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KChan Saves the World > KC Optho and Oral > Flashcards

KC Optho and Oral Flashcards

1
Q

*4 physical exam findings suggestive of acute angle closure glaucoma (AACG)

A
  • increased IOP
  • shallow anterior chamber
  • mid-fixed dilated pupil
  • decreased VA
  • Hazy Cornea
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2
Q

*4 physical exam findings suggestive of iritis

A

Ciliary flush
conjunctival injection
flare in ant chamber
small pupils
consensual photophobia
Decrease vision

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3
Q

*List 5 treatments for acute angle closure glaucoma and describe the mechanism of action of each

A

Timolol - decreases production of aqueous humor
Pilocarpine - pupil constriction, keeps canal of Schlemm open to drain AqH
Apraclonidine - block production of AqH
Prednisolone - decreases inflamm
Diamox - decrease production of AqH
Mannitol - decrease ICP (osmotic gradient)

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4
Q

*Anatomic features that predispose to AACG

A
  • Shallow anterior chamber
  • Family history of angle-closure glaucoma
  • Female
  • Hyperopia (farsightedness)
  • Medications (e.g. alpha/beta adrenergic agonists, anticholinergic agents)
  • Race (angle-closure glaucoma more prevalent in populations of Asian descent)
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5
Q

*Describe a pupillary block and why this causes glaucoma

A

The lens is located too far forward anatomically and rests against the iris, resulting in pupillary block, a condition in which aqueous humor can no longer flow through the pupil. Pressure builds up behind the iris, relative to the anterior chamber, causing the peripheral iris to bow forward and cover all or part of the anterior chamber angle.

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6
Q

*3 pharmacological mechanisms to treat AACG

A

DECREASE PRODUCTION
INCREASE OUTFLOW
Contract vitreous volume

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7
Q

*4 topical medications for AACG

A
  • Beta-blocker (e.g. timolol): decreases Aq production, 30 mins onset
  • Alpha-blocker (e.g., apraclonidine) increase AQH drainage and decrease production
  • Miotic (e.g. pilocarpine) to help “unlock”, can give q15mins
  • Prednisolone
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8
Q

*2 indications for mannitol or acetazolamide in a patient with AACG

A
  • Abnormal vision
  • Intraocular pressure significantly elevated (>40 mmHg)
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9
Q

*4 atraumatic painful red eye conditions

A
  • Conjunctivitis
  • Keratitis
  • Uveitis
  • Scleritis
  • Episcleritis
  • Orbital cellulitis
  • Endophthalmitis
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10
Q

5 causes of exophthalmos

A

Retro-orbital abscess, tumor, hyperthyroidism, retrobulbar hemorrhage, orbital compartment syndrome, foreign body, retrobulbar emphysema

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11
Q

List 5 causes of unequal pupils

A

Acute: Globe injuries, CN6 injury, CN3 injury, uveitis, acute angle closure glaucoma, pharmacologic (organophosphates, pilocarpine, cholinesterase inhibitors, anticholinergics), Horner’s syndrome
Chronic: previous surgery, synechiae (previous inflammation), Adies or Argyll’s pupils (syphilis)

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12
Q

Describe a +ve RAPD and list 6 differentials

A

Normal: both pupils restrict regardless of which eye is illuminated due to intact afferent and consensual pupillary reflexes
RAPD: Pathologic dilation of both eyes when a bright light is swung from the patient’s normal eye to affected eye. This is due to loss of afferent signal
Ddx optic nerve: unilateral optic neuropathies, demyelinating optic neuritis, ischemic optic neuritis,glaucoma
Ddx retinal: CRVO, CRAO, sickle cell, ischemia, retinal detachment, macular degeneration, vitreous hemorrhage

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13
Q

What is abnormal IOP? List 3 differentials

A

Abnormal >20
Ddx: glaucoma, hemorrhage, vitreous hemorrhage, orbital cellulitis/abscess, hyphema, hypopyon, space occupying retrobulbar pathology, endophthalmitis, trauma

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14
Q

List 6 reasons why you may not be able to elicit a red reflex

A

Box 19.5
See photo

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15
Q

What is the target pH when irrigation for a caustic eye injury

A

7

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16
Q

List 5 features that suggest a serious optho injury

A

Box 19.1
See photo

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17
Q

*Orbital cellulitis/retrobulbar abscess 4 historical signs

A

Absolute neutrophil count (ANC) of >10 000 cells/µL,
Moderate-to-severe periorbital edema (extending beyond the eyelid margins),
Absence of conjunctivitis as the presenting symptom,
Older than 3 years old,
Recent antibiotic use

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18
Q

*Orbital cellulitis/retrobulbar abscess 4 physical exam signs

A

Proptosis,
Ophthalmoplegia,
Pain with eye movement,
Chemosis,
Systemic signs of infection
Visual loss

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19
Q

*After CT, what is next best test for retrobulbar abscess?

A

Maybe MRI? Or does the question imply, if found a retrobulbar abscess on CT, you should re-check visual acuity. Not sure.

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20
Q

*Has loss of vision, suspicion of retrobulbar abscess – next best intervention

A

Immediate lateral canthotomy and cantholysis

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21
Q

*How do you perform a lateral canthotomy intervention (6 steps)

A
  1. Identify lateral canthus, cleanse and anesthetize
  2. Crush with hemostat for 1-2min
  3. Cut through crushed tissue with scissors
  4. Pull lower eyelid away from globe
  5. Strum tissues to find ligament
  6. Cut the inferior canthal ligament
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22
Q

*5 signs of globe rupture

A
  1. enophthalmos
  2. circumferential (360) subconj hemorrhage
  3. irregular pupil (tear drop)
  4. +ve sidel sign
  5. iridodialysis
  6. uveal prolapse
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23
Q

*Name 5 lid lacerations that require optho consult

A
  • Laceration with globe perforation
  • Laceration with orbital septal injury/Prolapsed fat
  • Canalicular laceration
  • Levator muscle/Levator tendon laceration
  • Canthal tendon laceration
  • Laceration involving lid margins
  • Laceration with tissue loss
  • Intraorbital foreign body present
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24
Q

*Indications for admission in hyphema?

A
  • Decreased vision
  • Hyphema greater than 50%
  • Sickle cell trait
  • Uncontrolled intra-ocular pressure
  • Anti-coagulation
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25
Q

*Recognize hyphema. What are the goals of treatment?

A

Close follow-up with ophthalmology within 48 hours is warranted to ensure injury does not result in other ocular issues, such as glaucoma, corneal damage, and hypotony. (and rebleeding)

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26
Q

*What is the treatment for hyphema?

A

In consultation with Ophthalmology:

  • Paralytic agent for the iris and ciliary body (e.g. homatropine or cyclopentolate)
  • Topical ophthalmic steroid drops (e.g. prednisone acetate)
  • Anti-fibrinolytic (e.g. aminocaproic acid)
  • Gentle ambulation permitted
  • Head of bed elevated 30 to 45 degrees to keep larger hyphema from clothing in visual axis
  • Analgesics
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27
Q

*Recognize globe rupture

A

picture

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28
Q

*Eye metal welder fluorescein - leaking out (Seidel test) Most likely diagnosis:

A

Globe perforation, or full thickness corneal injury

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29
Q

*3 management steps in globe perforation

A
  1. Bed rest (NO great evidence for this/vs avoid Valsalva
  2. Elevate head of bead (30 degree) (NO great evidence for this)
  3. Shield eye
  4. Analgesia - but no platelet inhibitors
  5. Antiemetics & sedatives should be used cautiously.
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30
Q

*Traumatic ball to eye. *photo shown. What is it called (traumatic hyphema). Most significant immediate complication and mechanism

A

Complication: acute angle closure glaucoma
Mechanism: Elevated IOP due to blockage of drainage through trabecular meshwork

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31
Q

*3 delayed complications of traumatic hyphema

A
  • Corneal staining
  • Persistent hyphema/re-bleeding
  • Uncontrolled intraocular pressure and optic nerve atrophy
  • Peripheral anterior or posterior synechiae/adhesions
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32
Q

*identify given images of fundoscopy:
a. CRVO
b. Retinal detachment
c. CRAO

A

What are the fundoscopy findings of CRAO, CRVO
CRAO - a prominent APD with a pale grey white appearance and a cherry red spot representing the fovea
CRVO - congestion of venous blood reads two dilated and tortuous veins, retinal hemorrhages and disc edema
Retinal Detachment - the retina appears out of focus at the site of the
detachment. In large retinal detachments with large fluid accumulation,
a bullous detachment with retinal folds can be seen

On ultrasound for retinal detachment you see a billowing hyperechoic line that may undulate with side-to- side movements of the eye

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33
Q

*2 anatomical locations that are most common for globe rupture.

A

Site of prior sx,
Behind insertion of rectus muscle
Limbus
Insertion optic nerve

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34
Q

*4 things to do to manage other than ophtho consult in globe rupture(you’ve done this already)

A
  1. Shield eye
  2. Antiemetics / analgesia
  3. IV Abx ie piptazo or ceftaz + cefazolin or vanco)
  4. Tetanus
  5. NPO
  6. ophtho consult –> OR

avoid checking IOP
If intubating consider ROC
need CT but still sensitivity (57-76%)

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35
Q

*Recognize retro-orbital hematoma on CT. What’s the management if loss of vision?

A

Immediate lateral canthotomy and cantholysis

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36
Q

*50 M, with presumed Acute Angle-Closure Glaucoma. 3 anatomic features of patient that predispose to AAGC.

A
  • Shallow anterior chamber
  • Family history of angle-closure glaucoma
  • Female
  • Hyperopia (farsightedness)
  • Medications (e.g. alpha/beta adrenergic agonists, anticholinergic agents)
  • Race (angle-closure glaucoma more prevalent in populations of Asian descent)
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37
Q

*Describe a pupillary block and why this causes glaucoma.

A

The lens is located too far forward anatomically and rests against the iris, resulting in pupillary block, a condition in which aqueous humor can no longer flow through the pupil. Pressure builds up behind the iris, relative to the anterior chamber, causing the peripheral iris to bow forward and cover all or part of the anterior chamber angle.

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38
Q

*What are 3 pharmacological mechanisms to treat AACG?

A

DECREASE PRODUCTION
INCREASE OUTFLOW
Contract vitreous volume

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39
Q

*What are 4 topical medications for AACG?

A
  • Beta-blocker (e.g. timolol): decreases Aq production, 30 mins onset
  • Alpha-blocker (e.g., apraclonidine) increase AQH drainage and decrease production
  • Miotic (e.g. pilocarpine) to help “unlock”, can give q15mins
  • Prostaglandin (e.g. latanoprost)
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40
Q

*What are 2 indications for mannitol or acetazolamide in a patient with AACG?

A
  • Abnormal vision
  • Intraocular pressure significantly elevated (>40 mmHg) or 50
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41
Q

*Traumatic causes of monocular diplopia

A
  • Lens dislocation
  • Iris injury (e.g. iridodialysis or tearing away of iris from its attachment to ciliary body)
  • Refractive error (e.g. corneal abrasion)
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42
Q

*What are five findings of AACG on physical exam?

A
  • Injected conjunctiva
  • Fixed, dilated pupil
  • Cloudy cornea
  • Shallow anterior chamber
  • Elevated IOP (e.g. tender, firm globe)
  • Decreased visual acuity
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43
Q

*4 Ddx atraumatic painful red eye

A
  • Conjunctivitis
  • Keratitis
  • Uveitis
  • Scleritis
  • Episcleritis
  • Orbital cellulitis
  • Endophthalmitis
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44
Q

*4 Treatments in the ED for CRAO

A
  • Direct digital pressure through closed eye lids
  • Medically reduce IOP
  • Anterior chamber paracentesis
  • Hyperbaric oxygen
  • Increase intra-arterial CO2 content
  • Consider intra-arterial or IV thrombolytic
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45
Q

*5 causes of painless LOV.

A

CRAO
Retinal detachment
Acute maculopathy (e.g. hemorrhage)
Central Retinal vein occlusion
Ischemic neuropathy (e.g. secondary to giant cell arteritis)
Nonischemic neuropathy (e.g. diabetes)
Functional vision loss
Vitreous detachment
TIA

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46
Q

*Name 4 clinical eye-related features of retrobulbar hemorrhage

A
  • Proptosis
  • Ophthalmoplegia/Weakness or restriction of extra-ocular movements
  • Decreased visual acuity
  • Increased intra-ocular pressure
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47
Q

*Woman unable to abduct her R eye. What CN is involved and what is the most likely diagnosis?

A

Cranial nerve VI/Lateral rectus palsy
Must rule-out raised ICP/Mass

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48
Q

*Man with ptosis, mydriasis & eye down/out CN III. What is the one worst diagnosis to rule out

A

Intracranial aneurysm

you get the dilation because the parasympathetic component that’s responsible for constriction is located on the outside and so if something is compressing it like an aneurysm you’ll probably get issues with your pupil before you start to get other symptoms from the nerve like ptosis

If its an ischemic issue like DM often pupil sparing

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49
Q

*Lady recently post-op from cataract surgery. What are exam findings of endophthalmitis? (5)

A

Pain
Decreased VA
Chemosis
Eyelid swelling
Ulcer
Conjunctivitis
Hypopyon

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50
Q

*What are exam findings of EKC

A

Severe conjunctival injection with punctate staining with fluorescein update

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51
Q

*What are symptoms of EKC

A

Pain, clear discharge, URTI sx,=

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52
Q

List 3 things that can be detected by fluorescein

A

Corneal abrasions, globe perforations, tarsal foreign bodies

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53
Q

List 4 topical ophthalmic medications, including 2 that cover pseudomonas

A

Erythromycin ointment, Polymyxin B/trimethoprim solution, azithromycin
Pseudomonal: ciprofloxacin, moxifloxacin, gentamicin, ofloxacin

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54
Q

List 10 causes of decreased vision post blunt trauma

A

Globe rupture, hyphemia, lens subluxation/dislocation, iridodialysis, traumatic uveitis, vitreous hemorrhage, retinal injury, orbital wall fracture, retrobulbar hematoma, optic nerve injury

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55
Q

List 10 causes of acute painless visual loss

A

Vascular occlusion (CRAO, CRVO), retinal detachment, vitreous hemorrhage, posterior vitreous detachment, hemianopsia due to stroke, pituitary tumor, macular degeneration, non-arteritic ischemic optic neuropathy, toxic-metabolic causes (ex. Ethylene glycol), hysteria

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56
Q

List 5 signs that a suggest that a corneal abrasion may actually be a corneal laceration or open globe

A

loss of anterior chamber depth, prolapse iris, irregularly shaped pupil, blood in anterior chamber, 360 subconjunctival hemorrhage, Seidel’s sign

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57
Q

List 3 indications for antibiotics in corneal abrasion

A

deep abrasion, organic or contaminated object, contact lens wearer, ICed

58
Q

Describe the grading of hyphemas

A

See photo

59
Q

List 3 risk factors for lens dislocation

A

Marfan’s, homocystinuria, myopia

60
Q

What is iridodialysis

A

Tearing of the iris from the ciliary body, often traumatic
See photo

61
Q

List 5 signs of an orbital fracture

A

Trouble with EOM, facial crepitus, enophthalmos, bruising, swelling, ptosis, diplopia on upward gaze, subcutaneous emphysema (when blowing nose)

62
Q

List 5 signs of orbital compartment syndrome

A

decreased visual acuity, positive RAPD, proptosis, subconjunctival hemorrhage, increased IOP, +RAPD

63
Q

Differentiate between herpes simplex keratitis and herpes zoster keratitis

A

Both: dendritic pattern with fluorescein staining
Simplex: associated with cold sores. Rx with topical acyclovir +/- systemic antivirals. Refer to optho
Zoster: associated with dermatomal vesicular rash (esp. at tip of nose) with iritis, uveitis. Needs systemic therapy; topical has limited effect. Optho consult; can be vision threatening.

64
Q

List 2 viral and 2 bacterial causes of conjunctivitis

A

Viral (many): adenovirus, entero, coxsackie, HSV, rubella
Bacterial: Moraxella, strep pneumo, haemophilus influenzae, neisseria gonorrhea, pseudomonas (contact lens)

65
Q

Differentiate between corneal ulcer, hypopyon, and endophthalmitis

A

Corneal ulcer is an infection in the cornea, usually from an abrasion that got infected. Needs optho, systemic antibiotics
Hypopyon is a collection of pus in the anterior chamber. Needs optho, likely surgery, systemic and topical Abx
Endophthalmitis is an infection of the globe itself, typically after surgery or perforate globe. This is a medical emergency that needs IV and intravitreal antibiotics

66
Q

Differentiate between iritis, episcleritis, scleritis, and keratitis

A

Iritis: perilimbal inflammation and flushing, photophobia, pain (consensual pain with light in non affected eye), cells and flare in anterior chamber. Often autoimmune. Rx with cycloplegics and referral to optho

Episcleritis: Superficial inflammation ontop of the sclera. Sectoral redness, not painful. Artificial tears + NSAIDs

Scleritis: Inflammation of the sclera. Painful. Vision loss. Often autoimmune of infectious. PO NSAIDs + optho as can lead to vision loss

Keratitis: Inflammation of the cornea. Punctate keratitis will have fluorescein uptake. Associated with UV keratitis. Supportive care; treated like a corneal abrasion

67
Q

Differentiate between a pterygium and a pinguecula

A

Pterygium: Chronic fibrovascular conjunctival growth on cornea growing from the nasal side of the eye
Pinguecula: Similar to pterygium but stops at the limbus and does not enter the cornea or visual axis

a pTerygium crosses the cornea like a t

68
Q

Differentiate between a style and chalazion

A

Style (hordeolum): inflammation or abscess in the eyelash follicle; at the eyelid margin
Chalazion: inflammation in meibomian gland causing a subcutaneous nodule within the eyelid

69
Q

List signs that suggest a post septal (vs pre septal) cellulitis

A

Fever, Limited EOM, proptosis, pain, decreased vision, RAPD

70
Q

What is dacrocystitis

A

inflammation of the lacrimal sac (medial corner of the eye) due to nasolacrimal duct obstruction. Managed with warm compresses and systemic antibiotics

71
Q

5 causes of painful vision loss

A

acute glaucoma, optic neuritis, GCA, uveitis, migraine, Terson’s syndrome (SAH + vitreous hemorrhage)

72
Q

List 5 risk factors for retinal detachment

A

myopia, intraocular surgery, previous RT, trauma, age related macular degeneration, diabetic retinopathy, sickle cell disease

73
Q

What is the difference between open and closed angle glaucoma

A

Open angle
- There is a blockage of the trabecular network so the venous system cannot drain
- AC looks normal, non tender, pressure <30
- Chronic, patients are asymptomatic, may be on topical drops to improve aqueous outflow
Closed angle
- The lens bulges anterior blocking the angle, then fluids builds up behind the iris, can eventually compromise arterial flow
- Can occur in patients with no prior history of glaucoma

74
Q

What is optic neuritis

A

Inflammation of the optic nerve
Etiologies: demyelination (MS), autoimmune, post vaccine, viral infections, sarcoidosis
Sx: +RAPD, gradual monocular visual loss, pain with eye movement, flashes
Managed: neuro-ophthalmologist. Methylprednisolone

75
Q

Localize the lesion for each of the following presentations:
1) bitemporal hemianopia
2) homonymous hemianopia

A

1) chiasmal
2) cerebral (post tract)

76
Q

What is Horner’s syndrome

A

ptosis, mitosis, anhidrosis due to a disruption of sympathetic innervation

77
Q

List 5 causes of Horner’s syndrome

A

Brainstem: neoplasm, stroke
Spinal: spinal cord injury
Arm pain: brachial plexus lesion, Pancoast tumor
Ear pain: carotid dissection
Hearing loss: infection

78
Q

*Traumatic causes of monocular diplopia

A

Lens dislocation
Iridodialysis
Corneal abrasion
Orbital floor fracture

79
Q

*Ddx for atraumatic monocular diplopia

A

Refraction problem in cornea, lens, vitreous, retinal wrinkle ex. Cataract, macular degeneration, diabetic retinopathy, posterior vitreous detachment

80
Q

*Fundoscopic findings for atraumatic monocular diplopia

A

Depends on the pathology, will see problem with part of the eye involved (FB, dislocation, tear, cloudiness etc) Should resolve when pinhole is used, unless retinal problem

81
Q

*Physical exam findings for INO, where is the lesion, what is the Dx

A

inability to adduct the eye on one side in the contralateral direction during lateral gaze that resolves during convergence (i.e., one cannot adduct the right eye when following the examiners finger laterally to the left, and vice versa)
Implicates a lesion in the medial longitudinal fasciculus (MLF) such as that typically found in patients with multiple sclerosis

82
Q

List 10 causes of binocular diplopia

A

EOM: thyroid myopathy, lupus, sarcoidosis, orbital cellulitis, retrobulbar hemorrhage, orbital tumor, orbital fracture
NMJ: myasthenia, botulism
CN palsies
Focal brainstem lesion: stroke, MS, tumors, aneurysms (esp if Horner’s!), dissection
Neuro disease: meningitis, migraine, Wernicke’s, cavernous sinus thrombosis, Miller-Fischer syndrome

83
Q

Define monocular and binocular diplopia

A

Monocular: Diplopia occurs whenever the affected eye is open; disappears when affected eye is covered and re-appears when unaffected eye is covered
Diplopia: Diplopia occurs when both eyes are open; disappears when either eye is covered

84
Q

Fill out the following chart of the cranial nerves (see photo)

A

see photo

85
Q

List 5 critical causes of a sore throat

A

Epiglottis, retropharyngeal abscess with airway compromise, peritonsillar abscess with airway compromise, Ludwig’s angina, angioedema, croup, Lemierre’s syndrome, ACS with referred pain

86
Q

*Middle aged gentleman on warfarin comes in with epistaxis. List 4 treatments to achieve hemostasis that is not packing

A
  • Silver nitrate (topical)
  • Tranexamic acid (topical)
  • Lidocaine/epinephrine (topical)
  • Surgical (topical)
87
Q

*3 arteries in the nose

A

Septal and posterior branches of Sphenopalatine artery
Anterior and posterior branches of ethmoidal artery
Superior labial branch of the facial artery

88
Q

*5 complications of posterior packing

A

1-Patient discomfort
2-Otitis media, sinus obstruction
3-Rebleeding
4-Dysrhythmias
5-Bradycardia
6-Aspiration
7-Stroke

TSS
Pressure necrosis
Contact dermatitis (if topical abx added)
Infection/cellulitis

89
Q

*Two treatments for otitis externa

A
  • Topical antibiotics (e.g. ciprofloxacin)
  • Topical steroids (e.g. hydrocortisone)
  • Clean canal
90
Q

*3 reasons for systemic antibiotics in otitis externa

A
  • Immunocompromised (e.g. diabetes, HIV)
  • Infection involving skin (e.g. cellulitis) and peri-auricular structures
  • Necrotizing (malignant) external otitis
91
Q

*Organism responsible for otitis externa

A

Otitis externa (OE) is usually caused by P. aeruginosa and S. aureus but can also be polymicrobial. Occurring most often in the summer and in tropical climates, it is also known as swimmer’s ear or tropical ear.

92
Q

*5 complications for malignant otitis externa

A
  • Skull base osteomyelitis
  • CNVII dysfunction (facial nerve paralysis)
  • Meningitis,
  • brain abscess
  • thrombosis of sigmoid sinus
93
Q

*2 patient populations at risk for malignant OE

A

Patients affected include older diabetics, those with acquired immunodeficiency syndrome (AIDS) and, rarely, immunocompromised children.

94
Q

*2 IV abx for malignant OE

A

ciprofloxacin, 400 mg IV q8h
tazo 4.5g IV q8h

95
Q

*25 month old male brought in for two day history of crying and nasal congestion. Normal vital signs and afebrile. What are two criteria required to diagnosis acute otitis media

A
  1. Acutely perforated tympanic membrane with purulent drainage
  2. All three of: acute onset of symptoms, signs inflammation, middle ear effusion.
96
Q

*What treatment approach would you recommend for AOM?

A
  • Pain management and antibiotic therapy (weight appropriate amoxicillin)
  • versus observation (shared clinical decision with parents)
    CPS said under 2 y need 10 days Abx
    Bugs
  • Streptococcus pneumonia
  • Haemophilus influenzae
  • Moraxella catarrhalis
97
Q

*What would you counsel the parents on when to return or obtain follow up?

A

Patients should be reevaluated in 3 days if there is no improvement. Treatment failure is defined by lack of clinical improvement in signs and symptoms, such as ear pain, fever, and TM findings of redness, bulging, or otorrhea. The reasons for treatment failure may include the wrong initial diagnosis or antibiotic resistance.

98
Q

*6 acute complications of AOM

A
  • Tympanic membrane perforation
  • Chronic otitis media
  • Mastoiditis
  • Meningitis
  • Labyrinthitis
  • Venous sinus thrombosis
  • Facial nerve palsy
99
Q

*List 2 clinical features that would suggest a posterior nosebleed

A

Sphenopalatine artery most common source of posterior epistaxis
- Bleeding persists with properly placed anterior nasal pack
- Pinching nose fails to stop/slow bleeding

100
Q

*Bike injury with obvious nasal fracture: Three indications to reduce.

A
  • Nasal obstruction from deviated septum
  • Airway compromise from deviated septum
  • Cosmetic concern/acute injury with minimal swelling, can trial reduction in ED
  • Potential cosmetic concern/arrange follow-up once swelling subsided
    • Deviation of nasal septum obscuring nares
    • Airway obstruction
    • < 6 hours and cosmetic defect
101
Q

*Three contraindications to reduction of nasal fracture

A
  • Severe comminution of nasal bones/septum
  • Associated fractures of orbital wall or ethmoid bone
  • Deviation of the nasal pyramid greater than half the width of the nasal bridge
  • Caudal septal fracture-dislocation
  • Open septal fractures
  • Fracture older than 3 weeks
    or
    • Basilar skull fracture
    • CSF otorrhea
    • HD unstable
    • Delay
    • Severely comminuted
102
Q

*Define chronic otitis media

A

Chronic otitis media refers to inflammation of the middle ear that persists for 6 weeks or longer, accompanied by discharge through perforation of an intact membrane.

103
Q

*4 intracranial complications of otitis media

A

lateral venous sinus thrombosis
Meningitis/encephalitis
Brain abscess
Extradural abscesses, subdural empyema

104
Q

*5 local complications of otitis media

A
  • Hearing loss
  • TM perforation
  • Cholesteatoma
  • Chronic effusion/otitis
  • Mastoiditis
  • Facial nerve paralysis
105
Q

*Mechanisms of complications of otitis media

A
  • Direct extension of infection through bone weakened by osteomyelitis or cholesteatoma
  • Retrograde spread by thrombophlebitis
  • Extension of infection along preformed pathways
106
Q

List 5 risk factors for OM in children

A

low SES, males, exposed to tobacco, craniofacial anomalies, prone position sleepers, pacifier users

107
Q

List 10 causes of epistaxis

A

Local: facial trauma, URTI, nose picking, allergies, low humidity, nasal polyps, foreign body, environmental irritants, neoplasms, septa deviation
Systemic: anticoagulant, pregnancy, barotrauma, hereditary hemorrhagic telangiectasia, bleeding disorders, rupture of internal carotid artery aneurysm, liver disease, diabetes, alcoholism, vitamin K deficiency
Idiopathic: habitual, familial

108
Q

List 2 causes of neck masses in each of the areas: central, anterior triangle, posterior triangle

A

Central: thyroid CA, thyroiditis, thyroglossal duct cyst, dermoid cyst, ranula, thymic mass
Anterior triangle: lymphoma, lymphadenopathy, sialadenitis, abscess, cancer, brachial cleft cyst, laryngocele
Posterior: lymphoma, cancer, cystic hygroma, Lemierre’s

109
Q

List indications for immediate antibiotics in pediatric OM

A

infants <6 mo, children with severe signs or symptoms, moderate-severe ear pain, >48 hours of symptoms, >39 temp, bilateral AOM, recurrent AOM, AOM with perforation, myringotomy tubes

110
Q

What is the dose and duration of antibiotics in pediatric OM

A

Amox 90mg/kg/day divided BID for 10 days of <2 years, 5 days if >2 years

111
Q

List 5 causes of sudden hearing loss

A

idiopathic in 70% of cases
Sensorineural: meningitis, Group A strep, syphilis, Epstein-Barr, Meniere’s disease, drug toxicity, trauma, vestibular schwannoma
Conductive: otitis media, cerumen impaction

112
Q

Describe the Rinne and Weber test for hearing loss

A

see photo

remember - conductive hearing loss - louder through the direct conduction to bone
Rinne First - conducitve or sensioneural, then weber to localize

113
Q

*7 non-infectious causes of parotitis

A
  • Collagen vascular disease
  • Cystic fibrosis
  • Alcoholism
  • Diabetes mellitus
  • Uremia
  • Xerostomia
  • Facial compression
  • Sarcoidosis
  • Sialolithiasis
  • Benign/malignant tumors
  • Drug-related disorders
    Trauma
    Juvinal recurrent parotitis
    Ductal stricture
114
Q

*What are 4 complications of parotitis?

A

Obstructive respiratory dysfunctions
Septicemia
Facial bone osteomyelitis
Septic jugular thrombophlebitis

115
Q

*You suspect he has bacterial parotitis. What is the appropriate antibiotic regimen?

A

Ampi-Sulbactam (is number 1 on uptodate)
I’d use tazo.

116
Q

*What is the one imaging test you would do?

A

CT facial bones

117
Q

*What oral lesions are associated with these systemic illnesses:
Measles
Bechet’s
HFM
Lupus
Kawasaki
Crohn’s
HHT

A

Measles: Koplik spots
Bechet’s: Aphthous ulcers
HFMD: Vesicular
Lupus (discoid): Red and white plaque on palate
Kawasaki: Strawberry tongue, dry cracked lips
Crohn’s: Aphthous stomatitis
HHT: Mouth telangiectasias

118
Q

*Patient with tooth pain; what are 7 things that can present with dental pain (specifically asked for dental and non-dental causes)?

A

Dental
- Dental carries
- Abscess
- Tooth fracture
Non dental
- Sinusitis
- Dysbarism
- Trigeminal neuralgia
- TMJ
- GCA
- Osteomyelitis
- Sialadenitis
- Trauma?

119
Q

*3 mandibular spaces that infection can spread in Ludwig’s angina?

A
  • Submandibular
  • Sublingual
  • Submental
120
Q

*2 mechanisms by which Ludwig’s angina can cause airway compromise

A

Airway occlusion
Difficulty with secretions

121
Q

*5 causes of Ludwig’s angina other than dental infections

A
  • Fractured mandible
  • Foreign body in floor of mouth
  • Laceration in floor of mouth
  • Tongue piercing
  • Traumatic intubation
  • Traumatic bronchoscopy
  • Secondary infections of oral malignancy
  • Submandibular sialadenitis
  • Peritonsillar abscess
  • Furuncles
  • Infected thyroglossal cyst
  • Sepsis
122
Q

*5 infectious causes of non-suppurative (i.e. non-bacterial) parotitis

A
  • Mumps
  • Influenza
  • Coxsackievirus
  • Epstein-Barr
  • Lymphocytic choriomeningitis
  • Parainfluenza
  • Herpes simplex
  • Cytomegalovirus
123
Q

*What is Ludwig’s angina?

A

“Progressive cellulitis of the connective tissues of the floor of the mouth and neck that begins in the submandibular space.”

124
Q

*List 4 physical exam findings suggestive of Ludwig’s angina

A
  • dysphagia,
  • odynophagia
  • neck swelling
  • neck pain
  • dysphonia
  • hot potato voice
  • dysarthria
  • drooling
  • tongue swelling
  • pain in floor of mouth
  • restricted neck movement
  • sore throat
  • crepitus
125
Q

*What is the most important immediate management step in Ludwig’s angina?

A

Probably want intubation as the answer here, eh?

“Flexible endoscopically guided oral or nasal intubation under sedation with topical anesthesia is the preferred method of airway control. Cricothyrotomy may be difficult…but is the procedure of choice if flexible endoscopic intubation cannot be accomplished.”

126
Q

*Ellis Classification and description

A
  • Class I: Enamel of tooth only, not painful
  • Class II: Expose yellow dentin, may be painful
  • Class III: Expose dental pulp, seen as red line or dot, exquisitely tender
127
Q

*Management of each type of Ellis #

A
  • Class I: Await dental evaluation on outpatient basis
  • Class II: Await dental evaluation on outpatient basis, but should be covered with a dressing of calcium hydroxide and aluminum foil or skin adhesive (e.g. Dermabond)
  • Class III: Early evaluation by dentist/endodontist
128
Q

*2 organisms implicated in Ludwig Angina

A

Anaerobes
S. aureus
Streptococcal species
Bacteroides

129
Q

*What antibiotic(s) are recommended in Ludwig Angina

A

Tazo+Vanco/Clinda (if allergic to Pen)

130
Q

*Management goals in periapical abscess

A

Analgesia - nerve block
antibiotics - PenV or clavulin

131
Q

*Name two potential spaces that could be infected after spread from periapical abscess

A

Potential Spaces in Neck
1. Parapharyngeal space
2. Retropharyngeal space
3. Danger space (retro-retropharyngeal)
4. Prevertebral
5. Submaxillary
6. Submental space
7. Sublingual
8. Buccal space

132
Q

*Antibiotics for “potential space” infection

A

Tazo+Vanco/Clinda (if allergic to Pen)

133
Q

How many permanent teeth are there? Describe the numbering

A

32 permanent teeth
8 in each quadrant: 1 central incision, 1 lateral incision, 1 canine, 2 premolars, 3 molars
Numbering starts in top right

134
Q

List 5 differentials for oral pain

A

tooth eruption, dental caries, pulpits, gingivitis, periodontal abscess, trigeminal neuralgias, TMJ pain, oral candida, sexually transmitted infection, ulcers, GCA

135
Q

List 3 medium that can be used to transport avulsed teeth

A

sterile saline, milk, saliva, Hank’s balanced salt solution (Toothsaver), oral rehydration solution

136
Q

What is a dry socket

A

Empty socket where previous clot after a tooth removal becomes dislodged
Managed with direct pressure, local anesthesia, packing with surgifoam

137
Q

List 5 medications that can cause gingival hyperplasia

A

anticonvulsants (phenytoin, valproic acid, carbamazepine), immunosuppressants (cyclosporine), calcium channel blockers (nifedipine, felodipine, amlodipine, verapamil, diltiazem)

138
Q

List 5 soft tissue spaces where a tooth infection can spread

A

Maxillary: canine (can lead to cavernous sinus thrombosis) or buccal space
Mandibular: submental (midline), sublingual, submandibular
- Infection of all three spaces is Ludwig’s angina

139
Q

What is Lemierre’s syndrome

A

Thrombophlebitis of the IJ with anaerobic bacteria, typically secondary to an oropharyngeal infection

140
Q

What bacteria is associated with Lemierre’s syndrome

A

fusobacterium necrophorum

141
Q

What is the treatment of Lemierre’s syndrome

A

Antibiotics (flagyl + penicillin, clinda)
Value of anticoagulation unknown

142
Q

Fill out CN involved in EOM and their palsy’s

A

KChan Saves the World (24 decks)

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