powerpoint EENT
Isa0730
PowerpointEENT2.pptxEye Evaluation
Evaluation of the Eyes
Routine Screening/Comprehensive Eye Exam
Every 1-2 years
>65 years old
without risk factors for eye disease
3-5 years after diagnosis
Patients with DM – type 1
At diagnosis and Annually
Patients with DM – type 2 to assess for diabetic retinopathy
Prior to Pregnancy and at first trimester
women with DM
Clinical Assessment and P.E.
PMHx and FamHx and ocular history
Medications
Systematic approach to examining the eyes and function
Visual acuity
Pupillary response
Intraocular pressure
Ocular alignments and extraocular movements
Visual fields
External structures
Anterior/posterior segments
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Evaluation of the Eyes
S/S of Eye Conditions
Red Eye
Bacterial, viral, allergic fungal infection
Vision Loss and Other Visual Disturbances
Decreased central or peripheral vision, metamorphopsia (distorted images), photopsia (light flashes), or vitreous opacities (floaters)
Ocular Disease
Ocular and Periocular Disease
Any discomfort in or around the eye and may be described as burning, aching, throbbing, boring, stabbing, or irritating
Foreign body sensation
Pain receptors in the eyelids, cornea, conjunctiva, and uveal tract will cause ocular or periocular pain
Any inflammatory disorder of the conjunctiva, superficial layers of the cornea, or uveal tract can cause ocular irritation, burning, discomfort, or frank pain
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Cataracts
An opacification of the lens that distorts the images that are projected onto the retina, resulting in difficulty seeing that may progress to complete loss of sight.
Intervention is indicated when visual acuity has been reduced to a level the client finds unacceptable or when diminished sight adversely affects the client’��s lifestyle.
Assessment findings include:
Blurred vision and diminished color perception (early signs)
Diplopia, reduced visual acuity, absence of the red reflex, and the presence of a cloudy white pupil (late signs)
Age-related: pain and eye redness
Gradual loss of vision
Cataracts
Cataracts
Considerations
The natural lens is surgically removed and (usually) replaced with an artificial lens, one eye at a time.
Administer preoperative eye medications; the client may need to administer the medications at home before the procedure.
After surgery, elevate the head of the client’��s bed 30 to 45 degrees and turn the client on his or her back or to the unaffected side.
Have the client wear an eye patch and orient the client to the environment.
Position the client's personal belongings on the unaffected side.
Maintain safety.
Provide home care instructions.
GLAUCOMA
What is it?
A disease of progressive optic neuropathy with loss of retinal neurons and their axons (nerve fiber layer) resulting in blindness if left untreated.
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And you thought glaucoma was a disease in which there was too much pressure in the eye! So did most ophthalmologists until several years ago.
GLAUCOMA
How do we diagnose it?
IOP is not helpful diagnostically until it reaches
approximately 40 mm Hg at which level the
likelihood of damage is significant.
Visual fields are also not helpful in the early stages
of diagnosis because a considerable number of neurons must be lost before VF changes can be
detected.
Optic nerve damage in the early stages is difficult
or impossible to recognize.
50% of people with glaucoma do not know it!
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The three mainstays of glaucoma diagnosis are inadequate. The actual intra-ocular pressure is too imprecise, and the changes in the visual field and the optic nerve occur too late to prevent most of the damage.
GLAUCOMA
Cup-to-disk ratio
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No two disks are alike. Signs suggesting glaucoma as seen in the right photo include a large cup, nasalization of vessels, and pallor of the cup. Note the peripapilary depigmentation on the right which can make the true cup:disk ratio difficult to estimate.
GLAUCOMA
Normal
DISK CUPPING
Glaucoma
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In glaucoma of all types, if not controlled. There is progressive enlargement of the cup, increased pallor of the base of the cup, and nasalization of the disk vessels.
GLAUCOMA
TREATMENT GOALS: Reduce pressure to less than or equal to 24 mm Hg with a minimum pressure reduction of 20% from the baseline.
OUTCOME MEASURES: Development of reproducible visual field abnormality or development of optic disc deterioration.
MEDICATIONS USED: beta-adrenergic antagonists,
prostaglandin analogues, topical carbonic anhydrase inhibitors, alpha-2 agonists, parasympathomimetic agents, and epinephrine.
OHTS parameters
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Narrow Angle Glaucoma
Onset: 50+ years of age
Symptoms
Severe eye/headache
pain
Blurred vision
Red eye
Nausea and vomiting
Halos around lights
Intermittent eye ache
at night
Signs
Red, teary eye
Corneal edema
Closed angle
Shallow AC
Mid-dilated, fixed
pupil
“Glaucomflecken”
Iris atrophy
AC inflammation
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The classical signs and symptoms of narrow angle glaucoma.
Narrow Angle Glaucoma
Mid-dilated, fixed pupil
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Mid-dilated, fixed pupils and cloudy corneas during an angle closure attack.
Open Angle Glaucoma Aka: chronic simple glaucoma (CSG) and primary open angle glaucoma (POAG)
Risk Factors
IOP Diabetes
Age Myopia
Race Gender
Family history Cardiovascular
Central corneal disease
thickness Hormones
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Open Angle Glaucoma
Onset: 50+ years of age
Symptoms
Usually none
May have loss of central
and peripheral vision
late
Signs
Elevated IOP
Visual field loss
Glaucomatous disk changes
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Remember: most patients with open angle glaucoma have no symptoms. This is the best reason to have periodic eye examinations with pressure checks and optic nerve evaluations.
Normal Tension Glaucoma (NPG, LTG, LPB, NTG)
Similar to OAG but IOP always < 21 mmHg
Higher prevalence of vasospastic disorders,
blood dyscrasias, autoimmune diseases
May be related to episodic hypotension,
hypothyroidism
A diagnosis of exclusion!!!
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Open Angle Glaucoma
HISTORY:
Positive family history
African American and Hispanic background
History of trauma
History of steroid use
Risk factors
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GLAUCOMA
Treatment
Medical
Surgical
Miotics
Beta-blockers
Carbonic anhydrase
inhibitors
Prostaglandin
analogues
Alpha-2 agonists
Argon laser trabeculoplasty
Trabeculectomy
Filtering procedure
Cyclocryotherapy
Cyclolaser ablation
Iridotomy
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No treatment works all the time!
Glaucoma
Considerations
Chronic Glaucoma
Medications that will decrease intraocular pressure will be prescribed. Explain to the client the possible need for lifelong medication use.
Instruct the client to avoid anticholinergic medications (prescribed for gastrointestinal conditions such as gastritis or ulcerative colitis; respiratory conditions such as asthma or chronic obstructive pulmonary disease; genitourinary conditions such as prostatitis or urethritis; and Parkinson disease) and to obtain permission from the physician before taking any over-the-counter medication.
Instruct the client to report eye pain, halos around lights, and changes in vision.
Tell the client that when maximal medical therapy has failed to halt progression of visual field loss and optic nerve damage, surgery will be recommended.
There are five main groups of glaucoma drugs, each acting in a different way to reduce IOP:
A) prostaglandin analogues (bimatoprost, latanoprost, and travoprost) increase uveoscleral outflow
B) beta-blockers consist of two main groups: selective (betaxolol) and non-selective (timolol, levobunolol), both of which decrease aqueous production
C) alpha-2 adrenergic agonists (apraclonidine, brimonidine) decrease aqueous production and increase uveoscleral outflow
d) carbonic anhydrase inhibitors decrease aqueous formation and can be applied topically (brinzolamide, dorzolamide), or systemically (acetazolamide, methazolamide)
E) parasympathomimetics (pilocarpine, carbachol) increases aqueous outflow through the trabecular meshwork by means of ciliary muscle contraction, and may open the drainage angle in angle-closure glaucoma by stimulating the iris sphincter muscle.
Conjunctivitis
Conjunctivitis
Inflammation of the conjunctiva, the transparent mucosal tissue that lines the eye and inner surface of the eyelids
Infectious: viruses and bacteria
Noninfectious: allergy, atopy, or exposure to toxins
Clinical Presentation
Viral: Recent URI or exposure to sick contacts (Adenoviral conjunctivitis)
Ocular S/S: acute onset of a red eye with excessive watery discharge, lymphadenopathy (screen for MRSA, HSV)
Bacterial: thick, purulent discharge, eyes are sticky/glued shut. These symptoms persist throughout the day but are worse in the morning
Allergic: headache, fatigue, possible fam Hx of atopy allergy, bilateral involvement, itching of eyes
Vernal and atopic: more severe s/s of severe itching, burning, and tearing, begins in childhood – resolves in the third decade, blepharospasm and photophobia. Discharge is often white, thick, and ropy
Medication toxicity: contact dermatitis of the lower lids with thickening and scaling of the skin is sometimes seen
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Etiology:
Chlamydia trachomatis and Neisseria gonorrhea- MOST COMMON IN NEWBORNS
Virus: adenoviruses – MOST COMMON in ADULTS & CHILDREN
Bacterial: S. Aureus - MOST COMMON IN ADULTS
IRRITATIVE: topical medications, wind, etc
Autoimmune: example: Sjogrens syndrome
Physical Exam
Visual acuity
Pupillary reaction and EOM’s intact
Edema of eyelids and matted eyelashes
Red eye, conjunctival injection
Foreign body sensation
* pt should not report photophobia and examiner should not see pupillary abnormalities in simple conjunctivitis
Conjunctivitis
Diagnostics
Thorough eye exam
Visual acuity testing
Gram-stained smears and cultures are necessary in the immunocompromised (including neonates) as well as in severe or unresponsive cases
PCR (chlamydial conjunctivitis)
Differential Dxs
Must consider other causes of conjunctival injection – may be benign to potentially sight-threatening
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Conjunctivitis
Management
Viral: artificial tears and cool compresses. Advise considered contagious as long as they are still tearing or for at least 1 week
Bacterial: use discretion in topical Abx Rx. Abx if suspect high infectivity rate (high-risk patients should always receive Abx) trimethoprim–polymyxin B or fluoroquinolone drops, 4 times a day for 1 week.
Systemic Abx for: H. influenzae,
gonoccocal or chlamydial infection
Allergic: avoidance of trigger, oral antihistamine preservative-free artificial tears, cool compresses, and removal of contact lenses. For severe cases addition of antihistamine-vasoconstrictor, mast cell stabilizers
Vernal and atopic: Avoid of triggers, mast cell stabilizers initiated 2 weeks before known allergic S/S develop
Medication toxicity: Eliminate toxic source, treat with preservative-free artificial tears. Short course of topical steroids
Ophthalmologic referral based on assessment of sight-threatening risk
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Prevention:
US Preventative Task Force Services Recommendation:
All newborn infants: Provide prophylactic ocular topical medication for the prevention of gonococcal ophthalmia neonatorum within 24 hours after birth
Preventive medications include 0.5% erythromycin ophthalmic ointment, 1.0% solution of silver nitrate, and 1.0% tetracycline ointment. All are considered equally effective; however, the latter two are no longer available in the United States.
Adults and Children: Frequent hand washing and hygiene
Management:
Avoid irritants
No contact lenses/ replace make-up
Allergic: Pantanol
Bacterial (NON Sexually Transmitted Infection): Tobramycin 3%, erythromycin ophthalmic ointment, etc.
Bacterial (Gonococcal): may need to be hospitalized for IV ABX, if no corneal lesions, ceftriaxone 1 g IM x1 and topical ophthalmic ABX
Neonates: base treatment on culture and sensitivity results
Erythromycin ethylsuccinate PO x 14 days
Special Considerations:
If suspect Herpetic: REFERRAL
Pregnancy or lactation: DO not prescribe doxycycline
If no improvement in 24 hours: REFERRAL
If sever pain, changes in visual acuity: REFERRAL
Blepharitis, Hordeolum, and Chalazion
Blepharitis, Hordeolum, and Chalazion
Blepharitis
Inflammation of the eyelids
Infectious or inflammatory
Chalazion
A chronic, sterile, lipogranulomatous inflammatory lesion of the meibomian gland
Hordeolum
An acute infection of one of the glands in the eyelid
The most commonly associated organism is S. aureus
Clinical Presentation
Blepharitis Sxs: due to ocular tear film instability and dry eye
Sxs: burning, foreign body sensation, tearing, photophobia, itching, redness, discharge, and swollen erythematous eyelids, often worse in the morning
Chalazion Sxs: usually non-painful,
Hordeolum Sxs: usually painful,
In both chalazion and hordeolum there may be cosmetic disfigurement and mechanical ptosis
If large, the lesion may mechanically press on the corneal surface to induce astigmatism and blurred vision
Copyright © 2017 by Elsevier Inc. All rights reserved.
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Blepharitis, Hordeolum, and Chalazion
P.E.
Inspect face, ocular adnexa, and eye (conjunctiva, sclera, palbera)
Inspect eye and lashes for discharge – suspicious for bacterial infection
Palpate eyelids for mass, pain assessment
Diagnostics
Based on clinical findings
Differential Dxs
Sebaceous carcinoma, basal cell carcinoma, squamous cell carcinoma (rare)
Eye syndrome
Conjunctivitis (viral, bacterial, or allergic)
Contact dermatitis
Atopic keratoconjunctivitis
Herpes simplex infection
Preseptal cellulitis
Acute dacryocystitis
Ocular rosacea
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Blepharitis, Hordeolum, and Chalazion Management
Blepharitis:
Warm compresses
Hygiene
Lid scrub kits
Warm water, diluted baby shampoo on cotton tip applicator
Erythromycin or bacitracin ointment
Artificial tears may also be beneficial
Hordeolum:
Self-limited
Frequent application of warm, moist compresses with light massage over lesion.
Daily lid hygiene with lid scrubs is also beneficial
Chalazium:
Self-limited
Chronic chalazium
may require steroid injection
OR surgically removed by ophthalmologist
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Corneal Abrasion
Defect of the epithelial layer of the cornea caused by a mechanical trauma to the surface of the eye
Etiology: Fingernails, paws, paper, branches
Foreign Body: rust, wood, plastic
Contact lens: Improperly fitting, dirty, over-worn, dry eyes with contact lens
RETINAL DETACHMENT
Marina Capak
Mentor: A. Žmegač Horvat
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pulled away from the underlying choroid
small areas of the retina torn =>
retinal tears or retinal breaks
retinal cells deprived of oxygen
if not promptly treated => permanent vision loss
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SYMPTOMS
floaters - bits of debris in field of vision that look like spots, hairs or strings
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SYMPTOMS
floaters
light flashes
shadow or curtain over a portion of visual field
blur in vision
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Can occur as a result of:
trauma
advanced diabetes
an inflammatory disorder, such as sarcoidosis
shrinkage of the jelly-like vitreous that fills the inside of the eye
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vitreous liquid leaks through retinal tear and accumulates underneath retina
retina can peel away from underlying layer of blood vessels
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Factors that may increase risk of retinal detachment:
aging - more common in people older than 40
previous retinal detachment in one eye
family history of retinal detachment
extreme nearsightedness
previous eye surgery
previous severe eye injury or trauma
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TREATMENTS
Retinal tears:
laser surgery (photocoagulation)
freezing (cryopexy)
Retinal detachment:
pneumatic retinopexy
scleral buckling
vitrectomy
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Presentation:
Excruciating pain, inability to open eye, photophobia, tearing, foreign body sensation
Usually unilateral
History of contact lens use, dry eyes
PE:
Increased lacrimation on affected side
Altered integrity of smooth cornea seen as irregular light reflex.
May be visible with the naked eye or with the use of fluorescein staining.
Diagnostic Test:
Fluorescein staining will show epithelial disruption on the cornea
Slit-lamp exam may be required by specialist to determine corneal penetration
Treatment:
Irrigation of normal saline to flush any foreign particles
Patching of eye no longer recommended
Avoid contact lens use until pain free and eye is healed
Topical ophthalmic ABX
Topical NSAIDS (use with caution)
Never use topical steroids- may delay healing
Tetanus Booster if indicated
Impaired Hearing
Impaired hearing is a defect in the detection and/or processing of sound waves
Affects both communication ability and personal safety and can be a socially isolating experience
Hearing loss occurs at all ages
Increases with advancing age
Requires different considerations in children than in adults
Clinical Presentation
Immediate specialist referral to an otolaryngologist or neurologist is indicated for patients with sudden hearing loss
May present as sudden, progressive, or fluctuating in nature
Assess whether unilateral or bilateral
Associated Sxs: otalgia, ear fullness, vertigo, tinnitus, or cranial neuropathies should be documented
Pts’s Med/Fam Hx and medication use should incorporate current and past treatments with oral and IV meds, OTC
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Impaired Hearing
P.E.
Perform a complete HEENT exam
Diagnostics (as indicated)
Rinne and Weber test
Screening audiogram
Tympanometric screening
MRI/CT scan
Differential Dxs
Sudden Causes
Idiopathic sensorineural hearing loss, infections, perilymphatic fistula, ischemia of the inner ear or retrocochlear structures, multiple sclerosis, autoimmune diseases, trauma, chronic renal failure, and sickle cell anemia
Chronic Causes
Presbycusis, noise exposure, familial factors, retrocochlear neoplasm, chronic otitis media, cholesteatoma, otosclerosis, hypothyroidism, diabetes, and chronic renal failure. Differential diagnosis for fluctuating hearing loss includes otitis media perilymphatic fistula, Meniere’s disease, multiple sclerosis, migraine headache, syphilis, autoimmune disorders, and sarcoidosis
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Impaired Hearing
Management (as indicated)
Remove cerumen impaction – spontaneous improvement in hearing
Treat underlying infection, other etiologies
Otolaryngology referral is indicated for patients with hearing deficit associated with trauma, congenital hearing loss, tumors, obstructions of the external auditory canal, nonhealing TM rupture, and otosclerosis. Treatment for otosclerosis may be stapedectomy or sound amplification
TM perforation may heal spontaneously or require a surgical patch or graft
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Earache: Differential Diagnosis
Otitis Externa: Inflammation of the lining of the external ear canal
Bacterial: Pseudomonas aeruginosa, Staph. Aureus, Group A Stre p. pyogenes Fungal agents: Candida, others Symptoms: Pain at external canal, acute, severe at times, pruritus; frequent swimming Physical Findings: Pain on pulling pinna or pressing on tragus Edema/erythema of external canal Whitish or green discharge
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External Canal
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http://www.med-ed.virginia.edu/courses/pom1/pexams/HEENT/
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Precipitants of Otitis Externa
Moisture : Swimming, Perspiration, High humidity
Water contaminated with bacteria*
High environmental temperatures
Mechanical removal of cerumen
Insertion of foreign objects
Cotton swabs, Fingernails, Hearing aids, Ear plugs
Other trauma to ear canal
Chronic dermatologic disease
Eczema, Psoriasis, Seborrheic dermatitis , Acne
Drying of the External Canal
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Otitis Externa
A cellulitis of the external auditory canal that may extend to the auricle (pinna)
“Swimmer’s ear”
A small percentage of patients with otitis externa will progress to malignant (necrotizing) otitis externa, which is a complication that is most often seen in people who are immunocompromised or who have comorbid conditions such as diabetes mellitus
Acute otitis externa is pain of the affected ear and auricle developing over 48 hours or less
Chief Sxs: pain, feeling of fullness, itching
Other signs and Sxs: drainage from the affected ear and hearing loss
Chronic otitis externa Sxs: primarily one of intense pruritus
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Otitis Externa
P.E.
Classic finding:
Pain and tenderness on palpation of the tragus and on repositioning of the auricle to allow inspection of the canal
Chronic O.E.
Erythematous and edematous ear canal
Often the canal is filled with debris and sloughed tissue
The TM may be erythematous, poorly visualized (edema, cerumen, or exudate blockage)
Advanced cases of acute otitis externa are often accompanied by complete obstruction of the canal, lymphadenopathy and hearing loss
Chronic O.E.
Dry ear canal, no exudates, thickened narrow canal with excoriations (scratching)
Diagnostics
Usually based on clinical exam alone
Culture of canal drainage with antibiotic sensitivities (when Abx Tx fails)
Microscopic analysis of drainage using potassium hydroxide (KOH) can identify a fungal etiology
Differential Dxs
Conditions that cause ear pain: drainage, inflammation, or hearing loss.
Patients with recurrent otitis externa should be evaluated to determine whether the episode represents a treatment failure rather than a recurrence
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Otitis Externa
Management
Goals:
Clear debris from the canal
Manage pain
Treat the infection and inflammation
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Differentiating Causes of Otorrhea
Otitis externa
Acute bacterial: Scant white mucus, occasionally thick
Chronic bacterial: Bloody discharge, especially in the presence of granulation tissue
Fungal: Typically fluffy and whitish, may be black, gray, bluish-green or yellow;
OM with perforated TM: Acute: Purulent white to yellow mucus with deep pain Serous : Clear mucus, especially in the presence of allergies Chronic: Intermittent purulent without pain
Cerebrospinal fluid leak: Clear, thin and watery discharge
Trauma-Bloody mucus
Osteomyelitis: Odor
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Otitis Externa Fungal
Left: Aspergillar: Otorrhea that looks like a fine white mat topped by black spheres.
Bacterial
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TX: Irrigation to remove debris; Drying
Topical Antibiotics:
Ear wick first 24-48 hrs
Topical otic antibiotics: Ofloxacin (Floxin), Cortisporin
Topical Analgesics: Auralgan otic 2-4 gtts
Oral Analgesics: Acetaminophen
Refractory to topical therapy: Oral antibiotics (Augmentin, Cipro, Dynapen, Keftab)
Fungal: Sulfanilamide powder, Otic Domeboro sol, Nystatin or Chlotrimazole
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Necrotizing Malignant Otitis Externa
> 65 years, mmunocompromised, DM
S&S: Similar to Otitis externa: severe pain and HA.
Does not respond to topical medications
Granulation tissue in posterior and inferior canal Cervical lymphadenopathy, TMJ involvement, facial nerve palsy or paralysis (Bell’s Palsy)
Infection extends into ear canal cartilage; Passes to temporal bone
Pseudomonas aeruginosa infection
Mortality reportedly as high as 20 to 53%. Immediate referral
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Normal TM TM Anatomy
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Key Recommendations For Practice
Diagnosis of AOM requires confirmation of acute onset, identification of signs of middle ear effusion, & evaluation for signs and symptoms of middle ear inflammation.
Antihistamines & decongestants should not be prescribed for children with AOM or otitis media with effusion. (OME)
Observation without antibiotic therapy is an option in selected children with acute otitis media.
Amoxicillin at a dosage of 80- to 90 mg/kg/ day should be the first-line antibiotic for most children with acute otitis media.
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KEY POINT:
Patients with OM who fail to respond to the initial tx within 48 -72 hours should be reassessed to confirm the diagnosis. If the diagnosis is confirmed, antibiotics should be started in patients for whom antibiotics were initially deferred, and a different antibiotic should be prescribed for patients already taking an antibiotic.
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Amoxicillin: 80-90 mg/kg/day, given orally in two divided doses. First-line drug. Safe, effective, and inexpensive
Amoxicillin/clavulanate (Augmentin) 90 mg of amoxicillin per/kg/day; 6.4 mg of clavulanate per/kg/day, given orally in two divided doses. Second-line drug. For patients with recurrent or persistent AOM, those taking prophylactic amoxicillin, those who have used antibiotics within the previous month, and those with concurrent purulent conjunctivitis
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Azithromycin (one dose; Zithromax) 30 mg per kg, orally. For penicillin allergy. One dose is as effective as longer courses
Azithromycin (3 day course; Zithromax Tri-pak) 20 mg/kg once daily, orally. Recurrent AOM
Azithromycin (five-day course; Zithromax Z-pak) 5-10 mg/kg once daily, given orally
For patients with penicillin allergy (type 1 hypersensitivity)
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Acute Otitis Media (AOM) Practice Guidelines.
Recommendation 1:Diagnosis
1. Recent, usually abrupt, onset of signs and symptoms of middle-ear inflammation and middle-ear effusion and
2. Middle-ear effusion with any of:
Bulging, Limited or absent mobility of the TM
Air fluid level behind the TM, Otorrhea and
Signs or sx of middle-ear inflammation, either:
Distinct erythema of the tympanic membrane or
Distinct otalgia (discomfort clearly referable to the ear[s] that results in interference with or precludes normal activity or sleep)
May have other SX
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AOM
Pathogens: Strep. Pneumoniae (32%) (DRSP = 17%-25%) Hemophilus Influenza: (28%) Moraxella Catarrhalis (8%) B-hemolytic strep: 2% Sterile or non-pathogens: 24% Viral: Some cases
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Practice Guidelines
Encourage the prevention of AOM through reduction of modifiable risk factors: reducing the incidence of URI, breastfeeding for at least the first six months; and avoiding supine bottle feeding and reducing or eliminating pacifier use in the second six months of life.
No recommendations for complementary and alternative medicine (CAM) for treatment of AOM are made based on limited and controversial data
http://www.aafp.org/patient-care/clinical-recommendations/all/otitis-media.html
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Persistent AOM: Clindamycin and tympanocentesis Levofloxacin (Levaquin) is effective (not approved for use in children)
Recurrent Acute Otitis Media: Most children improve with watchful waiting.
Antibiotic prophylaxis may reduce recurrence, there are no widely accepted recommendations for antibiotic choice or prophylaxis duration.
Minimizing risk factors (e.g., exposure to cigarette smoke, pacifier use, bottle feeding, daycare attendance) decreases recurrence.
Heptavalent pneumococcal vaccine (Prevnar) reduces the incidence of acute otitis media, but it does not reduce recurrence.
ADULTS: Same as children. Adjust dosages
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AOM Complications
Cholesteatomas-An abnormal skin growth in the middle ear behind the eardrum
Mastoiditis
Persistent,
Chronic OM,
Perforation,
Chronic OME
Brain abscess,
Meningitis,
Cholesteatoma
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Central TM Perforation Near-total TM Perforation
AOM Complications
Traumatic TM perforations
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Treatment of Recurrent Infections Prophylaxis? Placement of tympanotomy tubes; Myringotomy; Adenoidectomy, tonsillectomy or both
Chronic OM: Refer
Prevention
Sequelae
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Otitis Media with Effusion (O.M.E.)
Previously called serous OM
Causative Factors: Adenoidal Hypertrophy Recent URI, or OM; Allergies Deviated nasal septum
Symptoms: Hearing loss
Fullness in ears Snapping sensation No symptoms (if chronic)
Physical Findings: Fluid line, air bubbles, TM retraction Decreased or absent TM movement on insufflated otoscopy
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Practice Guidelines
Diagnosis
1. Presence of fluid in the middle ear without signs or symptoms of acute ear infection. OME is differentiated from acute otitis media The presence of persistent middle-ear fluid from OME results in decreased mobility of the tympanic membrane and is a barrier to sound
Pneumatic otoscopy as the primary diagnostic method for OME. OME should be distinguished from acute otitis media (AOM).
Tympanometry can be used to confirm the diagnosis of OME.
Population-based screening programs for OME are not recommended in healthy, asymptomatic children.
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OME
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Practice Guidelines
Document the laterality and duration of effusion, and the presence and severity of associated symptoms at each assessment of the child with OME.
Distinguish the child with OME who is at risk for speech, language, or learning problems from other children with OME and should more promptly evaluate hearing, speech, language, and need for intervention.
Manage the child with OME who is not at risk with watchful waiting for three months from the date of effusion onset (if known), or from the date of diagnosis (if onset is unknown).
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Antihistamines and decongestants are ineffective for OME and are not recommended for treatment. Antimicrobials and corticosteroids do not have long-term efficacy and are not recommended for routine management.
Hearing testing is recommended when OME persists for three months or longer, or at any time that language delay, learning problems, or a significant hearing loss is suspected in a child with OME. Language testing should be conducted for children with hearing loss.
Children with persistent OME who are not at risk should be re-examined at three- to six-month intervals until the effusion is no longer present, significant hearing loss is identified, or structural abnormalities of the eardrum or middle ear are suspected.
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If referred for evaluation by an otolaryngologist, audiologist, or speech-language pathologist, the referring clinician should document the effusion duration and the specific reason for referral (evaluation, surgery), and provide additional relevant information such as history of AOM and developmental status of the child.
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When a child becomes a surgical candidate, tympanostomy tube insertion is the preferred initial procedure; adenoidectomy should not be performed unless a distinct indication exists (nasal obstruction, chronic adenoiditis).
No recommendation is made regarding complementary and alternative medicine as a treatment for OME.
No recommendation is made regarding allergy management as a treatment for OME.
Treatment:
None or topical decongestant (Used by some practitioners, efficacy questionable)
nasal spray (for children 6 years old and older)
http://www.empr.com/rhinitisrhinorrhea-intranasal-products/category/131/0/ Intranasal products.
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A B C
D E F
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Otitis Media
Inflammation and or infection of the middle ear (bacterial, fungal, viral)
Produces inflammation with fluid
Most often associated with URI or allergies
The most frequent childhood infectious illness
Peak incidence between 6 and 15 months of age
Types
Acute otitis media (AOM), a rapid onset and short duration
Otitis media with effusion (OME) accumulation of serous fluid in the middle ear without acute inflammation
Precipitants: OME, barotrauma, allergy
Middle ear effusion (MEE) accumulation of serous fluid in the middle ear and can be associated with AOM
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Otitis Media
Clinical Presentation and P.E.
Otoscopic exam
Severity of symptoms (otalgia and fever)
Rapid onset otalgia, worse in a prone position, remains the common initial complaint of patients with AOM
Non-specific Sxs: ear rubbing, rhinorrhea, vomiting, diarrhea, and fever
Specific Sxs: linked with causative bacteria
PMHx, exposure to smoke, allergy Hx, lymphadenopathy, pneumatic otoscopy findings, TM presence of bulging with obscure landmarks/absence is important diagnostic finding
Diagnostics (as indicated)
Otoscopy findings of a bulging TM are classic
Tympanometry
Acoustic reflectometry
Examining the ear canal for otorrhea
Pain level
Rinne and Weber tests
Sinus X-ray study or a computed tomography (CT) scan of the sinuses
Allergy testing
CBC with diff
Tympanocentesis
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Otitis Media
Differential Dxs
Primary goal is to differentiate AOM from OME
Management
Specialist referral is recommended for children under 6 months of age OR a child who appears toxic
Pharmacotherapy
The need for antibiotic therapy is determined on an individual basis based on history and presentation
Generally amoxicillin is the preferred first-line medication
Analgesics: Acetaminophen or ibuprofen is preferred
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Dizziness and Vertigo
Dizziness and Vertigo
A Sx of an underlying condition that is classified by the categories of:
Vertigo
Presyncope/Syncope
Disequilibrium
Caused by an imbalance in the vestibular system that may result from lesions in the inner ear, vestibular nerve, brainstem, or cerebellum
Vertigo may result from lesions in the sensory pathways of the thalamus or cortex or stretch receptors in the neck
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Dizziness and Vertigo
Lightheadedness or presyncope/syncope is most commonly a result of a cardiovascular problem
Causes include orthostatic hypotension, vasovagal episodes, hyperventilation, and decreased cardiac output
Less common causes of lightheadedness are hypoglycemia and seizure activity
Dizziness is rarely a manifestation of impending stroke
Disequilibrium may result from
Visual impairment
Bilateral or unilateral vestibular loss
Proprioceptive loss
Impaired cerebellar function
Involvement of motor (frontal and basal ganglia) centers
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Dizziness and Vertigo
Clinical Presentation
Assess pt’s PQRST of Sxs
Obtain a general medical Hx
P.E.
Perform a general medical review as well as a review of medications, including herbals and over-the-counter drugs
Neurocognitive screen
Gait, balance, Rinne and Weber tests
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Dizziness and Vertigo
Diagnostics
Hallpike-Dix maneuver (if a vestibular lesion is suspected)
ENT/Neuro referral/consult
Audiology
Neuro imaging
MRI, CT, ECG, EEG
CBC and DIFF, TSH, glucose, BUN, creatinine, B12, RPR
Differential Dxs
Peripheral lesions include vestibular neuronitis, labyrinthitis, benign positional vertigo, Meniere’s disease, post-traumatic vertigo, acoustic neuroma, and ototoxic drug–induced conditions
Cardiac arrhythmias, critical aortic stenosis, vasovagal response, and orthostatic hypotension
Psychogenic causes
DM
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Dizziness and Vertigo
Management
Specialist referral is indicated when (1) there are positive neurological signs, (2) a suspicion of underlying cardiac disorder, (3) the diagnosis remains unclear, or (4) there is a lack of response to standard treatments
Aim – treat the underlying etiology
Manage – symptoms
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Noninfectious Rhinitis
Allergic: Adults and children Onset: Ages 10-20; Commonly seen in Adults ages 30-40; Ig-E mediated
Seasonal
Perennial (recurrent)
Aggravating factors:tobacco smoke, air pollution, sudden temperature changes
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Nonallergic Rhinitis
May be ACUTE or CHRONIC
viral
Bacterial
Irritant-related (often in the workplace)
Vasomotor
Hormone-related
Associated with medication use or overuse (rhinitis medicamentosum)
Atrophic (mostly in geriatric patients)
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Clinical Presentation of Rhinitis
Viral rhinitis
Accompanied by malaise, headache, sore throat, and occasionally fever
Allergic rhinitis
Itching in the nasal passages, conjunctivae, and roof of the mouth
Epiphoria (stringy, watery ocular discharge)
Sneezing, coughing, and a sore or burning throat
P.E: Allergic shiners, Pale edematous mucosa, nasal crease
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Clinical Presentation of Vasomotor Rhinitis
Vasomotor rhinitis (noninfectious rhinitis without eosinophilia)
Watery rhinorrhea, nasal congestion, “nasal” speech, and forced mouth-breathing
Onset of congestion is rapid in vasomotor rhinitis; patients typically complain of a pronounced, watery postnasal drip, as well as persistent nasal obstruction that may switch sides with each attack
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Management of Rhinitis
Viral rhinitis: treat symptomatically
Fever and headache may be treated with acetaminophen
Rhinorrhea may be treated with oral decongestants
Topical preparations
Intranasal ipratropium (Atrovent) nasal spray
Dextromethorphan for persistent coughs
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Treatment for Allergic Rhinitis
Avoidance or reduced exposure to offending allergens
Oral antihistamines: short-term treatment
Fexofenadine (Allegra) 60 mg bid OR 180 MG QD
Deslorotadine (Clarinex) 5mg qd , others
Combinations antihistamine/decongestant:
OTC:Pseudoephedrine; Dimetapp
Intranasal corticosteroids: long-term management
ZETONNA, OMNARIS (CICLESONIDE); NASONEX, FLONASE
Leukotriene receptor antagonists
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Treatment for Allergic Rhinitis (cont)
Systemic corticosteroids (rarely)
Cromolyn sodium (Nasolcrom)
Nasal spray (AFRIN)
Use no more than 3 days- WHY?
Afrin could give you a rebound effect after 3-5 days.
Rhinitis Medicamentosa (nasal spray addiction as a result of rebound congestion) is caused by the prolonged use of Afrin and other over-the-counter decongestant nasal sprays. The active ingredient in these sprays is a topical vasoconstrictor that temporarily reduces the size of the nasal turbinates, opens the nasal airway and provides decongestant relief from the rebound congestion.
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Complications:
Serous OM
Acute or chronic sinusitis
Respiratory infections
Considerations for immunotheraphy (hyposensitization)
Failure to respond to treatment, or side effects Perennial with daily antihistamine requirements
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Epistaxis: Children and Adults
Hemorrhage of the nasal mucosa
Etiology: 90% due to trauma or inflammation
Contributing Factors: Mucosal dryness, septal deviation, bleeding problems, chronic illnesses medications, cocaine, etc
Anterior/posterior epistaxis
Differential DX: Hemoptysis, hematemesis, chronic sinusitis, nasopharyngeal or paranasal sinus tumors
Kesselbach plexus
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Treatment:
Anterior epistaxis:
Pt sitting upright, with head bent forward, apply pressure x 10-15 min.
For persisting bleeding: vasoconstricting agents or chemical cauterization
Ice pack
Anterior nasal packing
Posterior epistaxis:
Refer to specialist
Prevention/Education
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Sinusitis
Inflammation of the paranasal sinuses
Undrained accumulation of pus
Caused usually by viral URI
Pathogens: Hemophilus Influenza, Strep. Pneumoniae, (25% PCN resistant in children) Moraxella catarrhalis
Differential Diagnosis: URI, rhinitis, nonbacterial sinusitis
Predictors: Maxillary toothache Abnormal transillumination Poor response to decongestants Purulent Discharge (By HX or PE)
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Etiology
The bacteria most commonly involved in acute sinusitis are part of the normal nasal flora
Streptococcus pneumoniae (30-40%)
Haemophilus influenza (20-30%)
Moraxella catarrhalis (12-20%)
Nosocomial sinusitis
Gram-negative organisms – including Pseudomonas aeruginosa (15.9%), Escherichia coli (7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae
PE
Facial Exam
Nasal
Assess the status of the nasal mucosa
Presence and color of nasal discharge
Sinus transilummination and palpation are of little predictive value
Sinusitis: Acute and Chronic
Bacterial:
Predisposing Factors:
Allergic rhinitis, common cold, environmental irritants, nasal polyps, deviated septum, dental abscess
Symptoms:
Purulent rhinorrhea
Facial pain, HA
P.E.:
Pain on palpation, purulent mucus, abnormal transillumination, may have middle ear abn. and eustachian tube dysfunction, post nasal drip
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Bacterial vs Viral
Facial pressure (1of 2 majors needed)
Congestion and/or obstruction
Purulent discharge
Hyposmia/anosmia
Cough not due to asthma in kids
Fever (acute only)
Headache
Fever (non acute)
Halitosis
Dental pain
Fatigue
Cough in adults
Otologic symptoms
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Imaging
Imaging studies are not necessary when the probability of sinusitis is either high or low – may be useful when the diagnosis is in doubt
Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels, and sinus opacification
Treatment
For nasal congestion/drainage: Positioning, steam inhalation
Analgesics: NSAIDS
Decongestants:
Topical Steroids: When secondary to allergic rhinitis
http://www.empr.com/rhinitisrhinorrhea-intranasal-products/category/131/0/ Intranasal products
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Tx of sinus inf. with antibiotics in the first week of sx is not recommended.
Antimicrobial:
Amoxicillin
PCN/Cephalosporin Resistant: Cefuroxime (Ceftin)
Augmentin
Other: Cipro, Biaxin
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SORT: Key Recommendations for Practice
Treatment of sinus infection with antibiotics in the first week of symptoms is not recommended.
Telling patients not to fill an antibiotic prescription unless symptoms worsen or fail to improve after several days can reduce the inappropriate use of antibiotics.
A diagnosis of acute bacterial rhinosinusitis should be considered in patients with symptoms of a viral upper respiratory infection that have not improved after 10 days or that worsen after five to seven days.
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Acute bacterial sinusitis
When to treat with an antibiotic: diagnosis may be made in adults with symptoms of a viral upper respiratory infection that have not improved after 10 days or that worsen after five to seven days.
When not to treat with an antibiotic: nearly all cases resolve without antibiotics. Antibiotic use should be reserved for moderate symptoms that are not improving after 10 days or that worsen after five to seven days, and severe symptoms.
Antibiotic duration: 10 days
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Failure to respond after 72 hours of antibiotics: reevaluate patient and switch to alternate antibiotics
First-line therapy: Amoxicillin
Alternative therapy:
Amoxicillin/clavulanate (Augmentin), cefdinir, respiratory quinolones : levofloxacin [Levaquin]
For beta-lactam allergy: TMP-SMX (Bactrim,, doxycycline, clarithromycin (Biaxin)
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Sinusitis (cont.)
Complications: Locally: Mucoceles, osteomylitis
Initially: Cellulitis, abscess
Intracranial: Abscess, meningitis
Serious findings:
Facial swelling
Erythema or cellulitis over invloved sinus (periorbital or forehead)
Vision changes such as diplopia
Difficulty with EOM
Any abnormal neuro signs
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Treatment: Children
Vaporizer, warm washcloth on face
Analgesics for pain, salt water nose drops (1/4 tsp salt to6 oz boiled water. Avoid antihistamines
Antimicrobial: (Drug of choice) Amoxicillin/(Amoxil) 40 mg/kg/day in 3 divided doses x 10 days or
Amoxicillin and potassium clavulanate (Augmentin) 40 mg/kg/day in 3 divided doses x 10 days or
Cefaclor (Ceclor) 20-40 mg/kg/day in 3 divided doses x 10 days or
Cefixime (Suprax) 8 mg/kg/day x 10 days or
TMP-SMX (Septra) 8 mg/kg TMP, 40 mg/kg SMX in 2 divided doses
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Sore Throat
Most Common: Pharyngitis (Viral) GABHS Pharyngitis: (Group A beta hemolytic strep)
Differential Diagnosis:
Infectious Mononucleosis
Influenza
Stomatitis
Gonococcal Pharyngitis
Oral Candidiasis (Trush)
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Pharyngitis
Inflammation of the pharynx, tonsils or both
Causative microbial agents and associated syndromes.
Viral or unknown cause (Most frequent)
GABHS Pharyngitis: (Group A beta hemolytic strep)
Clinical features:
Not possible to determine etiology by clinical features alone
Laboratory tests: Rapid streptococcal antigen- detection (rapid strep) test and throat culture
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Tonsillopharyngitis.
The diffuse tonsillar and pharyngeal erythema; nonnspecific finding that can be produced by a variety of pathogens.
Intense erythema, seen in association with acute tonsillar enlargement and palatal petechiae, is highly suggestive of group A b-streptococcal infection, though other pathogens can produce these findings.
Exudative tonsillitis, usually seen with GABA or Epstein-Barr virus infection.
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Pharyngitis: Viral
Intense erythema of the tonsillar pillar with accompanying bullae
Herpangina
Acute Viral illness
Sx similar to common cold
Prodrome of high fever (up to 106)
Systemic sysmptoms (malaise, HA, etc)
Oral vesicles and ulcers
Symptomatic tx
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Group A Beta-Hemolytic Streptococcal Pharyngitis: Clinical Findings
Correlation: Strong Tender enlarged anterior cervical lymph nodes Household contact
Scarlatina-form rash
Tonsillar exudates
Correlation: Moderate High fever
Acute onset Sore throat
Winter and spring
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Laboratory Tests:
Throat culture: Gold standard
Culture if 2-3 strongly or moderately correlated findings are present.
No cough, hoarseness or conjunctivitis is present. Culture symptomatic family members & close contacts or hx. of rheumatic fever
Rapid antigen detection tests (rapid strep test): 95% specificity, 76-87% sensitivity If negative, but strong suspicion of GABHS, do culture
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Management
General measures:
Acetaminophen, or Ibuprofen
ASA for adults
Warm saline gargles older children/adults Increase fluids Antibiotics if 4 positive strong or moderate correlated findings present
Do not use TCN, sulfonamides or trimethopim-sulfamethosaxole for strep. Pharyngitis
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Antibiotics:
Patients under 25 kg (55 lbs) Benzathine PCN G (Bicillin L-A) 600,000 u IM Patients over 25 kg (55 lbs) Benzathine PCN G (Bicillin L-A) 1.2 million u IM x1 (Observe client x 20 min. after inj.)
Or oral PCN: (Preferred, but compliance required) Pen VK oral suspension 25-50 mg/kg/day divided twice or 3x/day, x 10 days or 250 mg twice or 3x/day, x 10 days
Older children/adults: Pen V 250-500 mg po twice/day, x 10 days
Other:Azitromycin, Amoxicillin, Augmentin, Keflex
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If PCN allergic:
Child: Erythromycin ethyl succinate (EES 400 ) 40 mg/kg/day, 2-4 divided doses x 10 days (dosage varies with child weight, see tables)
Child: Erythromycin estolate 20-40 mg/kg/day, 2-4 divided doses x 10 days (dosage varies with child weight, see tables) NOT RECOMMENDED FOR ADULTS
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SORT: Key Recommendations for Practice
“Use of clinical decision rules for diagnosing GABHS pharyngitis improves quality of care while reducing unwarranted treatment and overall cost.
Penicillin is the treatment of choice for GABHS pharyngitis in persons who are not allergic to penicillin.
Treatment is not typically indicated in chronic carriers of pharyngeal GABHS.
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Modified Centor score
Score of 2 or 3: RADT or throat culture.
Score of 4 or higher : Consider Empiric treatment
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GABHS: Complications
Nonsuppurative: Rheumatic fever Posstreptococcal
Consultation/Referral Cervical adenitis Peritonsillar abscess Prolonged illness Retropharyngeal abscess
Suppurative: Cervical lymphadenitis Peritonsillar or retropharyngeal abscess Sinusitis Mastoiditis OM Meningitis Bacteremia Endocarditis Pneumonia
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COUNSELING AND PREVENTION:
Do not share eating utensils Good hand washing Change toothbrush after antibiotic taken for 3-5 days Do not return to work or school until 24-48 hrs after antibiotic treatment
Follow-up: Re-culture if pt. Remains symptomatic or has hx of rheumatic fever
If repeat culture positive treat once more; do not re-culture
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Infectious Mononucleosis
Epstein-Barr Virus (90%)
Cytomegalovirus (10%)
Ages: 15-19 , college students, military Symptoms: Fever, sore throat
Physical Findings:
Fever (90% )
Splenomegaly (50%)
Tonsillar/pharyngeal exudates (33%) Cervical lymphadenopathy (90%)
Palatial petichae (25-60%)
Rash (Sometimes)
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Management: Supportive In severe cases: Prednisone 40-60 mg/day on decreasing doses X 5 days
For pharyngitis: PCN V 250mg 3x/day, x10 days
If splenomegaly, exclude from sports x 6-8 weeks
Complications: Splenic rupture
Airway obstruction Neurologic complications
Prevention
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Antibiotics use in URIs: Summary SORT: Key Recommendations for Practice.
Clinical criteria for diagnosis of AOM include: abrupt onset of signs & symptoms, middle ear effusion, & signs or symptoms of middle ear inflammation.
A period of observation is appropriate for select children with AOM and non-severe symptoms.
Consider a diagnosis of acute bacterial rhinosinusitis if symptoms of a viral URI that have not improved after 10 days or worsen after 5-7 days.
It is not recommended to treat sinus infection with antibiotics in the first week of symptoms.
Telling patients not to fill an antibiotic RX unless symptoms worsen or do not improve after several days can reduce the inappropriate use of antibiotics.
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Test your knowledge
The most common cause of loss of vision in an adult over 45 years of age is?
A. presbyopia
B. Myopia
C. Trauma
D. age related macular degeneration
Answer:
A. presbyopia
Presbyopia is a normal age-related deficit in agin and the inablity to focus at a close range. This usually begins in the early 40’s
Macular degeneration is associated with loss o central vision; trauma is not common and myopia is nearsightedness and is common with younger people and not associated with advancing age.
Check you knowledge:
Sylvia, age 19, has a persistent sore throat, fever, and malaise not relieved with PCN therapy. What would you order next?
A. A throat culture
B. A monospot test
C. STD lab work
D. Do nothing a tell the patient to wait for the ABX to work
Answer
B. If a patient has a persisent sore throat, fever, and malaise not relieved with PCN, a monospot test should be performed to rule out mononucleosis (Epstein Barr Virus).
A rapid strep is ordered to confirm step infection of the throat.
Test you Knowledge:
The most common offending allergens causing allergic rhinitis are :
A. Pollens of grass, trees, and weeds
B. Fungi
C. Animal allergens
D. Food sensitivity
Answer:
A is correct
They all can contribute but most common to less common in descending order: pollens of grass trees and weeds
Fungi
Animal allergens
dust mites
Rhinitis affects 20% of the population
Test your knowledge:
Caroline, age 50, presents with soft, raised, yellow plaques on her eyelids at the inner canthi. She is concerned that they may be cancerous lesions. You tell her that they are probably:
A. Actinic Keratosis
B. Arcus senilis
C. xanthelasmas
D. Malignant melanomas
Answer:
C. Xanthelasmas: They appear most frequently in females in the 50’s.
They occur with both high and normal lipid levels and have no pathological significance .
Arcus senilis appears as grey-white arcs or circles around the limbus as a result of deposits of lipid material that make the cornea look cloudy.
Test You Knowledge:
Chronic sniffing, nasal congestion, nosebleeds, mucosal scabs, and septum perforation are signs of:
A. Chronic allergies
B. Cocaine abuse
C. Fungal Infection
D. Turbinate Hypertrophy
Pediatric Case Study:
A father bring his 6 month old infant to the clinic and tells the ARNP “ Lily has had a fever all night and has been crying for the last hour. The ARNP looks in Lily’s ears and notes that the tympanic membrane is red. How can the ARNP differentiate redness caused by otitis media from redness caused by crying?
Answer:
To differentiate redness associated with crying versus otitis media, the examiner needs to look for other clinical signs.
Primary bulging of the tympanic membrane
Motility of the tympanic membrane
Sensitivity
Color of fluid inside ear canal
