EENT (7%) Flashcards
CORNEAL ABRASION
Corneal abrasion is a medical condition involving the loss of the surface epithelial layer of the eye’s cornea.
Corneal abrasion is the most common ophthalmologic visit to the emergency department and is a commonly seen problem in urgent care.
CAUSE
- MC cause of corneal abrasion = ** trauma **
Corneal abrasions most commonly result from accidental trauma (e.g., fingernail scratch, makeup brush): Dirt, sand, sawdust, or other foreign body gets caught under eyelid.
FIRST STEP = CHECK VISUAL ACUITY
In corneal abrasion cases, visual acuity is usually fine
SIGNS / SYMPTOMS ⦁ Pain ⦁ Conjunctival injection (red) ⦁ Blurry vision (+/-) ⦁ Photophobia ⦁ Foreign body sensation ⦁ excessive squinting ⦁ reflex production of tears
In cases of corneal abrasions, the pupil is normal
Corneal abrasions are common and recurrent in people who suffer from corneal dystrophy.
- check for foreign body
- make sure to evert eyelids
DIAGNOSIS
** pain relieved with ophthalmic analgesic drops **
- if not relieved = something else, suspect iritis
⦁ Fluorescein staining of cornea
= see “ICE RINK” / Linear abrasions - fluorescein dye collects at site of abrasion
- apply numbing drops: Tetracaine or Proparacaine
- use saline on fluorescein strip - apply to conjunctiva
- use wood’s lamp to check for abrasion
- rule out corneal ulcer
⦁ Slit Lamp ** = technically best diagnostic test for corneal abrasion. If no slit lamp available = use fluorescein
TREATMENT
⦁ Sulfacetamide 10% solution drops / ointment
⦁ Erythromycin ointment
⦁ Polytrim B (Polymyxin B + Trimethoprim)
Ophthalmic antibiotics include ciprofloxacin 0.3%, ofloxacin 0.3%, gentamicin 0.3%, erythromycin 0.5%, polymyxin B/trimethoprim (Polytrim), and tobramycin 0.3%
- then f/u with ophtho
** ointment is preferred over drops for the management of corneal abrasions due to added benefit of lubrication **
Ointment is preferred over drops in children because it lubricates better and because the may drops sting
DO NOT PRESCRIBE TOPICAL ANESTHETIC AGENTS TO PATIENTS - Repeated use of these agents can cause corneal injury and vision loss.
- can also mask pain that could be due to a serious issue
if DIABETIC OR CONTACT LENS WEARER = need to cover for pseudomonas = can give CIPROFLOXACIN (Ciloxan) or TOBRAMYCIN (aminoglycoside) drops
Prophylactic broad-spectrum antibiotic eye drops are recommended in treatment of post-operative corneal abrasion = POLYTRIM (polymyxin B Trimethoprim)
In corneal abrasion, to reduce photophobia from corneal abrasion, anticholinergics like CYCLOPENTOLATE or HOMATROPINE are prescribed to enhance mydriasis and reduce pain from miosis.
- These drops are anticholinergic or parasympatholytic, meaning that they will block the parasympathetic system and enhance the sympathetic nervous system thereby preventing miosis, or pupillary constriction, and enhances mydriasis, or dilation. The mitotic action actually produces the pain in the eye due to the bright light and the ciliary body contracting to constrict the pupil.
It is critical to distinguish an abrasion from a corneal ulcer. Ulcers are deeper infections of the cornea that develop from corneal epithelial defects (ie: abrasions). Contact lens wearers are also at high risk for corneal ulcers. The hallmark of a corneal ulcer is a shaggy, white infiltrate within the corneal epithelial.
Corneal abrasions may be common after a surgery - The most common intra-operative and post-operative cause of corneal abrasions is due to patients rubbing their eyes during emergence from general anesthesia.
REGARDING PATCHING A CORNEAL ABRASION
- Sensory deprivation, such as patching an elderly patient’s eyes, may lead to an acute case of delirium.
- Even small alterations in the elderly patient’s environment can lead to confusion.
- In cases of corneal abrasions, an elderly patient should receive topical ophthalmic antibiotics. Although eye patching traditionally has been recommended in the treatment of corneal abrasions, multiple well-designed studies show that patching does not help and may hinder.
Patching of the eye after abrasion associated with organic material contamination is contraindicated due to increased risk of infection
EX: An 85-year-old nursing home patient was seen in a local physician’s office during the day for a corneal abrasion. The patient had antibiotic drops instilled, and the eye was patched. At 10: 00 p.m., the nursing staff calls reporting the patient is very confused. The most appropriate action is to
a) Remove the eye patch
b) Prescribe haloperidol
c) Have the patient taken to the emergency room
d) Reassure nursing staff and see patient next day
= A - REMOVE EYE PATCH!
CORNEAL ULCER
= (ULCERATIVE KERATITIS)
Corneal ulcer or ulcerative keratitis is an inflammatory condition of the cornea, USUALLY INFECTIOUS, involving disruption of its epithelial layer with involvement of the corneal stroma.
It is a common condition particularly in the tropics and the agrarian societies.
In developing countries, children with VITAMIN A DEFICIENCY are at high risk of corneal ulcers and may become blind in both eyes.
In ophthalmology, a corneal ulcer usually refers to having an INFECTIOUS ETIOLOGY while the term corneal abrasion refers more to physical abrasions.
It is critical to distinguish corneal abrasions from corneal ulcers
Ulcers are deeper infections of the cornea that develop from corneal epithelial defects (ie: abrasions).
Contact lens wearers are at high risk for corneal ulcers.
CAUSE OF CORNEAL ULCER / Ulcerative KERATITIS
⦁ MC cause = ** BACTERIA **
- Pseudomonas if contact lens wearer
⦁ Inflammation ⦁ Fungal infection ⦁ Viruses (HSV Keratitis, Zoster) ⦁ Protozoa - acanthamoeba if contact lens wearer ⦁ Exposure keratitis (ex: Bell's Palsy)
RISK FACTORS ⦁ corneal abrasions ⦁ contact lens wearer ⦁ eye burns ⦁ xerophthalmia (dry eyes) ⦁ eyelid disorders ⦁ steroid eye drops ⦁ vitamin A deficiency
SIGNS / SYMPTOMS ⦁ Pain*** ⦁ Photophobia ⦁ Reduced vision / blurred vision / vision loss ⦁ Tearing / purulent or watery discharge ⦁ Conjunctival erythema ⦁ Eyelid swelling (same symptoms as with corneal abrasion, but decreased vision more likely with corneal ulcer)
PHYSICAL EXAM
⦁ conjunctival erythema / injection
⦁ ** LIMBIC FLUSH ** = CILIARY INJECTION - red ring spreading from around the cornea
⦁ Bacterial Keratitis: ** HAZY CORNEA ** - White Hypopyon often present
DIAGNOSIS
⦁ SLIT LAMP = definitive
⦁ Fluorescein stain** = MC test
⦁ HSV keratitis = dendritic pattern - branching seen with fluorescein staining
The hallmark of a corneal ulcer is a
** SHAGGY WHITE INFILTRATE ** within the corneal epithelium.
Patient will present as a contact lens wearer with severe pain, redness, and photophobia. Eyes are injected with cloudy discharge unilaterally. A dense corneal infiltrate is visible with fluorescein staining.
TREATMENT
** All patients with corneal ulceration should be referred immediately to an ophthalmologist **
Immediate referral - if immediate referral is not possible, it is reasonable to start antibiotics without delay
Ophthalmic antibiotics include ciprofloxacin 0.3%, ofloxacin 0.3%, gentamicin 0.3%, erythromycin 0.5%, polymyxin B/trimethoprim (Polytrim), tobramycin 0.3%.
⦁ Fluoroquinolone drops (cipro, moxi, gatifloxacin) - DO NOT PATCH EYE
⦁ Tobramycin ointment or other aminoglycosides
⦁ If HSV Keratitis = topical antivirals: ** Trifluridine ** (viroptic), Vidarabine, Ganciclovir ointment, PO Acyclovir
Corneal ulcers are treated aggressively with antipseudomonal antibiotics and immediate ophthalmology consultation
⦁ Analgesics for pain (cyclopentolate, homatropine)
⦁ Topical steroids to reduce inflammation / swelling to prevent scarring
⦁ Corneal transplant surgery if scarring impedes vision
o Must be able to differentiate corneal ulcer from abrasion
o Corneal ulcers usually represent an infection deeper in the cornea by bacteria, viruses, or fungi as a result of a breakdown in the protective epithelial barrier
o Risk factor for contact lens wearers!
o Dendritic ulcer with fluorescein stain = Herpes Simplex Keratitis – common board review question.
Patient will present as → a 34-year-old contact lens wearer with severe pain, redness, and photophobia. Eyes are injected with cloudy discharge unilaterally. A dense corneal infiltrate is visible with fluorescein staining.
ACUTE OTITIS MEDIA
Inflammatory condition of the middle ear, with or without effusion
Otitis media = Infection of the middle ear caused by a virus or bacteria
Infection of the middle ear, temporal bone + mastoid air cells
** MC PRECEDED BY A VIRAL URI **
Is characterized by the presence of fluid in the middle ear, along with symptoms of inflammation
MC occurs in children due to straighter / shorter / narrower eustachian tube in childhood
Often time frame = 6 months - 3 years
6-18 months = peak age
- **Most commonly preceded by a viral URI –> causes eustachian tube edema –> negative pressure –> transudation of fluid + mucus in the middle ear from sinuses –> secondary colonization of bacteria + flora
Acute otitis media = rapid onset + signs / symptoms of inflammation
Otitis Media with Effusion = asymptomatic - no inflammation, but has drainage/discharge
Common bacterial causes include
⦁ Streptococcus pneumoniae** (MC) - 50%
⦁ Haemophilus influenzae - 30%
⦁ Moraxella catarrhalis - 10-15%
⦁ Strep pyogenes (GABHS - same organism as with strep throat, impetigo, acute sinusitis)
usually viral, but if bacterial, most likely strep pneumo.
RISK FACTORS
- Eustachian Tube (ET) Dysfunction
- young age (shorter / narrower / more horizontal ET)
- caretaker smoking
- bottle propping - bottle feeding while supine
- pacifier use
- day care attendance
- formula feeding / not being breastfeed
- family hx
- male gender (MC in boys)
** Children with an upper respiratory infection or those regularly exposed to smoke = at increased risk of developing ear infections
- breastfeeding = protective against OM
COMPLICATIONS = ** Conductive Hearing Loss **
- hearing loss may occur due to chronic inflammation, perforation of TM, or damage to anatomy of inner ear
CLINICAL MANIFESTATIONS
⦁ ear pain (otalgia)
⦁ fever (more often afebrile though)
⦁ accompanying URI symptoms
- may present with abrupt onset ear pain in young children along with
⦁ pulling/tugging at the ear
⦁ increased crying
⦁ poor sleep
⦁ conductive hearing loss / stuffiness
⦁ decreased appetite (sucking / chewing can aggravate inner ear pain)
PHYSICAL EXAM
⦁ red, bulging TM with effusion
⦁ decreased TM mobility with pneumatic otoscopy
** if bullae seen on TM = suspect MYCOPLASMA pneumoniae
- multiple ear infections can cause scarring of middle ear structures
- If TM perforation occurs = Rapid relief of pain + otorrhea (usually heals in 1-2 days)
TREATMENT
- 1st line = Amoxicillin (90mg/kg BID) x 10-14 days
- 2nd line = Augmentin (if resistant to amoxicillin) - SE = diarrhea
- If allergic to PCN = Azithromycin or
- Cephalosporin (ceftriaxone/Rocephin) if mild allergy to PCN (SE / reactions)
- if received Amoxicillin in last month = give Augmentin
- if not seeing any clinical improvement = switch to Augmentin
- can give ibuprofen / Tylenol for pain + fever
H. flu + M. cat = produce beta lactamases = PCNs won’t work
- if under 2 = just give abx
- educate parents with kids over the age of 2 about waiting prior to using antibiotics
symptoms usually spontaneously resolve in 2/3 of children by 24 hours, and` 80% in 2-10 days
- irrigation, then lay on affected side
for chronic / recurrent cases
- myringotomy (incision in eardrum) to help relieve pressure / fluid buildup
- tympanostomy tubes
OTITIS EXTERNA
= ** SWIMMER’S EAR **
- inflammation of the outer ear + ear canal
- seen more in ELDERLY and KIDS
CAUSE
⦁ EXCESS WATER or LOCAL TRAUMA
- that changes the normal acidic pH of the ear, causing bacterial overgrowth
frequent water exposure can slightly raise the pH, making the canal more favorable for bacterial or fungal overgrowth
Causes
⦁ Infectious - MC Pseudomonas (swimming)
⦁ Allergic
⦁ Dermal disease (eczema / psoriasis)
MC BACTERIAL ETIOLOGY = ** PSEUDOMONAS **
- other causes = Proteus, staph aureus, staph epidermidis, GABHS, anaerobes (peptostreptococcus)
IF FUNGAL = ** ASPERGILLUS **
Risk Factors
- swimming (pseudomonas)
- warm / wet environment
- overcleaning / cottonswabs
- seb derm / psoriasis / eczema
- otomycosis = fungal ear infection
- ** diabetes **
- too much ear wax
- any manipulation / damage to the ear (trauma)
** COMMONLY SEEN IN DIABETICS **
CLINICAL MANIFESTATIONS ⦁ 1-2 days of INTENSE EAR PAIN ⦁ PRURITUS in the ear canal ⦁ may have recently swam ⦁ AURICULAR DISCHARGE ⦁ feeling of pressure / fullness in ear ⦁ hearing usually preserved, may be decreased
generally presents with canal itching and pain with movement of the ear
vs Malignant Otitis Externa = severe, deep pain, greenish foul smelling discharge and hearing loss.
Otitis externa is an infection of the external auditory canal secondary to trauma or a consistently moist environment, which favors the growth of bacteria or fungi. It generally presents with canal itching and pain with movement of the ear. If the canal is closed, Weber is expected to lateralize to painful / blocked side (conductive hearing loss)
PHYSICAL EXAM
⦁ intense pain simply with traction of ear canal / tragus
⦁ external auditory canal erythema, edema + debris
- should see an edematous + erythematous ear canal
- may see yellow / brown / white / or grey debris
- should be no middle ear fluid (fluid behind TM - if you can see it through the debris/edema)
- the TM should be mobile (if you can see it)
If the canal is closed, Weber is expected to lateralize to the side of the blocked canal (conductive loss)
If the TM is not visible, only use drops that are not ototoxic in case of perforated eardrum - Ofloxacin is safe; do NOT use drops with aminoglycosides
Extremely painful - start with drops to clean/relieve some debris = very scabbed. Do not try to remove scabs
DIAGNOSIS: cultures are not routinely required for diagnosis of otitis externa; usually a clinical diagnosis with otoscopy
In contrast to acute otitis media, the tympanic membrane moves normally with pneumatic otoscopy in a patient with otitis externa****
⦁ ** CONDUCTIVE HEARING LOSS = Weber lateralizes to the infected ear **
TREATMENT
- protect ear from moisture
- drying agents can help - isopropyl alcohol or acetic acid (vinegar)**
- can use hydrogen peroxide to try to clean debris
*** IRRIGATE FIRST!!!! - then antibiotics
- topical antibiotics
1) Fluoroquinolone ± steroid
⦁ ciprofloxacin or ofloxacin ± dexamethasone or hydrocortisone
⦁ cipro HC = ciprofloxacin + hydrocortisone
⦁ ciprodex = ciprofloxacin + dexamethasone - all expensive!!!!
- but fluoroquinolones are ototoxic anyway, other than ofloxacin - usually can’t see TM with otitis externa
The initial treatment of otitis externa is ciprofloxacin.
2) Aminoglycoside combination
⦁ cortisporin* = neomycin + polytrim-B + HC
⦁ tobradex = tobramycin + dexamethasone
- do NOT use aminoglycoside combo unless can verify that TM is not perforated
3) If fungal = amphotericin B, clotrimazole, itraconazole
Patient will present as → a 4-year-old girl who has been complaining of progressively worsening ear pain and itchiness over the past week. Examination reveals left tragal tenderness and an edematous and closed canal. Weber lateralizes to the left.
BLEPHARITIS
inflammation of the lid margin
erythema, crusting, scaling, swelling
often associated with conditions such as ⦁ ROSACEA ⦁ SEBORRHEIC DERMATITIS ⦁ ECZEMA ⦁ PSORIASIS ⦁ DOWN SYNDROME ⦁ ALLERGIC CONTACT DERM
affects BOTH EYELIDS
can have anterior or posterior blepharitis
POSTERIOR BLEPHARITIS = more common
- due to Meibomian gland dysfunction (critical for eye lubrication)
- Inflammation of inner portion of eyelids
- Seen in chronic inflammatory skin conditions such as rosacea + seb derm
ANTERIOR BLEPHARITIS = less common
- get inflammation at the base of the eyelashes
- More often occurs in females and tends to be in younger patients
- 2 types of anterior blepharitis = infectious (bacterial or viral) or seborrheic
MC bacterial cause of blepharitis = ** STAPH **
infectious [bacterial/viral} or seborrheic = more anterior
inflammatory skin conditions - rosacea/seb derm = posterior blepharitis
** ASSOCIATED WITH ROSACEA + SEBORRHEA **
Other possible causes of blepharitis = allergic contact dermatitis, eczema, psoriasis
Blepharitis is common in patients with eczema and down syndrome
SYMPTOMS
- generally have chronic recurrent symptoms that involve both eyes
⦁ red, swollen, itchy eyes
⦁ “pink eyes”
⦁ CRUSTING/MATTING of eyelashes, esp. in morning
⦁ light sensitivity (photophobia)
⦁ ** “RED RIMMING OF EYELID” **
⦁ gritty/burning sensation
⦁ excessive tearing (due to dry eyes - Meibomian gland dysfunction)
⦁ FLAKING/SCALING of eyelid skin
⦁ blurred vision
⦁ May have entropion/ectropion - especially with posterior blepharitis
Patient will present as → a 34-year-old female with crusting, scaling, red-rimming of eyelid and eyelash flaking along with dry eyes. The patient has a history of seborrhea and rosacea.
Blepharitis = usually a chronic course with intermittent exacerbations
EXAM
⦁ clinical diagnosis
⦁ SLIT LAMP = exam of choice
- can help distinguish between anterior + posterior blepharitis
- If not available = can use penlight or otoscope lamp
Major findings on exam = pink/irritated eyelids, may have crusting/scaling
TREATMENT
⦁ EYELID HYGIENE = mainstay of tx
- warm compresses
- lid massages (esp for Meibomian gland dysfunction)
- lid washing (baby shampoo)
- artificial tears (for dryness)
IF NOT RESPONDING TO CONSERVATIVE TX
- can apply topical abx (erythromycin or bacitracin ointment, azithromycin solution)
- systemic abx for severe/unresponsive cases: tetracyclines, azithromycin
HORDEOLUM
abscess of the EYELID MARGIN
PAINFUL
90-95% of the time = ** STAPH **
- can be external or internal
External = infection of the eyelash follicle or external sebaceous glands near the lid margin
Internal = inflammation/infection of the Meibomian gland
SIGNS / SYMPTOMS
⦁ Usually presents as a painful, erythematous mass
⦁ Painful, warm, swollen red lump on eyelid margin
⦁ think H(ordeolum) for Hot (warm to touch)
DIAGNOSIS
⦁ Clinical
TREATMENT
⦁ WARM COMPRESSES = mainstay of tx
- eyelid hygiene
- most naturally resolve/drain on their own
- can add erythromycin/bacitracin ointment if draining
- can refer to ophtho for I+D if not spontaneously draining/improving with conservative measures after 48 hours
- can give oral doxycycline if patient has a hx of recurrent hordeolums
HORDEOLUM VS CHALAZION
⦁ Hordeolum = Stye = Painful and “Hot”- think “H” for Hot = Hordeolum.
⦁ Patient will present with a painful, warm (hot), swollen red lump on the eyelid (different from a chalazion which is painless)
Hordeolum are infections of the glands of the eyelid while a chalazion is a sterile, chronic inflammation that results from a blocked meibomian gland.
CHALAZION
chaLAZYon = lazy - DOESN’T HURT (unlike hordeolum)
PAINLESS granuloma of the internal Meibomian gland –> focal eyelid swelling
larger, firmer, slower growing, less painful than hordeolums
Nontender eyelid swelling - RUBBERY NODULE
Chalazion occur more commonly in the upper eyelid because of the presence of more sebaceous glands.
A chalazion, also known as a meibomian gland lipogranuloma, is a cyst usually in the upper eyelid that is caused by inflammation of a blocked meibomian gland, which is a sebacious gland (not infection, unlike hordeolums)
Chalazia differ from styes (hordeola) in that they are subacute and usually painless nodules.
They may become acutely inflamed, but unlike a stye, chalazia usually sit inside the lid rather than on the lid margin.
Unlike a stye, a chalazion tends to have a more gradual onset, is less painful, and affects the middle part of the eyelid.
Patient will present with a foreign-body sensation in one eye. Over the last few weeks, has had gradually increasing painless swelling around upper or lower eyelid. Examination shows a nontender discrete nodule on upper or lower eyelid. There is no evidence of injection or discharge and visual acuity is normal.
DIAGNOSIS
⦁ clinical
Will present as a hard, nontender eyelid swelling, often NOT very red.
Treatment
⦁ EYELID HYGIENE
- warm compresses
- Antibiotics usually not necessary
- in extreme cases = can inject steroids, Incision + curettage, or surgery for large chalazions that are affecting vision
Recalcitrant and recurrent chalazia should be biopsied to rule out carcinoma of the meibomian gland or basal cells.
MALIGNANT OTITIS EXTERNA
NECROTIZING EXTERNAL OTITIS
- A severe form of otitis externa that presents in DIABETIC and IMMUNOCOMPROMISED patients
- An invasive infection of the external auditory canal and skull base
- **typically occurs in the elderly + patients with DM (most likely uncontrolled) + immunocompromised / HIV
- MC bacterial agent = ** PSEUDOMONAS ** (gram negative rod / bacilli)
- 2nd MC cause = staph aureus
Malignant otitis externa, or necrotizing external otitis, is an uncommon form of otitis that occurs primarily in immunocompromised patients and early diabetic patients, particularly when DM is being poorly managed.
It typically begins as a case of acute otitis externa, which is characterized by ear pain, swelling of the ear canal, and occasionally decreased hearing.
CLINICAL MANIFESTATIONS ⦁ otalgia - pain more severe than with otitis externa ⦁ otorrhea - drainage / discharge ⦁ hearing loss ⦁ green foul smelling discharge
Unlike acute otitis externa, malignant otitis externa is potentially fatal and commonly presents with severe, deep pain, greenish foul smelling discharge and hearing loss.
COMPLICATIONS
⦁ Osteomyelitis of the base of the skull
⦁ Mastoiditis
⦁ TMJ osteomyelitis
⦁ Cranial nerve palsies (CN palsies)* (CN 7)
⦁ can develop Trismus** = pain with chewing
MOE is caused by extension of the outer ear infection into the bony ear canal and soft tissues deep to the bony canal and can result in skull base osteomyelitis and multiple cranial nerve palsies.
DIAGNOSIS
⦁ ** CT WITH IV CONTRAST **
⦁ Elevated ESR
⦁ Positive culture
TREATMENT = - no role for topical abx!!
The offending pathogen is almost always PSEUDOMONAS, and, unlike acute otitis externa, malignant otitis externa requires oral or IV antibiotics.
The initial treatment of malignant otitis externa is CIPROFLOXACIN***
⦁ CIPRO bid po x 6-8 weeks
⦁ pip/tazo (as pseudomonas is growing more resistant)
⦁ steroids to reduce itching / inflammation
PHARYNGITIS
Pharyngitis is the inflammation of the pharynx, a region in the back of the throat.
In most cases = painful, and MC cause of sore throat
MC CAUSE = Viral - Adenovirus, Rhinovirus, Enterovirus, EBV, RSV, Influenza, Zoster, etc.
Symptoms = sore throat; pain with swallowing / phonation
- other symptoms = based on etiology
o BACTERIAL PHARYNGITIS
- MC cause = ** GABHS - Strep pyogenes **
STREPTOCOCCAL PHARYNGITIS, also known as strep throat = infection of the back of the throat including the tonsils caused by GABHS (group A beta hemolytic strep = strep pyogenes)
TRANSMISSION = respiratory droplets
SYMPTOMS ⦁ fever ⦁ ** sore throat ** ⦁ red tonsils or tonsillar exudates ⦁ enlarged lymph nodes ⦁ headache ⦁ pain with swallowing ⦁ fatigue / malaise ⦁ +/- nausea / vomiting ⦁ may have "scarlet fever" -diffuse sandpaper-like rash (more common in kids)
Symptoms begin 1-3 days after exposure
Symptoms last 7-10 days
NO COUGH
NO RHINORRHEA
CENTOR CRITERIA
1) age: 3-15 = 1 point (15-44 = 0 points, > 44 = -1 point)
2) fever > 100.4 (38) = 1 point
3) tender cervical anterior lymphadenopathy = 1 point
4) tonsillar swelling or exudates = 1 point
5) no cough = 1 point
DIAGNOSIS
- clinical
- rapid strep test: if negative and still suspected = throat culture (usually sent off regardless)
- throat swab culture = gold standard
COMPLICATIONS
⦁ Rheumatic Fever (preventable with antibiotics)
⦁ Post-strep Glomerulonephritis (not preventable with antibiotics)
⦁ Peritonsillar abscess, Cellulitis
TREATMENT
⦁ 1st line = PCN VK or IM Benzathine PCN G (Bicillin)
- usually give amoxicillin in real life…
⦁ 2nd line = Azithromycin (if allergic to PCN)
⦁ 3rd line = Keflex
- fluids, saline gargles, NSAIDS / Tylenol
PROPHYLAXIS
⦁ Antimicrobial prophylaxis with PENICILLIN is indicated for streptococcal pharyngitis in children with prior rheumatic fever.
o VIRAL PHARYNGITIS
- Less likely exudative
- MC Cause = Adenovirus
- Others = CMV, EBV (mononucleosis), influenza, HSV
Infectious mononucleosis: Caused by EBV = characterized by malaise, fever, severe sore throat, splenomegaly
- Rash with penicillins
- Diagnosed by atypical lymphocytes, heterophile agglutination test (monospot)
- Splenic rupture possible with trauma/contact sports
SYMPTOMS
⦁ sore throat
⦁ fever
⦁ red eyes
DIAGNOSIS
⦁ clinical
⦁ rapid strep swab to r/o strep throat
⦁ throat culture = gold standard (r/o bacterial or fungal causes)
TREATMENT
⦁ supportive - Tylenol / Ibuprofen for fever, fluids, etc.
o FUNGAL PHARYNGITIS (THRUSH / CANDIDA)
MC Cause = patients using inhaled steroids
- counsel patients to rinse mouth after use of inhaled steroids.
SYMPTOMS
⦁ sore throat
⦁ dysphagia
⦁ Cheesy white patches in the oropharynx
⦁ Seen in AIDS patients and small children
DIAGNOSIS
⦁ clinical
⦁ KOH prep or wet mount
⦁ throat culture = gold standard
TREATMENT
⦁ Clotrimazole troches, Miconazole, Ketoconazole, Fluconazole
⦁ Nystatin swish
PTERYGIUM
⦁ ELEVATED ⦁ SUPERFICIAL ⦁ FLESHY ⦁ FIBROVASCULAR ⦁ TRIANGULAR SHAPED growth
⦁ GROWING (unlike pinguecula - doesn’t grow)
⦁ “ fibrovascular mass “
⦁ MC location = inner corner/nasal side of the eye -
⦁ grows laterally towards the cornea
RISK FACTORS
Associated with
⦁ increased UV EXPOSURE in sunny climates
⦁ Also associated with increased exposure to Sand, Wind, and Dust
⦁ Allergens
- basically anything that causes chronic irritation
Asymptomatic = no pain, no discharge
DIAGNOSIS
⦁ clinical
- Look for an elevated, superficial, fleshy, triangular-shaped “growing” fibrovascular mass
TREATMENT
⦁ None - observation for most
⦁ artificial tears if needed
- most = asymptomatic
In most cases, treatment is supportive with topical vasoconstrictors, saline drops, and protection from sunlight. Surgery is reserved for cases in which vision is being affected
⦁ surgery
- if pterygium starts to impede vision (can move onto the cornea)
Patient will present as → a 65-year-old male Hispanic farmworker who is brought to you by his concerned wife. She reports he has had this “thing” on his left eye for years and refuses to seek care. He denies pain or discharge from the affected eye. Physical exam reveals an elevated, superficial, fleshy, triangular-shaped fibrovascular mass in the inner corner/nasal side of the left eye.
PINGUECULA
⦁ YELLOW, ELEVATED NODULE = fat / protein
- hyaline, elastic nodules that appear yellow
- can affect both sides of the cornea, but MC on the
- ** NASAL SIDE *** (just like pterygium)
⦁ ** DOES NOT GROW ** (unlike pterygium)
Causes
⦁ SUN EXPOSURE
⦁ chronic trauma / irritation
⦁ chronic dryness
- generally asymptomatic
DIAGNOSIS
⦁ clinical
TREATMENT
⦁ none - observation for most
⦁ If pingueculitis occurs = still no treatment is necessary!! a short course of NSAID drops or steroids may help
⦁ May be excised for cosmetic purposes or if inflamed and not responsive to NSAID / steroid drops
LUDWIG’S ANGINA
- Cellulitis of the sublingual + submaxillary spaces in the neck
- MC secondary to dental infections (strep viridans and oral anaerobic infections)
Ludwig’s angina is a bilateral abscess / infection of the submandibular space that consists of two compartments in the floor of the mouth, the sublingual space and the submylohyoid (submaxillary) space
This infection most commonly arises from an infected second or third mandibular molar tooth.
● The infection begins in the floor of the mouth. It is characteristically an aggressive, rapidly spreading “woody” or brawny cellulitis involving the submandibular space.
● The infection is a rapidly spreading cellulitis without lymphatic involvement and generally without abscess formation.
● Both the submylohyoid and sublingual spaces are involved.
● The infection is bilateral
usually in elderly/debilitated patients
precipitated by dental procedures
**Swelling of the soft tissues and elevation / posterior displacement of the tongue causes airway obstruction
CAUSES/ETIOLOGIES ⦁ 90% of cases are odontogenic ⦁ Strep Viridans ⦁ staph ⦁ strep ⦁ bacteroides
Ludwig’s Angina = typically a POLYMICROBIAL infxn
CLINICAL MANIFESTATIONS ⦁ swelling + erythema of upper neck + chin ⦁ pus on floor of mouth ⦁ tongue elevation ⦁ fever ⦁ chills ⦁ malaise ⦁ mouth pain ⦁ stiff neck ⦁ drooling ⦁ dysphagia ⦁ may lean forward to open airway
- rarely abscess is present
PHYSICAL EXAM
On physical examination, patients with Ludwig’s angina have tender, symmetric, and “woody” induration, sometimes with palpable crepitus, in the submandibular area
⦁ ** “WOODY” induration
⦁ Palpable crepitus
Crepitus = grating, crackling or popping sounds and sensations experienced under the skin and joints or a crackling sensation due to the presence of air in the subcutaneous tissue.
Patients with Ludwig’s angina typically present with fever, chills, and malaise, as well as mouth pain, stiff neck, drooling, and dysphagia, and may lean forward to maximize the airway diameter.
Increased risk of Ludwig’s in immunocompromised: DM, HIV, transplant patients, alcoholics, etc.
DIAGNOSIS
⦁ ** CT = test of choice **
Ludwig’s angina has airway compromise as a potential complication, and requires careful monitoring and rapid intervention for prevention of asphyxia and aspiration pneumonia.
TREATMENT
- admit
- antibiotics
- airway management
⦁ ** Unasyn (Ampicillin + Sulbactam) **
⦁ Penicillin G + Metronidazole
⦁ Clindamycin
TREATMENT FOR LUDWIG VAN BEETHOVEN = UNASYN (unison!)
SIALOLITHIASIS
Sialolithiasis is a condition in which calcifications called salivary stones form in the duct of a salivary gland
- A calcified mass or sialolith forms within a salivary gland
CAUSE
- sialoliths made up of calcium and other minerals are naturally found in the saliva
- When saliva ducts—tiny openings in your mouth that produce saliva—become blocked, those minerals can build up and harden beneath the surface of the skin
PATHOPHYSIOLOGY
- salivary glands secrete saliva through tiny ducts in the mouth to help lubricate the mouth + also to moisten / soften food
- the quick flow of saliva + the antibacterial properties in the saliva both help prevent bacterial infections
- Flow can be reduced by ⦁ dehydration ⦁ chronic illnesses (sjogrens) ⦁ certain medications - which can cause calcium / mineral deposits to settle in the walls of the salivary duct
–> build up of deposit blocks the path of saliva –> even more reduced salivary flow –> further stagnation can allow calcium / phosphorus / electrolytes to precipitate out even more —> STONES (sialoliths) - grow over time in vicious cycle
Reduced salivary flow that is now blocked by sialolith allows BACTERIA to move from the mouth into the salivary duct –> inflammation + swelling –> can further compress the salivary duct –> worsens the problem!
MC bacteria = staph aureus
MC LOCATION = SUBMANDIBULAR GLAND = WHARTON’S DUCT**
- Less commonly the parotid gland (Stensen’s duct)
- rarely the sublingual gland or a minor salivary gland
Sialolithiasis = a common condition characterized by recurrent enlargement of a salivary gland, usually TRIGGERED BY FOOD. They occur most often in the submandibular glands.
** PERIPRANDIAL or POSTPRANDIAL SALIVARY GLAND PAIN + SWELLING **
SYMPTOMS
⦁ pain
⦁ erythema of the floor of the mouth
⦁ swelling
⦁ tenderness of the affected gland
⦁ recurrent enlargement of salivary gland that is triggered by food** (MC Submandibular gland = Wharton’s Duct)
⦁ PERIPRANDIAL colicky swelling and pain
- won’t have tenderness / swelling of neck as much as with Ludwig’s angina
Sialolithiasis can lead to chronic sialadenitis due to poor salivary flow.
Sialadenitis is most commonly due to sialolithiasis that in turn leads to Staphylococcus aureus infection.
DIAGNOSIS
⦁ clinical
⦁ can confirm with CT / US / MRI
TREATMENT o Conservative ⦁ hydration - increase fluid intake ⦁ warm compresses ⦁ Sialogogues (tart/hard candies, lemon drops, xylitol containing gum or candy - stimulation of salivation ⦁ gland massage ⦁ avoid anticholinergic drugs***
- for more severe cases
⦁ extracorporeal shock wave lithotripsy
⦁ endoscopic removal of stone
⦁ gland excision
PAROTITIS = SIALADENITIS
Sialadenitis = Bacterial infection of the parotid or submandibular salivary glands –> inflammation of salivary gland(s)
CAUSES ⦁ Sialolithiasis = MC - salivary duct gets plugged ⦁ dehydration ⦁ chronic illness (sjogrens) ⦁ gland hyposecretion
usually affects UNILATERAL PAROTID GLAND
MC in people in 50s-60s, but can occur at any age
Unlike Sialolithiasis (where MC gland = submandibular), the MC gland for sialadenitis = Parotid = PAROTITIS
** MC PATHOGEN = STAPH AUREUS **
- Others:
⦁ Strep viridans
⦁ H. flu
- or mixed aerobic / anaerobic pathogens
Viral pathogens (mumps / HIV) = then called Parotitis
PATHOPHYSIOLOGY
- salivary glands secrete saliva through tiny ducts in the mouth to help lubricate the mouth + also to moisten / soften food
- the quick flow of saliva + the antibacterial properties in the saliva both help prevent bacterial infections
- Flow can be reduced by ⦁ dehydration ⦁ chronic illnesses (sjogrens) ⦁ certain medications - which can cause calcium / mineral deposits to settle in the walls of the salivary duct
–> build up of deposit blocks the path of saliva –> even more reduced salivary flow –> further stagnation can allow calcium / phosphorus / electrolytes to precipitate out even more —> STONES (sialoliths) - grow over time in vicious cycle
Reduced salivary flow that is now blocked by sialolith allows BACTERIA to move from the mouth into the salivary duct –> inflammation + swelling –> can further compress the salivary duct –> worsens the problem!
SYMPTOMS
⦁ acute pain / swelling / erythema near gland
⦁ pain / swelling particularly worse when eating
⦁ tenderness at duct opening
⦁ may have PUS drainage if duct is massaged
⦁ local pain
⦁ dysphagia
⦁ trismus –> reduced opening of jaw due to spasms of muscles during mastication
⦁ painful to open mouth
⦁ may develop FEVER / chills if severe
⦁ can develop into abscess
Chronic sialadenitis = less painful, and causes gland to enlarge over time, not as erythematous on overlying skin
- chronic sialadenitis = more caused by fibrosis due to an acute infection, or a chronic disease such as sjogrens
- can lead to recurrent sialadenitis infections
- acute sialadenitis = bacterial infection likely due to stone or bout of dehydration
DIAGNOSIS
⦁ Clinical - based on swollen salivary gland / symptoms
⦁ Culture of pus drainage
- can get CT / US / MRI to confirm and to check for abscess / stone / tumor / deeper infection, etc.
⦁ CT scan (non-contrast) = definitive - to assess for associated abscess / extent of tissue involvement
- often find stone
⦁ can do ultrasound
TREATMENT ⦁ sialogogues (tart hard candy to increase salivary flow) ⦁ hydration ⦁ massage ⦁ warm compresses ⦁ good oral hygiene ⦁ if abscess present --> drainage!
⦁ IV Antibiotics
- Dicloxacillin or Nafcillin or Keflex
- Add metronidazole or clindamycin if severe
- may need IV vanco - especially if elderly population
Patient will present as → a 39-year-old female complaining of episodic left-sided jaw pain and swelling. The symptoms are typically aggravated by eating or by the anticipation of eating. Over the last 2-days, the patient has been experiencing worsening pain, redness, and fever. On physical exam, the left salivary gland is exquisitely tender. High-resolution noncontrast computed tomography (CT) scanning reveals a left-sided salivary gland stone.
OCULAR FOREIGN BODY
1ST CHECK VISUAL ACUITY
Patient will present as → complaining of right eye pain and irritation. He states that he wasn’t wearing glasses, and while trimming his driveway with his weedwacker “something flew into my eye.” Visual acuity is 20/20. Pupils are equal, round, reactive to light and accommodation. Extraocular movements are intact. On physical examination you note a tearing, red, and severely painful eye.
SYMPTOMS ⦁ foreign body sensation ⦁ tearing ⦁ red ⦁ painful ⦁ inability to open eye due to foreign body sensation
Inspect the eye thoroughly to identify if foreign body is present; use fluorescein staining if necessary
Metallic foreign bodies may leave a RUST RING
- If you can’t remove the foreign body easily = refer to the ophthalmologist
DIAGNOSIS
⦁ Full inspection of lids, conjunctiva and cornea
⦁ fluorescein staining may help
⦁ ** SLIT LAMP ** - assists in identification + removal
- X-ray or CT of may be necessary if there is evidence of penetration of the globe, or if foreign body was metal
TREATMENT
⦁ FOREIGN BODY REMOVAL = topical anesthetic + try irrigation - 2L of saline or for 20 minutes
- This is particularly helpful in the case of multiple superficial foreign bodies (eg, sand).
⦁ if irrigation doesn’t work, try swab moistened with proparacaine.
⦁ If swab doesn’t work = REFER
⦁ Treat with topical antibiotic ointment (erythromycin) or sodium sulfacetamide
- no patches!
- do NOT send patients home with topical anesthetics
Intraocular foreign bodies require immediate surgical removal by an ophthalmologist
Rust ring — After removal of a foreign body containing iron there is often a residual rust ring and reactive infiltrate. Patients with rust ring should be treated as patients with corneal abrasions. The rust ring itself is not harmful and will usually resorb gradually.
If patient was working with metal and metal piece is in eye or corneal abrasion present or patient has foreign body sensation = needs TETANUS VACCINE = every 5 years
THEN REFER TO OPHTHO…ALWAYS
ECTROPION
EVERSION OF THE EYELID MARGIN - away from the globe
- the eyelid + eyelashes turn outward
CAUSES ⦁ MC seen in the elderly (aging) - can also occur due to ⦁ burns ⦁ congenital anatomical abnormalities ⦁ scars ⦁ infections ⦁ CN 7 palsy ⦁ posttraumatic / postsurgical changes
PATHOPHYSIOLOGY
- due to relaxation of the orbicularis oculi muscle
Ectropion occurs when the eyelid turns outward exposing the palpebral conjunctiva
- tends to be bilateral
- corneal + conjunctival exposure => dryness => excessive tearing
SYMPTOMS ⦁ irritation ⦁ conjunctival injection ⦁ photophobia/increased sensitivity ⦁ DRY / painful eyes ⦁ EXCESSIVE TEARING ⦁ sagging of eyelid
DIAGNOSIS = clinical
TREATMENT
⦁ ARTIFICIAL TEARS / ocular lubricants
⦁ can do surgical correction = definitive treatment
Patient will present as → a 72-year-old with complaints of dry eyes coupled with excessive tearing. On exam the conjunctiva appear red and the left eyelid is turned outward.
ENTROPION
INVERSION OF THE EYELID MARGIN - towards the globe
- eyelid and lashes turn inward
- MC seen in elderly
CAUSE
⦁ may be caused by orbicularis oculi muscle spasm
- can be caused by ⦁ aging* ⦁ burns ⦁ scars ⦁ previous surgeries ⦁ skin diseases ⦁ infections ⦁ muscle weakness (CN 7 palsy)
Entropion (inversion of an eyelid) is caused by age-related tissue relaxation, postinfectious or posttraumatic changes, or blepharospasm.
SYMPTOMS ⦁ excessive tearing ⦁ eye pain ⦁ irritation ⦁ redness ⦁ decreased vision if the cornea is damaged
COMPLICATIONS
May cause corneal abrasions/ulcerations, erythema, tearing, and increased sensitivity
DIAGNOSIS = clinical
TREATMENT
⦁ lubricating eyedrops/artificial tears
⦁ Can tape lower lid
⦁ can do surgical correction = definitive treatment
Patient will present as → a 75-year-old with a foreign body sensation and tearing of his right eye. On physical exam you note a red, irritated, right eye in association with an inverted eyelid.
KERATITIS
Keratitis is a condition in which the cornea becomes inflamed.
CAUSES
⦁ Infectious keratitis can be caused by bacteria, viruses, fungi, or parasites
⦁ Viral infection of the cornea is often caused by HSV, which frequently leaves a dendritic ulcer
- epithelial herpes keratitis = MC type of herpes keratitis
- types = epithelial, stromal, endothelial, neuropathic
⦁ Bacterial infectious keratitis - improper CONTACT LENS wear is the largest risk factor
- Pathogens include Staph aureus, Pseudomonas, Strep pneumo, etc.
SYMPTOMS The condition is often marked by ⦁ moderate to intense pain ⦁ impaired eyesight ⦁ photophobia ⦁ red eye ⦁ 'gritty' sensation
DIAGNOSIS
⦁ Fluorescein staining
⦁ Slit lamp
The diagnostic finding in bacterial keratitis is a CORNEAL OPACITY or INFILTRATE (typically a round white spot) in association with red eye, photophobia, and foreign body sensation.
Viral infection of the cornea is often caused by HSV, which frequently leaves a “DENDRITIC ULCER”
TREATMENT
o Bacterial
- requires urgent ophthalmological referral and prompt initiation of topical bactericidal antibiotics (ideally after obtaining cultures)
⦁ ciprofloxacin 0.3%, ofloxacin 0.3%, gentamicin 0.3%, erythromycin 0.5%, polymyxin B/trimethoprim (Polytrim), tobramycin 0.3%.
- refrain from wearing contact lenses
o Viral
- HSV = topical antivirals: ** Trifluridine ** (viroptic), Vidarabine, Ganciclovir ointment, PO Acyclovir
- MOA = inhibit viral DNA polymerase ==> DNA chain termination
Patient will present as → a 37-year-old female with an intense, tearing pain in her right eye. She was recently placed on topical corticosteroids for suspected allergic conjunctivitis. On visual inspection the conjunctiva appears red. A fluorescein stain of the eye exhibits a shallow ulcer with a dendritic appearance and irregular borders
PHOTOKERATITIS
Photokeratitis = It is analogous to a sunburn of the cornea and conjunctiva
Photokeratitis is caused by excessive exposure of the eye to ultraviolet light.
RISK FACTORS
⦁ exposure to sun-tanning lamps
⦁ welding
⦁ sun activities - ex: skiing
DIAGNOSIS
⦁ Fluorescein staining
- “ superficial punctate keratitis “
diagnosed based on a history of ultraviolet light exposure and superficial punctate keratitis on fluorescein staining.
TREATMENT
⦁ analgesia
⦁ cycloplegia - reduce ciliary spasm and pain
⦁ erythromycin ointment
ophthalmology follow-up in 1 to 2 days
Fortunately, most patients with ultraviolet keratitis make a full recovery with supportive care alone. It is important to emphasize proper eye protection when in situations that pose a risk to eye damage, such as tanning in this patient
ACOUSTIC NEUROMA
VESTIBULAR NEUROMA
CN VIII NEUROMA
VESTIBULAR SCHWANNOMA
Acoustic Neuroma = Vestibular Neuroma = CN VIII Neuroma = Schwannoma = Neurilemmoma
BENIGN TUMOR that develops from SCHWANN CELLS
Schwann cells = type of glial cells = surround and support the neurons of the nervous system
Acoustic neuroma is a type of schwannoma that is located in the internal acoustic meatus, thereby affecting CN8
Acoustic schwannomas are commonly found in adults
3rd MC brain tumor found in adults
3 parts to a neuron
⦁ dendrite = receives signals from other neurons
⦁ soma = cell body - has all main organelles
⦁ axon = transmits signal to next neuron
SCHWANN CELLS
- synthesizes “MYELIN” = fatty substance that forms insulating sheaths around parts of axon
A schwannoma is a nerve sheath tumor composed of Schwann cells that produce MYELIN on peripheral nerves.
- the myelin sheath plays important role in conducting electrical impulses (action potentials):
- action potentials propagate along axons when ion channels move sodium ions into the cells
- there are no sodium ion channels within myelin sheath
- NODES OF RANVIER = gaps between myelin = tons of ion channels
- action potential therefore able to jump from node to node, leaping over schwann cells / myelin sheath == saltatory conduction = much faster signal conduction
Schwann cells express a gene: NEUROFIBROMIN 2 = encodes a protein called “merlin”
- in schwann cells, merlin acts as a TUMOR SUPPRESSOR = prevents schwann cells from dividing uncontrollably
SCHWANNOMA = schwann cells start dividing uncontrollably; cause = unknown, but due to lack/decreased amount of merlin = due to lack of neurofibromin 2
Schwannoma = solitary benign tumor found around peripheral nerves
- usually benign - don’t invade surrounding tissue structure - don’t metastasize to distant locations
Most often arise around CN 8 (vestibulocochlear nerve) = vestibular schwannomas or acoustic neuromas
Vestibular schwannomas, also known as acoustic neuromas, arise at the CEREBELLOPONTINE ANGLE from cranial nerve VIII (between the cerebellum and lateral pons). They may cause local compression of cranial nerves V and VII with associated symptoms and signs.
- less often - schwannomas can arise around nerves in the legs, arms or trunk, often compressing the nerves around which the tumor is located
Schwannomas grow really slowly
a small number of schwannomas are related to NEUROFIBROMATOSIS TYPE 2 = mutation on NF2 (neurofibromin 2) => inactivates merlin => schwann cells divide uncontrollably => schwannomatosis (multiple schwannomas in several locations)
Bilateral acoustic schwannomas are a typical finding in neurofibromatosis type 2
SYMPTOMS
⦁ SENSORINEURAL hearing loss = MC (CN 8)
⦁ tinnitus (CN 8)
⦁ problems with balance / vertigo / unsteady gait (CN 8) [ vs Meniere’s = complete ataxia - can’t get up]
⦁ facial numbness / weakness / paralysis depending on if nearby nerve is compressed (CN 7) - may also have loss of taste in anterior 2/3 of tongue
⦁ loss of corneal reflex (blink reflex) (CN 5) - may also have loss of sensation around the mouth and nose, and paralysis of the muscles of mastication
⦁ may have nausea / vomiting / headache
Sensorineural hearing loss = lateralizes to normal ear, and AC > BC
- inner ear disorders: presbycusis (MC), chronic loud noise exposure, CNS lesions (acoustic neuroma), Labyrinthitis, Meniere’s
** Unilateral sensorineural hearing loss = an acoustic neuroma until proven otherwise **
Sensorineural hearing loss + Tinnitus + Vertigo / ataxia - may have N / V / HA - loss of corneal blink reflex - may have facial numbness / weakness - *** LOSS OF HIGH TONE HEARING *** (unlike Meniere's = loss of LOW tone hearing) - ** MRI ** = GOLD STANDARD - TX = Surgical resection
DIAGNOSIS
⦁ ** MRI ** (best imaging choice = gold standard)
⦁ CT
If bilateral neuromas = suspect neurofibromatosis II
⦁ Biopsy
o histology = biphasic appearance = alternating regions that show 2 different cell patterns
- Antoni A = hypercellular = tons of tightly packed Schwann cells with elongated or spindle shaped nuclei
- Antoni B = hypocellular = loosely packed schwann cells
- Schwannomas stain positive for S100 proteins (marker of schwann cells)
TREATMENT
⦁ surgical resection
⦁ radiotherapy for those who cannot have surgery
Small or non-growing tumors can be observed with serial MRI scans
Stereotactic radiation therapy tends to be used for patients who are elderly, those with smaller tumors, or those who cannot undergo surgery for medical reasons.
Patient will present as → a 42-year-old male with a history of neurofibromatosis type II complains of nausea, vomiting, headache, continuous disequilibrium, and a slowly progressive unilateral hearing loss in his right ear. On physical exam, the patient has decreased sensation to touch on the right side of this face.
EPIGLOTTITIS
TRUE EMERGENCY!!!!
- Inflammation of the epiglottis => can interfere with breathing
- MC CAUSE WAS = HIB (haemophilus influenza B)*
- gram negative rod
- has been a decrease in incidence due to vaccination
NOW MC CAUSE = STREP PNEUMO / STAPH / GABHS
- other causes ⦁ GABHS - MC ⦁ staph aureus ⦁ strep pneumo ⦁ strep agelectiae ⦁ strep pyogenes ⦁ M. cat
Non-HIB seen more commonly in adults (esp crack, cocaine use)
MC in children 3 months - 6 years*
Males = 2X more common
DM = risk factor
generally sudden in onset (acute)
SYMPTOMS
⦁ DROOLING
⦁ MUFFLED, HOT POTATO VOICE*
3 D’s = DYSPHAGIA, DROOLING, DISTRESS
⦁ fever
⦁ odynophagia (difficulty / painful swallowing)
⦁ inspiratory stridor (also with croup)
⦁ dyspnea
⦁ hoarseness
often in TRIPOD POSITION - leaning forward
Patients sit with neck hyperextended and chin protruding (sniffing dog position)
DO NOT EXAMINE THE PATIENT - could cause spasm
BE PREPARED TO INTUBATE - do not give IV ABX prior to intubation, as this could also cause spasm
DIAGNOSIS
⦁ Laryngoscopy = definitive diagnosis - provides direct visualization, however, could induce bronchospasm!
⦁ LATERAL NECK XRAY - STAT - THUMBPRINT SIGN
TREATMENT
Secure airway - call anesthesiology and prepare to establish airway, transfer to OR to perform exam
- tracheostomy if necessary to maintain airway
⦁ maintain airway + supportive management = place child in comfortable position and keep them calm.
Admit for observation ==> humidified O2, IV antibiotics (ceftriaxone + clindamycin), and IV corticosteroids
⦁ Dexamethasone to decrease airway edema, and be prepared to intubate
⦁ IV ABX = Ceftriaxone (most likely HIB) or Vanco for anti-staph - call ID specialist for regional coverage/most likely etiology
EX:
Your patient is a 45 year old male that is not immunized. He presents with a fever of 102, dysphagia, drooling, and shortness of breath. Lungs are clear. O2 Sat 100%. Pulse 102. RR-24. Soft tissue neck reveals a thumb sign. All of the following are acceptable management plans except:
A Give a Racemic Epinephrine aerosol treatment and discharge the patient home on steroids = NO
B Begin Vancomycin and Ceftriaxone
C Intubate the patient in the operation room
D Consult anesthesia or ENT
Question 36 Explanation:
In the treatment of epiglottitis racemic epinephrine can help momentarily, but ultimately the patient needs to be intubated and admitted to the hospital. Airway protection is the mainstay of treatment. The patient usually needs to be intubated for 2-3 days prior to weaning attempts. The role of steroids is controversial. Vancomycin helps with anti-staph coverage and Ceftriaxone covers the most common organism haemophilus influenza type B. Anesthesia and/ or ENT should be consulted for airway management.
Patient will present as → a 3-year-old who is brought into the emergency room by her parents. The child has had a high fever, sore throat, and stridor. She has a muffled voice and is sitting up on the stretcher drooling while leaning forward with her neck extended. The patients parents are adamantly against vaccinations, claiming that they are a “government conspiracy.” You order a lateral neck x-ray, which shows a swollen epiglottis.
EYE CHEMICAL BURNS
OPHTHO EMERGENCY!!! - every minute counts!
Irrigation must be started immediately!!!
Alkali burns = worse that acids!
- due to liquefactive necrosis = alkaline chemicals denature proteins + collagen –> thrombosis of vessels
- Ex: fertilizers, household cleaners, drain cleaners
Acidic burns
- coagulative necrosis = H+ precipitates the protein barrier
- ex: cleaners, batteries
Chemical injuries to the eye represent one of the true ophthalmic emergencies
While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or acidic compounds.
ALKALINE burns = more common + more DANGEROUS
Bilateral chemical exposure is especially devastating, often resulting in complete visual disability.
o ACID CHEMICAL BURN
⦁ results in ** protein coagulation **
⦁ limited depth of injury
o ALKALINE CHEMICAL BURN
⦁ results in ** liquefaction necrosis **
⦁ lipophilic
⦁ penetrates faster than acidic burns
⦁ can rapidly damage cornea / iris / lens
⦁ can result in blindness
TREATMENT
Immediate, prolonged irrigation, followed by aggressive early management and close long-term monitoring, is essential to promote ocular surface healing and to provide the best opportunity for visual rehabilitation
⦁ 1ST = remove any particulate material –> Immediate irrigation with NS or LR
- LR is ideal due to its pH of 6-7.5 = closer to the pH of tears (7.1) than NS (4.5 - 7.0), and LR is less irritating to the eyes
- initial step even before complete exam when a patient presents with a chemical eye injury
- irrigate x 30 minutes, or at least 2 L of fluid
- A lid speculum should be placed and topical anesthesia applied
- Irrigation may be administered by a handheld bottle or through IV tubing with an irrigation lens
⦁ 2ND = check pH with a pH strip + check visual acuity after irrigation
- irrigation discontinued when the pH reaches 7.0 - 7.3
Any particulate matter should be removed prior to irrigation if it is a reactive substance such as ammonium hydroxide crystals since fluid may dissolve these causing more injury. The upper lid should be everted to check for any particulate matter
⦁ 3RD = give MOXIFLOXACIN + cycloplegic agent (ex: atropine drops)
⦁ 4TH = Ophtho f/u
