Top Ten Eye Emergencies

1. Top Ten Eye Emergencies

2. Anterior Ischemic Optic Neuropathy
● What else besides AION could be number one?
● A-AION ranks as the prime medical emergency
in ophthalmology.
● There being no other disease in which
prevention of blindness depends so much on
prompt recognition and early treatment.

3. Anatomy of AION
● Ischemic optic neuropathy is classified based on
the pattern of the blood supply.
○ Anterior part: optic nerve head, which is
supplied by primarily the posterior ciliary artery
circulation (AION).
○ Posterior part: Supplied by multiple sources
other than posterior ciliary artery circulation
(PION)

4. Classification
● Both AION and PION can be subdivided into arteritic vs non-arteritic etiologies.
● Anterior ischemic optic neuropathy (AION): acute ischemia of the optic nerve head. Two types:
○ Arteritic Ischemic Optic Neuropathy (AAION): due to GCA
○ Non-arteritic ischemic optic neuropathy (NAION): NOT due to GCA
● Posterior ischemic optic neuropathy (PION): involvement of part of the rest of the optic nerve. 3 types:
○ Arteritic PION: due to GCA
○ Non-arteritic PION: not due to GCA
○ Surgical PION: a complication from a surgical procedure

5. Background
● From here on out we’ll focus on Arteric AION. This is much more emergent than NA-AION.
● PION is very rare and is generally a diagnosis of exclusion.
● A-AION is almost invariably due to GCA, but rarely other types of vasculitis can cause it (eg Lupus,
Herpes Zoster).
● GCA is a systemic vasculitis that generally involves medium and large arteries. It has a special
predilection for the temporal artery.

6. Background
● In the eye, GCA has a special predilection for posterior ciliary artery, resulting in thrombotic occlusion.
● Since the posterior ciliary artery is the main source of blood supply to the optic nerve head, occlusion of
the posterior ciliary artery results in infarction of a segment or the entire optic nerve head.
● That results in development of A-AION and in massive visual loss.

7. Demographics
● Age: GCA generally only occurs on either elderly or late middle aged patients.
● Gender: GCA is almost 3 times per common in women.
● Race: GCA is more common in caucasians, but does occur in other races.

8. Clinical Features
● Ocular Symptoms:
○ Transient vision loss (Amaurosis Fugax) is both an important symptom and an ominous sign.
○ It can sometimes be elicited by induced postural hypotension.
○ But most patients with GCA lose vision suddenly and without warning.
○ Diplopia and Ocular pain are considered symptoms of GCA but are relatively rare.
● Systemic Symptoms:
○ Most patients with GCA will have systemic symptoms
○ Anorexia / weight loss
○ Jaw Claudication
○ Headache, Neck pain, Scalp Tenderness, bulging Temporal Artery
○ Myalgia, malaise, and even anemia.

9. Clinical Features
● One in five patients with vision loss and biopsy proven GCA have zero systemic symptoms!
● Most patients have severe vision loss, but some patients only have mild vision loss and therefore near
normal vision does not rule out GCA.
● Most cases of GCA will have an APD.
● Anterior segment is usually normal on exam. Occasionally there can be signs of anterior segment
ischemia such as hypotony and anterior chamber cells, leading to a misdiagnosis of uveitis.

10. Optic Disc Changes
● Over two thirds of patients have a
diagnostic chalky white optic disc
appearance.
● After disc edema resolves, the optic
nerve takes on a glaucomatous
cupping appearance.

11. Optic Disc Changes
Fundus photograph of right eye with arteritic AION
during the early phase the typical white optic disc
edema.

12. Optic Disc Changes
Fundus photographs of right eye with A-AION: (A)
Before developing A-AION, (B) one week after
developing A-AION with chalky white optic disc
edema and (C) 4 months later showing optic disc
cupping with a cup/disc ratio of 0.8 (note no cup in
A).

13. Fundus Findings
● Retinal Cotton Wool Spots
● Central retinal artery occlusion
○ CRA occlusion is not uncommon in patients with GCA. It is usually combined with posterior ciliary artery
occlusion because the posterior ciliary artery and central retinal artery share a common trunk.
○ Consider GCA in any patient over 50 with a central retinal artery occlusion.
● Choroidal ischemic lesions
○ Visible on fluorescein angiography during the early phase of GCA.
○ It is critical to acquire an FA during the early stage, as these ischemic lesions will not be visible on FA later.

14. Fundus Findings
● Cilioretinal artery occlusion
○ The posterior ciliary artery supplies the cilioretinal artery (when it’s present).
○ A-AION with a retinal infarct in the region of the cilioretinal artery is a classic clinic picture of GCA.
○ Sometimes cilioretinal artery occlusion can occur without visible disc edema. These patients are sometime
misdiagnosed as having branch retinal artery occlusions and therefore untreated, leading to catastrophic loss
of vision is the contralateral eye as well.

15. Classic Diagnostic Picture of GCA

16. Laboratory Tests
● Markedly elevated ESR (erythrocyte sedimentation rate) is the classic lab finding.
○ There are numerous reports of normal ESR in patients with biopsy proven GCA.
● CRP (C-reactive Protein) is a more reliable indicator of GCA.
○ CRP is 100% sensitive for GCA, vs 92% for ESR.
○ The combination of markedly elevated ESR and CRP was shown to be 97% specific for GCA.
● Other lab findings such as anemia, elevated WBC count, elevated hemoglobin and hematocrit levels,
and thrombocytosis can be helpful.
● Unfortunately no test is individually 100% sensitive and specific.

17. Treatment
● Treatment of A-AION is actually treatment of GCA.
○ It is unlikely that the patient will regain vision with treatment. The goal of treatment is to prevent further vision
loss, especially in the contralateral eye.
● To prevent bilateral blindness, two things are crucial:
○ Early diagnosis
○ Immediate and adequate steroid therapy
● The set of clinical criteria most strongly suggestive of GCA in order are: Jaw Claudication, CRP > 2.45,
Neck pain, ESR > 47
■ A combination of the ESR and CRP is 97% specific (best indicator of all).
● If there is a reasonable index of suspicion for GCA, the patient must be treated ASAP. A biopsy can
confirm the diagnosis later.

18. Treatment
● IV steroids are no more effective than oral steroids
● Patient’s require high dose oral steroids (averaging around 80 mg/day of oral prednisone).
● The oral steroids are maintained until ESR and CRP decrease to normal stable levels. Usually this
takes 2-3 weeks.
● Steroids are then tapered slowly to low dose levels. ESR and CRP levels are used as guides during the
taper. If they increase, steroids must be increased again.
● Patients should probably never stop low dose steroids. To do so risks recurrence and blindness.

19. Retinal Artery Occlusion
● A symptomatic retinal artery occlusion is an
emergency.
● Patient’s often have silent concurrent
ischemic strokes.
● All patients with a CRAO or symptomatic
BRAO should be evaluated for a stroke.
● Unfortunately no treatment has been shown to
be effective in improving visual outcome.

20. Etiology
● Blockage may be caused by:
○ Emboli
○ Vasculitis (including GCA)
○ spasms

21. Risk Factors
● Risk factors are similar to the those of Ischemic Stroke.
○ Older age
○ Male gender
○ Smoking
○ HTN
○ Obesity
○ Diabetes
○ Hyperlipidemia
○ Cardiovascular disease
○ Coagulopathy

22. Presentation
● Patient’s typically describe sudden, painless, vision loss that occurs over seconds.
○ Occasionally this is preceded by amaurosis fugax
● Patients with CRAO usually have vision loss over entire visual field
● Patient with BRAO may have sectoral vision loss
● No light perception vision should raise suspicion for ophthalmic artery occlusion

23. Presentation
Patients with a cilioretinal artery sparing may have
20/20 vision.

24. Examination
● An APD may be present in a CRAO or an ophthalmic artery occlusion
● Fundus may appear normal early in the course
○ “You see nothing and the patient sees nothing”
● The fundus whitens due to edema secondary to the ischemia. The fovea appears cherry red because it
has no overlying nerve fiber layer.
○ This finding may take several hours to develop.
● Patient’s arteries may have box carring, Hollenhorst plaques, platelet fibrin plugs, or large calcific
plaques.

25. Box Carring
● The retinal vessels may show segmented blood flow or “box carring.”

26. Hollenhorst plaque
● Cholesterol emboli
● Hollenhorst plaques are bright and refractile
lesions within retinal blood vessels.
● Golden to yellow orange crystals.
● Often occur at bifurcations
● Originate from atherosclerotic lesions, usually
from the carotid.

27. Fibrin-Platelet Emboli / Plug
● Dull elongated plug.
● Often multiple small particles
● Also most often originate in the carotid

28. Calcific Emboli
● Relatively rare
● Originate from calcific aortic stenosis or calcific
valvular heart disease.
● Single, white, non-refractile lesions.

29. Retinal Emboli

30. Diagnosis
● Diagnosis is usually made clinically based on the presentation and exam findings.
● Ancillary tests can be useful to confirm the diagnosis and help determine prognosis.
○ OCT
■ Hyperreflectivity of inner retina, hyporeflectivity of outer retina.
○ FA
■ Delayed filling of arteries and delayed AV-transit
○ ERG
■ Characteristic dimunation of the b-wave.

31. Diagnosis: OCT in CRAO

32. Differential Diagnosis
● Ophthalmic artery occlusion.
○ Vision is usually NLP
○ No cherry red spot as the choroid is also occluded.
● Carbon Monoxide poisoning can cause a cherry red spot.
● Ocular ischemic syndrome may present with symptoms of transient vision loss.
○ Eye will also likely have injection, uveitis, neovascularization, optic nerve edema, and retinal hemorrhages.

33. Treatment
● There are no evidence based therapies that have demonstrated efficacy in improving visual outcomes.
● Refer any patient with a CRAO or symptomatic BRAO for an urgent stroke work up.
○ Asymptomatic BRAO’s are lower risk, and evidence is less clear on whether they need a urgent referral.
● Ocular massage: may cause embolus to move distally
○ Apply gonioscopy lens and hold pressure for 5 seconds, then release for 5 seconds

34. Treatment
● IOP reduction: also may cause an emoblus to move distally
○ Anterior chamber paracentesis
○ Eyedrops
● Increasing Carbon Dioxide to induce vasodilation.
○ Patient is instructed to breathe into a bag to increase CO2 concentration.
● Monitor patient for neovascularization of the:
○ Iris
○ Retina
○ Angles

35. Retinal Detachment
● Everyone here is probably pretty familiar with
these, yet Mac on RD’s are still missed
frequently by ophthalmologists and
optometrists.
● We also know the treatment:
○ Refer to retina!
● Today we’ll talk about how to make sure we
don’t miss any retinal tears or retinal
detachments.

36. Retinal Detachment
● Patients at risk for RD:
○ High myopia
○ Aphakia
○ History of RD in fellow eye
○ Family history of RD
○ Lattice
● Most common Precursors to rhegmatogenous retinal detachments:
○ PVD
○ Retinal holes (symptomatic and asymptomatic)
○ Lattice Degeneration

37. PVD
● PVD is usually the critical event that leads to retinal tears and detachments.
○ Between 8-26% of patients presenting with an acute PVD are found to have a retinal tear at the time of initial
examination.
○ Of the remaining patients, there is a 2-5% risk of a retinal tear being diagnosed in the weeks that follow.
These retinal breaks may have been new or missed.
■ Of these patients, 80% had either:
● Vitreous hemorrhage or pigment cells in vitreous at time of initial exam
● New symptoms prompting a return visit
● Have a low threshold for referring patients to retina if you are unable to get a good view of the entire
retina.

38. Symptomatic Retinal Breaks
● These are either:
○ Breaks caused by vitreoretinal traction in a
patient with a new PVD.
○ Breaks associated with new onset flashes/
floaters.
● 50% will lead to RD!
● Symptomatic operculated breaks usually do not
progress to detachment unless the vitreous
remains adherent to the retina surrounding the
break.

39. Asymptomatic Retinal Breaks
● Asymptomatic operculated holes and round
holes rarely lead to retinal detachment.
● Sometimes patients with pre-existing retinal
holes develop a symptomatic PVD. There is no
consensus on treatment.
● Asymptomatic horseshoe tears have a 5%
chance of RD and should be treated.

40. Acute Third Nerve Palsy
● Acute TNP can be caused by numerous conditions:
○ Compressive lesions:
■ Tumors
■ Posterior communicating artery aneurysms
● Life-threatening emergency!
○ Post-traumatic
○ Post-infectious
○ Ischemic oculomotor palsies
■ Microvascular or “diabetic palsy”
○ Complex Migraines
○ Orbital inflammatory syndromes (eg Orbital Pseudotumor).

41. Acute Third Nerve Palsy: Presentation
● The primary symptom is diplopia.
○ Mixed horizontal and vertical binocular diplopia.
○ The pattern of image separation is the key to diagnosis.
● Pain or headache
● Ptosis
○ Sometimes ptosis covers the pupil and prevents the patient from experiencing diplopia.
● Pupillary dilation
○ Patients may complain of glare with bright lights or difficulty reading due to accommodative deficit.

42. Physical Findings: Horizontal and Vertical Deviation
● Exotropia results from weakness of medial rectus
● Vertical deviation results from weakness of superior rectus, inferior oblique, and inferior rectus.
● Superior oblique and lateral rectus are unaffected. Therefore most patients have a downward and
outward deviation of the affected eye.
○ Classic presentation is “down and out.”
● The eye movement deficits should be apparent on exam, even in a partial TNP.
○ Very mild cases may require maddox rod testing to elicit latent deviation or phoria.

43. Physical Findings: Horizontal and Vertical Deviation

44. Physical Findings: Horizontal and Vertical Deviation

45. Physical Findings: Ptosis
● Ptosis results from weakness of the levator palpebrae.
● Ptosis is often complete with the upper lid blocking the pupil.
● In cases with milder ptosis, it can be evaluated by measuring Margin reflex distances:
○ MRD1: distance from light reflex to upper lid margin (normally 4-5 mm).
○ MRD2: distance from light reflex to lower lid margin (normally 5 mm).
○ Levator palpebrae weakness reduces MRD1, but not MRD2.
○ Ptosis from ocular sympathetic palsy (eg Horner’s Syndrome) causes reduction of both MRD1 and MRD2.
○ Pseudoptosis from contralateral seventh nerve lesion causes increased MRD1 and MRD2 on the side
opposite to the apparent ptosis.

46. Physical Findings: Pupillary Dilation
● Pupillary dilation and sluggish or absent reaction to light results from involvement of the
parasympathetic fibers that originate in the Edinger-Westphal subnucleus of the third cranial nerve
complex.
● The size difference between the two pupils should be greater is bright light, and lesser in dim light.
○ The opposite is true for Horner’s Syndrome.
○ Anisocoria that remains the same in bright and dim light is often physiologic.

47. Assessment
● Recommendations for managing acute TNP’s are based on whether they are “internal” or “external.”
○ Internal TNP: pupil involvement
○ External TNP: extraocular muscle involvement (including ptosis)
● Treatment Recommendations:
○ Internal TNP with no external involvement (i.e. isolated dilated pupil):
■ Usually caused by tonic pupils or exposure to dilating medications.
■ Risk of aneurysm is minimal, neuroimaging is not required.

48. Assessment
● Treatment Recommendations (cont.):
○ Partial external TNP without internal involvement (“pupil sparing partial TNP”):
■ Risk for aneurysm is not well defined. Pupil involvement may develop over time.
■ MRI with MRA is recommended in the acute setting.
■ If scans are negative, patient must be followed. Look for alternative causes like myasthenia gravis.
■ If the patient has a negative or inadequate MRA and pupil development occurs later, then catheter angiography is
recommended.
○ Complete external TNP without internal involvement (“pupil sparing complete TNP”).
■ Most likely vasculopathic and may be observed.
● The pupil must be re-examined within one week.
■ TNP’s usually improve within a few weeks to months.
■ If no improvement in 8-12 weeks, recommend neuroimaging.

49. Assessment
● Treatment Recommendations (cont.):
○ Partial external and partial internal dysfunction.
■ MRI and MRA must be performed.
■ If scans are negative, follow patient for progression. Consider catheter angiography.
○ Complete external, partial internal dysfunction.
■ Similar risk of aneurysm (perhaps slightly lower) compared to partial external and partial internal.
■ MRI/MRA must be performed.
○ Complete or partial external with complete internal involvement.
■ Highest risk of aneurysm!
■ Immediate MRI/MRA, and if negative then catheter angiography.

50. Bacterial Keratitis
● Approximately 30,000 cases of microbial keratitis per
year in the U.S.
● Incidence is rising!
● A major cause of vision loss due to corneal
opacification.
● The WHO recognizes bacterial keratitis as a silent
epidemic.

51. Bacterial Keratitis
● The pattern of microbial keratitis varies with geographic region and local climates.
● The bacteriological profile shows huge disparities amongst populations living in both western countries
and developing countries.
● 80% of of bacterial corneal ulcers in the U.S. are caused by:
○ Staphylococcus aureus
○ Streptococcus pneumoniae
○ Pseudomonas species

52. Bacterial Keratitis
● Bacterial keratitis is rare in normal eyes. Most patients have predisposing risk factors such as ocular
surface disease or immunosuppresion.
● According to insurance data in the US, the most common predisposing risk factors are:
○ Contact Lens use
○ Trauma
○ HIV

53. Bacterial Keratitis
● Management
○ Start with obtaining a careful history:
■ Degree of symptoms
■ Medication allergies?
■ Identify any predisposing factors
● Contact lens use or misuse?
● Prior viral keratitis?
● Hot tub?
● Immune status?
● History of MRSA?
● Trauma?
● Current use of eye drops?

54. Bacterial Keratitis
● Exam:
○ Perform a careful exam including visual acuity, external exam, and slit lamp exam.
○ Pay particular attention to the following on external exam:
■ Any exposure issues that may have caused the infection or prevent healing?
● Eyelid closure
● Globe position
■ Check corneal sensitivity
■ General appearance of patient
■ Make note of any skin conditions

55. Bacterial Keratitis
● Exam:
○ Pay particular attention to the following on slit lamp exam:
■ Eyelid margins: check for ulcers, inflammation, and trichiasis
■ Conjunctival discharge?
■ Filtering bleb? Tube erosion?
■ Scleral nodules, thinning, or inflammation?
■ Cornea:
● Document the lesion’s location, density, size, shape, character of infiltrate margin (eg suppuration, feathery, necrosis, soft,
crystalline), and edema.
● Check for dystrophies
● Check for prior scars

56. Bacterial Keratitis
● Diagnostic tests: cultures and smears
○ The majority of community acquired cases of bacterial keratitis resolve with empiric therapy.
○ However antibiotic resistances are on the rise and the majority of MRSA is also resistant to fluoroquinolones.
○ Therefore cultures are the standard of care for sight threatening ulcers, especially for any large central corneal
infiltrate extending into the middle or deep stroma.
■ Also consider performing cultures these settings:
● Chronic ulcers that are unresponsive to empiric therapy.
● Atypical clinical features suggestive of fungal, amoebic, or mycobacterial keratitis.
● Trauma from vegetable matter
● If the patient wore contact lenses in a hot tub.

57. Bacterial Keratitis
● Performing Cultures:
○ Choose the right tools:
○ Corneal scraping (A) can be performed with a
Kimura spatula (B), blade (C), culturette swab
(D) or calcium alginate swab (E).

58. Bacterial Keratitis
● Culture media:
○ Saboraud agar (A) for fungal culture
○ chocolate agar (B) for aerobes
○ blood agar (C) and thioglycolate broth (D) for
aerobes and anaerobes
○ viral transport media (E) for viral and
Chylamydia culture
○ sterile saline (F) to transport specimens that
require plating in the lab with otherwise
unavailable media.
○ Glass slides (G) should be used to create
smears for microbial stains.

59. Bacterial Keratitis
● Antibiotics
○ Most providers initiate treatment with a 4th generation fluoroquinolone.
○ Assessing response to treatment is critical. Switch to fortified antibiotics ASAP if any worsening is noted.
■ A combination of fortified vancomycin and fortified tobramycin is recommended.
■ It used to be common to use fortified cephazolin and fortified tobramycin, and some providers still do use this regimen.
However, neither cephazolin nor tobramycin cover MRSA. If treatment with a 4th generation fluoroquinolone has
already failed, then there is a good chance the patient has MRSA.
■ Start with a loading does of using both drops every 15 minutes for the first hour, then alternate each drop every 30
minutes (so they get each one every hour).
■ Reduce therapy when possible because toxicity from fortified antibiotics will slow healing.

60. Bacterial Keratitis
● Even if the ulcers are properly treated with
topical antibiotics, clinical outcomes are often
poor due to scarring.
● There we are always looking for ways to mitigate
the inflammatory response without risking
healing.

61. Bacterial Keratitis
● Anticollagenases
○ Tetracyclines have been shown to be beneficial in reducing scarring in animal laboratory models.
○ Unfortunately no high quality studies demonstrated this effect in humans.
○ Despite that, doxycycline is widely used as an adjuvant.
● Amniotic Membrane Grafts (Prokera)
○ Small studies have shown benefits, but no large or high quality studies have been performed.
○ May limit penetration of suspensions like besivance.

62. Bacterial Keratitis
● Steroids
○ The subject of a long debate! Steroids can reduce scarring, but also risk worsening infections.
○ Largest study to date is SCUT: Steroids for Corneal Ulcers Trial.
■ All patients in SCUT had culture proven bacterial keratitis and had been on moxifloxacin for 48 hours before starting
steroid drops.
■ For most patients there was no difference in outcome.
■ Certain subclasses may benefit from starting steroids within 2-3 days
● CF or worse vision at presentation
● Pseudomonas ulcers
■ Other subclasses did worse with steroids
● Nocardia infections (10% of all K ulcers in US) demonstrated worse scarring with steroids.

63. Bacterial Keratitis
● Nocardia Keratitis
○ Often looks and behaves like a
fungal ulcer.
○ Avoid steroids in ulcers with satellite
lesions or feathery borders.

64. Bacterial Keratitis
● This is fairly common presentation of a severe
case of Pseudomonas Keratitis.
● Recommend performing culture and starting
steroid drops if it grows out pseudomonas.

65. Open Globe
● If you find an open globe, stop the exam and
refer immediately.
● Do not manipulate the eye or check IOP.
● Tell the patient not to eat or drink anything.
● Place a rigid eye shield.

66. Open Globe
● Not all open globes are obvious.
● Anytime you see a patient with an eye injury get a careful history.
○ Grinding or hammering are the most common causes of IOFB’s.
● With blunt trauma, rupture often occurs under the rectus muscles.
○ Significant blunt trauma should considered a ruptured globe until proven
otherwise.
● Posterior ruptures are often not visible on exam. Look for deepening of the
AC (compared to fellow eye), vitreous hemorrhage, and low IOP.

67. Acute Angle Closure Glaucoma
● Angle-closure glaucoma (ACG) is a group of
diseases in which there is reversible
(appositional) or adhesional (synechial) closure
of the anterior-chamber angle.
● The angle closure may occur in an acute or
chronic form.
● We’re going to focus on Pupillary Block.

68. Acute Angle Closure Glaucoma
● Symptoms:
○ Pain
○ Nausea
○ Blurred vision
○ Headache
● Signs:
○ Corneal Edema
○ Shallow AC
○ Fixed mid-dilated pupil
○ IOP usually over 30

69. Acute Angle Closure Glaucoma
● Pupillary block is the most common mechanism
of angle closure.
● Is caused by resistance to aqueous humor flow
from the posterior to anterior chambers at the
pupil.
● Aqueous humor accumulates behind the iris
increasing its convexity causing angle closure.

70. Acute Angle Closure Glaucoma
● Risk Factors:
○ Female Gender
■ Women 2-4 times more likely to have ACG
○ Hyperopia
○ History of ACG in fellow eye
■ If a patient has ACG on one eye, the other eye has a 40-80% of chance of developing ACG over the next 5 to 10
years.
○ Asian or Inuit ethnicity.
○ Use of angle narrowing medications:
■ It’s possible that any medication with anticholinergic side effects could precipitate ACG in at risk individuals:
phenothiazine, antihistamines.
■ Topical dilating drops can induce pupillary block in at risk patients.

71. Acute Angle Closure Glaucoma
● Treatment:
○ The immediate goal is to decrease the IOP, which can usually be done medically.
○ Initiate treatment with oral or topical carbonic anhydrase inhibitors, topical beta-blockers, and topical alpha-
agonists.
○ Pilocarpine can break the pupillary block, it may not work until the IOP is below 40.
■ Confirm that pupillary block is the mechanism causing elevated IOP before instilling pilocarpine. Cholinergic agents
like pilocarpine shallow the AC and narrow the angle. Therefore they can worsen phacomorphic or malignant
glaucoma.
○ Hyperosmotic agents can be used if these modalities fail.
■ Oral glycerol or oral isosorbide are relatively safe but take time to work. Oral glycerol can be dangerous in diabetics.
■ IV Mannitol is safe in diabetics and works quickly. But it is dangerous in any patient with borderline cardiac or
pulmonary status.

72. Acute Angle Closure Glaucoma

73. Acute Angle Closure Glaucoma
● Other treatments:
○ Occasionally you can break the pupillary block simply by indenting the cornea with a cotton tip applicator or
gonioscopy lens.
○ Anterior chamber paracentesis can be used to acutely lower IOP and allow the pupil to constrict, thereby
breaking the attack.

74. Endophthalmitis
● A purulent inflammation of the vitreous, usually
due to infection.
● Progressive vitritis is the hallmark.
● Types:
○ Exogenous
■ Acute postoperative
■ Chronic postoperative
■ Bleb associated
■ Post intravitreal injection
■ Traumatic
○ Endogenous
■ Rare, patients usually very sick.

75. Endophthalmitis
● Acute Post-operative
○ Refers to infectious endophthalmitis shortly after ocular surgery (usually cataract).
○ Most present in 1-2 weeks, usually 3-5 days after surgery.
○ Rapidly progressive
■ Early recognition is key!
○ Initial Symptoms:
■ Pain in 75% (25% have no pain!).
■ Red eye in 80%
■ Swollen lid in 35%
■ Blurred vision in 95%
■ Discharge

76. Endophthalmitis
● Acute Postoperative
○ Common Signs
■ Corneal edema
■ Hypopyon
■ Vitreous inflammation
■ Retinitis
■ Blunting of red reflex
■ Anterior chamber cells with fibrin

77. Endophthalmitis
● Treatment
○ Patient must be sent to a retina specialist emergently.
○ If the patient has HM vision or better, they will be treated by vitreous tap and intravitreal antibiotics.
○ If vision is LP or worse, then immediate pars plana vitrectomy is necessary.

78. Alkali Burn
● Alkaline compounds cause saponification of the fatty acids in cell membranes, which
penetrates the ocular surface epithelium as well as deeper cellular structures.
● Corneal and conjunctival epithelium, goblet cells, stromal keratocytes, corneal extracellular
matrix, blood vessels, ciliary body and trabecular meshwork may be damaged.

79. Alkali Burn
● Clinical features:
○ Symptoms:
■ Ocular pain
■ Lacrimation
○ Signs:
■ Mild Cases: epithelial erosion, corneal haze,
conjunctival injection.
■ Moderate cases: cornea may opacify with slight
ischemia of limbus.
■ Severe cases: significant ischemia of the sclera,
avascularity of the limbus, blanching of conjunctiva
and severe corneal haze.

80. Alkali Burns
● Complications
○ Eyelid scarring
○ Corneal opacification
○ Severe dry eye
○ Corneal ulcer
○ Perforation with potential secondary intraocular
infection
○ Conjunctival scarring
○ Symblepharon or ankyloblepharon
○ Aqueous dynamic changes with increased or
decreased intraocular pressure
○ Cataract and phthisis bulbi

81. Alkali Burns
● Treatment
○ Immediate irrigation of the eye until and cul-de-sac until pH returns to neutrality (7.0)
○ If pH is not returning to 7, check for foreign bodies and sweep fornix.
○ Cederroth solution is preferable to saline for irrigation, but use whatever you have available.
○ Once pH returns to normal, perform a full ocular examination
○ If there is no limbal whitening or epithelial defects then the patient may be treated conservatively:
■ Antibiotic drops QID
■ Prednisolone QID
■ Preservative free lubrication
■ Follow up in 3-5 days

82. Alkali Burns
● Treatment
○ If after irrigation there is limbal whitening or an epithelial defect, then the patient must be treated aggressively:
■ Prednisolone q1h
■ Antibiotic drops qid
■ Consider 1 drop of atropine in clinic
■ Vitamin C 1000mg orally bid
■ Aggressive lubrication with preservative free drops
■ Oral doxycycline if the patient is a candidate (over 8 y/o and not pregnant)
■ Follow patient daily, paying particular attention to IOP
■ Amniotic Membrane Graft

83. Orbital Cellulitis
● Orbital cellulitis is a relatively uncommon infective
process involving ocular adnexal structures posterior to
the orbital septum.
● If treated early, orbital cellulitis has a good prognosis.
But if not treated early it can lead to blindness and
death.
● Can affect both adults and children, but is more
aggressive in pediatric cases.

84. Orbital Cellulitis
● Presentation:
○ Eyelid edema
○ Erythema
○ Chemosis
○ Proptosis
○ Blurred vision
○ Fever
○ Headache
○ Double vision
○ History of upper respiratory tract infection is very common
■ 90% of cases occur as extensions from sinusitis

85. Orbital Cellulitis
● How to distinguish from preseptal cellulitis?
○ Decreased visual acuity
○ APD
○ Proptosis
○ Limited ocular mobility (diplopia)
○ Fever
○ History
■ Patients with preseptal cellulitis should have a reason for developing it:
● Direct inoculation such as bug bite or eyelid trauma
● Spread from stye, sinusitis, impetigo, etc.
■ If a convincing event or reason for preseptal cellulitis cannot be elicited, then suspect orbital cellulitis.

86. Orbital Cellulitis
● Case:
○ 9 year old female presented to her pediatrician
with four days of left eye pain, swelling, and
mild headache. She was diagnosed with
preseptal cellulitis and started on amoxicillin.
○ After 4 days she did not improve so returned to
the pediatrician. The pediatrician switched her
to augmentin, ordered a CT scan, and referred
to ophthalmology.

87. Orbital Cellulitis
● Exam was remarkable for eyelid swelling and
reduced ocular motility. When asked the
patient endorsed diplopia.

88. Orbital Cellulitis
● The patient also had mild proptosis

89. Orbital Cellulitis

90. Orbital Cellulitis
● Treatment:
○ Hospital admission with IV antibiotics
○ Sometimes surgical drainage is necessary, especially in adults because the infections are frequently
polymicrobial.
○ Lumbar puncture may be necessary if the patient develops meningeal signs or symptoms.

91. Orbital Cellulitis
● Post-Treatment: