HEENT Flashcards
Common complaints of blepharitis
Burning Watering FB sensation Crusting and matting of the lashes Red lids Sometimes red eyes Sometimes pain
What are the two categories of anterior blepharitis?
Staphylococcal
Seborrheic- chronic scaling of the eye that leads to irritation
DDx of blepharitis
Bacterial or viral conjunctivitis Contact lens complications Rosacea Allergic or contact dermatitis Preseptal cellulitis Chalazion Hordeolum Dry eye syndrome Basal cell carcinoma, eyelid
Dx and tx of blepharitis
First, apply a warm compress to the eyelid to clean the eye, and do this repeatedly
Abx ointment
-Erythromycin TID x7 days
-Sulfacetamide ointment q4hrs x7 days
Which form of conjunctivitis is more common?
Viral > bacterial
What are the four clinical factors associated with viral conjunctivitis
Age 6 yrs or older
Presentation in April thru November
No d/c or watery d/c
No glued eye in the morning
Hx of bacterial conjunctivitis
Pts complain of eyelids sticking together
Itching, burning or gritty FB sensation
Family members may be infected as well
Acute onset, minimal pain
Staphylococcal and streptococcal species are most common
Presentation of allergic conjunctivitis
Very similar in appearance to viral conjunctivitis, but accompanied by nasal congestion, sneezing, eyelid swelling and sensitivity to light. Both eyes are affected. Not contagious
PE of conjunctivitis
Erythematous- conjunctiva
May see pus drainage across the eye
Photophobia is minimal
Hx of recent URI is typically associated with a viral cause
Dx of conjunctivitis
Do visual acuity and consider fluorescein stain if corneal abrasion or ulceration suspected, or risk of FB
Still need to check for FB
Be sure no risk of chlamydial conjunctivitis
If neonate- immediate referral- if suspect N. gonorrhea or chlamydial infection
Tx for conjunctivitis
Viral- supportive care with artificial tears prn, cold compresses
Bacterial
-Polytrim (trimethoprim/sulfa): 1 drop q3h while awake for 5-7 days
-Gentamicin: 2 drops q4h while awake for 5-7 days
-Ciloxan (cipro): 2 drops q4h while awake for 5 days
-Ocuflox (ofloxacin): 2 drops q4-6h for 5 days
Choice depends on cost to pt and allergies. Ciloxan and Ocuflox better for contact lens associated conjunctivitis
Causes of corneal abrasion
Dry eye
FB injury
contact lens wear
Traumatic abrasion- fingernails, animal paws, pieces of paper or cardboard, makeup applicators, hand tools, branches or leaves
Pathophys of corneal abrasion
Occurs because of a disruption in the corneal epithelium or a scrape to the corneal surface
Procedure of fluorescein stain
Use anesthetic drops before stain procedure
Burns for 20-30 seconds
PE findings of corneal abrasion
Dx can be confirmed with slit lamp exam and fluorescein installation
Pt complains of eye pain and inability to open eye d/t FB sensation
Often pts are too uncomfortable to work, and pain may interfere with sleep
Photophobia may be present
Excessive tearing
What to do for a PE to look for corneal abrasion
Examine eye with lids retracted in order to fully look at the cornea as well as conjunctiva
Assess visual acuity
Apply a topical anesthetic to do a full exam
DDx of corneal abrasion
Uveitis
Keratitis
Glaucoma
Prognosis of corneal abrasion
Prognosis usually excellent with full recovery of vision and is expected with minor abrasion within 24-48 hrs
Extensive or deep abrasions may require a week to heal
If abrasion is in central line of vision, monitor with ophthalmology
Bacterial keratitis from overnight use of contact lens can become infected with P. aeruginosa, pneumococcus, moraxella and staphylococci
-Treat with moxifloxacin 1 drop TID for one week
Tx of corneal abrasion
Traditionally, topical abx are used for prophylaxis even in noninfected corneal abrasions not related to contact lenses, but this practice has been called into question. Gentamicin or Tobramycin have been used as well
Treat pain with topical NSAID drops. Ketolorac- 1 drop q6h prn for pain
Ice packs for 24 hrs prn, then warm compresses
Health maintenance- corneal abrasion
Persons who work in high-risk occupations such as auto mechanics, metalworkers, or miners should wear protective eyewear
Contact sports such as hockey, racquetball, pts who farm and ski should also wear protective eyewear
Pts with large abrasions should be reexamined freq by ophthalmologist until healing occurs
Pt complaints with FB
Pain (relieved sig with topical anesthesia) FB sensation Photophobia Tearing Red eye
What is your first step in trying to remove a FB from an eye?
Only try touching with Q-tip if you think you can remove the FB
What’s your second option for FB removal in the eye if the first one doesn’t work?
Needle
What is applied to the before and after FB from eye removal?
Antibiotic Polytrim Ocuflox Tobrex Ciloxan Bacitracin ointment
What to do with rust rings that remain in the cornea after removal of a metallic FB
May require removal with a rust ring drill
F/u every 2 days until the epithelial defect is well-healed
What should be updated after FB removal in the eye
Tetanus booster if not immunized in past 7 years
Background information in primary open angle glaucoma
Multifactorial optic neuropathy
Chronic and progressive
Acquired loss of optic nerve fibers
This develops into the presence of open anterior chamber angles, visual field abnormalities, and IOP that is too high
Silent onset with no sx or complaints until late
What to pay attention to in primary open angle glaucoma
Past ocular hx Previous surgery Ocular or head trauma PMH (CAD, DM, HTN) Current meds RFs
Who is at the highest risk for primary open angle glaucoma?
Advise screening by eye specialist for AAs and elderly
What does ocular hx usually include for primary open angle glaucoma?
Hx of eye pain or redness Multicolored halos HA Previous eye dz Uveitis Ask about FHx
Diagnostic testing for primary open angle glaucoma
Lab tests to r/o other causes of optic neuropathy in pts
-CBC
-ESR
-Serology for syphilis
Golman tonometry
Gonioscopy: microscope used in conjunction with a slit lamp that measures the anatomical angle of the eye’s cornea and slit lamp
-These tests would be done by an eye specialist
PE findings of primary open angle glaucoma
If IOP rises above 21 mm Hg, the % of pts developing vision loss increases rapidly
Optic disc cupping and nerve fiber layer losses of up to 40% have been shown to occur before actual visual field loss has been detected
Pathophys of primary open angle glaucoma
The aqueous humor passes through the pupil and drains through a special membrane called the trabecular meshwork
In open angle glaucoma, the flow of this liquid becomes impaired
Too much abnormal pressure damages the optic nerve, which can eventually lead to blindness
General approach to primary open angle glaucoma tx
Current medical therapy for primary open-angle glaucoma is limited toward lowering IOP
If one med is inadequate in reaching the target pressure, a second med should be chosen that has a different MOA so that the two-drug therapy will have an additive effect
Tx for primary open angle glaucoma
Beta-adrenergic blockers: Timoptic, Betoptic-S, Betagan
Adrenergic agonists: Alphagon
Carbonic anhydrase inhibitors- Truspot, Azopt
Antiglaucoma combos- Tomoptic/Alphagon
Prostaglandin analogs: Xalatan, Lumigan
Miotic agents: Pilocar, Ocusert
Acute angle closure glaucoma
A condition in which the iris is apposed to the trabecular meshwork at the angle of the anterior chamber of the eye
This blocks the outflow of aqueous from the eye which causes a rapid rise in IOP
Hx/PE of acute angle closure glaucoma
Sudden eye pain, blurred vision and N/V
Halos around lights
<10% of glaucoma in the US are d/t acute angle closure glaucoma
PE of acute angle closure glaucoma
Examine with ophthalmoscope, tonometry, and gonioscopy
Tonometry may show as high as 40-80 mm Hg
Ophthalmoscopy may reveal a swollen optic disc
Gray atrophy of the stroma of the iris provides further evidence of a prior attack
Tx of acute angle closure glaucoma
Definitive tx is laser iridotomy or surgical iridectomy
Intended to prepare the pt for laser iridotomy
Cornea should be treated with osmotic agents, pupil constricted, and IOP lowered to prevent acute damage to the optic nerve
What meds lower IOP in acute angle-closure glaucoma?
Acetazolamide given as a state dose of 500 mg IV followed by 500 mg PO. A dose of a topical BB (i.e., carteolol, timolol) will also aid in lowering IOP
What does laser iridotomy do?
Creates an opening in the iris through which aqueous humor trapped in the posterior chamber can reach the anterior chamber and the trabecular meshwork
Pathology of exudative macular degeneration
Pathologic choroidal neovascular membranes (CNMV) develop under the retina. The CNMV can leak fluid and blood and if left untreated, cause a centrally blinding disciform scar
What can contribute to the worsening of age-related
Smoking
HTN
Obesity
Dietary fat intake
Hx of age-related macular degeneration
Painless, progressive blurring of the central visual acuity, which can be acute or insidious in onset
This leads to a central scotoma in which the pt’s visual acuity falls below reading level and legal driving level
Peripheral visual acuity is usually retained
Hard exudates
Lipid deposits which are produced from lipoprotein leakage from blood vessels. When hard exudates are present, one should think of a vasculopathy, seen usually in conditions with chronic vascular leakage
Drusen
Waste material and composed of proteins, lipids and many other trace elements such as zinc
PE findings of exudative AMD
Subretinal fluid Pigment epithelial detachments Subretinal hemorrhages Drusen present Choroid neovascular tissue may be seen as yellow-green subretinal discoloration
Tx of exudative AMD
Until the start of anti-VEGF agents, ophthalmologists used thermal laser destruction or photodynamic therapy of the choroid neovascular tissue as the primary tx
Now, two new drugs: FDA approval of Ranibizumab, but it’s still expensive, and bevacizumab, which is still considered off-label
Aflibercept is indicated for exudative to bind and prevent activation of vascular endothelial growth factors (VEGF-A)
Non-exudative macular degeneration
Characterized by the presence of atrophy that can be associated with severe central visual field loss
Peripheral vision is preserved
90% of pts with ARMD have dry ARMD, which is a slower progression
Usually affects those >50 yo
Tx/followup of non-exudative macular degeneration
10-20% of those with dry ARMD can progress to wet ARMD
One trial showed favorable results when treating dry ARMD with large doses of antioxidant multivitamin therapy (vit A, C, E, zinc, and copper)
F/u for macular degeneration
Support groups and counseling Low-vision aids Handheld or stand magnifiers for reading Talking watches Computers that use large type face
When does optic neuritis typically first occur?
In young adulthood and is commonly the first manifestation of MS, but ON can occur in isolation
Occasionally, ON can result from an infectious process involving the orbits or paranasal sinuses
Optic neuritis
A demyelinating inflammation of the optic nerve that often occurs in association with MS and neuromyelitis optica (NMO)
PE findings of optic neuritis
Rapidly developing impairment of vision in 1 eye, or less commonly, both eyes
Retro-orbital or ocular pain, exacerbated by eye movement
Pain may precede vision loss
Decreased pupilary light reaction in the affected eye
Marcus Gunn pupil
Abnl color vision
Central scotoma with visual field testing
Papillitis (swollen optic disc) in 33% of pts with ON
With time- the optic nerve may become pale
Lab diagnosis for optic neuritis
Do blood tests to exclude causes of optic neuropathy other than optic neuritis
-ESR
-Thyroid function testing
-ANA
-Angiotensin-converting enzyme
MRI is highly sensitive for and specific in the assessment of inflammatory changes in the optic nerves
DDx for optic neuritis
Acute angle closure glaucoma Interstitial keratitis Optic nerve sheath meningioma Anterior ischemic optic neuropathy Compressive neuropathy Sarcoidosis Sudden visual loss Thyroid opathlmopathy Toxic/nutritional optic neuropathy
Prognosis for optic neuritis
Visual function begins to improve 1 wk to several weeks after onset, even without any tx
Permanent residual deficits in color vision and contrast and brightness sensitivity are common
Tx for optic neuritis
IV steroids to speed the rate of recovery, BUT do little to affect ultimate visual acuity
Treat pain with pain meds
Determine with workup whether pt has brain lesions on MRI that indicate high risk for MS. Immunomodulators can improve risk of reoccurrence of optic neuritis for pts with MS
Causes of orbital cellulitis
Can be an extension of an infection from the paranasal sinuses, eyelids, dental infections
Direct inoculation of the orbit from trauma or surgery
Hematogenous spread from bacteremia
What are 90% of cases of orbital cellulitis due to?
Ethmoid sinusitis
Aerobic bacteria are most frequently responsible in ethmoid sinusitis
Anaerobic bacteria from maxillary sinus- bacteroides (from mouth)
Eyelid infections can cause orbital cellulitis from S. aureus, S. pneumoniae, S. pyogenes
Hx/PE of orbital cellulitis
Fever, malaise Hx of recent sinusitis Recent dental work Recent infection/sepsis Swollen conjunctiva Decreased vision Pain on eye movement Lid edema
Labs/dx of orbital cellulitis
CBC-WBC >15,000 with a shift to the left
BCx should be drawn prior to giving abx
Culture should be ordered of purulent drainage from the eye or from the orbital abscess
High-resolution CT scan with contrast infusion
MRI may be helpful in defining orbital abscesses
Tx of orbital cellulitis
Pt should be promptly hospitalize for tx until the pt is afebrile and has clearly improved
Consider orbital surgery in every case of subperiosteal or intraorbital abscess formation
Pt needs to be monitored daily and treated with IV abx started and continued for 1-2 wks then oral abx for 2-3 wks
-Nafcillin (staph and strep coverage)
-Cefotaxime (H. influenzae, Moraxella)
-Vanc, clinda, or TMP-SMX (for MRSA)
-Metro (for anaerobes)
What is different in papilledema in contrast to other causes of optic disc swelling?
Vision is well preserved with acute papilledema
Onset of papilledema
Bilateral and may develop over hours to weeks
Cause of papilledema
Rare brain tumor
Brain infection: brain abscess, meningitis, encephalitis
Severe HTN
Pseudotumor cerebri or benign intracranial HTN
Optic nerve glioma (unilateral papilledema)
Meds (minocycline, lithium, corticosteroid withdrawal)
Cerebral edema
PE findings of papilledema
Papilledema on retinal exam
Peripheral vision affected in some pts
Wider blind spot near the nose
Afferent pupil defect- pupil is slow to react to light
Sixth nerve palsy: double vision and eyes not tracking well together
Small hemorrhages on the nerve fiber layer detected with the green light on ophthalmoscope
Signs/hx of papilledema
HA
Visual changes- vision turns gray briefly or described as if a “veil has fallen over the eyes” with position changes
Presents as a bilateral phenomenon and may develop over hrs to wks
Pulsatile tinnitus
Neck and back pain
Nausea with vomiting
Labs/rads of papilledema
Brain CT or brain MRI CBC Blood sugar ESR RPR
F/u diagnostic of papilledema
LP should be performed following nl MRI to assess opening pressure of the CSF and to obtain CSF for analysis to r/o neoplastic and infectious etiologies. May provide therapeutic benefit
Tx of papilledema
Tailored to the underlying pathologic process
Diuretics: Diamox may be useful in selected cases, esp in cases of idiopathic intracranial HTN
Corticosteroids may be effective in cases of inflammatory disorders
