4 MARK QUESTIONS

DISEASES OF CONJUNCTIVA:

Symblepharon

Spring catarrh (Feb 2009, Feb 2014)

Aetiology, signs and treatment of phlyctenxular conjunctivitis

Geographical ulcer

Ophthalmia Neonatorum

DISEASES OF CORNEA:

Hypermature cataract.

Keratoconus.

Corneal blindness.

Indications of keratoplasty.

Herpes simplex keratitis

Describe anatomy of cornea

Keratic precipitates.

Management of Keratoconus

Acanthamoeba keratitis

Entropion

fascicular ulcer
herpes simplex keratitis

DISEASES OF SCLERA:

Episcleritis

DISEASES OF UVEAL TRACT:

Staphylomas (Aug 2013)

Endophthalmitis

Sympathetic ophthalmia.

Granulomatious uveitis - clinical features and management.

DISEASES OF LENS:
Write notes on:

Treatment for myopia.

Posterior synechiae.

Zonular cataract

Hypermetropia (Feb 2015,Aug 2013)

Different types of hypermetropia.(Feb 2013)

Complicated cataract (2008)

Post operative complications of cataract surgery

Subluxation of Lens.

Types of astigmatism

Lens induced glaucoma

Staphyloma

Pseudophakia
Sturm’s conoid
Complicated cataract

management of complicated cataract

GLAUCOMA:

Field defects in primary open angle glaucoma.

Management of open angle glaucoma

Hypertensive iridocyclitic crisis

Acute congestive glaucoma.

Describe field defects in chronic simple Glaucoma with diagram.

Causes or variations in intraocular pressure in iridocyclitis.

Management of Absolute glaucoma

DISEASES OF VITREOUS:

Vitreous Haemorrhage.

DISEASES OF RETINA:

Retinopathy of prematurity.

Nyctalopia.
Anti VEGF (Vascular Endothelial Growth Factor) agents

Applanation tonometry.

Diabetic retinopathy.

Stages of retinopathy of prematurity.

Stages of retinoblastoma

Describe Fundus picture in Retinitis Pigmentosa.

Fundus features of diabetic retinopathy

Central Retinal Artery Occlusion

Photocoagulation ( correction )

Central Retinal Artery Occlusion

Hypermetropia

optic atrophy

Fundus findings in central retinal vein occlusion

NEURO-OPHTHAL:

Thyroid eye disease.

Optic neuritis
Lagophthalmos

Endophthalmitis
Marcus Gunn pupil
Esotropia
OCUL MOTILITY AND STRABIS:

Mydriatics and cycloplegics.

DISORDERS OF EYELIDS:

Blepharitis.

Applied Anatomy of Eye lids.

Chalazion

. Causes and investigation of Chalazion (Feb 2014)

ectropion

DISEASES OF LAC APP:

Congenital dacryocystitis

. Anatomy of lacrimal drainage system.

DISEASES OF ORBIT:

Orbital cellulitis.( ,2008, Feb 2010)

OCULAR INJURIES:

Xerophthalmia

Iridodialysis

Chalcosis

Extraocular muscles(2008)

Ocular manifestations of Acquired Immuno Deficiency Syndrome.\

Vision 2020 (2008,Aug 2009,2017,Aug 2013).

----------

Common causes of blindness in India, Hypertensive

iridocyclitic crisis. WHO grading system for trachoma
.Pupillary reflexes. Functions of eye bank. Proptosis .
Tonometry. Eye camps . . Carbonic Anhydrase
Inhibitors.Disciform Keratitis. . Leukocoria in children.
Types of blindness and WHO definition of blindness
Post operative Complications of cataract surgery
Chronic dacryocystitis ( Dieseases of tear duct )

1. Sturm’s conoid 2 3. Entropion – classification, complication,

management 4. 5. Optic neuritis
what is Sturm's Conoid?
 The configuration of rays refracted through the astigmatic surface (toric surface) is called
Sturm's conoid and the distance between the two focal lines is known as focal interval of Sturm.

What is regular astigmatism?

Regular astigmatism

Each meridian in the regular astigmatic eye has a uniform curvature at every point across the entrance
of the pupil. This is the most common type of astigmatism in which the symptoms included are blurry vision,
headaches, and light sensitivity, to name a few.26-Apr-2021

What is mixed astigmatism?

Mixed astigmatism is when an eye has both types of astigmatism at the same time. Figure 2: On the
left is a diagram of an eye with mixed astigmatism showing that the light entering the eye through different
regions of the cornea focuses in two points, but neither point is on the retina.

What is the interval of Sturm?

Sturm interval - the distance between the anterior and posterior focal lines in a spherocylindrical
lens combination
What is cross cylinder?
The cross cylinder is a lens having the effect of two cylindrical lenses, one convex the other concave,
of equal strength, placed with their axes at right angles to each other. It is mounted in a ring, which has a
small round handle, easily rotated between the thumb and finger.
What is against the rule astigmatism?
“Against-the-rule” astigmatism occurs when the horizontal meridian of the cornea is steepest—the
horizontal meridian of the football is the steepest curve.01-Sep-2013

2. Describe uses of fluorescein in ophthalmology. 2.

Lagophthalmos. 3. 4. 5. Aphakia.

Fluorescein is a diagnostic contrast agent particularly used in various ophthalmic procedures, such as checking for any
corneal or vessel abnormalities. The application of fluorescein also extends to bioimaging of whole anatomic
structures and even further to cellular components in immunohistological staining. This article outlines the
indications, mechanism of action, adverse event profile, and contraindications for fluorescein to guide the healthcare
team in evaluating ophthalmic abnormalities, infection, and pathophysiology, among other conditions.

Objectives:

 Identify the mechanism of action of fluorescein.

 Describe the possible adverse effects of fluorescein.

 Review the appropriate monitoring for patients receiving fluorescein.

 Summarize interprofessional team strategies for improving care coordination and communication to advance
fluorescein and improve outcomes.

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Indications
Fluorescein is a dye used particularly as a fluorescent agent in diagnostic procedures at various levels.

 Ophthalmology

o Fluorescein has extensive use in routine ophthalmic tests. This usage ranges from applanation
tonometry, gonioscopy, and contact lens fittings to angioscopy/angiography of retina and iris
vasculature. In the first scenario, after an anesthetic and a fluorescein strip are applied to the eyes, a
tonometer is placed on the cornea to determine the intraocular pressure of one eye at a time.
Applanation tonometry utilizes fluorescein to produce semicircles that aid in the measurement of
the dial reading. For improved detection of any breaks in the vasculature or associated retinal
conditions, fluorescein angiography stains the blood vessels of the retina and iris to provide a
detailed image of the posterior view of the eye. One study on retinopathy of prematurity (ROP)
relies on fluorescein angiography to evaluate treatment efficacy between two different drugs on
peripheral retina vasculature. Unlike plain fundus photographs, fluorescein angiography also
pinpointed vascular loops, blunting, dilatation, and capillary dropout.[1] Additionally, fluorescein
produces remarkable contrast to determine if any corneal abrasions, epithelial keratitis, herpes
simplex keratitis, or corneal foreign bodies are present. If the epithelium of the cornea is not intact,
aqueous humor leaks through and mixes with the fluorescein dye to reveal a corneal abrasion or
other corneal abnormalities. In a study assessing dry eyes, fluorescein was useful in measuring the
stability of the tear film. Despite any significant differences between using a standard strip or small
volumes of liquid dye, fluorescein proved effective in augmenting any breaks in the tear film that
occurs in dry eye disease.[2]

 Bioimaging 

o The remarkable fluorescence of fluorescein permits considerable insight into the identification of
non-diseased tissues, tumor-affected tissues, or histological markers. For example, fluorescein can
serve as a contrast agent in surgical procedures for nonspecific identification of anatomic
arrangements. Fluorescence of healthy tissue of the focused region differentiates it from nearby
normal tissues and aids the surgeon in removing or repairing necessary tissues while also
protecting vital structures. A surgery repairing hand anatomy may need fluorescein to highlight the
 nerves specific for fine motor skills or to differentiate blood vessels of a certain section.
[3] Furthermore, in a study using microendoscopy to find dysplasia in colorectal tissue, fluorescein
was preferred to proflavine, especially due to its ability to highlight crypt structures with greater
sensitivity, intensity, and uniformity. Identification of structures on a deeper, finer level expands
the nonspecific functionality of fluorescein and eases the process of diagnostic procedures.[4] Its
range of use can be from a bundle of nerves to an individual blood vessel, and further to tissue
abnormalities, and even further to the molecular level.

 Conjugate Species/Biomarker

o Fluorescent microscopy allows for the identification of microorganisms or cellular components,

such as proteins, in immunohistological staining. In the most common indirect method of
immunohistochemistry, Enzyme-Linked Immunosorbent Assay (ELISA) uses fluorescein to act as
a fluorescent conjugated to secondary antibodies. Moreover, certain compounds commonly modify
or combine with the original fluorescein structure to adjust the attachment of the fluorescent tag to
specific macromolecules. The combination of water-soluble chitosan derivative with a fluorescent
tag created glycol chitosan fluorescein-isothiocyanate (GC-FITC), which showed to be a sufficient
agent used for bio-imaging when compared to its commercial equivalents. Even at a lower
concentration, the biocompatibility of the molecule as well as the strong affinity to the cell surface,
through a strong electrostatic interaction, offer efficient cell staining, namely, for the identification
of lipid rafts.[5] On a clinical level, a cardiology study exhibits the use of fluorescein as a
fluorescent tag/biomarker in cardioscopy for the detection/monitoring of coronary artery disease
(CAD). Fluorescein is injected into the circulatory system, and its fluorescence is observable
throughout cardiomyocytes in terms of tissue fluid flow. Through molecular bioimaging,
fluorescein plays a role in the status of patients with CAD experiencing angina pectoris or other
cardiovascular issues or who have undergone treatment with stents.[6]

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Mechanism of Action
As an ocular disclosing agent, fluorescein sodium dissolves readily in aqueous alkaline solutions, responds to 465 to
490 nm at cobalt blue light, and fluoresces at 520 to 530 nm as bright green. The compound contains a conjugated
system that illuminates when electrons spend a prolonged time in an excited state.

When using fluorescein to stain cells, its charged ends attract to the hydrophilic ends in the cell membrane to form a
strong electrostatic bond. One or more of the charged ends of fluorescein may then be modified for greater interaction.
[5]

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Administration
Ophthalmic administration of fluorescein starts with a paper strip with one tip stained with fluorescein. The paper strip
is moistened with saline water, then placed on the conjunctiva or inferior fornix. The patient may blink a few times to
spread the dye across the eye.

Fluorescein solution may be administered orally and requires 10-15 minutes before appearing. Although the solution
is bitter, combining it with sugar or a beverage can increase palatability.

Intravenous injection of fluorescein sodium occurs at the antecubital vein. The dye appears almost immediately in the
retina and choroidal vessels (in 7 to 14 seconds). In the case of anaphylaxis, IV access is still necessary for
epinephrine. 

After administration, the examiner can extinguish the room light to view the fluorescence of the dye under cobalt blue
light.[7]

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Adverse Effects
Common: paresthesia of lips, change in taste (orally), severe eye irritation (ophthalmic), severe nausea, vomiting,
abdominal pain, chest pain, and extravasation.

 Mild: urine discoloration, skin inflammation/discoloration at the injection site 

  Moderate: rashes, urticaria, syncope/dizziness/hypotension, angioedema, chest pain

 Severe: nerve palsy, seizure, bronchospasm, pulmonary edema, anaphylaxis[7]

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Contraindications
Hypersensitivity to fluorescein formulation prevents its application. Furthermore, even though more research is
needed to determine side effects on a fetus, pregnancy may be considered a relative contraindication.[7]

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Monitoring
Fluorescein has no known significant drug interactions. Under ophthalmic examination, contact lens removal is
necessary with the use of fluorescein to avoid unnecessary staining. Fluorescein completely clears through urine
excretion 2 to 3 days after injection.[7]

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Toxicity
Fluorescein toxicity is low. Proper doses of epinephrine and antihistamines can manage cases of significant
hypersensitivity after flushing the affected area with plenty of water. Prevention of anaphylaxis is possible by
providing a minimal dose of fluorescein to determine if a minor reaction would occur.

If enough fluorescein is issued intravenously, precaution is necessary for nursing mothers because another route of
excretion is through human milk, causing it to turn yellow.

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Enhancing Healthcare Team Outcomes

Because fluorescein administration is for diagnostic purposes, its use is most commonly by specialists, especially
ophthalmologists and surgeons, and general practitioners, where nurses and/or medical assistants may also assess
proper dosage for the desired procedure. Not all health professionals readily operate with a fluorescent agent. Nurses
can assist in the procedure via preparation, monitoring for adverse effects, and post-procedural care. INterprofessional
coordination will result in optimal results when using fluorescein for diagnostic purposes. [Level 5]

What are some uses for fluorescein?

Fluorescein is a xanthene dye that is highly fluorescent, detectable even when present in minute quantities.
Used forensically to detect traces of blood, in analytical chemistry as an indicator in silver nitrate
titrations and in microscopy. It has a role as a radioopaque medium and a fluorescent dye.

Lagophthalmos describes the incomplete or abnormal closure of the eyelids and has many different causes. This
activity reviews the evaluation and management of lagophthalmos and highlights the role of the interprofessional team
in evaluating and improving the care of patients with this condition.

Objectives:

 Identify the etiology and epidemiology of lagophthalmos.

  Describe the appropriate history, physical, and evaluation of lagophthalmos.

 Explain the management options available for lagophthalmos.

 Outline interprofessional team strategies for improving care coordination and communication to advance
lagophthalmos and improve outcomes.

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Introduction
Lagophthalmos describes the incomplete or abnormal closure of the eyelids. A full eyelid closure with a normal blink
reflex is necessary for the maintenance of a stable tear film and healthy ocular surface. Patients who are unable to
blink and completely close their eyes are at risk of corneal exposure, evaporation of the tear film, and subsequent
exposure keratopathy. This can progress to corneal ulceration and perforation. Therefore it is essential to recognize the
signs of lagophthalmos early and investigate the causes and begin treatment. The primary cause of lagophthalmos is
facial nerve paralysis, which leads to paralytic lagophthalmos.[1] 

There are many etiologies associated with facial nerve paralysis; hence a detailed history and workup are necessary to
determine treatment of the underlying cause. The purpose of treating lagophthalmos is two-fold: to prevent further
corneal exposure and to improve eyelid function. Any asymmetry in a person's face will likely have a psychological
impact. Therefore the patient needs to regain an appearance acceptable to themselves.[2]

Treatment can be divided into medical and surgical modalities. Medical treatment consists of improving the quantity,
quality, and stability of the tear film. Surgical procedures can be dynamic or static and focus on reestablishing eyelid
function or eyelid coverage. The choice of treatment and reconstruction method will depend on the location, severity,
etiology of lagophthalmos, as well as patient factors of age, health, and their expectations.

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Etiology
Paralytic Lagophthalmos

Facial nerve paralysis is the cause of paralytic lagophthalmos, of which there are many underlying aetiologies outlined
below.

Infection:

 Otitis (external, otitis media)

 Mastoiditis

 Viral (herpes simplex, herpes zoster, influenza, coxsackievirus, polio, mumps, mononucleosis)

 Bacteria (Tuberculosis, syphilis, leprosy, cat scratch disease, Lyme disease, botulism)

 Fungal (Mucormycosis)

 Immunocompromised (AIDS)

Trauma:

 Facial injuries

 Birth trauma

 Fractures to the skull base, temporal bone fracture

Tumour:

 Parotid lesion

 Cholesteatoma

 Facial nerve tumor

  Schwannoma

 Teratoma

 Neurofibromatosis Type 2

 Fibrous dysplasia

 Haemangioblastoma

 Acoustic neuroma

 Sarcoma

 Leukemia

 Meningioma

 Carcinoma (primary or metastatic) 

Metabolic:

 Diabetes mellitus

 Hypertension

 Vitamin A deficiency

 Hyperthyroidism

 Toxic:

 Thalidomide

 Alcohol excess

 Arsenic

 Tetanus

 Diphtheria

 Carbon monoxide

Iatrogenic:

 Parotid surgery

 Mastoid surgery

 Post-immunization

 Post-tonsillectomy/adenoidectomy

 Embolization

 Mandibular block anesthesia

 Antitetanus serum

 Dental surgery

 Eyelid surgery (excessive tissue removal from blepharoplasty)

 Squint surgery (vertical muscle recession surgery)

Neurological:

 Millard-Gubler syndrome
  Foix-Chavany-Marie syndrome

Congenital:

 Mobius syndrome

 Goldenhaar syndrome

 Ichthyosis 

Idiopathic:

 Bell's palsy

 Amyloidosis

 Temporal arteritis

 Guillain-Barre syndrome

 Multiple sclerosis

 Myasthenia gravis

 Sarcoidosis

 Osteopetrosis

 Thrombotic thrombocytopenic purpura

 Hereditary hypertrophic neuropathy

 Melkersson-Rosenthal syndrome

Cicatricial Lagophthalmos

Lagophthalmos is due to scarring to the eyelids. The upper and lower eyelids consist of seven structural layers. From
anteriorly, these are skin and subcutaneous tissue, orbicularis oculi, orbital septum, orbital fat, retraction muscles,
tarsal plate, and conjunctiva. Injury to any of these tissues can cause incomplete eyelid closure. Causes include:

 Solar elastosis

 Chemical burns

 Ocular cicatricial pemphigoid

 Steven-Johnson syndrome

 Trauma 

Nocturnal Lagophthalmos

Lagophthalmos, which occurs during sleep, is termed nocturnal lagophthalmos and can cause similar symptoms of dry
eyes and exposure keratopathy. The diagnosis can be challenging as there is clinical overlap with blepharitis, and the
patient may not be aware of lagophthalmos during slumber. Patients can report insomnia, and exacerbated symptoms
upon waking, either in the morning or during the night. 

Incomplete Blink and Lagophthalmos

An incomplete blink with consequent lagophthalmos is seen in patients with Parkinson disease and ocular myopathies
like myotonic dystrophy and chronic progressive external ophthalmoplegia.

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Epidemiology
Facial nerve paralysis occurs in 30 to 40 people per 100,000 annually in the United States.[3] The most common
cause is Bell palsy and is responsible for up to 80% of cases. Bell palsy is an acute, unilateral facial nerve paralysis
that resolves spontaneously over time. There is no known cause; however, it may have an association with viral
infections. Symptoms experienced can include earache, hyperacusis, deafness, taste alterations, paresthesia of the
cheek, mouth, and ocular pain. Fortunately, there is an excellent prognosis, with up to 84% of patients recovering full
function of their facial nerve.[4]

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Pathophysiology
Eyelid retraction is usually acquired and associated with thyroid eye disease.[5] The Müller muscle is stimulated and
results in a bilateral asymmetric stare in hyperthyroid patients. Lymphocyte and mast cells can infiltrate the Muller
muscle and levator, with secondary fibroblastic proliferation, which leads to the classic appearance of superior
temporal eyelid retraction (lateral flare).[6]

Facial nerve (seventh cranial nerve) paralysis from any cause will result in lagophthalmos (without eyelid retraction).
The more common etiologies include Bell palsy, sarcoidosis, cerebral ischaemic event, and post-surgical tumor
excision. Orbicularis oculi paralysis will lead to the unopposed action of the levator. For the lower lid, this will cause
loss of tonus, which will result in a scleral show and a progressive ectropion. Epiphora (tearing) occurs due to lacrimal
pump malfunction and increased reflex lacrimal secretion secondary to corneal exposure.[7]

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History and Physical

The clinical history is very important and should aim to determine the underlying etiology of the lagophthalmos. If the
patient had recent surgery or trauma to the eye, orbit, face, or head, then this should be ascertained. Previous
infections in history should be reviewed, especially if it was herpes zoster. A detailed medical history will help to
reveal any systemic causes, such as thyroid disease or obstructive sleep apnea. The history of acute facial nerve
paralysis is a sudden unilateral loss of facial motor function. This results in a distinctive facial asymmetry.

If the lesion is the lower motor neuron, then the complete hemiface is affected; upper motor neuron lesions will spare
the frontalis muscle, and hence the forehead is not affected. For a lower motor neuron lesion causing complete facial
paralysis, patients will have a loss of forehead, nasolabial folds, ptosis of the eyebrow, lower lid ectropion, upper lid
retraction, lagophthalmos, oral droop, problems with speech, and possibly emotional distress due to the physical
effects.

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Evaluation
Clinical Examination

The patient should be observed for external signs such as incomplete blink, exophthalmos, eyelid malposition, degree
of Bell's phenomenon. The degree of lagophthalmos can be measured by asking the patient to close their eyes and
checking if there is a space between the upper and lower eyelid margins. If there is lagophthalmos, the vertical height
at the greatest distance of the palpebral fissure should be measured, and any scleral or corneal show documented. All
cranial nerve function should be then examined, especially those governing ocular motility and the orbicularis oculi
muscle. 

On the slit lamp, the conjunctiva should be assessed for injection or chemosis, followed by examination and testing
the cornea for sensitivity. The presence of punctate epithelial erosions or epithelial defects can be highlighted with
fluorescein staining, with special attention focussed on the inferior cornea where lid excursions terminate. The tear
breakup time should be recorded.

Further Investigations

Laboratory and imaging studies are determined based on what the underlying etiology could be. If there is suspicion
of thyroid eye disease, thyroid function tests along with CT orbital imaging may become necessary in the presence of
exophthalmos. If there are fluctuating and progressive neurological signs, then CT/MR neuroimaging is indicated to
rule out hemorrhage or tumor. 

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Treatment / Management
Management of lagophthalmos involves both medical and surgical approaches with the aim of treating the underlying
condition leading to exposure keratopathy and protection of the ocular surface.

Medical

Artificial tears without preservatives can be administered frequently in order to improve the patient's tear film. The
ointment can be applied at night time or during the day if there is severe corneal exposure. Taping of the eyelids at
night can offer additional ocular surface protection without resorting to surgery.[8] There are also moisture chamber-
type glasses which can aid in maintaining a stable tear film and improve symptoms.[9] The volumizing hyaluronic
acid gel has been used for tissue expansion for immediate management of cicatricial ectropion in cases of
lagophthalmos e.g. congenital ichthyosis.[10]

Surgical

A stepwise approach is recommended based on the severity and duration of the lagophthalmos. A close follow-up
with the frequent examination is necessary.

Tarsorrhaphy 

When there is corneal exposure and recovery is expected within a matter of weeks, a temporary tarsorrhaphy can be a
good option. In the majority of cases, the cornea can be protected adequately by closing the lateral one-third of the
eyelids. A small opening should remain so that the cornea can be continuously assessed and required topical
medications can be administered. Loosening of the sutures can occur over time, resulting in inadequate ocular surface
protection. Complications include trichiasis and poor cosmesis from scarring.

Gold/Platinum Weight Implantation

If there is no full lid closure, gold or platinum weight can be implanted into the upper eyelid in patients with paralytic
lagophthalmos. This will result in a gravity-dependent enhancement of eyelid closure.[11] Gold was initially used
because it is inert. Platinum has a higher density which translates to a slimmer profile, decreased visibility, and
improved cosmesis. It is also less likely to induce inflammatory reaction compared to gold, and decreased rates of
extrusion. [12] Preoperatively the correct weight is chosen by taping weights onto the external lid superior to the
tarsus and observing the effect on eyelid closure. The ideal weight should allow for full lid closure, opening, and
avoid ptosis in primary gaze. 

Upper Eyelid Retraction and Levator Recession

Patients with lagophthalmos secondary to upper eyelid retraction (i.e. from thyroid eye disease) can have recession
surgery of the upper eyelid retractor muscles (levator palpebrae superioris and Müller’s muscles). Full-thickness skin
grafts or advancement flaps can be options for patients with postsurgical lid shortening e.g. after upper lid
blepharoplasty. In addition, scar band releases and tarsal-sharing procedures can be suitable for cicatricial
lagophthalmos.[13] 

Lower Eyelid Tightening and Elevation

Lower eyelid laxity occurs in facial nerve paralysis and floppy eyelid syndrome. Lid tightening procedures such as
lateral tarsal strip will lead to improved apposition of the lower eyelid to the globe and decrease scleral exposure and
epiphora symptoms.[14] If there is persistent corneal exposure after medical therapy and upper eyelid surgery, lower
eyelid elevation with retractor muscle recession can be an option. A spacing graft from the autologous ear, nasal
cartilage, or hard palate grafts can be sutured in place to achieve further elevation.[15][16] If there are cicatricial
changes a full-thickness skin graft and/or mucous membrane graft could be needed.[17]

Ancillary Surgical Procedures 

Severe lagophthalmos secondary to facial nerve paralysis may require midface elevation. This can be achieved with a
variety of techniques, such as using autogenous fascia slings. Other approaches to reanimate the face include
temporalis muscle transposition, nerve grafts, palpebral springs, suborbicularis oculi fat lifts, and soft tissue
repositioning.[18]

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Differential Diagnosis
Bell's palsy is a diagnosis of exclusion; more serious causes of facial palsy will need to be ruled out. The more serious
causes are listed in the etiology section of this article. It is important to consider whether the lesion location is lower
or upper motor neuron. Bilateral cortical innervation of the upper facial muscles will result in complete facial
paralysis for lower motor neuron lesions in most cases. Therefore asking the patient to raise their eyebrows is very
useful in assessing the functions of frontalis and orbicularis oculi. Lower motor neuron lesions include Bell's palsy
and Ramsay Hunt syndrome. Upper motor neuron lesions causing facial nerve paralysis include cerebral ischaemic
event, multiple sclerosis, intracranial hemorrhage, or neoplasia. An atypical presentation, recurrent or progressive
symptoms, additional neurological findings, lack of spontaneous resolution, and/or history of head, neck, or cutaneous
malignancy are risk factors necessitating further workup.

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Prognosis
The prognosis of lagophthalmos depends on the underlying etiology. Mild exposure keratopathy has a very good
prognosis, especially if due to Bell's palsy, in which the majority of patients have spontaneous resolution. Severe
cases can lead to corneal scarring, perforation, and visual loss. 

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Complications
Complications can range from relatively mild, involving dry eye signs and symptoms, to corneal abrasions, persistent
epithelial defects, ulceration, microbial keratitis, and corneal scarring. Corneal perforation can occur leading to visual
loss. Band keratopathy can occur as a result of chronic exposure keratopathy. 

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Deterrence and Patient Education

There are multiple challenges for patients with lagophthalmos with which to cope with. Patient education is vital to
reduce complication risks with self-management regimes. These mainly consist of managing dry eyes, lid taping
technique, and if due to facial palsy additional factors such as eating and drinking, speech, facial expression, and
psychological impact. Providing patients with relevant educational material, and also directing them to support groups
can be beneficial to patients' wellbeing and outcome. 

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Pearls and Other Issues

Facial nerve paralysis is the main cause of lagophthalmos. There are several grading systems in use, with the House-
Brackmann grading scale (HBGS) being widely used as a measure of facial nerve function.[19] Patients with grade 1
to 3 have full eyelid closure and those with grade 4 to 6 are at risk of exposure keratopathy. Alternative grading scales
include the Sunnybrook and Yanagihara systems, which have been found to score at the same agreement level.[20] 

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Enhancing Healthcare Team Outcomes

A multi-disciplinary team approach is required for timely accurate patient evaluation, management, and long-term
rehabilitation of patients with lagophthalmos. Members of the team can include emergency, stroke, and family
physicians, ophthalmologists, ENT surgeons, radiologists, neurologists, maxillofacial surgeons, nursing staff, speech
therapists, dieticians, pharmacists, and physiotherapist.

Presentation of lagophthalmos due to different etiologies can present to an emergency as well as primary care staff,
hence familiarity with the assessment and management is essential for clinicians. Nursing staff working on head and
neck wards will need to recognize the signs and symptoms of facial nerve paralysis. Pharmacists will need to verify all
dosing, medication checks, and liaise with medical staff in administering the medication. Rehabilitation will closely
involve physiotherapists, speech and language therapists, and dieticians in patients with lagophthalmos secondary to
facial nerve paralysis. A psychologist can also aid the patient's recovery from the psychological impact of facial nerve
paralysis.[21] An interdisciplinary approach can provide a holistic and integrated management system in
lagophthalmos patients and lead to improved outcomes. [Level 5]

Lagophthalmos Evaluation and Treatment

By Scott D. Lawrence, MD, and Carrie L. Morris, MD
Edited by Ingrid U. Scott, MD, MPH, Sharon Fekrat, MD, and Christine C. Nelson, MD
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This article is from April 2008 and may contain outdated material.
Proper eyelid closure and a normal blink reflex are essential to maintaining a stable tear film and a healthy
corneal surface. Patients affected with lagophthalmos are unable to fully close their eyelids, and they may
describe symptoms of dry and irritated eyes. Common morbidities of lagophthalmos are corneal exposure and
subsequent keratopathy, which may progress to corneal ulceration and infectious keratitis. It is important to
recognize lagophthalmos early in the patient’s course and begin treatment as soon as possible. The choice of
therapy requires an understanding of both the etiology and expected duration of the lagophthalmos.

Initial Evaluation
Taking the history. A careful history should seek to determine the etiology of the lagophthalmos. Any recent
trauma or surgery involving the head, face or eyelids should be documented. Past infections should be reviewed,
with particular attention to any history of herpes zoster infection. It is also important to document any past
symptoms suggestive of thyroid disease or obstructive sleep apnea.
Testing the lids and globe. Ask the patient to look down and gently close both eyes. Lagophthalmos is present
when a space remains between the upper and lower eyelid margins in extreme downgaze. Document the degree
of lagophthalmos by measuring this space, in millimeters, with a ruler. Also, record the blink rate as well as the
completeness of the blink. Carefully test cranial nerve function, paying particular attention to ocular motility and
the strength of the orbicularis oculi muscle. The latter can be assessed by evaluating the force generated on
attempted eyelid closure. Also, the presence and quality of the Bell’s phenomenon should be noted, as the
cornea is better protected when the eye rolls upward on attempted closure of the eyelids.
Testing the cornea. Next, test corneal sensitivity by applying soft cotton to the unanesthetized cornea and
comparing the blink reaction with that of the fellow eye. Conduct a slit-lamp exam that focuses on the presence of
punctate epithelial erosions or abrasions highlighted with fluorescein staining, and pay particular attention to the
inferior cornea where lid excursion ends. Also, record the tear breakup time. Any epithelial defects or corneal
ulcers should be carefully documented. 

Etiology
Facial nerve. The facial nerve (seventh cranial nerve) innervates both the frontalis muscle, which raises the
eyebrow, and the orbicularis oculi muscle, which closes the eyelids. Loss of function of the facial nerve inhibits
eyelid closure as well as the blink reflex and the lacrimal pumping mechanism. In addition, the facial nerve
innervates the muscles of facial expression including the zygomaticus muscles, which elevate the cheeks as well
as the corrugator supercilii and procerus muscles, which depress the eyebrow. These muscles play an important
role in maintaining facial symmetry. Facial nerve weakness may result from a host of causes:

 Trauma. The facial nerve is susceptible to blunt trauma or laceration along its bony course. Fractures to
the skull base (petrous portion of the temporal bone) or mandible can damage the nerve or one of its
branches. Neurosurgical procedures present additional risk.
 Cerebrovascular accidents. The facial nerve receives its blood supply from the anterior inferior
cerebellar artery. It is most susceptible to ischemic damage just proximal to the geniculate ganglion.
 Bell’s palsy. This is an idiopathic facial nerve palsy that is thought to be associated with an acute viral
infection or reactivation of herpes simplex virus.
 Tumors. Acoustic neuromas in the cerebellopontine angle and metastatic lesions are most commonly
associated with lagophthalmos. MRI with gadolinium best characterizes the mass.
 Infectious, immune-mediated causes. Less common causes of lagophthalmos include Lyme disease,
chickenpox, mumps, polio, Guillain-Barré syndrome, leprosy, diphtheria and botulism.
 Möbius’ syndrome. This rare, congenital condition is characterized by cranial nerve palsies (especially
sixth and seventh cranial nerve palsies), motility disturbances, limb anomalies and orofacial defects.

Eyelids. The upper and lower eyelids contain seven structural layers. Beginning anteriorly, these comprise 1)
skin and subcutaneous tissue, 2) orbicularis oculi muscle, 3) orbital septum, 4) orbital fat, 5) muscles of
retraction, 6) tarsus and 7) conjunctiva. Damage to or degeneration of any of these tissues may inhibit good
eyelid closure. Related causes of lagophthalmos include:

 Cicatrices. Chemical or thermal burns, ocular cicatricial pemphigoid, Stevens-Johnson syndrome or

mechanical trauma may cause scarring of the soft tissues or retractor muscles.
  Eyelid surgery. Excessive removal of eyelid skin or muscle (e.g., blepharoplasty, tumor excision) can
lead to lagophthalmos of the upper eyelids or retraction of the lower eyelids. Overcorrection in ptosis
repair has also been implicated.
 Proptosis. Exophthalmos of one or both globes may inhibit eyelid closure. Also, retraction of the upper
and lower eyelids is a common feature of thyroid ophthalmopathy that may increase the degree of
lagophthalmos.
 Enophthalmos. Posterior displacement of the eye may affect eyelid apposition and closure. Acquired
causes include socket contracture (orbital blowout fractures); orbital fat atrophy (trauma, infection,
inflammation, aging or a wasting disease such as linear scleroderma or HIV-AIDS); a phthisical or
prephthisical eye; or scirrhous carcinomas leading to contraction of orbital fat.
 Floppy eyelid syndrome. This condition is the result of severe laxity and flexibility of the superior and
inferior tarsal plates, and it may be associated with obstructive sleep apnea.

Symptoms
Lagophthalmos patients commonly complain of foreign body sensation and increased tearing. Pain may be
worse in the morning due to increased corneal exposure and dryness during sleep. Patients often note blurry
vision, which results from unstable tear film. In cases of advanced keratopathy and corneal ulceration, the
symptoms and presentation may be severe.

Workup and Treatment

A stepwise approach based on the severity and expected duration of the lagophthalmos is recommended. Most
important is close follow-up with frequent examination of the cornea.
Medical treatment and supportive care for corneal exposure. Nonpreserved artificial tears should be
administered frequently (at least four times per day) in order to supplement the patient’s tear film. Ointments can
be applied to the cornea once at bedtime or throughout the day in cases of severe corneal exposure. Moisture
goggles also may be used. As the corneal surface normalizes, ointments may be replaced with 0.5 percent or 1
percent methylcellulose formulations. When choosing a lubricant, the patient’s ability to accept visual blurring
caused by the viscosity of the lubricant should be considered. Infectious corneal ulcers should be treated with
appropriate antibiotic therapy. Also, the surgeon may elect to patch the eye closed or place a Frost suture for
temporary protection of the cornea.
Tarsorrhaphy. When recovery of the eyelid closure is expected within a few weeks, a temporary tarsorrhaphy
achieves narrowing of the interpalpebral fissure. In most cases, the cornea can be protected adequately by
suturing the lateral one-third of the eyelids together. Ideally, a small opening remains so that the patient can
retain useful vision, the health of the cornea may be assessed and lubrication or antibiotic therapy can be applied
to the eye.
When a protracted clinical course is evident, a permanent tarsorrhaphy may be performed by abrading the eyelid
margins at the site of the sutures to create intermarginal adhesions. The sutures are removed in 10 to 14 days. If
the patient regains useful function of the orbicularis oculi muscle, the adhesions can be lysed.
A limitation of tarsorrhaphy is that loosening of the sutures may occur, resulting in inadequate lid coverage of the
cornea. Trichiasis and poor cosmetic appearance represent additional risks.
Gold weight implantation. Gold weights can be implanted into the upper eyelid to treat paralytic lagophthalmos.
This procedure enhances eyelid closure in a gravity-dependent fashion. Gold has been considered an ideal
substance because it is inert and tends to not show through the thin skin of the eyelid. In cases of allergy,
platinum may be used.
Gold weights range from 0.6 to 1.6 g and come in 0.2-g increments. The appropriate weight is chosen
preoperatively by taping weights of varying sizes onto the external lid above the tarsus and observing the closing
and opening of the lids. Properly chosen, the ideal weight will allow full closing and opening of the lids, while
avoiding ptosis in primary gaze. Gold weight implantation is usually well-tolerated. However, astigmatic shift as
well as migration and/or extrusion of the gold weight may occur.
Upper eyelid retraction and levator recession. Recession of the upper eyelid retractors (levator and Müller’s
muscles) is a useful procedure in patients with lagophthalmos related to upper eyelid retraction from thyroid
ophthalmopathy. Also, a combination of full-thickness skin grafts, advancement flaps, tarsal-sharing procedures
and release of scar bands can be performed on patients with lagophthalmos from cicatricial or postsurgical lid
shortening.
Lower eyelid tightening and elevation. Laxity of the lower eyelid may occur in conditions such as facial nerve
palsy and floppy eyelid syndrome. A tightening procedure such as a lateral tarsal strip will improve apposition of
the lower eyelid to the globe and decrease tearing.
Patients who continue to have exposure of the cornea despite medical therapy and upper eyelid restructuring
may also benefit from lower eyelid elevation. Here, the lower eyelid retractor muscles may be recessed from their
insertion on the inferior tarsal border. An additional spacing graft may be sutured in the lid to achieve further
elevation. Autologous ear cartilage, nasal cartilage or hard palate grafts are often used. In cases with a cicatricial
component, a full-thickness skin graft and/or collagen or mucous membrane graft may be needed.
Ancillary surgical procedures. In cases of severe lagophthalmos related to facial nerve palsy, elevation of the
midface may be achieved using a variety of materials including autogenous fascia slings and/or Coapt Endotine
Midface implants. Facial reanimation procedures include temporalis muscle transposition/ transfer, nerve grafts
and anastomoses, palpebral springs, soft tissue repositioning and suborbicularis oculi fat lifts. Each approach
has been used effectively in patients with facial nerve palsy.
___________________________
Dr. Lawrence is an ophthalmology resident at the University of Tennessee in Memphis. Dr. Morris is doing an
ASOPRS fellowship in oculoplastics at the University of Tennessee and Vanderbilt University.

What is lagophthalmos?
Lagophthalmos is a condition that prevents your eyes from closing completely. If the problem
only happens when you sleep, it’s called nocturnal lagophthalmos.

The condition itself is usually harmless, but it does leave your eyes vulnerable to damage.

Lagophthalmos can also be a symptom of more serious conditions, so it’s important to

contact your doctor if you have trouble blinking or closing your eyes to sleep.

Symptoms of lagophthalmos
The main symptom of lagophthalmos is being unable to close your eyes. If you have
nocturnal lagophthalmos, you might not even know it. Look for these additional symptoms in
one or both eyes if you think you have lagophthalmos:

 increased tears
 foreign body sensation, which is the feeling that something is rubbing against your
eye
 pain or irritation, especially in the morning

Causes of lagophthalmos
A variety of things can cause lagophthalmos, but they mostly fall within two categories.

The first is damage to the seventh cranial nerve, which controls the muscles in your eyelid.
This is also known as the facial nerve. Many things can cause damage to the facial nerve,
including:

 injury, either from blunt trauma or a deep cut

 stroke
 Bell’s palsy
  tumors, especially acoustic neuromas
 Möbius syndrome
 autoimmune conditions, such as Guillain-Barré syndrome

The second group of causes involves damaged eyelids, which can result from the following:

 scarring from burns, injuries, or certain medical conditions, such as Stevens-Johnson

syndrome
 eyelid surgery
 floppy eyelid syndrome

Protruding and sunken eyes can also lead to lagophthalmos.

Diagnosing the cause of lagophthalmos

Using your medical history and a physical exam, your doctor will try to figure out the
underlying cause of lagophthalmos. Make sure you tell your doctor about any recent injuries
or infections they don’t know about.

Your doctor will also probably perform some tests. You may be asked to look down while
trying to close your eyes. Your doctor will measure the space between your eyelids with a
ruler. They might also record how often you blink, and how much your eyes close when you
do. The amount of force you use to close your eyes can also help your doctor figure out if
the facial nerve is involved.

They’ll probably also do a slit lamp exam, which involves using a microscope and bright light
to look get a better look at your eyes. Your doctor may also do a fluorescein eye stain test to
see if there are any signs of damage to your eye.

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Treatment options for lagophthalmos

There are several surgical and nonsurgical treatment options for lagophthalmos.

Surgical treatment

Changing the position of either the top or bottom eyelid can treat or improve the symptoms
of lagophthalmos. Another procedure involves implanting gold weights into the upper eyelid,
which allows the eyes to close using gravity.
If lagophthalmos is caused by a temporary condition, your doctor may suggest tarsorrhaphy.
This involves temporarily sewing your eyelids together, either completely or partially.
Keeping the eye covered helps to prevent any additional damage to it while you recover from
the underlying condition.

If the underlying condition is going to take some time to heal, your doctor may do a
permanent tarsorrhaphy. They’ll likely leave a small opening so you can still see. Once
you’ve healed, your doctor will enlarge the opening.

For severe lagophthalmos related to a paralyzed facial nerve, your doctor may suggest a
procedure that provides more support for the eyelid. These include nerve and muscle
transfers, implants, and facial reanimation procedures.

Nonsurgical treatment

Nonsurgical treatment options tend to focus on treating the symptoms of lagophthalmos,

rather than the condition itself. Applying artificial tears (Visine Pure Tears, Refresh)
throughout the day can help to prevent your eyes from drying out and itching. You can also
apply a protective ointment to your cornea throughout the day to prevent scratches.

If you have nocturnal lagophthalmos, moisture googles may help protect and moisturize your
eyes while you sleep. You can also keep a humidifier nearby while you sleep for added
moisture. Your doctor may suggest putting small weights on the outsides of your eyelids to
keep them closed. Surgical tape can provide the same effect.

Are there any complications with

lagophthalmos?
Untreated lagophthalmos leaves your eyes vulnerable to scratches and other injuries
because they aren’t protected by your eyelids.

Ongoing exposure of your eyes can also lead to exposure keratopathy, which has the same
symptoms as lagophthalmos. Exposure keratopathy can eventually cause your cornea, the
clear front part of your eye, to either swell or thin. It can also cause a corneal ulcer.

Surgery to treat lagophthalmos may also have complications. Tarsorrhaphy can leave
permanent scarring, while gold weight implants can start to move away from their original
placement. Make sure you follow your doctor’s post-surgery instructions to avoid additional
problems.
 Living with lagophthalmos
Lagophthalmos isn’t a dangerous condition, but it can eventually lead to eye problems. Work
with your doctor to figure out the underlying cause. Depending on the cause, you can treat
lagophthalmos with either surgery or products to help keep your eyes moisturized and
protected.

Abstract 

Purpose

To describe our experience treating a cohort of unilateral aphakic infants with contact lenses in the Infant
Aphakia Treatment Study (IATS).

Materials and methods

Fifty-seven of the 114 infants in the IATS were randomized to contact lens wear; all were followed until age 5
years, although a few had lapses in care. An examination under anesthesia, including keratometry, was
performed at the time of enrollment and at approximately 1 year of age; keratometry was performed again at 5
years of age. A traveling examiner assessed visual acuity at approximately 1 year of age and again at 4.5 years
of age.

Results

Twenty-four treated eyes (46%) wore silicone elastomer (SE) contact lenses, 11 eyes (19%) rigid gas permeable
(GP) contact lenses and 17 eyes (29%) wore both lens types at various points of time. Median logMAR visual
acuity was +0.70 (interquartile range (IQR), +0.30 to 1.20) in the SE group and 2.03 (IQR, +0.20 to 2.28) in the
GP group at age 4.5 years. The mean (±SD) keratometric power of the treated eyes was 46.3±2.8 diopter (D) at
baseline, 44.6±2.3 D at 1 year of age, and 44.3±1.7 D at 5 years of age. Keratometric astigmatism of treated
eyes was 1.98±1.37 D at baseline, 1.62±0.98 D at 1 year of age, and 2.00±1.00 D at 5 years of age. Thirteen
contact lens-related adverse events occurred among 7 patients after age 1 year.

Conclusions

A cohort of infants with unilateral aphakia successfully wore contact lenses with relatively few adverse events.

Abstract and Figures

We describe our experience correcting a cohort of infants with contact lenses in the
Infant Aphakia Treatment Study. Fifty-seven infants 1-6 months of age were
randomized to contact lens wear. An examination under anesthesia was performed
at the time of enrollment and at approximately 1 year of age. A traveling examiner
assessed visual acuity at approximately 1 year of age. Forty-two treated eyes (74 %)
were fitted with silicone elastomer (SE) contact lenses; 12 eyes (21 %) with rigid gas
permeable (RGP) contact lenses, and 3 eyes (5%) wore both lens types. Median
visual acuity was +0.80 logMAR in both lens type-wearing groups. The mean (± SD)
keratometric power of the treated eyes was 46.3±2.8 D at baseline and 44.6±2.3 D
at 1 year of age for a mean decrease of 0.2±0.2 D/mo. Keratometric astigmatism of
treated eyes was 1.98±1.37 D at baseline and 1.62±0.98 D at 1 year of age for a
mean decrease of 0.05±0.2 D/mo. The mean RGP lens base curve at baseline was
47.62 D±2.62 D versus 47.00 D±3.50 D at 12 months after surgery. Children wearing
SE lenses required a mean of 10.9 replacements (range 2-24) compared to 16.8
replacements (range 8-32) for children wearing RGP lenses. Three adverse events
occurred. Contact lenses were worn successfully with relatively few adverse events
by a cohort of infants with unilateral aphakia. The visual acuity results were identical
independent of the contact lens material or modality. RGP lenses needed
replacement more often than SE lenses.

3. 1. Ophthalmia Neonatorum. 2 3. Endophthalmitis. 4. 5.

Adela Matejcek, MD and Ran D. Goldman, MD FRCPC

Author information Copyright and License information Disclaimer

This article has been cited by other articles in PMC.

Abstract
Conjunctivitis is an inflammatory disease characterized by conjunctival erythema, swelling, and
discharge.1 Ophthalmia neonatorum (ON), also called neonatal conjunctivitis, is an acute, mucopurulent infection
occurring in the first 4 weeks of life,2 affecting 1.6% to 12% of all newborns,3,4 caused by chemical, bacterial, or viral
processes.3 Before the 1880s, ON was the primary cause of neonatal blindness and the term ophthalmia
neonatorum was used only for cases of conjunctivitis due to Neisseria gonorrhoeae.5,6 In 1881, Dr Carl Siegmund
Franz Credé, a German obstetrician, introduced ocular prophylaxis with 2% silver nitrate at birth, which resulted in a
dramatic reduction in the incidence of neonatal gonococcal conjunctivitis from 10% to 0.3%. 5,7 In recent years, there
has been increasing debate about the necessity of “Credé’s prophylaxis” given that the prevalence of sexually
transmitted infections has declined, treatment of ON has improved, and prophylaxis carries a certain risk of
developing antibiotic resistance. As a result, ocular prophylaxis has fallen out of practice in some countries in the
developed world, which has led to the reemergence of sight-threatening infections. 8 In the current Canadian context,
the evidence supports that ocular prophylaxis should remain the standard of care 5; however, debate and controversy
have emerged around this issue in Canada.9

Go to:

Causes of ON
Causes of ON include the following.

Chemical conjunctivitis
Chemical conjunctivitis accounts for most cases of ON,4 presenting as a mild, purulent conjunctivitis within the first
24 hours of life. It is most commonly associated with silver nitrate prophylaxis, or secondary to prophylaxis with other
agents such as erythromycin or tetracycline. 3 Chemical conjunctivitis is a self-limiting condition that does not require
any diagnostic tests or treatment.10

Non–sexually transmitted bacteria

Non–sexually transmitted bacteria account for 30% to 50% of cases of ON. 5 The most commonly isolated
microorganisms are listed in Box 1. The role of Staphylococcus aureus is unclear, as it is commonly cultured from the
eyes of asymptomatic infants.1 Most cases of bacterial ophthalmia can be treated with topical antibiotics
(aminoglycosides, polymyxin B sulfate–trimethoprim solution, macrolides, or fluoroquinolones). 1,3,11 Ophthalmia
neonatorum caused by Pseudomonas is rare but can present with eyelid edema, erythema, and purulent discharge
causing corneal perforation, endophthalmitis, blindness, and possibly death. 3,4 Presumptive diagnosis can be made
from Gram stain results, and a definitive diagnosis is based on conjunctival culture results. 4 Systemic antibiotics have
poor penetration into the anterior chamber of the eye, and thus both systemic and topical aminoglycoside antibiotics,
and occasionally subconjunctival injections, are required for effective treatment. These infants require isolation and
assessment by an ophthalmologist.3

Box 1.

Causes of ophthalmia neonatorum

Causes of ophthalmia neonatorum include the following:

 Chemical

 Bacterial

 Chlamydia trachomatis

 Neisseria gonorrhoeae

 Haemophilus species

 Streptococcus pneumoniae

 Staphylococcus aureus

 Staphylococcus epidermidis

 Streptococcus viridans

 Escherichia coli

 Pseudomonas aeruginosa

 Other

 Viral

 Adenovirus

 Herpes simplex virus

Sexually transmitted bacteria

Chlamydia trachomatis: Sexually transmitted bacteria including C trachomatis account for up to 40% of all cases of
ON in Canada.3,5 An infant born vaginally to a mother with chlamydial cervicitis has a 50% to 75% chance of
acquiring the bacteria in the nasopharynx, rectum, vagina, or conjunctiva. 12 Of neonates with proven exposure to
chlamydia, 30% to 50% will develop conjunctivitis.13 The prevalence of chlamydial infections is higher in the spring
and summer months.14 The incubation period is typically 1 week after delivery; however, it varies from 5 to 14 days or
earlier if membranes ruptured prematurely.15 The clinical manifestations vary from mild conjunctival injection with
scant watery discharge to severe mucopurulent discharge with eyelid edema, chemosis, and pseudomembrane
formation.6,13 Loss of vision is very rare. Most cases of chlamydial infections resolve spontaneously without
complications, but, if left untreated, superficial corneal vascularization and conjunctival scarring can
occur.13 Newborns with conjunctivitis should have specimens of their conjunctiva and pharynx sent for culture. The
American Academy of Pediatrics recommends a 14-day course of systemic erythromycin (50 mg/kg/d, divided in 4
doses).16 Topical therapy is not indicated.13 Erythromycin has a 10% to 20% failure rate and thus some infants will
require a second or occasionally a third course of erythromycin. 11 Parents should be informed of the potential risk of
pyloric stenosis and counseled on monitoring.13 A small study has demonstrated that a short course of oral
azithromycin (20 mg/kg once daily for 3 days) might be an effective treatment alternative; however, further studies
are needed.17 The infant’s mother and her sexual partners should be treated for chlamydia. 3

Neisseria gonorrhoeae: Neisseria gonorrhoeae accounts for less than 1% of all reported cases of ON in Canada.5 In
the absence of adequate prophylaxis, 30% to 42% of infants born by vaginal delivery to infected mothers will develop
gonococcal ON.6 The transmission rate is higher in mothers with concomitant chlamydial infection. 18 Infants born to
mothers with known gonococcal infection should be treated with a single parenteral dose of cefotaxime or
ceftriaxone.5,7 If left untreated, gonorrheal ON can lead to corneal scarring, ulceration, panophthalmitis, and
perforation of the globe within 24 hours.7 The disease typically presents with profound chemosis, edema of the
 eyelids, and abundant purulent discharge that might be blood-tinged from superficial hemorrhage within 2 to 5 days of
birth; however, it can manifest up to 2 to 3 weeks after delivery. 6,7 Infants with gonorrheal ON should be hospitalized,
treated with frequent irrigation of the conjunctiva and intravenous or intramuscular administration of ceftriaxone (25
to 50 mg/kg, to a maximum dose of 125 mg), and evaluated for disseminated gonococcal disease (eg, arthritis, sepsis,
meningitis).1,3,4 The infant’s mother and her sexual partners should be treated for gonorrhea. 1

Viral conjunctivitis
Viral conjunctivitis is most commonly caused by adenovirus and herpes simplex virus. 1,6 Infants with adenovirus ON
might present with petechial hemorrhage or occasionally with large subconjunctival hemorrhages. 1 Lymphadenopathy
is associated with approximately 50% of cases of viral conjunctivitis. 1 Infants with conjunctivitis caused by herpes
simplex virus might be diagnosed late, as they are commonly treated empirically for chlamydial or gonococcal
infection.6 Herpetic lesions on the borders of the eyelids are common and present 6 to 14 days after birth. 6 These
infants require diagnostic evaluation, including lumbar puncture, and assessment by an ophthalmologist. Treatment
includes systemic acyclovir (60 mg/kg in divided doses 3 times a day) for 14 days, coupled with topical ophthalmic
solution (ie, 1% trifluridine, 0.1% iododeoxyuridine, or 3% vidarabine). 16,19

Go to:

Preventing conjunctivitis
The Canadian Paediatric Society recommends that ocular prophylaxis with 1% silver nitrate, 0.5% erythromycin
ointment, or 1% tetracycline hydrochloride be given to all newborns, including those born by cesarean section, in the
first hour after birth.5 It is important to note that routine ocular prophylaxis does not prevent chlamydial ON; and that
although gonorrheal ON has become relatively rare with the introduction of ocular prophylaxis, it must continue to be
considered, given its high propensity to cause severe ocular destruction and blindness. 3

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Updated: Mar 03, 2021 
 Author: Michael A Puente, Jr, MD; Chief Editor: Andrew A Dahl, MD,
FACS  more...

Background
Neonatal conjunctivitis, also known as ophthalmia neonatorum, presents
during the first month of life. It may be aseptic or septic and, if left
untreated, may be blinding.
Aseptic neonatal conjunctivitis most often is a chemical conjunctivitis that is
induced by silver nitrate solution, which has been used at birth since the
late 1800's for prophylaxis of infectious conjunctivitis (a procedure known
as Credé's prophylaxis). Chemical conjunctivitis is becoming less common
owing to the use of erythromycin ointment or povidone iodide in place of
silver nitrate solution for the prophylaxis of infectious conjunctivitis

Ophthalmia neonatorum
The CMGs are guidelines on the diagnosis and management of a range of common and rare, but
important, eye conditions that present with varying frequency in primary and first contact care.

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 Aetiology

Ophthalmia Neonatorum (ON) (conjunctivitis of the newborn) occurs within the first month of life. It is a
bacterial, chlamydial or viral infection acquired during passage through an infected birth canal. Since April
2010 it is no longer a notifiable disease in the UK.

Historically, the commonest agent was Neisseria gonorrhoeae (also known as ‘gonococcus’, and a cause
of sexually-transmitted disease). The use of silver nitrate drops as prophylaxis was introduced in the C19,
although abandoned in the UK in the 1950s. Gonococcal ON develops in approx. 30-50% of newborns
exposed to gonococcal infection during delivery

Nowadays a more usual agent, also sexually acquired by the mother, is Chlamydia trachomatis. Babies
born to women with untreated chlamydial infection at delivery have a 30-50% chance of developing ON

The incubation period is usually as follows:

 C. trachomatis: 5-14 days

 N. gonorrhoeae: 3-5 days
The prevalence of ON differs in different parts of the world and is dependent mainly upon socio-economic
conditions, level of knowledge about general health, standard of maternal healthcare as well as the type of
prophylactic programme used. UK incidence is:

 C. trachomatis: 6.9 per 100,000 live births

 N. gonorrhoeae: 3.7 per 100,000 live births
In low income countries, very much higher incidences have been reported

Other bacteria that cause ON

include Haemophilus, Streptococcus, Staphylococcus and Pseudomonas species

Viral infections (less common) can be caused by herpes simplex virus, adenovirus or enterovirus

The neonatal conjunctiva is particularly vulnerable to infection because of the lack of immunity and the
absence of local lymphoid tissue at birth

Predisposing factors

Infection of the maternal birth canal as the result of sexually-transmitted disease

This infection may be asymptomatic, especially in the case of C. trachomatis

Symptoms

(Usually described by mother):

 redness
 discharge (may be profuse in gonococcal infection)
 swelling of lids (may be severe)
 symptoms usually bilateral

Signs

Lids

 oedema (may impede examination of ocular surfaces)

Conjunctival features
 mucopurulent conjunctivitis – discharge may be profuse in  C. trachomatis infection. Danger of
infection of clinician when prising open lids
 NB: in neonatal C. trachomatis infection there are no follicles as in adults, because of the
neonate’s lack of lymphoid tissue
 conjunctival oedema (‘chemosis’)
 conjunctival membrane in severe cases
Corneal features

 cornea can be involved, especially in N. gonorrhoeae infection. This organism can pass through
intact corneal epithelium. Perforation may result
 signs usually bilateral; may be asymmetrical

Differential diagnosis

 By definition, conjunctivitis occurring within the first month of life is ON

 Congenital obstruction of the nasolacrimal duct(s) is often associated with epiphora, discharge and
recurrent conjunctivitis (see Clinical Management Guideline on Nasolacrimal Duct Obstruction)

Management by optometrist

Practitioners should recognise their limitations and where necessary seek further advice or refer
the patient elsewhere

GRADE*  Level of evidence and strength of recommendation always relates to the

statement(s) immediately above

Non pharmacological
None

Pharmacological
None

Management category

A1: emergency (same day) referral to ophthalmologist; no intervention ON may result in a severe
and progressive conjunctivitis with corneal complications and be associated with potentially
serious systemic infection

Possible management by ophthalmologist

Diagnosis

 conjunctival cultures for bacteria (N. gonorrhoeae requires special media)

 conjunctival scraping for Gram stain (bacteria) and Giemsa stain (for C. trachomatis)
 Polymerase Chain Reaction (PCR) studies
Treatment

Bacterial conjunctivitis

 systemic penicillin G or a cephalosporin for  N. gonorrhoeae

 topical erythromycin sometimes given in addition
 other topical antibiotics, including azithromycin or chloramphenicol
 frequent irrigation until discharge ceases
 Chlamydial conjunctivitis

 systemic erythromycin
 topical azithromycin
Herpetic conjunctivitis

 systemic and topical antiviral, e.g. aciclovir

Endophthalmitis is a purulent inflammation of the intraocular fluids (vitreous and

aqueous) usually due to infection. Serious intraocular inflammatory disorder resulting
from infection of the vitreous cavity. Progressive vitritis is the hallmark of any form of
endophthalmitis.
What causes endophthalmitis?
Endophthalmitis is the term used to describe severe inflammation of the tissues inside the eye. The
inflammation is typically due to infection by bacteria (eg. Staphylococcus species, Streptococcus species,
Gram-negative bacteria) or fungi (eg. Candida, Aspergillus).
What are the signs of endophthalmitis?

The most common symptoms of endophthalmitis are:

 eye pain that keeps getting worse after surgery, an injection or injury to the eye.
 red eyes.
 white or yellow pus or discharge from the eyes.
 swollen or puffy eyelids.
 decreased, blurred or lost vision.

What Is Endophthalmitis?
 Symptoms

 Causes

 Diagnosis

 Treatment

 Complications

 Prevention
 Outlook

Overview
Endophthalmitis, pronounced “end-opf-THAL-mi-tis, is the term used to describe severe
inflammation inside the eye. Inflammation is caused by an infection. It may occur with certain types
of eye surgery or if the eye has been pierced by an outside object.

Endophthalmitis is very rare, but if it occurs, it’s an urgent medical emergency.

Symptoms of endophthalmitis
Symptoms occur very quickly after infection. They will typically occur within one to two days, or
sometimes up to six days after surgery or trauma to the eye. Symptoms include:

 eye pain that becomes worse after surgery or injury to the eye
 decreased or loss of vision
 red eyes
 pus from the eye
 swollen eyelids

Symptoms may also occur later, such as six weeks after surgery. These symptoms tend to be milder
and include:

 blurred vision
 mild eye pain
 trouble looking at bright lights

If you notice any of these symptoms, see a doctor right away. The sooner endophthalmitis is treated,
the less likely it is to cause continued and serious vision problems.

Causes of endophthalmitis
There are two main types of endophthalmitis. One is exogenous endophthalmitis, meaning infection
goes inside the eye through an outside source. The second is endogenous endophthalmitis, meaning
infection spreads to the eye from another part of the body.

Exogenous endophthalmitis is the most common form. It can occur as a result of a cut to the eye
during surgery or by piercing of the eye by a foreign body. Such cuts or openings make it more likely
infection will travel inside the eyeball.
Exogenous endophthalmitis is seen more frequently with specific eye surgeries. One is cataract
surgery. This isn’t necessarily due to the surgical procedure itself. Cataract surgery is the most
common eye surgery performed, so there are more possibilities for this surgery to result in
endophthalmitis.

Other surgeries that result more frequently in this type of infection are those done within the eyeball
itself. This is called intraocular surgery.

Risk factors for exogenous endophthalmitis include extra loss of fluid behind the eye, poor wound
healing, and a longer surgery time.

After a piercing eye trauma, risk factors for endophthalmitis include:

 having the foreign object, or a piece of the object, remain in your eye
 waiting more than 24 hours to repair the cut
 being in rural settings, where you’re more likely to get soil in your eye
 damage to the lens

People who’ve had certain types of surgery for glaucoma, such as glaucoma filtering, are at life-long
risk of developing endophthalmitis.

Diagnosis
Your doctor, usually an ophthalmologist (a doctor specializing in eye health), will likely do several
things to find out if symptoms are from endophthalmitis. They will look at your eye and test your
vision. They may order an ultrasound to see if there are any foreign objects in the eyeball.

If an infection is suspected, your doctor may perform a test called a vitreous tap. This involves using a
tiny needle to take some fluid out of your eyeball. The fluid is then tested so your doctor can tell the
best way to treat the infection.

Treatment of endophthalmitis
Treatment ofendophthalmitis depends in part on the cause of the condition.

It’s most important to get an antibiotic into the eye as soon as possible. Typically, antibiotics are
placed right into the eye with a tiny needle. A corticosteroid may be added in some cases to reduce
swelling. Only in very rare and more serious cases are general antibiotics given.

If there’s a foreign body in the eye, it’s equally important to remove the object as quickly as possible.
Never try to remove an object from your eye by yourself. Instead, seek immediate medical attention.
Symptoms often begin to improve within several days of starting treatment. Eye pain and swollen
eyelids tend to improve before vision gets better.

Complications from treatment

Complications from endophthalmitis treatment can be reduced by following your doctor’s eye care
advice. In particular, be sure you know how and when to put in any prescribed eye drops or antibiotic
eye ointment. If an eye patch is prescribed, you should also know how and where to place the patch.
You may need tape to keep the patch in place.

Be sure to keep all follow-up eye appointments with your doctor.

Prevention of endophthalmitis
Use protective eyewear when doing anything that could cause an object to fly into your eye, such as
sawing wood, or during contact sports. Protective eyewear may include:

 goggles
 eye shields
 helmets

If you have eye surgery, follow your doctor’s postoperative instructions. That can help reduce your
risk for infection.

Outlook
Endophthalmitis is a complex condition with a potentially serious outcome for your vision. Declining
vision and possibly the loss of an eye may occur. The likelihood of these events is greatly reduced if
the condition is treated right away. It’s a medical emergency that requires immediate and appropriate
medical attention. If treated correctly and right away, the outlook for endophthalmitis is usually
considered to be good.

Abstract
Go to:

Introduction
Endophthalmitis is one of the most devastating diagnoses in ophthalmology. It is a serious intraocular inflammatory
disorder affecting the vitreous cavity that can result from exogenous or endogenous spread of infecting organisms into
the eye.1 With any breaching of the ocular bulbus, the potential exists for introducing an infectious inoculum large
enough to cause an intraocular infection. This is most commonly seen after intraocular surgery but can also occur as a
complication of penetrating ocular trauma or from the adjacent periocular tissues.
Endogenous endophthalmitis is less common and occurs secondary to hematogenous dissemination and spread from a
distant infective source in the body. In patients with endogenous endophthalmitis, predisposing risk factors usually
exist.2–6

In most cases, independent of its origin, the presentation of endophthalmitis consists of reduced or blurred vision, red
eye, pain, and lid swelling.3,5,7,8 Progressive vitritis is one of the key findings in any form of endophthalmitis, and in
nearly 75% of patients a hypopyon can be seen at the time of presentation 1 (see Figure 1). Progression of the disease
may lead to panophthalmitis, corneal infiltration, and perforation, affection of orbital stuctures, and phthisis bulbi.

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Figure 1

Anterior chamber inflammation, mild corneal edema, and hypopyon in bacterial endophthalmitis.

In general, the incidence of endophthalmitis has decreased in recent decades 9 and, fortunately, endophthalmitis is
rare.7,9,10 Nonetheless, its evident severity and indistinct prognosis require timely and effective treatment to provide
satisfactory visual results.

Go to:

Pathogenesis and clinical presentation

Exogenous endophthalmitis

Postoperative endophthalmitis
Endophthalmitis after ocular surgery is the most common form of the condition. Cataract surgery is by far the most
frequently performed intraocular surgery.11 Approximately 90% of postoperative endophthalmitis cases develop after
this procedure7,9,10 with an incidence following such surgery ranging from 0.08% to 0.7%. 10,12–15 A recently published
meta-analysis indicates that the endophthalmitis rate seems to have increased during the last two decades. 16 According
to these data, the rate of endophthalmitis following cataract surgery was about 0.09% during the 1990s and 0.27% in
2000.16 Greater use of clear corneal incision has been debated as a potential reason for this. Experimental data indicate
that with this technique wound architecture seems to be less stable, thus allowing fluctuations in the intraocular
pressure and potentially easier entry of bacteria through a less completely sealed wound. Some studies found a three-
to four-fold risk for endophthalmitis after clear cornea cataract surgery compared with scleral tunnel incisions. 17,18 In
contrast, Lalwani et al reviewed 73 endophthalmitis cases after clear cornea cataract surgery and compared them with
the data from the Endophthalmitis Vitrectomy Study (EVS), in which scleral tunnel and clear cornea incisions were
used. They found that time to endophthalmitis diagnosis was longer in clear cornea cataract surgery cases but clinical
features, causative organisms, and visual acuity outcomes were similar to those reported in the EVS. 19

Wound integrity also seems to be an important feature influencing the risk for developing endophthalmitis in pars
plana vitrectomy. In general, the incidence of endophthalmitis after pars plana vitrectomy is low (0.03%–
0.05%).10,20 Nevertheless, recent data indicate that the use of sutureless small incision techniques (eg, 23- or 25-gauge
incision size) is significantly associated with a higher rate of postoperative endophthalmitis than the sutured 20-gauge
technique.21

However, endophthalmitis can also complicate other ocular surgeries and procedures such as intravitreal
injections.22,23 Some data suggest that penetrating keratoplasty, trabeculectomy, and glaucoma drainage device
implantation have a higher risk of being complicated by endophthalmitis than cataract surgery. 24–26 Regarding
glaucoma filtering surgery, endophthalmitis is reported to occur after 0.2%–9.6% of trabeculectomies, 24,27–32 and its
incidence seems to increase with the rising use of antifibrotic agents, such as mitomycin-C or 5-fluorouracil. 27–
29,32,33
 Endophthalmitis rarely occurs after external ocular surgeries including scleral buckling, pterygium excision,
removal of corneal sutures, and strabological interventions. 34–38

In general, secondary intraocular lens placement seems to be associated with the highest risk for developing
endophthalmitis (0.2%–0.37%) and pars plana vitrectomy with the lowest (0.03%–0.05%). 10,20

Preoperative risk factors include eyelid abnormalities, blepharitis, conjunctivitis, cannuliculitis, lacrimal duct
obstructions, contact lens wear, and ocular prosthesis in the fellow orbit. 39–42

The ocular surface and the adnexa are considered the primary sources of infection in postoperative
endophthalmitis.41 However, contaminated agents or surgical equipment used perioperatively may also be a source of
infection.43–45 In addition, perioperative variations seem to have some impact on postoperative endophthalmitis rate;
different intraocular lens (IOL) materials potentially act as vectors for bacterial spread into the eye 11,46,47 and
viscoelastic substances, such as sodium hyaluronate, or hydroxypropylmethylcellulose may facilitate transmission of
bacteria to the eye.48,49

Knowledge about the cause of endophthalmitis is essential because the spectrum of organisms may change,
warranting different therapeutic approaches. Bacteria infections are the most common cause of postoperative
endophthalmitis, and Gram-positive isolates account for most cases.7,10,15,50 Fungal infections may also occur,
particularly in association with the use of contaminated ocular irrigation fluids. 43,51

Postoperative endophthalmitis can be either sterile or infectious. In the EVS, only 69.3% of cases met the criteria for
laboratory-confirmed infection.7 The reasons that more than 30% of cases failed to obtain positive results from culture
vary and include low microbial counts, spontaneously sterilizing during the ocular inflammatory response of certain
strains (eg, Staphylococcus epidermidis), or even noninfectious inflammations.7,10,15,50,52

In addition, the etiology of endophthalmitis might differ depending on the location in the world where the disease
occurs. Whereas the microbiologic spectrum in Europe or in the US seems to be generally comparable, 7,46 it might be
very different in other parts of the world. According to the EVS, 94.2% of culture-positive endophthalmitis cases
involved Gram-positive bacteria; 70% of isolates were Gram-positive, coagulase-negative staphylococci, 9.9%
were Staphylococcus aureus, 9.0% were Streptococcus species, 2.2% were Enterococcus species, and 3% were other
Gram-positive species. Gram-negative species were involved in 5.9% of cases. 7 In contrast, a recent survey from India
reported that Gram-positive bacteria accounted for only 53% of postoperative endophthalmitis cases, but 26% were
Gram-negative isolates and 17% were of fungal origin.53

The advent of new therapeutic strategies for treating age-related macular degeneration, diabetic macular edema, and
uveitis has led to a dramatic increase in intravitreal drug application. The risk of endophthalmitis after intravitreal
injection is of rising concern.23 Recent data, albeit limited, indicate that coagulase-negative staphylococci, as in
postoperative endophthalmitis, appear to be the predominant pathogens in the development of endophthalmitis after
intravitreal injection.23 Less common organisms, including Streptobacillus parasanguis, Mycobacterium chelonae,
and Streptobacillus species, as well as cases of noninfectious (sterile) endophthalmitis, especially in the context of
intravitreal triamcinolone acetonide injections, have been reported in the literature. 22,23,54

The majority of patients with postoperative endophthalmitis present with an acute onset and within seven days after
surgery.7,55 Chronic postoperative endophthalmitis is characterized by insidious inflammation and appears less
common than the acute variety. Such cases can occur in the early postoperative period but usually manifest several
weeks or month after surgery and often include less virulent bacteria and fungal pathogens.

Depending on the infecting organism, a correlation is thought to exist between clinical presentation and microbiologic
spectrum. Gram-positive, coagulase-negative micrococci seem to cause less severe infections compared with more
virulent Gram-negative and “other” Gram-positive organisms. 7 Streptococcal endophthalmitis often results in earlier
onset and notably worse outcomes than infections by staphylococcal species. Endophthalmitis cases that failed to
obtain positive results from culture tended to have a later onset and a better visual outcome. 55–59

More severe infections are correlated with loss of red fundus reflex, afferent papillary defect, and light perception
only at the time of initial presentation.7 The presence of corneal infiltrates or cataract wound abnormalities are more
strongly associated with more virulent Gram-negative and “other” Gram-positive organisms. 7 In addition, when more
virulent pathogens are involved, signs and symptoms of endophthalmitis might be apparent earlier. 7 This is important
because these cases seem to be significantly correlated with a worse visual outcome.

Specific factors influencing bacterial adhesion, including IOL material and surface irregularities, might have a role in
the development of certain forms of endophthalmitis. S epidermidis carrying the intercellular adhesion locus might
play a part in the pathogenesis of some forms of endophthalmitis. 60,61

In most cases the diagnosis of endophthalmitis is made on clinical grounds. Any eye with inflammation that is out of
proportion to the previous surgical trauma or greater than the predicted postoperative clinical course must be
suspected as indicating postoperative endophthalmitis. If doubt cannot be erased, frequent observations should be
conducted until the clinical course can be determined. Symptoms can be variable, from very little inflammation in the
anterior chamber and the anterior portion of the vitreous to extremely painful panopthalmitis with no fundus view,
corneal edema, or complete anterior chamber hypopyon7,24,50 (see Figure 2).

Figure 2

Leukocornea as a result of massive corneal edema and complete hypopyon in advanced Staphylococcus aureus endophthalmitis.
According to the EVS, hypopyon can be seen in nearly 75% of patients, whereas ocular pain, often regarded as
pathognomonic for endophthalmitis, was absent in 25% of patients. 7 In the European Society of Cataract and
Refractive Surgeons Endophthalmitis Study (ESCRS) of prophylaxis for postoperative endophthalmitis after cataract
surgery, hypopyon was present in 80% of culture-proven cases and 56% of unproven cases, resulting in an overall
incidence of 72%.55 Most common presentations include decreased vision, ocular pain and redness, corneal edema,
and vitritis. In addition, retinal vasculitis, retinal hemorrhages, and posterior pole hypopyon may
occur7,24,50 (see Figure 3).

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Figure 3

Posterior hypopyon in bacterial endophthalmitis imaged with Optomap widefield fundus imaging.

Posttraumatic endophthalmitis

Endophthalmitis is an important complication of open globe injury. About 25% of endophthalmitis cases are a result
of ocular trauma and these are more often associated with a poorer visual outcome than otherwise similar globe
injuries.8 After posttraumatic endophthalmitis, only 22% to 42% of patients obtain a final visual acuity of 20/400 or
better.62–64

The risk for developing endophthalmitis after sustaining open globe injuries is estimated at about 7%. 1,8,65 Increasing
risk factors for endophthalmitis after ocular injury are dirty wound, lens capsule rupture, older age, initial presentation
with a delay of more than 24 hours, and the presence of intraocular foreign bodies. 8,66–69 The incidence of
endophthalmitis in cases of penetrating ocular trauma has been reported to range from 3.3% to 30% and after
intraocular foreign body from 1.3% to 61%.8,63

A recent study from China, including 4968 eyes with open globe injury, found an incidence of posttraumatic
endophthalmitis of 11.9%,70 which is consistent with previous published data within the range of 2.6% to 54.2%. 70–
73
 In contrast, no evident correlation is found between the results of intraocular content culturing and development of
posttraumatic endophthalmitis. Ariyasu and colleagues found that 33% of open globe injuries were culture-positive
when aqueous was sampled, but none of these patients developed endophthalmitis. 66 In contrast, the prevalence of
culture-negative cases of posttraumatic endophthalmitis has been reported to range from 17% to 42%. 67,68,74–
76
 Therefore, some authors do not suggest routine culture in all cases of open globe injury. 67

Bacillus and Streptococcus are common species found in penetrating trauma with an intraocular foreign body. 68 This
is important because Bacillus species are associated with more aggressive infection and are especially common in
intraocular foreign bodies with organic composition.64 Other species isolated include S.
epidermidis, Propionibacterium acnes, Pseudomonas and Streptococcus species, Gram-negative organisms, fungi,
and mixed pathogens.8,64,70

Initial evaluation of posttraumatic endophthalmitis must exclude occult or retained foreign bodies. If the fundus view
is inadequate, computed tomography or, in eyes with self-sealing or previously sutured wounds, ultrasound may be
helpful. Magnetic resonance imaging must be avoided because a retained foreign body might be magnetic.

Posttraumatic endophthalmitis may also be a result of contagious spread from an infected corneal, scleral, or adjacent
wound.8,68–70 Depending on the virulence of the infecting organism, posttraumatic endophthalmitis may occur within
hours after the trauma or up to several weeks after injury. 8,68–70 Signs and symptoms must be evaluated with regard to
the degree of traumatic injury and include decreased vision, pain greater than expected, lid swelling, corneal ring
ulcer, anterior chamber inflammation, hypopyon, vitritis, or frank purulence.

Endogenous endophthalmitis

Unlike the origin in exogenous endophthalmitis, where the pathogen enters from outside the body into the eye, in
endogenous endophthalmitis the infection is secondary to hematogenous spread from a distant infective source within
the body. The endogenous form of endophthalmitis accounts for approximately 5% to 10% of endophthalmitis
cases.3,4,77–80 It occurs when microorganisms in the bloodstream get into the eye, cross the blood–retina barrier, and
infect the ocular tissue. Because of the higher blood flow, choroids and ciliary body are the primary focuses of
infection in the eye with secondary involvement of the retina and vitreous. 3,5,79,81

Risk factors for the development of endogenous endophthalmitis are mainly related to immunosuppression or to
procedures that increase the risk for blood-borne infections. Most common factors include immunosuppressive
diseases, such as diabetes mellitus, HIV infection, cancer, renal failure requiring dialysis, cardiac disease, long-term
use of broad-spectrum antibiotics, steroids and other immunosuppressive drugs, major surgery, especially intra-
abdominal surgery, intravenous hyperalimentation, indwelling intravenous catheters, and intravenous drug abuse. 3,4,77–
80
 Liver abscesses have been reported as the most common infectious origin, 3,82–84 followed by pneumonia,
endocarditis, soft tissue infection, urinary tract infections, meningitis, septic arthritis, and orbital cellulitis. 3

Causative organisms of endogenous endophthalmitis may be bacteria, as well as fungi, and rarely parasites. In contrast
to exogenous forms of this disease, in endogenous endophthalmitis fungal pathogens play an important
role.3,4,85 However, the infecting organisms vary with geographic location.

In Europe and the US, Streptococcus species, S. aureus, and other Gram-positive bacteria account for two-thirds of
bacterial endogenous endophthalmitis cases and Gram-negative isolates are found in only 32% of cases. 4,79 These
numbers differ significantly from East Asia, where most cases of endogenous endophthalmitis are caused by Gram-
negative organisms. In these areas, Klebsiella isolates count for 80% to 90% of positive cultures.3,83 This difference
might be attributable to the higher incidence of cholangiohepatitis and liver abscess in East Asian people than in the
Western population.3,82–84 However, during the last two decades, the number of endogenous ocular infections due to
Gram-negative pathogens has dramatically increased in the Western world. 79 In contrast with its prominent role in
acute postoperative endophthalmitis, S. epidermidis is only rarely found to cause endogenous endophthalmitis. 3

Fungal endophthalmitis has become an increasing issue in western countries. Candida albicans followed

by Aspergillus are the predominant species.3,85 Candida species are a part of the human flora where they exist as
commensals on the mucosal surface of the respiratory, gastrointestinal, and female genital tracts. 86 Where the immune
system is compromised these organisms potentially become pathogenic. Candida species are the most common cause
of nosocomial fungal infections.87–89

Candida chorioretinitis and endophthalmitis occur predominantly as a result of candidemia seeding the eye; cases in
otherwise healthy individuals have rarely been reported.90,91 Prospective studies demonstrated that patients with
candidemia have a risk of developing endogenous fungal endophthalmitis of up to 49%. 2,81,92,93 However, a recently
published study demonstrated that in patients with disseminated fungal disease, Candida chorioretinitis and
endophthalmitis occurred in approximately 2.5% of cases. 94 These data might indicate that the current trend for
prophylaxis and early treatment, as well as new drugs and treatment strategies for Candida infections, have decreased
the incidence of fungal ocular complications dramatically. 94,95 Other isolates commonly found in endogenous fungal
endophthalmitis are Cryptococcus and Fusarium species. 85,90

Clinical findings in endogenous endophthalmitis may be similar to those in infections of exogenous origin. They
include decreased vision, ocular pain, conjunctiva injection, hypopyon, corneal edema, vitritis, and reduced fundus
view secondary to inflammation. Especially in cases of fungal infection, a subacute onset of floaters and blurred
vision may be associated with ocular discomfort and photophobia. 94 In Candida infections, localized fluffy creamy
white retinal or subretinal nodules may be associated with vitreous haze. 86,94 (see Figure 4). Early or peripheral fungal
lesions may be asymptomatic, with patient referral for ocular consultation based on a positive blood culture or
diagnosis of a systemic fungal infection. When more virulent pathogens are involved, widespread areas of
perivascular infiltrates and hemorrhages with necrosis and retinal infarction can be seen. 5,8,96,97 In panophthalmitis, the
whole globe and the orbital tissue may be involved.5,84

Figure 4

Localized epiretinal infiltrates of fluffy creamy white appearance in Candida endophthalmitis.

Go to:

Management and perspectives

The prognosis of endophthalmitis, whether of exogenous or endogenous origin, is often poor. In general,
endophthalmitis is recognized as an ominous disease, which runs a potentially devastating course, leaving only very
limited visual function in many patients. Therefore, early diagnosis and treatment with antimicrobial therapy are
fundamental to optimize visual outcome. In addition, the anticipated rise in ocular surgeries, as well as growing
evidence that the rates of postoperative endophthalmitis might increase, underscore the importance of identifying
effective methods of prophylaxis for improving surgical safety.

If endophthalmitis occurs, in most cases the diagnosis is based on clinical findings. Therapy is usually initiated
empirically while microbiologic testing is being performed.

Early intervention is required and justified. With the introduction of intraocular sampling and intravitreal injection of
antimicrobial agents, as well as the possibility for vitrectomy, management of endophthalmitis has entered a new era.
The availability of such an armamentarium allows better management of endophthalmitis. However, knowledge about
the likely organism that causes endophthalmitis, as well as the antimicrobial drug apt to be most effective, remains
paramount.

Exogenous endophthalmitis

Historically, treatment of exogenous endophthalmitis was consisted mainly of intravenous antibiotics. 1 Nevertheless,
most systemically administered antibiotics do not reach sufficiently high intraocular concentrations for effective
treatment of severe intraocular infections such as endophthalmitis. Amore effective way to achieve a high
concentration of an antimicrobial substance within the eye and the infected tissue is intravitreal drug application.
Therefore, the intravitreal injection of antibiotics has become the primary method of administration in the treatment of
exogenous endophthalmitis.1,98,99

Unless there is no other unequivocal result from culturing, endophthalmitis therapy should cover Gram-positive
organisms, which play a predominant role in exogenous endophthalmitis. Gram-negative coverage is also important
because these organisms are associated with higher virulence and poorer outcome.

Current antibiotic standard protocols for intravitreal application are empirically based and include the peptide
antibiotic vancomycin (1.0 mg/0.1 mL) for Gram-positive coverage, 7 in combination with the β-lactam antibiotic
ceftazidime (2.25 mg/0.1 mL) for Gram-negative coverage. 7 In patients sensitive to β-lactam drugs, amikacin (400
μg/0.1 mL), an aminoglycoside antibiotic, might be considered instead of ceftazidime. However, a degree of retinal
toxicity of amikacin has been reported.100,101

Gram-positive organisms reportedly have a 99% susceptibility to vancomycin. 102 Consequently, it has become a
valuable component of endophthalmitis treatment. However, recently cases of vancomycin-resistant strains in
endophthalmitis have been reported,103,104 and emerging resistance of Gram-positive pathogens to vancomycin is a
concern.105,106 In addition, the EVS showed that only 89.5% of Gram-negative isolates were sensitive to amikacin or
ceftazidime;7 in India, susceptibility of Gram-negative bacteria to amikacin or ceftazidime has been reported as being
only 68% and 63%, respectively.107

Use of fluoroquinolone antibiotics has been widely discussed as a potential alternative to current antibiotic treatment
protocols. In particular, the recently developed third- and fourth-generation fluoroquinolones, such as levofloxacin
and moxifloxacin, with their enhanced activity against Gram-positive pathogens, offer broad-spectrum activity that
covers most organisms commonly encountered in bacterial endophthalmitis. 108

Moxifloxacin, and fluoroquinolones in general, penetrate well into the eye. After topical administration at two-hourly
intervals, moxifloxacin reaches mean aqueous concentrations of 2.3 μg/mL. 109 A recent study demonstrated that
anterior chamber levels achieved using moxifloxacin are higher than those obtained with any other topically
administered fluoroquinolone antibiotic. 109 Nevertheless, intravitreal concentrations are 10 times lower than those in
the anterior chamber. These levels are too low for effective treatment of intraocular infections. 110 Systemic
moxifloxacin does not exceed anterior chamber concentrations. It reaches intravitreal concentrations 10 times higher
than levels achieved by topical use, but to reach S. aureus and certain fluoroquinolone-resistant strains, higher
concentrations are needed.111 Therefore, direct intraocular application of such antibiotics seems useful.

Moxifloxacin is available as an unpreserved ophthalmic solution and covers both Gram-negative and -positive
pathogens, including those most often implicated in the development of exogenous endophthalmitis. 112 An additional
potential advantage of moxifloxacin for intraocular use might be the administration of only a single substance into the
eye.

Several studies have investigated the potential use of fourth-generation fluoroquinolones, and especially moxifloxacin,
as prophylaxis for and treatment of endophthalmitis. 113–119 In addition, pharmacokinetic data suggest intravitreal
moxifloxacin is a useful alternative to current treatment protocols. 120 Its safety has been demonstrated both in
vivo and in vitro.113–117 An argument against use of moxifloxacin for the treatment of endophthalmitis may be that
antibiotics from this group are widely used as topical antibiotics for treating superficial ocular infections and for
preoperative prophylaxis. Moreover, concern exists about the emerging resistance of S. aureus and other Gram-
positive isolates to third- and fourth-generation fluoroquinolones because of prophylactic use before and after
intraocular surgery.53,121–123

These reports must be considered seriously, but it is noteworthy that sensitivity testing was determined in vitro and
minimal inhibitory concentrations were based on serum levels (8 mg/mL). Recent data from toxicologic testing on
ocular tissue indicate that moxifloxacin in doses up to 150 μg/mL did not result in significant toxicity on several
ocular cell types.113,114,116,117,124 Therefore, in vivo resistance appears to be very unlikely.

However, until these issues are resolved and its therapeutic role in endophthalmitis treatment is further elucidated,
moxifloxacin should only be used in combination with an agent that is more reliable against Gram-positive pathogens.

A potential use of moxifloxacin for intracameral endophthalmitis prophylaxis in cataract surgery seems to be more
reasonable. The ESCRS demonstrated that the prophylactic use of intracameral antibiotics helps to reduce the
incidence of postoperative endophthalmitis after cataract surgery by 75%. 55 Therefore, prophylactic intracameral
application of the β-lactam cefuroxime, together with the peptide antibiotic vancomycin, has become a beneficial and
widely accepted practice for intracameral endophthalmitis prophylaxis in cataract surgery. 125

However, in addition to the potential benefits, clinicians must consider that antibiotics from both groups are the
mainstay of intravitreal treatment of endophthalmitis. 7 Consequently, one might argue that they should be reserved for
this indication and not used for prophylaxis.

Due to its broad-spectrum properties, moxifloxacin is one of the most promising candidates in endophthalmitis
prophylaxis as an intracameral adjunct during cataract surgery. Nevertheless, further investigations will have to clarify
the role of moxifloxacin in this context.

Systemic fluoroquinolones and antibiotics in general have been discussed as adjunctive systemic treatments for
postoperative endophthalmitis. In 1995, the EVS evaluated the role of systemic antibiotics and pars plana vitrectomy
in the treatment of postoperative endophthalmitis. 7 The results of this study demonstrated that intravitreal antibiotics
need not be supplemented with intravenous antibiotics in either acute or subacute postoperative endophthalmitis. 7

Subconjunctival antibiotics may temporarily provide therapeutic levels to the anterior segment but, in general, they do
not penetrate sufficiently into the vitreous cavity.126 Further, large retrospective studies did not reveal an additional
benefit compared with intravitreal antibiotic application.127,128

Corticosteroids are commonly used as adjunctive treatment in bacterial as well in fungal endophthalmitis. These
agents are given to modulate the inflammatory response to infection that might help to reduce secondary damage.
Topical and subconjunctival steroids are widely accepted. However, use of steroids given via the systemic and
intravitreal routes in the treatment of endophthalmitis remains controversial. A prospective, randomized trial
demonstrated significantly less inflammation in endophthalmitis cases after intervention when 400 μg dexamethasone
was applied intravitreally.129 In contrast, visual outcome after 12 weeks was not affected.129 A recent study found a
trend toward better visual acuity with adjunctive dexamethasone in a smaller series of patients with
endophthalmitis.130 Other studies did not find any significant effect on inflammation or visual acuity. 131 Conversely, a
retrospective, nonrandomized trial of 57 patients with postoperative endophthalmitis found a significantly worse
visual outcome when intravitreal dexamethasone was added to therapy. 132

Pars plana vitrectomy offers several potential benefits for endophthalmitis treatment. Results from the EVS showed
that immediate vitrectomy provides a clear benefit in a well-defined subgroup; patients with light perception only at
the time of presentation had a significant, threefold improved chance of obtaining a visual acuity of 20/40 after
vitrectomy.7 For diabetic patients with hand movement or better vision, at least a trend toward better final visual
acuity after vitrectomy could be documented compared with vitreous tap and biopsy. 7 One reason for this may be that
vitrectomy results in a reduction of pathogens, toxins, inflammatory materials, and opacities. Furthermore, vitrectomy
enables samples to be obtained for culture.

A potential disadvantage of vitrectomy in endophthalmitis treatment might be that this technique is not ubiquitous and
therefore effective treatment might be delayed. In addition, visualization of intraocular structures might be difficult,
and vitrectomy might become desperate in highly inflamed eyes. Data from different studies are inconclusive, and the
overall benefit of vitrectomy in endophthalmitis is still under discussion. 7,133,134 However, the EVS addressed the
relative effectiveness of immediate pars plana vitrectomy.7
One prognostic factor for the final visual outcome seems to be the type of infecting organism isolated and, in one
study, if no or equivocal growth was detected in culture, 80% of cases obtained a final visual acuity of 20/100 or
better.56 Infections with coagulase-negative staphylococci have also been associated with a final visual acuity of
20/100 or better in the EVS population (84%).56 Due to their ability to induce significant inflammation, S. aureus,
streptococci, and Gram-negative isolates seem to result in a worse visual outcome. Other strong predictors for poor
visual outcome are initial visual acuity of light perception only, older age, corneal ring ulcers, compromised posterior
capsule, abnormal intraocular pressure, afferent papillary defect, rubeosis iridis, and absence of the red fundus
reflex.56

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Endogenous endophthalmitis
In contrast with exogenous endophthalmitis, endogenous endophthalmitis requires systemic antimicrobial therapy.
The primary source of infection in endogenous endophthalmitis is outside the eye, but within the body. Therefore,
systemic cultures should be obtained.

Identification of the causative pathogen by blood, urine, or cerebrospinal fluid culture is successful in more than 75%
of endogenous endophthalmitis cases.3,4,135 Positive cultures from vitreous samples can be achieved much less
frequently in endogenous endophthalmitis than in exogenous endophthalmitis. 3,4,135 However, especially in fungal
endophthalmitis, the value of obtaining an ocular culture should not be underestimated because it may be the sole
source of microbial growth. In addition to cultures, in certain cases and for fastidious organisms, fungal/bacterial
DNA in intraocular fluid can be detected by polymerase chain reaction assay. 136–138

The role of vitrectomy in endogenous endophthalmitis is not exactly defined. One reason for this could be that data
from the EVS may not be applicable because the spectrum of causative organisms differs significantly in endogenous
endophthalmitis. Although systemic and intravitreal antibiotics may be sufficient in milder forms of infection,
vitrectomy seems to be helpful in severe cases of endogenous endophthalmitis because more virulent organisms, such
as endotoxin-producing Streptococcus and Bacillus species, are commonly involved.3,4 In addition, material from
vitrectomy may provide a better source for culturing.

Patients with endogenous endophthalmitis need to have the type and extent of their disease diagnosed, complications
detected, and underlying systemic cause or risk factors defined. A major target of antimicrobial therapy in endogenous
endophthalmitis treatment is the source of infection, which is often guided by culture and susceptibility of the
infecting organism.

Systemic antimicrobial therapy is the mainstay of endogenous endophthalmitis treatment. In most cases, treatment is
initiated empirically and the infecting organism presumed to be that causing systemic infection. For intravitreal
antibiotic application in bacterial infections, as with exogenous endophthalmitis treatment, vancomycin (1.0 mg/0.1
mL) for Gram-positive coverage or in combination with the β-lactam antibiotic ceftazidime (2.25 mg/0.1 mL) or
amikacin (400 μg/0.1 mL) is recommended for Gram-negative coverage. In general, systemic therapy must be
continued for several weeks to ensure eradication of the infection.

Fungal endophthalmitis

Only a small number of exogenous endophthalmitis cases are thought to be fungal. However, in some tropical
countries, up to 50% of central corneal ulcers are caused by fungi, 139–142 and a recent review of more than 40 cases of
exogenous fungal endophthalmitis revealed that almost 50% of these cases were associated with fungal
keratitis.99 (see Figure 5). Therefore, exogenous fungal infections of the eye are of increasing concern.

Open in a separate window

Figure 5

Exogenous fungal endophthalmitis with corneal ulcer.

If exogenous fungal endophthalmitis occurs, it is mostly caused by molds
(mainly Fusarium and Aspergillus species).99 Nevertheless, most cases of fungal endophthalmitis are a result of
endogenous fungal spread into the eye. The most commonly reported causes of endogenous fungal endophthalmitis
are Candida species (>50%) followed by Aspergillus and Fusarium species.8,90,143–145

In endogenous fungal endophthalmitis, treatment should be instituted as soon as the diagnosis is made, under close
supervision by the attending physician. Treatment guidelines for mild forms of fungal chorioretinitis and vitreitis
suggest systemic antifungal therapy combined with serial ophthalmologic examinations. 146,147 Surgical intervention
combined with systemic and intraocular antifungal drug application is warranted in cases of moderate or severe
vitreous involvement.146,147

Most current treatment protocols recommend amphotericin B (5–10 μg/0.1 mL) and triazoles as primary therapeutic
options. Both can be given systemically and intravitreally. However, the intraocular penetration of amphotericin B
after topical or systemic treatment is limited, and intraocular use is associated with retinal toxicity. 148 In addition,
many fungal pathogens affecting the human eye are not susceptible to these agents. 90,143 Recently developed second-
generation triazole derivates (eg, voriconazole) seem to be promising alternatives. Voriconazole can be given either
systemically or intravitreally. It penetrates well into the ocular tissue after systemic administration. 149 Severe systemic
side effects seem to be less common than with amphotericin B and several in vitro studies indicate that the safety
profile of voriconazole after intravitreal application may be superior to that of amphotericin B. 150–154 The general in
vitro susceptibility of Candida, Aspergillus, and Fusarium species to voriconazole are almost 100%.90 Numerous case
reports indicate that voriconazole treatment has been successful where amphotericin B or fluconazole has failed, even
in cases of drug-resistant fungal keratitis and endophthalmitis. 152,155–160

In a situation where adequate and timely treatment is essential, eyes with endogenous fungal endophthalmitis may
achieve a far better final visual acuity than eyes with bacterial infections. 6,161 In a larger series of endogenous fungal
endophthalmitis cases, 65% of eyes achieved 20/400 or better acuity. 2 Nevertheless, in endogenous fungal
endophthalmitis the organism isolated is critical for prognosis. Candida endophthalmitis seems to result in better
outcomes than endoophthalmitis caused by Aspergillus or other fungi.2,5

Another potential treatment for endogenous fungal endophthalmitis is caspofungin, the first member of a recently
introduced new class of antifungal agents known as the echinocandins. 162,163 Because of their different mechanism of
action, these agents are an important therapeutic alternative to currently available antifungal treatments for invasive
fungal infections. Caspofungin has potent antifungal activity against Candida and Aspergillus species, which are the
predominant fungal pathogens in fungal endophthalmitis. Recent reports suggest that systemic caspofungin combined
with voriconazole might be an effective treatment of endophthalmitis caused by Candida, Acremonium,
and Aspergillus species.159,164–166 However, the intraocular penetration properties of caspofungin after intravenous
application remain unclear.167,168 One patient with advanced endogenous endophthalmitis failed to respond to
caspofungin, and after nine days of a standard systemic dosage, no caspofungin could be detected intravitreally. 167

Clinical experience with caspofungin in endophthalmitis treatment is limited. To date, no data are available on the
potential intraocular use of caspofungin. First results from in vitro testing seem to be promising169 but need further
clarification in vivo. Nevertheless, due to their unique mechanism of action and their high activity against yeasts and
mold, including those commonly affecting the eye,170–172 caspofungin and other emerging drugs of this group might
become more prominent in future treatment strategies for fungal endophthalmitis.

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Conclusion
Endophthalmitis is one of the most devastating complications after ocular surgery or trauma and in people with
systemic infection. Treatment of endophthalmitis remains challenging. Early diagnosis and treatment are essential to
optimize visual outcome. Intravitreal antimicrobial drug application achieves the high intraocular substance levels
needed for effective endophthalmitis treatment.

Vitrectomy seems to provide several substantial benefits in the treatment of endophthalmitis and remains accepted as
a treatment option which is supplementary to intravitreal antimicrobial therapy in patients with moderate or severe
disease. The EVS addressed the relative effectiveness of immediate pars plana vitrectomy after postoperative
endophthalmitis.7 However, a general advantage of vitrectomy in endophthalmitis is still under discussion.
In general, for exogenous endophthalmitis treatment, intravitreal antibiotics need not be supplemented with
intravenous antibiotics. In contrast, most cases of endogenous endophthalmitis, where the primary focus of infection is
outside the eye, require systemic antimicrobial therapy. Supplementary intravitreal drug application and vitrectomy
may be supportive.

In fungal endophthalmitis, vitrectomy and intravitreal amphotericin B are indicated in case of severe vitreous
involvement. Recent advances in therapy using antimycotic drugs, including the second-generation triazole agent
voriconazole and the echinocandin caspofungin, may offer new treatment options to manage fungal endophthalmitis,
but these drugs need further evaluation.

Abstract
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Introduction
Endophthalmitis means bacterial or fungal infection inside the eye, involving the vitreous and/or aqueous humors.
Most cases of endophthalmitis are exogenous, and organisms are introduced into the eye via trauma, surgery, or an
infected cornea. Endogenous endophthalmitis occurs when the eye is seeded via the bloodstream. Patients usually
have symptoms from their underlying systemic infection, but sometimes present only with eye symptoms.

Endophthalmitis does not serve as a source of bactaeremia or fungaemia. Infection remains confined to the eye. In
panophthalmitis, infection spreads from the globe of the eye to the adjacent soft tissues of the orbit.

Most cases of endophthalmitis present acutely, with hours to a few days of symptoms. These cases are medical
emergencies, as delay in treatment may result in permanent vision loss.

Go to:

Types of Endophthalmitis
Endophthalmitis may be divided into several categories (Table 1). Regardless of category, treatment requires the
prompt intra-ocular injection of antibiotics and, in some cases, a vitrectomy as well.

TABLE 1

Types of endophthalmitis, common pathogens, and treatment

Type Most common pathogens Intial Vitrectomy Need to Initial systemic

intravitreal necessaryc remove antibioticsb
treatmenta artificial
intra-
ocular
lens?

Acute post- Coagulase-negative Intravitreal Yes, if severe No, unless Value

cataract staphylococci (70% of cases), vancomycin plus infection or fungal unknown,
other Gram-positive cocci ceftazidime fungal aetiology rarely given
(25%) aetiology
Type Most common pathogens Intial Vitrectomy Need to Initial systemic
c
intravitreal necessary remove antibioticsb
treatmenta artificial
intra-
ocular
lens?

Chronic Propionibacterium acnes Intravitreal Varies Yes No

post- vancomycin
cataract

Post- Coagulase-negative Intravitreal Yes, if severe No Moxifloxacin or

injection staphylococci, viridans vancomycin plus infection similar?
streptococci ceftazidime

Bleb-related Streptococci, Haemophilus Intravitreal Most cases No Moxifloxacin or

influenzae vancomycin plus similar?
ceftazidime

Post- Bacillus cereus, coagulase- Intravitreal Most cases Varies Intravenous

traumatic negative staphylococci (fungi vancomycin plus (always if vancomycin
in some cases) ceftazidime (plus fungal) plus either
amphotericin if ceftazidime or
fungi suspected) ciprofloxacin

Endogenous Staphylococcus aureus, Intravitreal Yes, nearly No Intravenous

bacterial streptococci, Gram-negative vancomycin plus all cases antibiotics
bacilli (e.g. Klebsiella) ceftazidime (or tailored to
amikacin) systemic
 Type Most common pathogens Intial Vitrectomy Need to Initial systemic
c
intravitreal necessary remove antibioticsb
treatmenta artificial
intra-
ocular
lens?

infection

Candida Candida species Intravitreal Yes, if vitritis Often Yes

amphotericin (or
voriconazole)

Mould Aspergillus, Fusarium Intravitreal Yes Yes Yes

amphotericin

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a
Intravitreal antibiotics are given at the end of a vitrectomy case in the operating room, or as an office procedure without a vitrectomy (see
text). Whereas initial therapy is empirical, subsequent injections may be tailored to culture results.
b
Systemic antibiotics alone are not effective in treating endophthalmitis, except for most cases of Candida chorioretinitis without vitritis.
They are indicated in endogenous endophthalmitis and fungal endophthalmitis. Whether they are beneficial as adjunctive therapy in
exogenous bacterial endophthalmitis is unknown (see text).

See text for exceptions.

c

Acute post-cataract endophthalmitis

Cataract surgery is one of the most common eye operations performed worldwide, and acute post-cataract
endophthalmitis complicates this procedure in c. 0.1% of cases 1–7. In the USA and Europe, nearly all cases are caused
by bacteria, whereas in tropical regions such as India, 10–20% of cases are caused by fungi 8.

Ocular surface bacteria contaminate the aqueous humor in 7–43% of cataract operations, but endophthalmitis is rare 9–
11
. This may be because the aqueous humor has a rapid turnover time (100 min). The vitreous humor does not
regenerate, so it is more susceptible to infection. During cataract surgery, the lens pulp is removed but the posterior
lens capsule is left intact. Inadvertent breaks in this capsule increase the endophthalmitis risk 14-fold 6,12. Other
endophthalmitis risk factors include clear corneal incision and silicone rather than acrylic intra-ocular lenses (IOLs) 13.

Symptoms occur within 1 week postoperatively in 75% of cases, and include decreased vision (95%), red eye (80%),
and eye pain (75%) 14. Patients feel otherwise well and are afebrile. On physical examination, vision is decreased,
eyelids are normal to slightly swollen, the conjunctiva is injected, and a hypopyon is present in >80% of cases 15.
There are white blood cells in the aqueous humor and vitreous humor, so the view of the retina is hazy. In 80% of
patients, the view is so obscured that retinal vessels cannot be seen 16.
Diagnosis
Endophthalmitis is a clinical diagnosis, supported by culture of intra-ocular fluids, although a negative culture occurs
in 30% of cases. The differential diagnosis is sterile intra-ocular inflammation. This may occur as a reaction to
surgery, and is typically greatest on the first postoperative day, whereas endophthalmitis usually occurs on day 2 or
later. Toxic anterior segment syndrome, another sterile inflammatory condition, is associated with instrument-cleaning
problems or with solutions used during surgery 17,18.

The vitreous humor is sampled through either a vitrectomy or a needle aspirate; the aqueous humor is sampled
through a needle aspirate. Needle aspirates can be performed as an office procedure. A vitrectomy is performed in the
operating room with a vitrector, which cuts and aspirates the vitreous humor while this is being replaced by saline.
The result is c. 100 mL of dilute vitreous washings, which may be vacuum-filtered through a 0.45-μm filter; the filter
paper can then be cultured. Gram stains are positive in 40–50% of cases. Gram stains may reveal pigment granules
from the iris or retinal pigment epithelium, and these may resemble Gram-positive cocci but are more refractile.
Vitreous cultures are more likely to be positive after vitrectomy than vitreous aspirate (90% vs. 75%); aqueous
cultures are positive in 40% 16. Only the aqueous humor is positive in 4% 19.

Molecular diagnostic techniques have been used to improve the sensitivity of pathogen detection. A multicentre
European study of over 16 600 cataract operations evaluated 29 endophthalmitis cases by both culture and PCR, and
found that PCR increased the detection of pathogens from 14 to 20 20. In a study from France of 100 post-cataract
endophthalmitis cases, the sensitivities of PCR and culture were similar with initial intra-ocular samples, before
antibiotics had been injected 21. However, PCR was much more sensitive than culture (70% vs. 9%) in subsequent
vitrectomy samples, reflecting either the inhibitory effect of the previously injected antibiotics, or the fact that PCR
does not distinguish living from dead organisms. In a study from Brazil of 11 patients with endophthalmitis, cultures
were positive in 75% and PCR was positive in 91% 22. This study also tried to evaluate the specificity of PCR; none of
the 12 vitreous controls were positive, but two of 50 aqueous samples were. A study from Japan also found improved
sensitivity with PCR: of 19 patients with endophthalmitis, 18 were positive by PCR and only ten by culture 23. Control
samples were positive by PCR in 6% of 50 patients with uveitis, although in none of 40 patients without intra-ocular
inflammation.

Microbiology
The major pathogens are coagulase-negative staphylococci (70%), Staphylococcus aureus (10%), streptococci (9%),
other Gram-positive cocci, including enterococci and mixed bacteria (5%), and Gram-negative bacilli (6%). The fact
that Gram-positive bacteria cause >95% of cases reflects the usual pathogenesis, i.e. contamination of the aqueous
humor with surface bacteria during surgery. In tropical regions such as India, fungi may cause 10–15% of
postoperative endophthalmitis cases.

Treatment
The most important component of therapy is the direct injection of antibiotics into the eye. The injection is performed
after a sample of vitreous humor is taken for Gram staining and culture. Initially, broad-spectrum antibiotics are used
empirically: intravitreal vancomycin 1 mg/0.1 mL normal saline plus either ceftazidime 2.25 mg/0.1 mL or amikacin
0.4 mg/0.1 mL. If there is no improvement in 48 h, a repeat intravitreal injection may be given with either vancomycin
or ceftazidime, depending on culture results. Repeated injections of amikacin are avoided, owing to concerns about
retinal toxicity.

The second component of treatment is vitrectomy. Vitrectomy surgically debrides the vitreous humor, similarly to
draining an abscess, and is the fastest way of clearing infection in eyes with fulminant endophthalmitis. However,
vitrectomy is performed in the operating room, whereas a needle aspirate (for culture) is performed in the office:
intravitreal antibiotics are given at the end of a vitrectomy case or after vitreous aspirate. A multicentre prospective
trial, the Endophthalmitis Vitrectomy Study (EVS), tried to answer the question of whether a vitrectomy was
necessary in the treatment of post-cataract endophthalmitis, prior to intravitreal injection of antibiotics 14. The EVS
randomized 420 patients into ‘tap’ (needle aspirate or biopsy of vitreous humor) and vitrectomy groups, with both
groups receiving intravitreal antibiotics after the procedures 14. Vitrectomy decreased the rate of severe vision loss
from 47% (tap group) to 20% (vitrectomy group) in patients who presented with the worst vision (light perception
only). No apparent benefit was seen in patients who presented with hand motion or better vision, although the study
design may have obscured a possible benefit: two-thirds of patients in the ‘tap’ group actually received a vitreous
‘biopsy’ in the operating room, with a vitrector. We favour vitrectomy for all patients who present with severe vision
loss or rapidly worsening vision, or who are likely to have endophthalmitis caused by virulent bacteria such as
streptococci.
Systemic antibiotics are not effective in treating endophthalmitis: intravitreal antibiotics must always be given.
Whether systemic antibiotics provide any additional benefit to intravitreal antibiotics is unknown. The EVS also tried
to answer this question, but the choice of systemic antibiotics used in the study, amikacin plus ceftazidime, was
poor 14. These antibiotics have poor activity against staphylococci, the cause of 80% of post-cataract endophthalmitis
cases, and amikacin does not cross the blood–eye barrier, and so reaches minimal levels in the vitreous humor.

Visual outcome
The visual outcome is highly correlated with the bacteriology. Streptococci of any type produce severe
endophthalmitis with a poor chance of visual recovery, whereas coagulase-negative staphylococci cause milder
endophthalmitis in general. Overall, 50% of eyes with post-cataract endophthalmitis recover 20/40 vision, and 10%
are left with no useful vision (5/200 or less).

Chronic post-cataract endophthalmitis

Chronic post-cataract endophthalmitis is usually caused by Propionibacterium acnes, and presents as a persistent low-
grade inflammation in the anterior chamber. Patients present with decreased vision in the affected eye, and half also
have eye pain, which is usually mild. On examination, there are white blood cells in the aqueous humor, sometimes a
hypopyon, a characteristic white plaque on the posterior lens capsule, and usually inflammation in the anterior
vitreous humor.

Intra-ocular cultures may be negative, although culture of the white capsular plaque is often positive. Treatment with a
combination of removal or exchange of the IOL, total capsulectomy, vitrectomy and intravitreal antibiotics (e.g.
vancomycin) has been the most successful approach. Treatment regimens that leave the original IOL in place have a
40–50% relapse rate.

In rare cases, this entity is caused by fungi, and treatment is different (see below).

Post-injection endophthalmitis

Intravitreal injections of anti-vascular endothelial growth factor agents (e.g. bevacizumab, ranibizumab, and
pegaptanib) are given to treat neovascular macular degeneration. Injections may be repeated monthly for several
months, and each injection carries a small risk of causing endophthalmitis. The number of cases of post-injection
endophthalmitis is increasing as the use of this treatment increases, and at a tertiary eye centre in Australia there were
more cases of post-injection endophthalmitis than of post-cataract endophthalmitis between 2007 and 2010 24. The rate
of endophthalmitis per injection is low, with reported rates varying from 0.025% to 0.2% 25–28. A study using a
Medicare database of 40 903 injections found an endophthalmitis rate of 0.09% per injection 29.

Symptoms are eye pain and decreased vision, and examination reveals vitreal inflammation. In one large study, all 23
patients with presumed endophthalmitis had pain and vitritis developing 1–6 days after injection (average: 3.4 days),
and 78% had hypopyon 28. Cultures were positive in only seven cases. A study in England of 47 post-injection
endophthalmitis cases found that patients presented an average of 5 days after injection (range: 1–39 days), and
positive cultures occurred in 60% 25.

Gram-positive bacteria cause >95% of culture-positive cases 30. Coagulase-negative staphylococci cause c. 60% of
cases and viridans streptococci cause 25% 24,30. This is a much higher rate of streptococcal endophthalmitis than in
post-cataract cases. Viridans streptococci (Streptococcus mitis/Streptococcus oralis) also caused an outbreak of 12
cases of post-injection endophthalmitis in Florida, owing to contamination of bevacizumab syringes made up by a
single compounding pharmacy 31. Eleven of the 12 patients were left with minimal vision, count fingers, or worse.

Diagnosis and treatment are the same as for post-cataract endophthalmitis (see above). Visual outcomes are poor in
cases caused by streptococci.

Bleb-related endophthalmitis

A filtering bleb is a treatment for glaucoma. It is a surgically created scleral defect, covered only with conjunctiva,
that allows excess aqueous humor to be absorbed into the systemic circulation. Because only conjunctiva separates the
ocular surface flora from the aqueous humor at the bleb, endophthalmitis may occur at any time. The risk of
endophthalmitis is c. 1.3% per patient-year 32. One study reported an average onset at 2 years postoperatively (range: 1
month to 8 years) 33. Streptococci, including Streptococcus pneumoniae, cause 50% of cases. Haemophilus
influenzae, Moraxella catarrhalis, S. aureus and coagulase-negative staphylococci are other pathogens 33.
Vitrectomy and intravitreal antibiotics (e.g. vancomycin plus ceftazidime) are indicated. The value of a systemic agent
as adjunctive therapy has not been studied, but it seems reasonable to give an oral quinolone, such as moxifloxacin,
that achieves good vitreous levels and treats the major pathogens. The visual outcome varies, depending partly on the
pathogen: 40% achieve 20/40 vision or better, whereas 30% lose all vision in the affected eye 34.

Post-traumatic endophthalmitis

Endophthalmitis occurs in 3–10% of cases after penetrating trauma to the eye, although early surgical repair and
prophylactic systemic antibiotics may reduce this incidence to <1% 35. Risk factors for the development of
endophthalmitis include metal rather than glass or blunt trauma injuries, retained intra-ocular foreign bodies,
disruption of the lens, and delay in primary repair of >24 h.

Bacillus cereus is a major pathogen in post-traumatic endophthalmitis, and causes a fulminant infection with very
poor visual outcome 36. Onset of symptoms (eye pain, red eye, and decreased vision) usually occurs within 12–24 h of
the injury. Findings include marked intra-ocular inflammation and often a ring corneal infiltrate. Other causes of post-
traumatic endophthalmitis are coagulase-negative staphylococci, streptococci, Gram-negative bacilli such
as Klebsiella and Pseudomonas, and moulds 37,38.

Treatment should be aggressive, with vitrectomy, intravitreal antibiotics (e.g. vancomycin plus ceftazidime), and
systemic therapy.

Endogenous bacterial endophthalmitis

Endogenous bacterial endophthalmitis arises from bacteraemic seeding of the eye. Endocarditis, usually caused by S.
aureus or streptococci, accounts for 40% of endogenous endophthalmitis cases in the USA, and other cases are
associated with urinary tract infections, indwelling central venous catheters, illicit injection drug use, and procedures
such as endoscopy that can cause transient bacteraemia. In Taiwan, Singapore, and other East Asian nations, liver
abscess caused by Klebsiella pneumoniae is the source of 60% of cases of endogenous endophthalmitis 39.

Many patients present with eye symptoms (pain and blurred vision) rather than symptoms of their underlying
infection; this was true of half of the patients in one study 40. Blood cultures are positive in 75% of cases, as are
vitreous cultures 40. Common pathogens in western countries include S. aureus (25%), streptococci (30–50%,
primarily Streptococcus pneumoniae, Streptococcus milleri group, and group A and B streptococci), and Gram-
negative bacilli such as Escherichia coli (30%). In Asia, K. pneumoniae causes the majority of cases.

Treatment of the underlying source of bacteraemia with systemic antibiotics is necessary, but this will not effectively
treat the endophthalmitis: intravitreal antibiotics and, usually, a vitrectomy are necessary.

Candida endophthalmitis

Endogenous Candida endophthalmitis
Most cases of Candida endophthalmitis are endogenous, occurring as a complication of candidaemia. The
candidaemia usually occurs in hospitalized patients, often as a complication of an indwelling central venous catheter.
Other risk factors include total parenteral nutrition, broad-spectrum antibiotics, neutropenia, recent abdominal surgery,
and glucocorticoid therapy.

Candidaemia seeds the highly vascular choroid first, so the initial manifestation is usually chorioretinitis or
choroiditis. There may be minimal or no vitreous inflammation at first. Infection in the choroid and retina is often
painless, so, unless the lesions are near the macula, patients with early Candida chorioretinitis may have no
symptoms. As the infection worsens, vitritis develops, and patients develop decreased vision. With inflammation
spreading to the aqueous humor, eye pain may also be a presenting symptom.

Often, the literature distinguishes Candida chorioretinitis from Candida endophthalmitis, the latter term being

reserved for those cases with significant vitritis. A term that includes both Candida chorioretinitis and
endophthalmitis (i.e. vitritis) is ocular candidiasis.

The prevalence of ocular candidiasis in candidaemia must be evaluated by prospective studies. In such studies, the
incidence varies from 2% to 26%, with most cases being attributable to chorioretinitis and only 0–6% having
significant vitritis (i.e. ‘endophthalmitis’) 41–44. In a multicentre trial involving 370 patients with candidaemia, possible
or probable ocular involvement occurred in 16%, with most having chorioretinitis as the manifestation and only 1.6%
being classified as having endophthalmitis (i.e. with significant vitritis) 41.
Outpatients may also present with endogenous Candida endophthalmitis, and some of these patients have a recent
history of hospitalization and a recent indwelling central venous catheter. However, most outpatients who present
with Candida endophthalmitis have a history of illicit intravenous drug use. In a study from Australia, 70% of 27
patients presenting with fungal endophthalmitis between 2001 and 2007 were injection drug users 45. Candidaemia is
often transient in injection drug users and in patients with recent indwelling central venous catheters, so patients may
present with decreased vision as their only symptom. They may be misdiagnosed initially as having a sterile uveitis,
unless a history of intravenous drug use or recent hospitalization is obtained.

The diagnosis of ocular candidiasis is made on the basis of eye examination and confirmed with vitreous culture.
Vitreous culture is usually not necessary in patients who have known candidaemia and eye findings compatible with
chorioretinitis. Funduscopic examination shows white fluffy lesions in the choroid or retina, sometimes with vitritis
(endophthalmitis). There may be so much vitritis that the retina may be obscured. A ‘string of pearls’ or ‘snowballs’
may be seen in the vitreous humor, representing clumps of infection within the inflamed vitreous humor. In
outpatients who present with eye findings but do not have a history of known candidaemia, diagnosis must be
suspected by clinical appearance (fluffy white infiltrates in the retina or vitreous humor, often with marked vitritis),
and confirmed by vitreous culture.

Candida albicans is the most common cause of ocular candidiasis, causing 92% of cases in one review; Candida
tropicalis was the second most common cause 46.

All patients with ocular candidiasis must be followed closely by an ophthalmologist, as some patients worsen despite
therapy. In a multicentre study of 370 patients with candidaemia who received either voriconazole or amphotericin
followed by fluconazole, 18% of the 60 ocular candidiasis cases developed while antifungal therapy was being
given 41. For most patients with chorioretinitis alone, the lesions will respond to the systemic antifungal therapy.
Patients who have significant vitritis (endophthalmitis) require a vitrectomy and intravitreal amphotericin (or
voriconazole), in addition to systemic antifungal therapy with an agent that crosses the blood–eye barrier, such as
fluconazole (if susceptible), voriconazole, or amphotericin.

Exogenous Candida endophthalmitis
Exogenous cases are rare, and most cases occur following surgery. Inflammation may initially be greatest in the
anterior chamber, before involving the vitreous humor.

Candida parapsilosis is the most common species, especially in postsurgical outbreaks. The reason is most likely that
this species appears to survive well in irrigation fluids and on prosthetic materials 47. An outbreak in the USA in 1983
affecting 13 patients in different states was traced to a balanced salt solution used during ophthalmic surgery that was
contaminated during manufacture 48.

Treatment includes intra-ocular injection of either amphotericin or voriconazole, vitrectomy, and systemic
voriconazole or fluconazole (if the organism is susceptible). The dose of intravitreal amphotericin is 5–10 μg in 0.1
mL of sterile water, and the dose of intravitreal voriconazole is usually 100 μg in 0.1 mL of sterile water. If infection
follows cataract surgery, it is often necessary to remove the IOL as well. Systemic therapy with high-dose fluconazole
(400–800 mg daily, assuming normal kidney function) is also indicated for susceptible strains, or voriconazole for
fluconazole-resistant but voriconazole-susceptible strains.

Mould endophthalmitis

Two-thirds of patients with mould endophthalmitis lose useful vision, but the prognosis may be improving with the
use of newer antifungal agents.

Exogenous mould endophthalmitis

Mould endophthalmitis is usually exogenous, occurring after eye surgery, after eye trauma, or as a result of
keratomycosis (fungal corneal infection). Aspergillus and Fusarium are the most common aetiological agents.

Postoperative mould endophthalmitis is rare in western countries. When it does occur, it often presents subacutely,
and diagnosis may be delayed. In one review that included ten cases of postoperative mould endophthalmitis, 60%
presented ≥2 months after surgery 49. In tropical regions such as India, moulds have caused >20% of postoperative
endophthalmitis cases in some series 8,50, and 80% of cases present within 4 weeks of surgery. Outbreaks of
postoperative mould endophthalmitis have also occurred.

Post-traumatic mould endophthalmitis is also more common in India than in the USA or Europe. Moulds caused 14%
of 113 culture-positive post-traumatic endophthalmitis cases in a series from India 51. In another series from India, the
average time to presentation after eye trauma was 7 days 52. Aspergillus was the most common mould isolated in both
of these series.

Mould infection of the cornea (keratomycosis) may lead to endophthalmitis as the mould grows through the cornea
and into the aqueous humor. Keratomycosis was the aetiology for half of all exogenous mould cases in a series from
Florida, and eye surgery and trauma each accounted for 25% of cases 49. Many cases of keratomycosis are associated
with contact lens wear. Fusarium is the most common cause of endophthalmitis resulting from keratomycosis in many
series. Some of these cases reflect the international outbreak of Fusarium keratitis that occurred in 2004–2006, related
to one brand of contact lens cleaning solution. In this outbreak, 6% of keratitis cases developed endophthalmitis 53,54.

The clinical presentation of exogenous mould endophthalmitis may be subacute, as noted above. Slit lamp
examination of the eye often shows hypopyon and clumps of thick white material in the anterior chamber, particularly
after trauma or surgery. There may be vitritis. When endophthalmitis complicates keratitis, slit lamp examination will
show the corneal infection, and often shows filaments extending from the back of the cornea into the aqueous humor.

Diagnosis is made by culture of the aqueous humor as well as the vitreous humor. Treatment requires surgery to clean
out thick material, if present, in the aqueous humor, vitrectomy for significant vitritis, intracameral and intravitreal
injections of antifungal agents (amphotericin or voriconazole), and systemic voriconazole therapy. Systemic
voriconazole achieves very good intra-ocular levels, of c. 40% of serum levels. Unless the fungus is known, the initial
intra-ocular injection should be amphotericin; subsequent injections may be voriconazole for sensitive fungi. Repeated
intra-ocular injections of voriconazole (if the organism is susceptible) or amphotericin can be given, at least 48 h
apart. Voriconazole is preferred for susceptible strains, as it appears to be less irritating than amphotericin. If there is
an IOL, this must be surgically removed. In cases related to keratomycosis, a corneal transplant is almost always
necessary.

Several case reports have described salvage with posaconazole for cases of Fusarium keratomycosis-related
endophthalmitis in which other therapies have failed 55,56. Itraconazole is not recommended, as it does not achieve good
levels in the vitreous humor; and fluconazole should not be given, as it has poor activity against moulds. Systemic
amphotericin has significant toxicity, and is rarely used to treat exogenous fungal endophthalmitis, but may be
considered as adjunctive therapy in those rare cases of azole-resistant fungal endophthalmitis in which other therapies
have failed.

Endogenous mould endophthalmitis

Endogenous mould endophthalmitis is rare. It usually occurs in severely immunocompromised patients with
fungaemia, or in injection drug users. Aspergillus and Fusarium are common aetiological agents. Hospitalized patients
with mould fungaemia are usually very ill, and may not be able to complain of eye symptoms. In a retrospective study
at a Texas cancer centre, only 27% of the 15 patients with mould endophthalmitis survived for >4 weeks 57. Often, the
diagnosis of mould endophthalmitis is missed during life. In an autopsy study of 85 orthotopic liver transplant
recipients, Aspergillus endophthalmitis was noted in 7%, but only one of six patients was diagnosed ante-mortem 58. In
contrast, injection drug users who have endogenous mould endophthalmitis are usually well except for their eye, with
no evidence of systemic infection. In these patients, fungaemia is usually transient, occurring only at the time of
intravenous drug injection.

In immunocompromised patients, treatment must include systemic antifungal therapy, with the choice (e.g.
amphotericin or voriconazole) tailored to optimize treatment for the fungaemia. Vitrectomy and removal of any IOL,
followed by intravitreal amphotericin or voriconazole (for susceptible strains), should be performed if the patient is
able to tolerate surgery. If too ill for surgery, the patient should have intravitreal injection of amphotericin or
voriconazole, with repeated injections as needed. In injection drug users with no evidence of ongoing fungaemia,
vitrectomy, intravitreal antifungal injection and systemic therapy should be given.

Go to:

Conclusion
Endophthalmitis is a medical emergency. The most important component of therapy is intravitreal injection of
antibiotics. Vitrectomy is also important in many cases, and leads to improved visual outcomes in patients who
present with significant visual loss. Vitrectomy should also be performed in cases that have failed to respond to initial
intravitreal injection. Systemic antibiotics are necessary to treat the underlying infection in endogenous
endophthalmitis, and as adjunctive therapy in exogenous fungal endophthalmitis. Visual prognosis is partly related to
the virulence of the pathogen. The best outcomes usually occur in cases that are either culture-negative or are caused
by coagulase-negative staphylococci, and the worst outcomes typically occur in endophthalmitis caused by
streptococci, Bacillus species, and moulds. Even in cases of severe endophthalmitis caused by virulent pathogens,
however, prompt therapy may save useful vision. Even light perception vision is considered to be useful to a blind
patient.

Endophthalmitis
is an infection inside the eye that can either be acute or chronic, meaning that
it can develop very rapidly which is most common, or develop slowly and
persist for long periods of time.
DOWNLOAD FACT SHEET     LARGE-PRINT VERSION

Symptoms
Endophthalmitis causes the white of the eye to be inflamed. There may be a white or yellow
discharge on or inside the eyelid, and the cornea may show a white cloudiness. There may also
be a layer of white cells (hypopyon) present within the anterior chamber of the eye between the
iris and the cornea. (Figure 1) Endophthalmitis is usually a very serious problem and prompt
examination by an ophthalmologist is essential to make an appropriate diagnosis and initiate
treatment.

Enlarge
Figure 1. Hypopyon is an accumulation of white blood cells in the anterior chamber of the eye and corneal infiltrate associated with
infectious endophthalmitis. Image courtesy of ©Retina Image Bank, contributed by Aleksandra V. Rachitskay, MD, Cole Eye Institute,
Cleveland Clinic. 2014. Image 16250.

Other symptoms include:

 Eye pain and redness

 Decreased vision
 Trouble looking at bright lights (photophobia), usually sudden onset

Causes
Acute cases of endophthalmitis are caused by gram-positive (or less frequently gram-
negative) bacteria and are most often seen within 6 weeks after surgery or trauma to the
eye.

Chronic cases that occur outside of the 6-week window are often related to a previous
surgery and are commonly caused by slowly progressive infections such as
Propionibacterium acnes or fungus.

Finally, systemic infections can spread to the eye causing endogenous endophthalmitis. This
is often associated with systemic fungal or gram-negative bacterial infections. Patients who
are debilitated, septicemic (bacteria in the bloodstream), and who have weakened immune
systems are particularly susceptible, especially after surgical procedures.

RISK FACTORS

Loss of vitreous gel (also referred to as vitreous humor), disrupted posterior capsule, poor wound
closure, and prolonged surgery are risk factors for developing endophthalmitis. The incidence
following penetrating trauma is 4–13% and may be as high as 30% after injuries in rural settings.
Risk factors for endophthalmitis after trauma include:

 Retained intraocular foreign body (having foreign material remain in your eye following an
injury)
 Delayed surgery (longer than 24 hours) to repair a full-thickness laceration
 Rural setting (soil contamination)
 Damage to the lens during trauma

Diagnostic testing
To determine what organism has caused the infection, a biopsy of the fluid within your eye
needs to be obtained. This fluid is then sent to the laboratory for a determination and to
decide on the best treatment.

Treatment and prognosis

 In acute cases, treating endophthalmitis is an emergency and needs to be performed as
soon as possible. The procedure performed will depend on your vision. If your vision is very
poor, you will need to undergo an emergency surgery called a vitrectomy to remove the
infectious debris from your eye and to inject antibiotics or antifungal agents directly inside
your eye. Cases with better vision may only require an injection of antibiotics or antifungal
agents in the office. In rare cases, only antibiotic eye drops are required.
The prognosis depends on the cause, duration, and type of organism that caused the
infection. Outcomes are often less favorable for traumatic cases involving gram negative
organisms. Some cases involving gram positive bacterial infections after cataract surgery
fare better. Eyes with endophthalmitis often require frequent examinations to obtain the best
outcomes.


o A-Z

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What is Endophthalmitis?
Leer en Español: 

¿Qué es la endoftalmitis?

By Reena Mukamal

Reviewed By Jeffrey Whitman

Edited By David Turbert

Nov. 20, 2019

What Is Endophthalmitis?
Endophthalmitis is an infection of the tissues or fluids inside the eyeball. It is an urgent medical emergency. If you
have symptoms, see an ophthalmologist as soon as possible. Endophthalmitis can blind you if it’s not treated
quickly.

What Causes Endophthalmitis?

There are two main types of endophthalmitis:
Exogenous Endophthalmitis. This is the most common type of endophthalmitis. With this type, the source of
the infection comes from outside the body. Bacteria or fungi gets inside the eye from surgery, an injection into the
eyeball or an eye injury. Puncture wounds to the eye are the most likely cause of endophthalmitis.
Symptoms usually begin within only a few days of an eye procedure or injury. When symptoms begin quickly like
this, it is acute endophthalmitis.
The infection can also develop more slowly. When symptoms take longer to emerge, it is chronic
endophthalmitis. This happens when specific types of bacteria or fungi enter the eye.
Endogenous Endophthalmitis. This is the second main type of endophthalmitis. It starts as an infection in
another part of the body and spreads to the eye. For example, this can happen with a urinary tract infection or
blood infection.

What Are the Symptoms of Endophthalmitis?

The most common symptoms of endophthalmitis are:

 eye pain that keeps getting worse after surgery, an injection or injury to the eye
 red eyes
 white or yellow pus or discharge from the eyes
 swollen or puffy eyelids
 decreased, blurred or lost vision

Eye injections and cataract surgery are two of the most frequent eye procedures. Both can cause
endophthalmitis, though it is not common. If you do have these symptoms, see your ophthalmologist right away.
The infection can get worse very quickly.

How Is Endophthalmitis Diagnosed and Treated?

Your ophthalmologist will perform several tests to diagnose your symptoms. They will look at your eye and test
your vision. They will also ask about any recent surgeries, eye procedures or injuries. If you’ve had an eye injury,
your doctor may order an ultrasound to see if there are any foreign objects in your eye.
If your doctor suspects you have an infection, he will perform a test called an aqueous/vitreous tap. This test
involves using a tiny needle to take some fluid out of your eyeball. The fluid is then sent to a laboratory to test
whether there is an infection.
Treatment is an injection of antibiotics or antifungal medicine into the eye. You may also get a steroid to reduce
swelling and inflammation caused by the infection. With more serious infections, you may have vitrectomy
surgery. Your ophthalmologist removes vitreous gel from your eye. Then he injects medicine that prevents
infection.

You Can Prevent Endophthalmitis.

 Use protective eyewear when doing things around the house that can injure the eye. This
includes things like sawing wood.
 Wear appropriate eyewear and safety gear during contact sports.
  Follow your doctor’s home care instructions after eye surgery or an eye injection. For example,
wash your hands before putting in eye drops. Don’t let the eyedrop bottle touch the eye, which can
contaminate the dropper.

4. II. Write notes on : (6 x 5 = 30) . 2. Esotropia. 3. 4.. 5. Marcus

Gunn pupil.

Marcus Gunn pupil is indicative of a defect in the afferent pathway of the light reflex. To avoid the high morbidity
associated with this condition, it must be promptly diagnosed and the cause should be treated. This activity reviews
the evaluation of Marcus Gunn pupil and highlights the role of the interprofessional team in evaluating and treating
patients with this condition.

Objectives:

 Describe the etiology, epidemiology, and pathogenesis of Marcus Gunn pupil.

 Summarize the relevant history and physical examination of patients with Marcus Gunn pupil.

 Review the evaluation process of patients with Marcus Gunn pupil.

 Outline the prognosis and interprofessional care of patients with Marcus Gunn pupil.

Access free multiple choice questions on this topic.

Go to:

Introduction
Marcus Gunn pupil (MGP) is the term given to an abnormal pupil showing aberrant pupillary response in certain
ocular disorders. In literature, the term is often used synonymously with Marcus Gunn phenomenon or relative
afferent pupillary defect (RAPD).[1] After exposure to bright light, a normal pupil constricts.[2]A Marcus Gunn pupil,
on the other hand, has a relative weakness of the afferent limb of the pupillary light reflex compared to the other eye
because of which when light is rapidly transferred from the normal eye to the eye with MGP, the MGP dilates instead
of constricting. It is named after Scottish Ophthalmologist Robert Marcus Gunn.[3] Hirschberg first noted this
phenomenon in the case of unilateral retrobulbar optic neuritis.[3] The presence of a relative afferent pupil defect
(RAPD) is the hallmark of a unilateral afferent sensory abnormality or bilateral asymmetric visual loss.

An afferent pupillary response is characterized by:[4]

1. Constriction of pupils of both eyes when the light stimulus is applied to the normal eye

      2. Dilatation of pupils of both eyes when the light stimulus is rapidly transferred from the normal eye (after brief
light exposure to the normal eye) to the affected eye.

Go to:

Etiology
The relative afferent pupillary defect is seen in various disorders (see pathophysiology). All the causes may not cause
clinically appreciable RAPD.

The causes include:

Lesions of the Optic Nerve and Visual Pathway

 Lesions of the optic nerve[5]

 Lesions of the optic chiasm

 Lesions of optic tract[6][7]

  Lesions of pretectum[8]

 Glaucoma[1]

 Visual field defect[9]

Lesions of the Retina/Posterior Segment

 Retinal detachment[4][10]

 Central retinal vein occlusion (CRVO)[11]

 Central serous chorioretinopathy[12] (CSCR)- may not be clinically appreciable.

 Macular degeneration[13]

 Retinitis pigmentosa[14] (RP)

 Endophthalmitis

Induced RAPD of the Contralateral Eye

 Dense cataract[15] (see following discussion)

 Eye patching[16] of one eye

 Dark adaptation[16] of one eye

Miscellaneous

 Amblyopia[17]- may not be clinically appreciable.

 Anisocoria[18]

Lesions of the optic tract, pretectum, dense cataract, and eye patching/dark adaptation produce RAPD in the
contralateral eye.[15][16] RAPD will be induced in the smaller pupil when anisocoria is greater than 2 mm.[18]

Go to:

Epidemiology
There is no specific age and sex predilection for Marcus Gunn pupil in isolation. In a study conducted using binocular
pupilometer, 42% of the normal population showed an RAPD between 0.08 and 0.22 log units, and 6% had an RAPD
between 0.23 and 0.39 log units.[19] This occurrence of RAPD was justified due to the inaccuracy of measurement or
synaptic asymmetries of the visual pathway.

An RAPD is noted in more than 90% of cases of acute unilateral cases of optic neuritis, 91% cases of ischemic central
retinal vein occlusion (CRVO), more than 50% cases of retinal detachment involving the macula, and 23% cases of
primary open-angle glaucoma (POAG).[5][4][11][5][20]

Go to:

Pathophysiology
When a bright light is shone on one eye, its pupil constricts. This pupillary constriction is known as a direct light
reflex. Simultaneously, the pupil of the other eye also constricts. This response in the contralateral eye is known as a
consensual light reflex. The light reflex is mediated by retinal photoreceptors and subserved by four neurons.[21]

 First (sensory afferents) connects each retina with both pretectal nuclei located in midbrain at the level of
the superior colliculus. Impulses from the nasal half of retina decussate in the optic chiasm and pass via
contralateral optic tract to reach the contralateral pretectal nucleus. Impulses from the temporal half of retina
travel via the ipsilateral optic tract to reach the ipsilateral pretectal nucleus. It is estimated that the fibers
decussate within the chiasm in a ratio of crossed to uncrossed fibers of 53:47.[22] According to a new
model, there may be a partial crossing of temporal fibers in the chiasm in addition to the crossing of nasal
fibers, leading to larger input from one eye into the contralateral optic tract.[7]
  Second (internuncial) connects each pretectal nucleus to both Edinger-Westphal nuclei. Thus uniocular light
stimulus evokes bilateral pupillary constriction. This consensual light reflex results in an almost similar
amount of pupillary constriction since pupillomotor output to both the eyes is the same.[23]

 Third (preganglionic motor) connects the Edinger-Westphal nucleus to the ciliary ganglion. These fibers
pass through the inferior division of the oculomotor nerve.

 Fourth (postganglionic motor) innervate sphincter pupillae via short ciliary nerves.

The relative afferent pupillary defect is usually seen in lesions of the afferent arm of the light pathway. When the light
is shifted from the normal eye to abnormal eye, the total pupillomotor input is reduced, hence the amount of pupillary
constriction is less when compared to stimulation of the normal eye.[24] This difference in pupillomotor input gives
rise to relative afferent pupillary defect.

RAPD in Lesions of the Optic Nerve

Ischemic optic neuropathies, such as arteritic ischemic optic neuropathy (AION), Nonarteritic ischemic optic
neuropathy (NAION) causes RAPD via optic nerve ischemia and infarction secondary to optic nerve edema. Other
diseases causing such asymmetric or unilateral damage of optic nerve resulting in RAPD include glaucoma, optic
neuritis, retrobulbar neuritis, and traumatic optic neuropathy.

RAPD in Lesions of the Optic Tract [6] [7]

The axons of the retinal ganglion cells from the nasal retina decussate in the optic chiasm joining the temporal fibers
of the other side. In addition, there may be a partial crossing of temporal fibers in the chiasm.[7] Thus there is an
asymmetry of pupillomotor input into the optic tracts. There is larger input from one eye to the contralateral tract.
Thus patients with unilateral lesions of the optic tract show a marked relative afferent pupillary defect in the eye
contralateral to the lesion. It usually occurs in the eye with temporal field defect.

RAPD in Lesions of the Pretectum [8]

The asymmetry of pupillomotor input extends from the optic tract to the pretectal nucleus. Hence lesions of pretectum
produce RAPD in the contralateral eye. The relative afferent pupillary defect in such situations is without the
associated loss of visual acuity, color vision, or visual field. This is because just before fibers reach lateral geniculate
body (light pathway), few fibers (pupillary reflex) go to the pretectum. Hence for the lesions at the brachium of the
superior colliculus (just before the fibers reach the pretectal nucleus), vision is not affected. 

RAPD in Glaucoma and Visual Field Defects [1] [9]

In conditions such as glaucoma, RAPD occurs secondary to damage to retinal ganglion cells and loss of retinal nerve
fiber layer.[25] At least 26% of retinal ganglion cells should be damaged to elicit an RAPD.[26] An RAPD will be
noticed only in asymmetric severity of the glaucomatous damage. An RAPD may be noted even before the appearance
of diagnostic glaucomatous visual field defects.[27] It was shown that central 30 degrees of the visual field is the most
effective for pupillomotor input, and the contribution of the visual field asymmetry outside of 30 degrees to the
relative afferent pupillary defect is clinically negligible.[9]

RAPD in Retinal Disorders [4] [10] [11] [12] [13] [14]

RAPD occurs secondary to the death of photoreceptors and viable retina.[13] The central retina is the most effective
for pupillomotor input.[28] The light stimulus to the central retina elicits a greater pupillary response than the same
stimulus applied to the peripheral retina. The detachment of each peripheral quadrant of the retina causes 0.35 log
units of a defect, and detachment of macula causes 0.68 log units of a defect.[10] However, this is only an estimate as
the standard deviation was in the range of +/- 0.65 log units.[10] Ischemic CRVO usually produces 0.9 to 1.2 log units
of a defect (usually more than 0.7 log units), and non-ischemic CRVO produces less than 0.6 log units of a defect.
[11] A Macular disease does not usually cause RAPD unless it is very severe.[29] For a given RAPD, visual acuity is
impaired to a far greater magnitude in macular disease, whereas, in optic neuropathy, vision loss may corroborate with
the quantification of RAPD.[12] Localized macular dystrophies/degenerations and diffuse retinal dystrophies such as
retinitis pigmentosa usually do not show an RAPD response unless the disease is asymmetric. Even in that case, the
RAPD may be subclinical. However, variants such as unilateral retinitis pigmentosa can show an RAPD usually of
<0.3 log units.[14] CSCR may cause mild RAPD (usually ≤ 0.4 log units, some cases may have RAPD up to 0.9 log
units), which improves with the resolution of the subretinal fluid.[12]

Induced RAPD

RAPD in Cataract [15]
Detection of RAPD in the case of cataracts is controversial. RAPD in cataracts usually indicates underlying damage to
the afferent visual pathway (damage of the optic nerve or the retina, or visual pathway) and not due to cataract in
itself. Since the time of Galen, RAPD was noted to indicate poor visual gain post-cataract surgery.[3] A dense cataract
causes an RAPD in the contralateral eye by increasing the pupillomotor effectiveness of the stimulus light likely due
to increased intraocular light scattering by the cataract.[15] Peripheral photoreceptors may be stimulated by diffusely
scattered light, and the light may bounce back again on the retina due to reflection by the posterior surface of the
cataract.[15] Also, a dense cataract may induce dark adaptation of the affected eye.[15] A mature cataract has been
noted to induce a mean of 0.44 log units (maximum 0.6 log units) of a defect in the contralateral eye. However, the
contralateral RAPD disappears after the extraction of the cataract.[15]

RAPD in Eye Patching and Dark Adaptation [16]

A ptotic eyelid or eye patch increases retinal sensitivity due to dark adaptation and causes a false RAPD of up to 1.5
log units in the uncovered eye. The contralateral physiological afferent pupil must be allowed to resolve prior to
commenting on the pupil. In most of the cases, this induced RAPD disappears within 30 minutes of examination in an
illuminated room or removal of the eye patch.

Miscellaneous

RAPD in Amblyopia [17]

According to classic teaching, in amblyopia, there is no structural abnormality of the retina or the optic nerve, and
hence RAPD should not be found. However, a study on amblyopic eyes showed that 'easily visible' RAPD (>0.3 log
units) was noted in 29 of 55 subjects (52.7%), and a total of 45 of 55 patients (81.8%) had RAPD. Most of the cases
had RAPD of a maximum of 0.6 log units. Some cases had minimal RAPD of <0.3 log units, which was detected by a
modification of the standard RAPD test. There is no definite proven hypothesis on the cause of RAPD in amblyopic
eyes. Various presumed hypothesis includes impairment of the function of the central retina[30] and impaired
development of X ganglion cells in the fovea of the amblyopic eye.[31] There is no correlation between the severity of
amblyopia and the grade of RAPD.

RAPD in Anisocoria [18] [32]

In anisocoria, the retina in one eye is shaded by iris more than the other. This difference in retinal illumination can
produce an RAPD in the eye with a smaller pupil. For every 1 mm difference in the size of pupils, a defect of 0.1 log
units of RAPD is noted. Hence a difference of 3 mm between the pupils produces a clinically detectable RAPD. This
artefactitious pupillary response can be alleviated by placing neutral density filters over the larger pupil at a rate of
1/10 of the log unit for every millimeter of anisocoria.

Go to:

History and Physical

Patients with RAPD can present with normal visual function[8][33] or may have symptoms of an underlying disorder.
RAPD is known to persist even when excellent recovery of vision has occurred after the resolution of an acute episode
of optic neuritis.[34] RAPD alone does not cause anisocoria.

Ocular Examination

1. Visual acuity: may range from perception of light (PL) to 20/20

2. Ocular alignment: patients with long-standing amblyopia may manifest sensory exodeviation.

3. Assessment of pupils: 

o A weaker initial constriction with greater redilatation

o An initial stall with greater redilatation

o An initial immediate dilatation, known as pupillary escape 

4. Pupillary escape is an evident and specific sign of RAPD.

5. Anterior segment examination: the presence of iris neovascularization should raise suspicion of ischemic
CRVO

6. Fundus evaluation: helps to identify underlying causes such as optic neuropathy (optic neuritis, ischemic
optic neuropathy), retinal detachment, retinal vascular occlusion, glaucoma, and others.
Supportive Tests: Color vision, contrast vision, Visual evoked potential, Visual fields evaluation, MRI in cases of
optic neuritis

Go to:

Evaluation
A relative afferent pupillary defect usually indicates disease in the pre chiasmal visual pathway.[3] The ability to
detect and quantify RAPD is an essential part of the neuro-ophthalmic examination.

Tests to Identify and Quantify RAPD

 Gunn test

 Kestenbaum-Gunn test / modified Gunn test

 Swinging flashlight test

 Pupillography

Use on neutral density filters and cross-polarized filters aid in the quantification of RAPD in conjunction with
swinging flashlight test or Modified Gunn test.[32][35][32]

Modified Gunn Test / Kestenbaum Gunn Test

In this test, the pupillary reaction to prolonged light exposure is assessed. When any patient has unilateral optic nerve
dysfunction or asymmetric involvement of optic neuropathy, with the patient in the light, covering the eyes
alternatively reveals, that pupil of the normal eye constricts when it is uncovered, and the abnormal eye is covered. In
contrast, the pupil of the eye with optic neuropathy dilates when it is uncovered, and the pupil of the normal eye is
covered. Here the size of pupils is measured.

Swinging Flashlight Test [36] [29]

Levatin modified the Gunn test for the detection of the relative afferent pupillary defect. He replaced alternate
covering of eyes with alternate flashlight stimulation. The swinging flashlight test is superior to the Marcus Gunn test
for the detection of RAPD.[37]

Procedure

1. In a semi-dark room, ask the patient to fix at a letter or pattern on the distance chart (looking at a near object
causes accommodative miosis)

2. Shine a penlight or indirect ophthalmoscope light into one eye from below the patient's eye at a distance of 5
to 10 cm.

3. After a pause of 3 seconds, quickly shift the light to the other eye.[38] Move the whole light from side to
side. Do not swing the beam from one central axis, as this can stimulate the near response.

4. Repeatedly alternate the light between the two eyes, with a pause of 3 seconds on each eye.

5. Look for the change in pupil size as light is alternated.

An eye with RAPD will dilate as the consensual dilatation response due to light moving off the good eye overpowers
the poor constriction (direct pupil light reflex) response from the affected eye.

Clinical grading of RAPD based on swinging flashlight test.[38] The grades are determined by averaging pupillary
responses over a minimum of six swings of the light.

 Grade I: A weak initial constriction and greater redilatation

 Grade II: An initial stall and greater redilatation

 Grade III: An immediate dilatation

 Grade IV: An immediate pupillary dilatation (followed by secondary constriction) following prolonged
illumination of a good eye for 6 seconds (bleaching of the normal eye)
  Grade V: An immediate pupillary dilatation with no secondary constriction following prolonged
illumination of a good eye for 6 seconds

Grade IV and V are elicited after bleaching the photoreceptors of the good eye to reduce its pupil power.

Special Situations

 Detection of RAPD in a fixed pupil [29] – when one pupil cannot react due to posterior synechiae, trauma,
or pharmacological miosis, we can still look for RAPD. In these situations, one should focus on the reactive
pupil.

For example –

1. If the afferent defect is present in the eye with a fixed pupil, when light is thrown onto the normal eye, its
pupil constricts. When the light is moved to the abnormal eye, the pupil in the normal eye dilates or
constricts less. Returning the light to the normal eye causes its pupil to constrict again.

2. If the normal eye has fixed pupil, here, shifting the light from this eye to the other, the reactive pupil will
dilate.

 In cases with subtle RAPD[17][29] – To unmask subtle RAPD, a Tilt test is performed.[39]

A neutral density filter of 0.3 log units is placed in front of the eye with suspected optic neuropathy. Then the
swinging flashlight test is performed. Placing the neutral density filter in front of the weak eye further decreases the
pupillomotor input of that eye and heightens the inter eye pupillomotor input difference. Thus RAPD is unmasked.

Quantification of RAPD  Using Neutral Density Filters [32] [38]

This is done by placing neutral density filters over the better eye and performing swinging flashlight test.

In this test, we dim the stimulus in the better eye by known amounts with neutral density filters (usually 0.3, 0.6, 0.9,
and 1.2 log units) and perform the swinging flashlight test until the two eyes are balanced and no RAPD is noted. The
density of the filter is recorded in log units as a measure of the size of the defect. The smallest defect that can be
measured with confidence is 0.3 log units. It is important to avoid light spill at the edge of the filters as the light is
swung from one eye to the other. It is difficult to visualize pupil beyond 1.2 log units of neutral density filter,
necessitating the examiner to peek around the filter to watch the pupillary reflex. During the first attempt, it is better to
overshoot the endpoint and induce an RAPD in the filtered eye; then, as one approaches the endpoint for the second
time, the readings can be made more accurately.

Kestenbaum’s pupil number [24]

In patients with unilateral optic nerve disease, with one eye covered and other eye exposed to bright light, the pupil of
affected eye settles at a larger diameter. This difference (in millimeters) in size of two pupils, is a measure of the
difference in pupillomotor input between the two eyes. It roughly corresponds to the relative afferent pupillary defect
measured in log units of neutral density filter.

Limitations

Swinging flashlight test is subject to various inconsistencies due to interindividual variability, the experience of
clinical performing the test, ambient light conditions, and cooperation of the patient and lack of precise criteria for
quantification. It is difficult to measure Kestenbaum's number or quantify relative afferent pupillary defect in children
due to hippus and in adults due to miosis and poor iris mobility.[24]

Pupillography [40]

Modern pupillography uses a computerized device to simulate the swinging flashlight test and allows more accurate
detection and quantification of RAPDs.[41] These are binocular pupillometers which provide information on pupil
diameter, pupil diameter vs. time curves, asymmetry in pupillary responses. The data studied in pupillography
includes average pupillary constriction amplitude (CA), constriction velocity (CV), and constriction onset latency
(COL). CA is the best parameter for detecting RAPDs and differentiating patients from normal subjects.[42]

Go to:

Treatment / Management
The treatment is directed towards the underlying cause.
 Go to:

Differential Diagnosis
Hippus

Random fluctuations of the pupil that are often observed under continual retinal illumination.[43]

Alternating Contraction Anisocoria

Direct pupillary constriction of the eye exceeds the consensual constriction of the contralateral pupil. This
phenomenon may be unilateral or bilateral. In one subset of unilateral contraction anisocoria, the pupillary response of
one side always exceeds that of the other eye. This subset is often confused with a relative pupillary afferent defect.
The cause is hypothesized to be a lesion at the posterior commissure and one or both brachia of the superior colliculus
due to damage of combination of both first and second-order neurons.[23]

Few diagnostic pearls:

1. RAPD with normal visual acuity, color vision, field defects suspect higher-order lesion at the level of the
pretectum

2. RAPD in one eye and contralateral field defects or specifically temporal field defects - optic tract lesion

3. RAPD and NVI (new vessels of the iris) - look for ischemic CRVO

4. RAPD and anisocoria - Repeat test after 30 minutes of light adaptation

5. Cataract and same eye RAPD - suspect posterior segment pathology

6. Cataract and contralateral eye RAPD - can be a transient phenomenon or posterior segment lesion of the
other eye such as recovered optic neuritis

Go to:

Prognosis
In optic neuropathy, RAPD magnitude often correlates with the degree of visual acuity loss, while in maculopathy,
vision is impaired to a greater magnitude compared to RAPD.[12]

In glaucoma – the presence of RAPD is objective evidence of visual field loss.[20] It is indicative of the earliest onset
of optic nerve damage in patients with optic nerve hypertension.[44] 

In retinal vein occlusion – An RAPD >0.9 log units is associated with extensive capillary nonperfusion and poor
visual acuity (Usually< 3/60).[11] A significant increase in RAPD in a patient with non-ischemic CRVO is an early
indicator of conversion to ischemic CRVO.

In retinal detachment – An RAPD usually occurs in retinal detachment involving the macula, and post-operative
visual acuity is usually lower in detachments involving the macula.[45]

In cataract – if the patient has RAPD in the same eye as cataract, then post-operative visual gain tends to be poor due
to associated defects in the anterior visual pathway.[15] A poor visual prognosis should always be explained if the eye
with cataract shows RAPD.

Go to:

Complications
The failure to detect this clinical sign results in complications secondary to the underlying etiology.

Go to:

Deterrence and Patient Education

Measurement of RAPD has proven value in the prediction of visual field loss in certain optic nerve and retinal
diseases.[5] RAPD is a very sensitive and specific test as a predictor of ischemia and in the differentiation of ischemic
and nonischemic central retinal vein occlusion.[11] Thus, this simple test for RAPD detection can be used to counsel
the patients.

Go to:

Enhancing Healthcare Team Outcomes

One should not be in a hurry to dilate the eye, as one might miss important pupillary signs. In a patient admitted in the
general ward or intensive care unit, the examination of pupillary reflexes by nurses and interns helps to identify
certain neuro-ophthalmic conditions and enable prompt referral to the ophthalmologist. Certain tumors such as
pituitary adenoma may remain silent and may be diagnosed on a detailed evaluation of a case with a relative afferent
pupillary defect.

Overview
Marcus Gunn pupil describes the finding during the swinging-flashlight test whereupon the patient's pupils appear to
dilate instead of constrict when the light swings from the unaffected "good" eye to the affected "bad" eye.
It is important to remember that there is no anisocoria in this case. The pupils remain the same size as each other at all
times.
Upon shining the light into the "good" eye, both pupils will constrict. However, when the light moves to the "bad" eye, the
full strength of the light will not be perceived and both pupils will appear to dilate.
The Marcus Gunn phenomenon is a relative afferent pupillary defect. That is to say, the "bad eye" can still perceive light
and respond to it, but not as much as the "good eye"; the bad eye is relatively less responsive than the good eye, but
both eyes are still responsive to light. If you shine the light in the bad eye, both pupils will constrict (due to the still-intact
consensual light response). However, if you shine the light in the "good eye", the pupils will constrict even more. It is as
if you are shining a light of lesser intensity at the bad eye.
In context of the swinging flashlight test, you first shine the light in the good eye, causing full pupillary contraction in both
eyes. Then you move the light to the bad eye. The bad eye perceives this same light as if were not as bright, and thus
causes the pupils to constrict less. This gives the illusion that both pupils are now dilating as a response to the light.
They are actually still constricting in response to the light, but constricting less than when the light was shining at the
good eye, because the bad eye perceives a dimmer light. But relative to the previous maximal dilation from shining the
light at the good eye, the pupils now dilate. Had you started with the light shining on the bad eye first, you'd see both
eyes constrict slightly. This distinguishes the Marcus Gunn Pupil from a total CN II lesion, in which the bad eye
perceivs no light. In that case, shining the light at the bad eye produces no effect. In any case the patient themselves
should report that they are totally blind in the unreactive eye.
Although the commonest lesion site is the optic nerve, severe retinal disease may also yield a Marcus Gunn pupil and
this sign should be taken as indication of a "pre-chiasmatic" visual defect.

What causes an esotropia?

Esotropia is caused by eye misalignment (strabismus). While strabismus can be hereditary, not all family
members will develop the same type. Some people develop esotropia, while others might develop eyes
that turn outward instead (exotropia).
Esotropia is a condition where one or both eyes turn
inward. The term derives from Greek, where ‘eso-‘ means
‘inward,’ and ‘trope’ means ‘turn.’

Approximately 1 to 2 percent of all people in the United States have esotropia, according to
the College of Optometrists in Vision Development.

Esotropia can take several forms, with some types developing in infancy and others
occurring in adulthood.

Fast facts on esotropia:

 Those with esotropia often look like they have crossed eyes.
 The condition is sometimes mistakenly referred to as lazy eye.
 Untreated esotropia may cause complications in both children and adults.
 Esotropia is a type of eye misalignment, known as strabismus.

What are the types?

 Esotropia may cause a range of complications, making early diagnosis and treatment
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important.

According to the American Association for Pediatric Ophthalmology and Strabismus

(AAPOS), esotropia can be classified by its frequency, the person’s age when it develops,
and whether it is related to eye-focusing or not.

The different classifications include:

Infantile

The infantile form of the condition begins during the first year of life. Infants with this
condition are unable to use their two eyes together.

If one of the eyes turns inward more often than the other, the child is at higher risk of
amblyopia, also known as lazy eye.

Infantile esotropia is usually treated with surgery, eyeglasses or,

sometimes, Botox injections. Correcting esotropia before a child is 2 years of age is often
very successful, with just a few children experiencing visual problems as they grow up.

Other eye problems associated with infantile esotropia include an upward drifting of the
eyes, farsightedness, and nystagmus, which is a jerking movement of the eyes.

Acquired

If esotropia develops later in life, it is known as acquired esotropia. It may result from
medical conditions, such as diabetes, or other eye problems, such as untreated
farsightedness.

Double vision is one of the leading complaints of those with the condition. It can make
everyday tasks difficult.

People with acquired esotropia can often successfully treat the condition with glasses and
vision therapy, although surgery may be necessary for some.

Accommodative
One of the most common forms of strabismus (crossed eye), accommodative esotropia is
characterized by eye crossing that occurs when the eyes are trying hard to focus to see
objects clearly.

This attempt at focusing is known as “accommodation.” People with accommodative

esotropia — also known as refractive esotropia — usually have farsightedness.

People can control accommodative esotropia by wearing prescription eyeglasses or contact

lenses. If this fails, they may require surgery.

Constant versus intermittent esotropia

 Esotropia causes one or both eyes to turn inwards.
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Image credit: Kakawere, (2010, March 20)

In addition to the types listed above, esotropia may be classified as constant or intermittent.

Constant esotropia is present all the time, while intermittent esotropia comes and goes.

For example, intermittent esotropia may only be noticeable when a person is:
  tired
 sick
 looking only at objects that are near
 looking only at objects that are far away

Symptoms
Symptoms of esotropia include:

 inward turning of the eyes

 crossing of the eyes
 lazy eye

People with esotropia may notice that they cannot focus their eyes on the same place at the
same time, and they may only be able to see objects fully with one eye.

Complications
Infants and young children may experience:

 loss of 3-D vision

 issues with depth perception
 amblyopia (loss of vision in the crossed eye)

However, if congenital esotropia is treated in infancy, such complications are less likely to be
experienced long-term.

Older children and adults that acquire esotropia can develop:

 diplopia (double vision)

 decreased binocular vision (the ability of the eyes to work together)
 depth perception issues

Causes
 Strabismus may be inherited in some cases, although not all family members will exhibit
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the condition, or the same form of the condition.

There are several forms of strabismus, with esotropia being the most common.

Some people are born with esotropia while others develop it later in life. There is a
hereditary component to strabismus, and the condition tends to run in families.
 However, not all family members will develop strabismus, and those that are affected will not
necessarily experience the same forms.

Risk factors

Some factors increase the risk of having esotropia, including:

 a family history of strabismus

 having another eye disorder, such as cataracts or glaucoma
 certain medical disorders, such as diabetes and overactive thyroid
 neurological conditions, including excessive fluid in the brain
 premature birth
 stroke

There are no known risk factors for childhood esotropia.

5. 1. Clinical features of Pseudophakia 2 3. 4 5. Post operative

Complications of cataract surgery. 6. Management of Chronic
dacryocystitis. 7. 8. Management of fascicular ulcer. 9. 10.
Cause & management of Geographical ulcer.

Pseudophakia
 Why do you need it?

 Signs you need a pseudophakic IOL

 Diagnosis

 Procedure

 Complications

 Outlook

Overview
Pseudophakia means “fake lens.” It’s a term that’s used after you’ve had an artificial lens
implanted in your eye to replace your own natural lens. This is done during cataract surgery.
The implanted lens is called an intraocular lens (IOL) or pseudophakic IOL.

Why do some people need a

pseudophakic IOL?
You’ll need a pseudophakic IOL if you have a cataract removed. A cataract is a clouding of
the lens — the clear part of your eye.

The lens helps focus light onto your retina. This is the layer of light-sensitive tissue in the
back of your eye.

As you get older, protein in your lens begins to clump together and form a cataract that
clouds your vision. The more the cataract grows, the blurrier your vision will become.

Cataracts become very common as people get older. By age 80, most people will have a
cataract. Replacing the clouded lens can restore clear vision.

What are the signs and symptoms that

you may need a pseudophakic IOL?
Signs that you have a cataract include:

 cloudy or blurred vision

 faded colors
 trouble seeing at night
 sensitivity to glare from sunlight, lamps, or headlights
 double vision in one eye
 frequent need to change your eyeglass or contact lens prescription
 a need for brighter light when you read or do other close-up activities

How is this diagnosed?

Your eye doctor can determine whether you need an IOL by doing an eye exam. You might
have one or more of these vision tests:
  Visual acuity test: This test checks your vision by having you read the letters on an
eye chart with one eye closed at a time.
 Slit-lamp exam: Your doctor uses a special lighted device to look for problems with
your iris, lens, and other structures in your eye.
 Retinal exam: Your doctor will first give you drops to dilate (widen) your pupils. This
makes it easier to examine your retina. Then your doctor will use a special device to
examine your retina and lens for signs of a cataract or other diseases.

What’s the procedure?

Surgery to replace the clouded lens is the main treatment for cataracts.

Before your surgery, your doctor will measure the size and shape of your eye to choose the
right lens. You’ll get drops to dilate your pupil. The area around your eye will be cleaned.

You’ll also get medication to numb your eye so you don’t feel any pain.

Your doctor will remove your clouded lens with one of these techniques:

 Phacoemulsification: Your doctor makes a tiny cut in the front of your eye. A probe
that sends out ultrasound waves is inserted into the cut to break up the cataract. The
pieces of the old lens are then suctioned out.
 Laser: Your doctor uses a laser to make a small cut in the eye and break up the
cataract for removal.
 Extracapsular cataract incision: Your doctor makes a larger cut in the front of the
eye and removes the whole cataract.

After your old lens comes out, your doctor will implant the new lens in the space it leaves
behind. The incision is then closed. A patch or shield will go over your eye to protect it while
it heals.

You can go home on the same day as your surgery, but plan ahead for a ride home. You’ll
need someone to drive you.

What are the complications for

pseudophakia and cataract surgery?
Possible side effects of pseudophakia include:

 too much or too little vision correction

  the lens is placed in the wrong position
 the lens moves out of place, blurring your vision
 fluid buildup and swelling in the retina, called Irvine-Gass syndrome

Risks of cataract surgery include:

 infection
 bleeding
 swelling and redness in the eye
 vision loss
 double vision
 increased pressure in the eye, which could lead to glaucoma
 retinal detachment

What’s the outlook?

Cataract surgery with pseudophakic IOL can improve vision in about 90 percent of people
who have the procedure.

Most implanted IOLs are monofocal. They can only focus at one distance — close up or far
away. However, multifocal lenses are also available for some individuals.

After your surgery, you’ll most likely need to wear glasses for reading or driving, depending
on which type of IOL you get.

[Postoperative complications in cataract surgery]

[Article in Romanian]

Marie-Jeanne Koos , Alina Muntean, Cristiana Lehaci

 1

Affiliations expand

 PMID: 12886680

Abstract
The paper is a statistical retrospective trial that evaluates the prevalence of postoperative complications of
the cataract surgery in the IInd Department of Ophthalmology Timisoara. The parameters of interest were
the type and the frequency of the postoperative complication encountered after the extracapsular cataract
extraction (ECCE) followed by a PMMA intraocular lens (IOL) implantation. The most frequent early
postoperative complications were endoepithelial comeal edema (20.8%), inflammatory complications
(uveitis) (8.72%), hemorrhagic complications (4.02%), and postoperative rise of IOP (8.05%). Out of late
complication, we encountered cystoid macular edema (1.34%), bullous keratopathy (1.34%), IOL malposition
(0.67%) and secondary glaucoma (1%).

6. 1. Lens induced glaucoma 2. Complicated cataract 3. Staphyloma 4. Management of

Absolute glaucoma 5. 6. 7. Photocoagulation 8. Central Retinal Artery Occlusion 9. Vision
2020 10. Indication for keratoplasty.
7. 1. Causes complication and management of ectropion. 2. Clinical features, prophylaxis and
management of Vitamin A deficiency. 3. Circulation of aqueous humor. 45. Causes, clinical
appearance and management of complicated cataract. 6. Different types of hypermetropia.
7. Types of optic atrophy. 8. Fundus findings in central retinal vein occlusion. 9. Clinical
features and management of herpes simplex keratitis. 10. How will you test pupil? Why it is
important?
8. 1. Medical management of primary open angle glaucoma. 3 8 1.5 2. Prevention and
management of corneal ulcer perforation. 3 8 1.5 3. Granulomatious uveitis - clinical
features and management. 3 8 1.5 4. Managment of diabetic retinopathy. 3 8 1.5 5.
Hypermetropia –management. 3 8 1.5 6. Sympathetic ophthalmia and its management. 3 8
1.5 7. Causes for blindness—management of trachoma. 3 8 1.5 8. Clinical features and
management of congenital glaucoma. 3 8 1.5 9. Viral keratits - clinical features. 3 8 1.5 10.
Ophthalmia neonatorum and its management.
9. \1. Draw cross section of the upper lid anatomy 2. Define ophthalmia Neonatorum and
management 3. 4. Lens induced Glaucoma 5. Describe the retinal function tests 6. Classify
Uveitis, management and complications of acute iridocyclitis 7. Various lasers used in
ophthalmology 8. Pathological myopia – recent trends in myopia correction 9. Clinical
features and management of Orbital Cellulitis 10.
10. 1. Aetiology and complications of blepharoptosis. 2. Aetiology, signs and treatment of spring
catarrh. 3. Discuss ocular manifestations and management of Vitamin A deficiency. 4.
Discuss features and management of episcleritis. 5. Classify Uveitis and describe the
management of acute iridocyclitis. 6. Discuss the management of acute angle closure
glaucoma. 7. Classification and clinical features of hypermetropia. 8. Describe the fundus
picture in AIDS. 9. Write briefly on Acanthameba keratitis. 10. Discuss different diagnosis of
leucocoria.
11. 1. Clinical features and management of Herpes Zoster ophthalmicus. 2. Sympathetic
Ophthalmitis. 3. Ophthalmia Neonatorum. 4. Sturm’s Conoid. 5. Fundus picture in central
retinal artery occlusion. 6. Pterygeum. 7. Dry eye. 8. Acanth ameba keratitis. 9. Vitreous
Hemorrhage. 10. Causes of Cherry red spot.
12. 1. Acute congestive glaucoma. 2. Ophthalmia neonatorum. 3. After cataract. 4. Recurrent
pterygium. 5. Eye banking. 6. Sympathetic ophthalmia. 7. Pathological myopia. 8. Malignant
tumours of the eye lid. 9.. 10. Toxic optic neuropathies.
13. 1. Clinical features of viral keratitis. 2. Viscoelastics. 3. Hardeolumexternum. 4. Goals of
vision 2020. 5. Treatment of pterygium. 6.
14. atbbbb
10 mark questions

DISEASES OF CONJUNCTIVITIS

Vernal keratoconjunctivitis.

DISEASES OF CORNEA:

Bacterial corneal ulcer – aetiopathogenesis and management.

Describe the aetiology, clinical features, diagnosis and treatment of hypopyon corneal ulcer.
(Aug 2013)

. Clinical features, diagnosis, investigations and management of corneal ulcer. (Aug 2015)

DISEASES OF SCLERA:

DISEASES OF UVEAL TRACT:

. Acute iridocyclitis – etiopathogenesis, clinical features and management. (Feb 2014)

. What is the differential diagnosis for acute red eye? Describe the clinical features and management
acute anterior uveitis (Iridocyclitis).

DISEASES OF LENS:

. Define myopia. Enumerate the types, clinical picture, complications and management of myopia.

. Define hypermetropia. Discuss its clinical features and management

Etiology and clinical varieties of Myopia. Signs and Symptoms. Management of Myopia.

Enumerate the pre-operative investigations for Cataract Surgery

Describe the clinical features diagnosis and management of senile cataract

Mention the causes of gradual loss of vision and discuss the management of senile cortical cataract.
(Feb 2015)

GLAUCOMA:

Describe the stages, clinical features of primary angle closure glaucoma and its management.

Write the differential diagnosis of Red eye and management of acute congestive attack of angle
closure glaucoma.

Discuss the etiology, clinical features field defects and management of primary open angle glaucoma
(Feb 2012)

Discuss clinical features, management of acute congestive Glaucoma.

Differential diagnosis of red eye. How will you manage acute congestive glaucoma?(Feb 2013, Feb
2016)

DISEASES OF VITREOUS:

DISEASES OF RETINA:

1. Discuss in detail about Retinal Detachment (RD)

2. Define Retinal detachment0, Aetiology, types, Clinical Features, investigation and treatment
of Retinal Detachment. (Feb 2012)
3. . Aetiology, clinical features and treatment of retinal detachment.
4. . Describe the pathogenesis, classification, clinical features and management of diabetic
retinopathy.(Aug 2011)
5. Describe the classification, clinical features of Hypertensive Retinopathy
6. . What are the causes of sudden loss of vision, what are the signs and management of retinal
detachment.(Feb 2014)
7. Write an essay on optic atrophy, its management

NEURO-OPHTHAL:

OCUL MOTILITY AND STRABIS:

DISORDERS OF EYELIDS:

DISEASES OF LAC APP:

Aetiology, clinical features and treatment of chronic decryocystitis.(Aug 2012)

Discuss the aetiology, clinical features, investigations and management of chronic dacryocystitis (Aug
2011)

DISEASES OF ORBIT:

OCULAR INJURIES

Describe the etiology, clinical features and management of Hypopyon corneal ulcer.

What are all the ocular manifestation of tuberculosis.

--------------------Abnormalities of pupillary reflex.optic neuritis.