysthyroid optic neuropathy (DON) is commonly caused by enlarged extraocular muscles at the orbital apex compressing the
optic nerve. Symptoms typically consist of desaturation of colors and blurring of central vision.
Visual acuity is usually reduced but not invariably.
Afferent pupil defect and optic disc edema are specific signs but are not always present.
Visual field defects can be central or paracentral.
This optic neuropathy is potentially reversible with appropriate treatment. It is more frequently developed by males, elderly, and
diabetic patients.
The optic disc may be normal, swollen or, rarely atrophic.
If the clinical features are sufficient, orbital imaging may not be necessary for diagnosis of GO.

Treatment
Treatment plan should be individually designed for each patient. An appropriate approach should be performed by a
multidisciplinary team of ophthalmologists, endocrinologists, radiologists, and orbital surgeons.
Any patient with symptoms or signs of orbitopathy in the high-risk group (elderly, male, diabetic, or smoker), positive family
history of orbitopathy, a recent history of progression, or any moderate inflammatory changes should be referred to the
ophthalmologist within a few weeks. Cases with reported color or central visual loss, progressive diplopia, rapid deterioration in
symptoms, or significant inflammatory scores should be urgently evaluated within a few days.

The first measure taken in all cases should be the cessation of smoking.
Thyroid disfunction should be managed adequately.
- Lubricants
- Topical anti- inflamatory agents
- Head elevation with 2-3 pillows during sleep to reduce periorbital edema
- Eyelid taping during the sleep may alleviate mild exposure keratopathy
- Systemic steroids are the mainstay of treatment for moderate and sever disease. Orbital steroid injections are
occasionally used to minimize systemic side effect.
- Alternatively, patients who are nonresponsive to corticosteroids may be treated with combination therapy of cyclosporin
A (5 mg/kg/day in 2 doses plus oral glucocorticoids), azathioprine, or specific monoclonal antibody agents.
- Low-dose fractionated radiotherapy may be used in addition with steroids or when steroids are contraindicated or
ineffective.

Surgical Treatment
- Once the disease has become inactive, several rehabilitative surgical procedures for patients with moderate to severe
ophthalmopathy may be used. Before offering surgery, patients should show evidence of disease quiescence over a
period of at least 6 months.
- Available procedures include orbital decompression for disfiguring proptosis; strabismus surgery for symptomatic
ocular motility restriction; eyelid recession for eyelid retraction causing lagophthalmos, exposure keratitis, and
disfigurement; and blepharoplasty for excessive soft tissue prominence of the eyelids

Orbital inflammations
Inflammatory processes of the orbit are favored by the abundance of fatty tissue, the proximity of the sinuses of the face, which is
easily infected, the communications of the orbit with neighboring structures (dental cavity, ear)
Etiopathogenesis

Inflammations of the orbit can occur:

- primary, from a wound at the level of the eyebrow region, penetrating eyelid wound, orbital wound with or without foreign
body, insect bites.
- secondary, by spreading a proximity infection or metastatically in general infectious diseases.
Proximity infections:
- sinusitis (frontal, maxillary, ethmoidal) In these cases, the infection is spread by contiguity, by lymphatic or venous route,
- dental diseases - the path of propagation is direct, lymphatic, venous, arterial (cold granulomas)
- otic disorders – middle ear, venous spread
- facial infections: boil, erysipelas, superinfected hordeolum, spread by lymphatic or blood
- intracranial infections: meningitis, brain abscess, when the propagation is direct bone, retrograde venous from the cavernous
sinus or through the perineural sheaths
- infections located inside the orbit: panophthalmia (inflammation of the eyeball), acute dacryocystitis, suppurative dacrioadenitis
(inflammation of the lacrimal gland), suppurative conjunctivitis.

General infectious diseases

In these cases, the infection spreads to the orbit through the bloodstream.
Examples: infections of upper respiratory tract ostomyelitis, sepsis, pyocyanin infection, pneumonia.
The most common pathological agents are: streptococcus, staphylococcus, pneumococcus.

Orbital cellulitis is an infection of the soft tissues and fat that hold the eye in its socket. This condition causes uncomfortable or
painful symptoms.

 
Preseptal cellulitis
Preseptal cellulitis is an infection of the subcutaneous tissues anterior to the orbital septum. It is considerably more common than
orbital cellulitis but rapid progression to the orbital cellulitis may occur.
Microorganism typically responsive are Staphylococcus aureus and Streptococcus pyogenes.
Diagnosis
The disease manifests with swollen, tender red eyelid that may be very severe.
Proptosis and chemosis are absent and Visual acuity, pupillary reflexand ocular motility are impaired. The patient is often
pyrexial.

Preseptal cellulitis

Orbital cellulitis
It’s not contagious, and anyone can develop the condition. However, it most commonly affects young children.
Orbital cellulitis is a potentially dangerous condition. When left untreated, it can lead to blindness, or serious or life-threatening
conditions.
Staphyloccocus aureus, Streptoccocul pyogenes, Streptoccocus pneumonia, Haemophylus influenzae are common causative
organism with infections originating typically from the paranasal ( especially ethmoid) sinuses.
Infections may spread from preseptal cellulitis and other sources mentioned above.

Symptomms consists of rapid onset of pain exacerbated by eye movements, swelling of the eye, malaise, and frequently visual
impairement and double vision. There is commonly recent history of nasal, sinus or respiratory symptoms,  a tooth infection or a
bacterial infection occurring anywhere in the body.

Sings
Pyrexia, often marked,
VA loss or impaired vision,
Pain in or around the eye,
Tender, firm, erythematous and warm eyelids, with chemosis and periocular edema, sometimes conjunctival haemorrhage,
Proptosis often obscured by lid swelling,
Painful ophthalmoplegia
Differential diagnosis
Infective dacryoadenitis, Cavernous sinus thrombosis, Carotid-cavernous fistula,
Rapidly progressive retinoblastoma in children, lacrimal gland tumor, metastatic lesions with inflammation, leukemia, Orbital
myositis, sarcoidosis, scleritis, etc…

Complications
- Ocular complications: optic neuropathy, exposure keratopathy, raised IOP, endophtalmitis and occlusion of the cental retinal
vein or artery.
- Subperiosteal abscess, most frequently located along the medial wall of the orbit.
- Intracranial complication uncommon but extremely serious, include meningitis, brain abscess and cavernous sinus thrombosis.
Investigtions
High-resolution CT of the orbit, sinuses and brain is vital to confirm the diagnosis and exclude a subperiosteal or intracranian
abscess.

Treatment
Hospital admission with urgent otolaryngological assessment and frequent ophthalmic review; delineation of the extent of
erythema of the skin usig an surgical marker.
Antibiotics are given intravenously ( cephalosporins), supplements by oral metronidazole to cover anaerobes. Intravenous
antibiotics should be continued until the patient has been apyrexial for 4 days, followed by 1-3 weeks of oral treatment.

Monitoring the optic nerve function is performed at least every 4 hours initially by testing VA, colour vision, light brightness
appreciation and pupillary reactions. Deterioration should promt the consideration of surgical intervention.
Surgery
Drenaige of an orbital abscess should be considered at an early stage.
An emergency lateral canthotomy shoud be considered in severe optic nerve compression.

Idiopathic orbital inflammation (IOI), also known as orbital pseudotumor and non-specific orbital inflammation, is an

idiopathic inflammatory condition that most commonly involves the extraocular muscles.
The exact etiology is not known but an association with many inflammatory/autoimmune diseases is reported.
Clinical presentation
Patients typically present with rapid-onset, usually unilateral (~90% of cases), painful proptosis and diplopia. Idiopathic orbital
inflammation is a diagnosis of exclusion; atypical presentation, poor response to treatment with corticosteroid and recurrence
should prompt biopsy to exclude other diseases. Pathology
Histologically acute lesions demonstrate lymphocytes (which can be mistaken for orbital lymphoma), plasma cells, and giant cell
infiltration.

 
Classification
Division into a number of subgroups according to location has been proposed:
1. lacrimal pseudotumor (dacryoadenitis)
2. anterior pseudotumor: in the fat immediately behind the globe
3. posterior pseudotumor: in the fat at the orbital apex but the cavernous sinus is spared
4. myositic pseudotumor (myositis): predominantly involve the EOMs and therefore mimic thyroid-associated orbitopathy
(TAO) but unlike TAO it also involves the tendons,
5. optic perineuritis: involvement of the optic nerve sheath
6. diffuse pseudotumor: affecting multiple compartments
The condition has been associated with other inflammatory and autoimmune conditions:

Radiographic features
*Imaging demonstrates enlargement of the muscle belly of one (or more) extraocular muscles typically with the involvement of
their tendinous insertions. Involvement of the tendinous insertion distinguishes it from thyroid-associated orbitopathy (TAO) in
which the insertion point is spared. .
Additional inflammation can be seen in surrounding tissues, including the orbital fat, lacrimal gland, and optic nerve sheath.
It can appear as an infiltrative mass and extends outside of the orbit via superior or inferior orbital fissures. Extension into
the cavernous sinus, meninges, and dura can occur. It is most commonly unilateral but can be bilateral in 25% of cases.

Treatment
Most cases resolve rapidly with treatment (usually corticosteroids suffice) although in a subset with more chronic progression
chemotherapy and radiotherapy may be required.
Differential diagnosis
One of the main differential diagnoses of idiopathic orbital inflammation is orbital lymphoma. There is considerable overlap
between these entities both clinically and radiologically. However, orbital lymphoma usually presents as a progressive orbitopathy
rather than acutely, is more often bilateral, and does not respond to corticosteroid.
Other imaging differential considerations include:
 orbital cellulitis: usually associated with an adjacent sinusitis or with a previous history of trauma/dental procedure 
 thyroid-associated orbitopathy (TAO): spares the tendinous insertions and not usually painful
 Tolosa-Hunt syndrome: related condition with the involvement of the cranial nerves in the cavernous sinus and resulting
ophthalmoplegia
 orbital sarcoidosis, orbital metastases, orbital rhabdomyosarcoma

Non-neoplastic vascular abnormalities

Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous
sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the
heart. This is a rare disorder and most commonly the form is of septic cavernous sinus thrombosis.
The cause is usually from a spreading infection in the nose, sinuses, orbital or preseptal
cellulitis,ears, or teeth. Staphylococcus aureus and Streptococcus are often the associated bacteria.
Features are of a rapid onset and may include severe headache, malaise, nausea and vomiting.
Cavernous sinus thrombosis symptoms include: unilateral or often bilateral congestion of facial,
conjunctival and retinal vein, decrease or loss of vision, chemosis, exophthalmos, and paralysis of
the cranial nerves which course through the cavernous sinus ( the third to sixth cranial nerves). This
infection is life-threatening and requires immediate treatment, which usually
includes antibiotics and sometimes surgical drainage. Aseptic cavernous sinus thrombosis is usually
associated with trauma, dehydration, anemia, and other disorders.
Treatment consist of intravenous antibiotics and sometimes surgical drainage.
 

Examination of the orbit

Ophthalmology Course no 4 .The lacrimal System. Conjunctiva 

I. THE DISEASES OF THE LACRIMAL SYSTEM 
The lacrimal system is made up of a secretory system, which produces tears, and an excretory system, which drains the tears. 
The  secretory system consists of the main lacrimal glands and the accessory lacrimal glands The lacrimal glands, which secretes
the tears, and its excretory ducts, which convey the fluid to the surface of the human eye  are paired exocrine glands, one for
each eye that secrete the aqueous layer of the tear film. It provises the reflex secretion stimulated by retinal illumination;
disappears at night and in extended darkness.
 The lacrimal glands are situated in the upper lateral region of each orbit, in the lacrimal fossa of the orbit formed by the frontal
bone.

 The lacrimal gland produces tears which are secreted by the lacrimal ducts, and flow over the ocular surface, and then into canals
that connect to the lacrimal sac. From that sac, the tears drain through the lacrimal duct into the nose. 
The gland has two sections, a palpebral lobe and an orbital lobe. 
The palpebral lobe lies close to the eye, along the inner surface of the eyelid; if the upper eyelid is everted, the palpebral
portion can be seen. 
The orbital lobe of the gland, contains fine interlobular ducts that connect the orbital lobe and the palpebral lobe.
Tears secreted collect in the fornix conjunctiva of the upper lid, and pass over the eye surface to the lacrimal puncta, small
holes found at the inner corner of the eyelids. These pass the tears through the lacrimal canaliculi on to the lacrimal sac, in turn to
the nasolacrimal duct.  

Exposure of the palpebral portion of the right lacrimal gland using a Desmarres retractor.

 
Nerve supply :
The lacrimal gland is innervated by the lacrimal nerve, which is the smallest branch of the ophthalmic nerve,
itself a branch of the trigeminal nerve (CN V). After the lacrimal nerve branches from the ophthalmic nerve it
receives a communicating branch from the zygomatic nerve.  
The parasympathetic innervation to the lacrimal gland increases the secretion of lacrimal fluid from the
lacrimal gland.  
The accessory tear glands provide basal tear secretion,  a permanent secretion. 
tears spread to the conjunctiva and cornea by blinking. 
Lacrimal fluid acts to the clean, nourish and lubricate the eyes. It
forms tears when produced in excess. 
 
 
The excretory system 
The lacrimal apparatus is the system responsible for the drainage
of lacrimal fluid from the orbit. 
After secretion, lacrimal fluid circulates across the eye, and
accumulates in the lacrimal lake – located in the medial canthus of
the eye. From here, it drains into the lacrimal sac via the upper and
lower  lacrimal canaliculi. 
The lacrimal sac is the dilated end of the nasolacrimal duct, and is
located in a groove formed by the lacrimal bone and frontal
process of the maxilla. Lacrimal fluid drains down the

nasolacrimal duct and empties into the inferior meatus of the nasal cavity.  

II. Diseases of the secretory system 

1. Dacryoadenitis refers to inflammation of the lacrimal gland and may be unilateral or bilateral. 
Lacrimal gland inflammation can be acute or chronic.  
Acute dacryoadenitis are frequently infectious and are typically unilateral. Infection most commonly ascends from the
conjunctiva, but also may be from the skin, penetrating trauma, or in bacteremia. The most common etiology for dacryoadenitis is
viral infection, with Epstein-Barr virus being the most common viral cause. Less common viral causes include adenovirus,
varicella zoster, herpes simplex, rhinovirus, cytomegalovirus or mumps.  
Bacterial forms tend to induce suppuration; the most common bacterial pathogen is Staphylococcus aureus.  

Picture: a): right upper lid swelling localized to lacrimal gland fossa – Sshaped ptosis. The swelling was
painless. 1(b): salmon patch appearance of conjunctiva. 1(c): MRI image showing soft tissue mass originating
from right lacrimal gland, extending around the lateral rectus muscle into extraconal space.
1(d): Histopathology (H&E stain). Low magnification: conjunctival infiltration  (long arrow) and dense
inflammatory aggregates in stroma (short arrows).

Chronic infectious dacryoadenitis is uncommon, with most cases attributed to Mycobacterium tuberculosis. 

1.1.Chronic inflammatory dacryoadenitis  are non-specific orbital inflammation , IG G4-related

disease,  Sjogren syndrome, sarcoidosis, Crohn disease, and granulomatosis with polyangiitis, neoplastic causes,
etc...  
A large portion of inflammatory cases remains idiopathic (=relating to or denoting any disease or
condition which arises spontaneously or for which the cause is unknown)  

Diagnosis 
Signs of dacryoadenitis include tenderness, edema, or erythema overlying the superolateral orbit, conjunctivitis with or without
chemosis, regional lymphadenopathy, proptosis of the globe.
Fever and malaise may be present. 

1.2. Acute dacryoadenitis frequently presents with erythema and tenderness over the superotemporal orbit, with enlargement
of the gland causing the lateral portion of the eyelid to fall, creating a characteristic S-shaped curve of the eyelid margin. There
can also be associated suppurative discharge from lacrimal ducts and pouting of the lacrimal ductules.  Inflammatory causes of
dacryoadenitis may present subacutely with typically painless swelling of the lacrimal glands and may be bilateral. 
 
Symptoms 
Symptoms of dacryoadenitis include pain in the superolateral orbit, pain with eye movements, ptosis or difficulty opening the
affected eye, redness of the eye, and possibly diplopia. 

Diagnostic procedures 
A contrast-enhanced computed tomography (CT) scan of the orbits will typically demonstrate enlargement of the affected lacrimal
gland with enhancement. 
If sarcoidosis is suspected, a chest radiograph is a screening tool to evaluate for lymphadenopathy or pulmonary disease. 

Medical therapy 
Depending on the severity of the presentation, therapy could range from warm compresses to  treatment of bacterial infection,
with or without the addition of systemic steroids. 
 
Close follow up is made to detect optic nerve involvemen, if there are  signs including decreased visual acuity, pain with eye
movements, relative afferent pupillary defect, or abnormal color vision. 
Acute viral dacryoadenitis is typically self-resolving within 4 to 6 weeks. The benefit of oral antiviral medications is uncertain.
Bacterial dacryoadenitis requires systemic antibiotic therapy. When purulence is present, obtaining cultures of the discharge can
guide antibiotic therapy. Abscess formation may necessitate surgical drainage. 
Corticosteroids will induce decrease in volume of an enlarged lacrimal gland from almost all sources of dacryoadenitis. 
Refractory cases of inflammatory dacryoadenitis may benefit from orbital radiotherapy, methotrexate, or rituximab.  
In patients with dacryoadenitis who respond to treatment but the lacrimal mass does not resolve by 3 months, a lacrimal gland
biopsy after appropriate scanning is necessary. 

Differential Diagnosis 
When focal swelling of the lacrimal gland is present, particularly in an older patient with an indolent course, it is important to
exclude malignancy.  
1.Thyroid eye disease (TED) may sometimes resemble dacryoadenitis, presenting with diplopia from restrictive inflammation of
the extraocular muscles. Typically, TED results in lid retraction rather than mild ptosis as is seen in dacryoadenitis. 
2. Other infectious conditions that can cause periorbital swelling, erythema, and pain must be considered, such as preseptal or
orbital cellulitis. Focal swelling of the upper eyelid may be due to chalazion or hordeolum, neither of which is associated with true
lacrimal gland enlargement. 

Complications 
Complications from infectious dacryoadenitis are rare; a lacrimal gland abscess may develop, or the infection may lead
to preseptal or orbital cellulitis. 
Tumors of the lacrimal gland - see the chapter on the orbit 

 
3. Dry eyes syndrome  : The tear film is important for good vision. 
The tear film is made of three layers: 
1.An oily layer : The oily layer is the outside of the tear film. It makes the tear surface smooth and keeps tears from drying up
too quickly. This layer is made in the eye’s meibomian glands. 

2. A watery layer : The watery layer is the middle of the tear film. It makes up most of the tears. This layer cleans the eye,
washing away particles that do not belong in the eye. This layer comes from the lacrimal glands in the eyelids. 

3. A mucus layer :The mucus layer is the inner layer of the tear film. This helps spread the watery layer over the eye’s surface,
keeping it moist. Without mucus, tears would not stick to the eye. Mucus is made in the conjunctiva. This is the clear tissue
covering the white of the eye and inside the eyelids. 

Normally, the eyes constantly make tears to stay moist. If the eyes are irritated, or while crying, the eyes make a lot of tears. Dry
eye occurs when either the eye does not produce enough tears or when the tears evaporate too quickly. 
The dry eyes occurs also when  something affects one or more layers of the tear film.  

*Dry eye syndrome (DES), also known as keratoconjunctivitis sicca (KCS), is the condition of having dry eyes. 

Dry Eye Symptoms : Typical symptoms of dry eye syndrome are dryness, burning and a sandy-gritty eye irritation that gets
worse as the day goes on 
Blurred vision, especially when reading 
Symptoms are worsened by activities in which the rate of blinking is reduced due to prolonged use of the eyes. These
activities include prolonged reading, computer usage, driving, or watching television. Symptoms increase in windy, dusty
or smoky  areas, in dry environments high altitudes including airplanes, on days with low humidity, and in areas where an air
conditioner. 
  Symptoms reduce during cool, rainy, or foggy weather and in humid places. 
There is a scratchy or gritty feeling like something is in the eye. 
There are strings of mucus in or around the eyes. It is painful to wear contact lenses. 

In the onset phase, there may be excessive tearing. 

Dry eye syndrome can occur at any age, and in people who are otherwise healthy. It is more common with older age, when the
individual produces fewer tears. It is also more common in women than in men. 
It is more common in  malnutrition results in a vitamin A deficiency. 

This can result from contact lens use, meibomian gland dysfunction, pregnancy, Sjögren syndrome (an autoimmune disease that
affects lacrimal and salivary glands) , vitamin A deficiency, LASIK surgery, and certain medications such as antihistamines, some
blood pressure medication, hormone replacement therapy, and antidepressants. Chronic conjunctivitis such as from tobacco
smoke exposure or infection may also lead to the condition. 
Diagnosis is mostly based on the symptoms and Schirmer tests. 
Treatment depends on the underlying cause. Artificial tears are the usual first line treatment. Stopping or changing certain
medications may help. The medication ciclosporin or steroid eye drops may be used in severe cases( for exemple Sjögren
Syndrome). Another option is lacrimal plugs that prevent tears from draining from the surface of the eye. 
If the condition is left untreated or becomes severe, it can produce complications that can cause eye damage, resulting in impaired
vision by affecting the cornea. 

4. Dacryocystitis is an infection or inflammation of the nasolacrimal sac, usually accompanied by blockage of the nasolacrimal
duct. Dacryocystitis can be acute or chronic and congenital or acquired.
When present, medial canthal swelling of dacryocystitis is usually located below the medial canthal tendon. Pain, swelling,
redness over the lacrimal sac at medial canthus Tearing, crusting, fever 
Digital pressure over the lacrimal sac may extrude pus through the punctum 

acute:
Chronic:

In chronic cases, tearing may be the only symptom 

Initial treatment is with warm compresses and oral antibiotics for mild or severe cases. The antibiotic is usually a 1st-generation
cephalosporin or penicillinase-resistant synthetic penicillin. If the infection does not respond as expected, consideration should be
given to methicillin-resistant Staphylococcus aureus (MRSA), and antibiotics changed accordingly. The abscess can be drained
and the antibiotics can be changed based on culture results if the initial antibiotic proves ineffective. 
Patients with chronic dacryocystitis usually present with a mass under the medial canthal tendon and chronic conjunctivitis.
Definitive treatment for resolved acute dacryocystitis or chronic conjunctivitis is usually surgery that creates a passage between
the lacrimal sac and the nasal cavity (dacryocystorhinostomy). 

 III. THE DISEASES OF CONJUNCTIVA 

Anatomy:
The conjunctiva  is a fine, translucent mucous membrane that lines the inside of the eyelids and covers the sclera. 
It covers the posterior surface of the lids and reflects to cover the anterior part of the sclera, then becomes continuous with the
corneal epithelium. At the lidmargin conjunctiva is continuous with the skin. 
It is highly vascularized. 

The conjunctiva can be divided into three regions:

1.the palpebral or tarsal conjunctiva: . The palpebral conjunctiva lines the eyelids
2.the bulbar or ocular conjunctiva: The bulbar conjunctiva is divided into scleral and limbal parts.  
3. conjunctival fornices (fornix). : are divided into the superior, inferior, lateral, and medial regions.

The conjunctiva has an average thickness of 33 microns. 

Conjunctiva of the Fornix: It is fold lining the cul-de-sac formed by conjunctiva covering the posterior surface of the lids to the
conjunctiva covering the anterior surface of the globe. The conjunctiva here is comparatively thicker and loosely attached in order
to allow free movement of the globe. 
The medial fornix is the shallowest and contains the caruncle and the plica semilunaris. 
The plica semilunaris is a small fold of bulbar conjunctiva on the medial canthus of the eye. It functions during movement of the
eye, to help maintain tear drainage. The plica semilunaris and lacrimal caruncle have a role of purifying stations  located upstream
of the drainage of tears. 
The lacrimal caruncle, or caruncula lacrimalis, is the small, pink, globular nodule at the inner corner (the medial canthus) of the
eye. It is made of skin covering sebaceous and sweat glands.  
 
 
Inflammatory pathology 
1.Conjunctivitis  
Conjunctivitis can be divided into infectious and noninfectious causes.  
Viruses and bacteria are the most common infectious causes.  

1.1Noninfectious conjunctivitis includes allergic, toxic, and cicatricial conjunctivitis, as well as inflammation secondary
to autoimmune diseases and neoplastic processes. 
 The disease can also be classified into acute, hyperacute, and chronic according to the mode of onset and the severity of the
clinical response.  
 
Subjective symptoms are: foreign body sensation, stinging or burning under the eyelids. 
Objective signs are common to inflammation of any mucosa: hyperemia, conjunctival secretion, tearing, papillary hypertrophy,
follicles, the presence of membranes or pseudomembranes, chemosis. 

Some conjunctivitis are accompanied by preauricular or submandibular adenopathy 

 Follicles and papillae are seen in palpebral part of conjunctiva. The palpebral conjunctiva is an area where reactive
pathology of the conjunctiva may be seen clinically. There are two types of changes that can occur in this region:
follicle formation and papilla formation. 
Follicles are thought to be identical to lymphoid follicles found elsewhere in the body. Follicle formation is characteristic of viral
and chlamydial infections as well as toxic conjunctivitis due to the application of certain topical medications.  
Papillae are composed of chronic inflammatory cells such as lymphocytes and plasma cells and are distinguished from follicles
by the presence of blood vessels at their center. Giant papillae are found in certain allergic diseases (e.g., vernal catarrh) and after
long-term use of contact lenses, ocular  prostheses, and cosmetic shells. 

1.2 Conjunctival hiperaemia 
Conjunctival injection or hyperemia is a nonspecific response with enlargement of conjunctival vessels induced by various
diseases. Conjunctival injection is an important diagnostic clue for infection or inflammation and can be utilized for the
monitoring of the disease progression and response to treatment. 
Superficial hyperemia of conjunctival inflammatory cause predominates on the palpebral conjunctiva and sac bottoms and
attenuates as it approaches the bulbar conjunctiva and the sclerocorneal limbus. 
Deep or perikeratic hyperemia predominates in the immediate vicinity of the sclerocorneal limbus. It may appear in isolation as a
dark red perilimbic ring or may be associated with superficial hyperemia. 

2. Bacterial conjunctivitis  
2.1 Acute conjunctivitis can be caused by numerous bacteria. Symptoms are hyperemia,
lacrimation, irritation, and discharge. Diagnosis is clinical. 
Bacterial conjunctivitis is usually caused by Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus species, or, less
commonly, Chlamydia trachomatis. Neisseria gonorrhoeae causes gonococcal conjunctivitis, which usually results from sexual
contact with a person who has a genital infection. 

2.2 Ophthalmia neonatorum (neonatal conjunctivitis) results from a maternal gonococcal and/or chlamydial infection.
Neonatal conjunctivitis occurs in neonates delivered through an infected birth canal.  These organisms may be spread from hand
to eye contact or through adjacent mucosal tissues colonization such as nasal or sinus mucosa. 
Neonatal conjunctivitis is watery or purulent ocular drainage due to a chemical irritant or a pathogenic organism.
Prevention with antigonococcal topical treatment at birth is routine.
The major causes of neonatal conjunctivitis (in decreasing order) are
-Ethiology 
-Bacterial infection
-Chemical inflammation
-Viral infection
Infection is acquired from infected mothers during passage through the birth canal. Chlamydial ophthalmia (caused by
Chlamydia trachomatis) is the most common bacterial cause. Gonococcal ophthalmia (conjunctivitis due to
Neisseria gonorrhoeae) accounts less then 1% of cases.
Chemical conjunctivitis is usually secondary to the instillation of topical therapy for ocular prophylaxis.
Conjunctivae are injected, and discharge (watery or purulent) is present.

Symptomatology 
Chemical conjunctivitis secondary to topical prophylaxis usually appears within 6 to 8 hours after instillation and
disappears spontaneously within 48 to 96 hours.
Chlamydial ophthalmia usually occurs 5 to 14 days after birth. It may range from mild conjunctivitis with
minimal mucopurulent discharge to severe eyelid edema with copious drainage and pseudomembrane formation. Follicles
are not present in the conjunctiva, as they are in older children and adults. 
Gonococcal ophthalmia causes an acute purulent conjunctivitis that appears 2 to 5 days after birth or earlier with
premature rupture of membranes. The neonate has severe eyelid edema followed by chemosis and a profuse purulent
exudate that may be under pressure. If untreated, corneal ulcerations and blindness may occur.

Laboratory diagnosis: Testing of conjunctival material for pathogens including gonorrhea, chlamydia, and,

sometimes, herpes.
Treatment :Systemic, topical, or combined antimicrobial therapy

Risk Factors (bacterial conjunctivis):

-Poor hygenic habits may increase the risk of infection  
- Poor contact lens hygiene 
-Contaminated cosmetics 
- Crowded living or social conditions such elementary schools 
- Ocular diseases including dry eye, blepharitis 
- Recent ocular surgery, or ocular foreign bodies 
- Chronic use of topical medications 
- Immune compromise 

Symptoms are typically, red eye unilateral but frequently spread to the opposite eye within a few days. Discharge is typically
purulent. 
Patients may complain of redness, discharge, crusting and sticking or gluing of the eyelids upon waking, blurry vision, light
sensitivity, irritation discomfort intolerance to contact lens.  
Almost all cases of acute bacterial conjunctivitis are self-limited and will clear within 10 days without treatment. 
Antibiotic treatment has been shown to decrease the duration of symptoms and speed the eradication of microorganisms from
the conjunctival surface. 
If neither gonococcal nor chlamydial infection is suspected, moxifloxacin 0.5% drops 3 times a day for 7 to 10 days or another
fluoroquinolone are used. 

A poor clinical response after 2 or 3 days indicates that the cause is resistant bacteria, a virus, or an allergy.  
Bacterial conjunctivitis are very contagious 
-Patients should be advised to Use hand sanitizer and/or wash their hands thoroughly after touching their eyes or nasal
secretions . Avoid touching the noninfected eye after touching the infected eye 
Avoid sharing towels or pillows . Avoid swimming in pools 
To avoid transmitting infection, physicians must:
-Use hand sanitizer or wash their hands properly (fully lather hands, scrub hands for at least 20 seconds, rinse well, and turn off
the water using a paper towel) 
-Disinfect equipment after examining patients 

2.3 Adult inclusion conjunctivitis is caused by sexually transmitted Chlamydia trachomatis.

Symptoms include chronic unilateral hyperemia and mucopurulent discharge. Adult inclusion conjunctivitis is caused by
Chlamydia trachomatis and,  in most instances, adult inclusion conjunctivitis results from sexual contact with a person who has a
genital infection. 
The disease has an incubation period of 2 to 19 days.
Most patients have a unilateral mucopurulent discharge.
The tarsal conjunctiva is often more hyperemic than the bulbar conjunctiva. Characteristically, there is a marked tarsal follicular
response. Occasionally, superior corneal opacities and vascularization occur. Preauricular lymph nodes may be swollen on the
side of the involved eye. Often, symptoms have been present for many weeks or months and have not responded to topical
antibiotics. 

Diagnosis :Clinical evaluation , Laboratory testing ,Chronicity (symptoms for > 3 weeks), mucopurulent discharge, marked tarsal
follicular response, and failure of topical antibiotics differentiate adult inclusion conjunctivitis from other bacterial
conjunctivitis. Smears and conjunctival scrapings should be examined microscopically  to identify bacteria. 

Treatment  
Azithromycin 1 g orally once only or either doxycycline 100 mg orally twice a day or erythromycin 500 mg orally 4 times a day
for 1 week cures the conjunctivitis and concomitant genital infection. Sex partners also require treatment.  

 
2.4 Hyperacute bacterial conjunctivitis presents with a severe copious purulent discharge and decreased vision . There is often
accompanying eyelid swelling, eye pain on palpation, and preauricular adenopathy. It is often caused by Neisseria gonorrhoeae
and carries a high risk for corneal involvement and subsequent corneal perforation and blindness. Treatment for hyperacute
conjunctivitis secondary to N gonorrhoeae consists of intramuscular ceftriaxone. 

3. Viral conjunctivitis 
Viruses cause up to 80% of all cases of acute conjunctivitis. Many cases are misdiagnosed as bacterial conjunctivitis. Between
65% and 90% of cases of viral conjunctivitis are caused by adenoviruses, and they produce 2 of the common clinical entities
associated with viral conjunctivitis, pharyngoconjunctival fever and  epidemic keratoconjunctivitis. 

  3.1Pharyngoconjunctival fever is characterized by abrupt onset of high fever, pharyngitis, and bilateral conjunctivitis, and by
periauricular lymph node enlargement. 
 
3.2 Epidemic keratoconjunctivitis is more severe and presents with watery discharge, hyperemia, chemosis, and ipsilateral
lymphadenopathy. Lymphadenopathy  is more prevalent in viral conjunctivitis compared with bacterial conjunctivitis. 
Other viruses that can be responsible for conjunctival infection include herpes simplex virus (HSV), varicella-zoster virus (VZV),
picornavirus (enterovirus , Coxsackie), poxvirus (molluscum contagiosum, vaccinia), and human immunodeficiency virus (HIV). 

3.3 Viral conjunctivitis secondary to adenoviruses is highly contagious. The virus spreads through direct contact via
contaminated fingers, medical instruments, swimming pool water. 
Symptomatology 
After an incubation period of about 5 to 12 days, conjunctival hyperemia, watery discharge, and ocular irritation usually begin in
one eye and spread rapidly to the other. Follicles may be present on the palpebral conjunctiva. A preauricular lymph node is often
enlarged and painful. Many patients have had contact with someone with conjunctivitis, a recent upper respiratory infection, or
both. 
 
3.4 In severe adenoviral conjunctivitis, patients may have photophobia and foreign body sensation due to corneal involvement.
Chemosis may be present. Pseudomembranes of fibrin and inflammatory cells on the tarsal conjunctiva, focal corneal
inflammation, or both may blur vision. Even after conjunctivitis has resolved, residual corneal subepithelial opacities (multiple,
coin-shaped, 0.5 to 1.0 mm in diameter) may be visible with a slit lamp for up to 2 years. Corneal opacities occasionally result in
decreased vision and significant halos. 
No effective treatment exists, artificial tears, topical antihistamines, or cold compresses may be useful in alleviating some of
the symptoms Available antiviral medications are not useful and topical antibiotics are not indicated. 

Picture: adenoviral conjunctivitis with conjunctival hyperaemia and significant pseudomembranes.: Adenoviral

conjunctivitis with conjunctival hyperaemia and significant pseudomembranes. Pseudomembranes can
be distinguished from true membranes as they do not bleed when removed. Both forms of membranes must
be gently removed by everting the eyelids and using either a cotton-tipped applicator or some sterile
forceps to help prevent tarsal scarring and relieve discomfort.

 
picture 2: Adenoviral conjunctivitis scar verted upper eyelid showing tarsal scarring in a patient with
a history of membranous adenoviral conjunctivitis. This patient did not have the membranes removed

during the acute episode.  

4. Allergic conjunctivitis 
Allergic conjunctivitis is an inflammatory response of the conjunctiva to an allergen. It is part of a larger systemic atopic reaction
and is usually seasonal with associated upper respiratory tract symptoms and complaints of redness and swelling of the
conjunctiva with severe itching and increased lacrimation. Presence of rhinitis often terms this process as allergic
rhinoconjunctivitis. 

Classification 
1.Vernal - of, or appropriate to spring 
2. Atopic - denoting a form of allergy or hypersensitivity reaction 
3. Perennial - chronic, year round 
4. Allergic conjunctivitis without involvement of the cornea: 
 1.acute allergic conjunctivitis 
2. seasonal allergic conjunctivitis (SAC) 
 3. perennial allergic conjunctivitis Symptoms occurring throughout all seasons (PAC) 
5.with involvement of the cornea: 
1. Vernal keratoconjunctivitis (VKC) 
2. Atopic keratoconjunctivitis (AKC) 
3. Giant papillary conjunctivitis 
This is not a true ocular allergy but rather an repetitive mechanical irritation, often in due to contact lenses, that is aggravated by
concomitant allergy. 

Signs and Symptoms 

Itching is the primary symptom where patients are constantly rubbing their eyes with temporary relief. The eyelids and
conjunctiva become edematous and diffusely hyperemic. Presentation is most often bilateral, due to the systemic nature of the
disease 
 
4.4.2 Seasonal/Perennial conjunctivitis 
Bilateral conjunctival injection, chemosis, watery discharge, and mild mucous discharge. 
Recur seasonally with the changes in pollens and allergens present.  Minimal or local inflammation often resolves and remits. 

4.5.1. Vernal keratoconjunctivitis (VKC) 

Bilateral bulbar conjunctival injection with associated watery and mucoid discharge. Patients develop a giant
papillary hypertrophy of only the superior tarsal conjunctiva, resembling “cobblestones”.   
Corneal involvements: limbal dots  that are small white-yellow chalky concretions around the corneal limbus;
corneal vernal plaques; or shield shaped ulcers of the cornea. he onset of symptomatology begins in childhood
and peaks at about 11-13 with acute exacerbations occurring more frequently during the spring and summer
months. Commonly the symptoms decreased ranging from 2-30 years of age. 
Untreated VKC can lead to eyelid thickening that ultimately leads to ptosis. Severe corneal involvement can
cause corneal neovascularization, thinning, ulceration, and infection. This can lead to vision loss. Conjunctival
scarring can also occur. 
 
4.5.2 Atopic keratoconjunctivits (AKC) 
Bilateral conjunctival injection with associated eczematoid belpharitis, watery/mucoid discharge, and boggy edema. Papillary
hypertrophy of superior or inferior tarsal conjunctival can occur with increased risk for eyelid thickening and scarring. In more
severe and untreated cases, patients can develop loss of eyelashes, conjunctival scarring, corneal neovascularization, ulcers or
scars, punctate epithelial keratitis. 
Similar to VKC, the onset of symptoms occurs during childhood but peaks during young adult and continues into the fifth decade
of life. The course remains chronic with periodic acute exacerbations.  
The  sequelae are similar to VKC with eyelid thickening or tightening. Conjunctival scarring can occur and involvement of the
cornea can lead to scarring, neovascularization, thinning, ulceration and infection. This can also develop into keratoconus or cause
vision loss. There can also be anterior or posterior subcapsular cataracts. 

4.5.3 Giant papillary conjunctivitis (GPC) 

The laterality of symptoms is associated with contact lens, or prostheses wear pattern. Most
notably, patients will have papillary hypertrophy of the superior tarsal conjunctiva. In long-
standing, untreated disease, the papillae will develop white fibrotic centers. In severe cases,
patients will have lid swelling and ptosis.  
This disease process is directly correlated with presence of risk factors.If left untreated,
GPC can cause acquired ptosis. 

Treatment 
Some additional measures can be used as adjunctive measures to improve symptom
management are as follows: 
-Artificial tears to dilute allergens 
-Cool compresses / ice packs 
-Avoid Allergens 
-Frequent clothes washing and bathing/showering before bedtime 
-Refer/consult allergy or dermatology for those who are not adequately controlled with topical medications and oral
antihistamines 
-Topical drops: antihistamines, Mast cell stabilizers, brief course of low-potency and low-frequency topical corticosteroids 
-In VKC and AKC, another adjunctive therapy is addition of topical cyclosporin 2%. If the VKC or AKC is not responsive to
topical therapy, supratarsal injection of corticosteroid can be considered. 
 
How to Differentiate Conjunctivitis of Different Origins 
History and Physical Examination 
Focused ocular examination and history are crucial for making appropriate decisions about the treatment and management of any
eye condition, including conjunctivitis. Eye discharge type and ocular symptoms can be used to determine the cause of the
conjunctivitis. 
*For example, a purulent or mucopurulent discharge is often due to bacterial conjunctivitis , whereas a watery discharge is more
characteristic of viral conjunctivitis; itching is also associated with allergic conjunctivitis. 
Bacterial vs. Viral:  a. bacterial, b. hyperacute bacterial conjuctivis, 3. Viral complications

 
5. Subconjunctival hemorrhage occurs when one or more blood spots appear on the white of the eye. The eye’s conjunctiva
contains a lot of tiny blood vessels that can break. If they break, blood leaks between the conjunctiva and sclera. This bleeding . 
These blood spots can look scary. But a subconjunctival hemorrhage is usually harmless and often heals on its own. 
Coughing, sneezing, straining, or other similar actions most commonly cause subconjunctival hemorrhages. This is because they
briefly raise blood pressure in the veins. That quick pressure rise can cause capillaries to break. 
Trauma to the eye can also cause subconjunctival hemorrhage. Even rubbing the eyes too hard might cause capillaries to break. 
Less common causes of subconjunctival hemorrhage include: 
-diabetes 
-high blood pressure 
-medicines :aspirin, anticoagulant 
Rarely, subconjunctival hemorrhage is caused by a blood clotting disorder or other blood problem that affects the whole body. 

   

Degenerative diseases of the conjunctiva 

1.Pinguecula  is a benign yellowish, raised growth on the conjunctiva. Is a common type of conjunctival stromal degeneration in
the eye. It appear in the bulbar conjunctiva near to limbus . A pinguecula is a deposit of protein, fat, or calcium. 
The exact etiology is unknown, but it may be associated with aging and excessive exposure to UV light. 
Pingueculae may enlarge slowly over time, but are a benign condition, usually requiring no treatment. Artificial tears may help
to relieve discomfort, if it occurs. If cosmesis is a concern, or if there is discomfort in contact lens use, surgical excision may be

done. Laser photocoagulation may also be used to remove pinguecula.  

 
2. A pterygium is a  triangular vascularized growth of bulbar conjunctiva that may spread across and distort the cornea, induce
astigmatism, and change the refractive power of the eye. Symptoms may include decreased vision and foreign body sensation. It
is more common in sunny, hot, dry climates.
To relieve symptoms caused by a pterygium, artificial tears or a short period of treatment with corticosteroid drops or ointments
may be prescribed. Removal is often indicated for documented growth, cosmesis, to reduce irritation, and to improve or preserve
vision. The technique with the best results to prevent recurrence is surgical removal of the pterygium followed by conjunctival
autograft and perhaps with cyclosporine drops. Following surgery a pterygium may recur in around half of cases. 

Tumors of the conjunctiva 

Tumors  that occur in the conjunctiva are generally recognized at a relatively early stage. Because many of these tumors have
typical clinical features, an accurate diagnosis can often be made by external ocular examination and slit-lamp biomicroscopy. A
diagnostic biopsy is not usually necessary in cases of smaller tumors that appear benign.  
In cases of larger lesions it may be appropriate to remove a portion of the tumor (incisional biopsy) to obtain a histopathologic
diagnosis. 
Most conjunctival tumors are epithelial or melanocytic in origin 

1.Conjunctival cysts don’t always cause symptoms, especially when they’re very small. 
As they grow, a range of symptoms can occur, including: 
-the feeling that something’s stuck in your eye 
-swollen eyelid 
-problems closing your eye 
If the cyst makes it hard to close theeye, can occur: dryness tearing itchiness and 
a burning sensation. 

Treatment is surgical     
 
Pigmented lesions of conjunctiva 
Pigmented lesions that arise from the conjunctiva include nevus, complexion-associated melanosis (CAM), primary acquired
melanosis (PAM), and malignant melanoma. All of these lesions arise from melanocytes. 
-Nevi represent more than 50 percent of conjunctival lesions and are the most benign of the pigmented lesions. Nevi usually
appear in childhood. Conjunctival nevi are very similar to those of the skin. Nevi should be monitored regularly. 
-CAM, also known as racial melanosis, is a benign lesion found among darkly pigmented individuals. 
It is typically observed around the limbus. On examination, the pigmentation appears flat and noncystic. It can cover the
conjunctiva extensively and increase in size with age; contrary to nevi and PAM, it is usually bilateral. 
-PAM is almost always unilateral. is a diffuse intraepithelial disease, so it appears as a thin dusting of pigment and is usually not
well circumscribed. 
Conjunctival malignant melanoma  is an uncommon but potentially devastating tumor that may invade the local tissues of the
eye, spread systemically through lymphatic drainage and hematogenous spread, and recur in spite of treatment. 
Conjunctival melanoma commonly presents as a thickened, raised, pigmented lesion with prominent feeder vessels and
surrounding areas of melanosis. 
 
Picture: Various presentations of conjunctival malignant melanoma (CMM)
A) Discrete, raised, pigmented lesion (B) Multifocal CMM (white arrows) in the setting of diffuse primary
acquired melanosis (C) Large, raised, pigmented CMM originating from inferior fornix (D) Large,
raised, amelanotic/mildly pigmented CMM .

  
 
 Practical works no 4-lacrimal sys

EXAMINATION OF THE LACRIMAL SYSTEM

1. Examination of the secretory function
2. Examination of excretory function

1. Examination of the secretory function

*It is being investigated using the Schirmer test. It is used when deficiency of tear secretion is suspected.
-The test measures the amount of tear fluid in the conjunctival sac.
-It is indicated for any patient who complains of dry eye or chronic irritated eyes.
-It is made of sterile filter paper, rounded at the ends, which at one end has a portion of about 3 mm bent, thus allowing
insertion into the lower conjunctival sac.
-The test can be performed under anesthesia (Schirmer2) or without anesthesia (Schirmer 1 test).
The Schirmer 1 test consists of measuring the length of the wet filter paper without prior anesthesia. If it is less than 10 mm, the
patient is considered to have a tear hyposecretion. If it exceeds 30 mm, the patient has tear hypersecretion. In this test, both the
basal and the reflex component of the secretion are measured.
Schirmer test 2 It is performed similarly, but after prior anesthesia. In this way the reflex component is eliminated, leaving only
the basal one. If after 3 minutes, the length of the wet filter paper is less than 10 mm, the patient has a basal hyposecretion.

2. Examination of excretory function

It is investigated by checking the permeability of the tear ducts. The procedure is used in both diagnosis and treatment. It
consists of injecting fluid through the upper or lower lacrimal point, from where it should normally flow into the lacrimal sac and
further through the nasolacrimal canal into the nasopharynx.
- It is applied to patients of any age who complain of tearing.
1.Local anesthesia is performed in the bottom of the conjunctival sac. The tear point is then dilated with the help of the dilator.
A lacrimal canunula is then advanced through the point and lower canaliculus..
2. A syringe with fluid (saline, weak antibiotic or fluorescein solutions) is attached to the lacrimal cannula. Apply pressure to
the syringe plunger. If the tear ducts are permeable, fluid drains into the nasopharynx and the patient feels the need to swallow. If,
when the fluid is introduced, a regurgitation of the fluid is produces and indicate lacrimal obstruction. If the fluid introduced
through the lower tear point flows back through the upper tear point, the obstruction is located at the level of the common tear
duct or at the entrance to the tear sac.

3. Radiological examinations
They are made to visualize the shape, volume, caliber and location of the tear obstructions.
PAHIMETRY - measurement of corneal thickness
It can be done using ultrasonic or optical methods.
1. Contact methods, such as ultrasound
2. Noncontact methods, such as optical biometrics or optical coherence tomography.
Normal values of the corneal thickess are 700 -900µm at the limbus and 500-560 µm at the center.

*Pachymetry is essential before refractive surgery to ensure sufficient corneal thickness to prevent abnormal corneal bulging, a
side effect known as ectasia.
The studies reported that corneal thickness measured by corneal pachymetry was an accurate predictor of glaucoma development
when combined with standard intraocular pressure measurements. As a result of this studes corneal pachymetry is now used to
better diagnose and detect early cases of glaucoma. Newer generation pachymeters have the ability to adjust intraocular pressure
which is measured by the thickness of the cornea.
The measurement of intraocular pressure is influenced by the thickness of the cornea, among other factors. Thin corneal eyes tend
to have pressures that are underestimated by tonometry, while thick corneal eyes tend to have overestimated
pressures.Conclusion: Patients should be considered at higher risk if they have a thin cornea and a lower risk if they have a thick
cornea
Clinical case:
CLINICAL CASE –  BILATERAL DACRYOADENITIS 
A 24-year-old male presented to the emergency department (ED) with complaints of bilateral eye pain, redness, and
photosensitivity for two days. The patient had been evaluated at another hospital the previous day where he
was treated with ciprofloxacin eye drops and neomycin/polymyxinB/hydrocortisone ophthalmic suspension. The
patient denied any improvement in symptoms.

On physical examination the patient was febrile with a temperature of 102.8°F. His orbital examination
revealed chemosis, injected sclera, edema of the upper and lower lids, and yellow discharge bilaterally [Figure
1] and [Figure 2]. Extraocular muscle movement was restricted in all directions. Visual acuity was 20/50 bilaterally.
Visual field testing was not possible secondary to upper and lower lid edema. Pupils were equally round and reactive
to light. Eye pressures by tonometry were within the normal range. Lymphadenopathy was present in both the
cervical and submandibular regions.
FIGURE 1 
Figure 1: Erythema and edema are greatest over the lateral one-third of the upper eyelids (photo was taken after the
application of flouroscein and with the patient's written permission)

 
FIGURE 2
Figure 2: Chemosis and injection of the sclera are present (photo was taken after the application of flouroscein and
with the patient's written permission)

 
Laboratory analysis revealed an elevated white blood cell count of 13,800 K/UL. A computed tomography (CT)
scan of the orbits was performed which showed bilateral enlargement and inflammation of the lacrimal glands
without evidence of orbital cellulitis [Figure 3] and [Figure 4]. After evaluation by an ophthalmology physician the
patient was discharged home on ofloxacin eye drops and oral amoxicillin/clavulanic acid. The patient was instructed
to discontinue his previous antibiotics and to follow up for reassessment.
Figure 3: Coronal CT image showing bilateral lacrimal gland inflammation (arrows)

 
Figure 4: Axial CT image showing bilateral lacrimal gland inflammation (arrows)
 
 The patient was reevaluated 4 days later and his symptoms had worsened. It was recommended that the
patient be admitted for intravenous antibiotics as well as further diagnostic assessment to better determine the
etiology for his symptoms. Blood cultures drawn from the patient's ED visit 4 days prior had no growth.
Eye culture results could not be located. A repeat CT scan of the orbits showed no progression to orbital
cellulitis.

 Rapid plasma reagin, cytomegalovirus immunoglobulin M antibody, measles antibody, and blood cultures
were all negative. The patient's cytomegalovirus immunoglobulin G antibody and mumps immunoglobulin G
antibody tests were positive suggesting previous but not active infection.
 Thyroid-stimulating hormone, thyroid stimulating immunoglobulin, neutrophil cytoplasmic antibody,
rheumatoid factor, antinuclear antibody, angiotensin- converting enzyme levels, and a chest radiograph
were also performed to determine if the patient's inflammation was secondary to an autoimmune process.
These tests were all negative. 
 The patient's symptoms were felt to be secondary to a bacterial infection so he was treated with
intravenous vancomycin and piperacillin/tazobactam. He was successfully discharged home on hospital day
3 with oral trimethoprim/sulfamethoxazole and ofloxacin ophthalmic drops.
 DISCUSSION
 Dacryoadenitis occurs in only one in 10,000 ophthalmic cases and may be acute, subacute, or chronic. It is
most common in children and young adults but may been seen in all age groups. Patients generally present
with redness, tenderness, warmth, and swelling of the lateral third of the upper eyelid.
A mucopurulent discharge, localized conjunctival injection, and chemosis may also be present.  
 Impaired vision, limited ocular movement, and pain with movement suggest an orbital cellulitis.
  CT can be used to determine if there is involvement of the orbital tissues. 
Dacryoadenitis may be caused by an obstruction occurring anywhere between the conjunctiva and the
lacrimal ductules. When it occurs acutely, it is usually due to infection, with viral etiologies such as mumps, measles,
influenza, mononucleosis, herpes, and cytomegalovirus occurring most commonly.  The most common bacterial
pathogen is Staphylococcus  aureus. Infections may also be caused
by Streptococcus pyogenes, Haemophilus influenza,  Neisseria   gonorrhea, Chlamydia trachomatis,
and Treponema pallidum.Fungal and parasitic infections are rare.  Infection may spread to the lacrimal

gland hematogenously, transneuronally, from the conjunctiva or via traumatic injury.