General ENT Flashcards
Tracheotomy v Tracheostomy
tracheOTomy: temporary airway or the actual surgical procedure
tracheoOSTomy: permanent or semi-permanent tracheo-cutaneous fistula
Indications for Tracheostomy
-Acute or chronic obstruction
(foreign body, laryngeal paralysis, cancer, trauma, craniofacial abnormalities, subglotic stenosis)
-prolonged intubation (to prevent tracheal stenosis).
-improved pulm toilet
-Prevent aspiration
- severe osa
Equipment needed for trach
Bovie, sens, tracheal dilatory, 15 blade scapel, Debakey’s, tracheal retractors, peanut, Army-Navy retractor, 2-0 silk sutures, cuffed tracheostomy tube or endotracheal tube, 10cc syringe, Mayo scissors
Relative CI for Trachs
- High PEEP and vent support preventing safe transport or preventing pt from safely tolerating apnea during exchange of the ET tube for the trach appliance
- Bleeding d/o’s
- Anatomy (see other card)
Anatomy RF for higher risk tracheostomy
♣ Body habitus
♣ Down syndrome (antlanto-occipital instability, prevents neck extension)
♣ Cervical spine fusions (prevent neck extension)
♣ High riding innominate at suprasternal notch
♣ High pressor requirements preventing adequate sedation during procedure 2/2 hypotension
Trachea anatomy, general
¬ 16-20 hyaline cartilaginous rings connected by fibromuscular membrane
¬ Start: Cricoid cartilage ~6th Cervical vertebra; End: Carina
¬ 10-13cm
¬ Runs superoanterior to inferoposterior
¬ Posterior trachea separated by eso by thin layer of connective tissue “party wall”
Trachea vasculature
¬ Superior trachea: Inf thyroid aa. branches
¬ Inferior: Bronchial aa. +3rd intercostal
¬ Inf. Thyroid venous plexus
Trach Complications: Intraop
♣ Hemorrhage/damage to great vessels ♣ PTX ♣ Pneumomediastinum ♣ Damage to party wall/tracheoesophageal fistula ♣ SC emphysema ♣ RLN injury ♣ Airway fire ♣ Cardiopulmonary arrest ♣ Post-obstruction pulm edema CHF Extravasation of fluid into alveoli in response to reduced PEEP
Trach Complications: Immediate post-op
♣ Obstruction ♣ Displaced tube ♣ Hemorrhage ♣ Wound infection ♣ SC emphysema
Trach complications: Delayed
♣ Stenosis/tracheomalacia
♣ Granuloma formation
♣ TEF
♣ Tracheoinnominate fistula
4 cardinal symp of CRS
- Ant/Post nasal mucopurulent drainage
- Nasal obstruction/blockage/congestion
- Facial pain/pressure/fullness
- Anosmia/hyponosmia (Cough in kids)
Samter’s Triad
- Asthma
- Nasal polyps
- NSAID sensitivity
Nasal obstruction DDX
- allergic rhinitis,
- chronic nonallergic (idiopathic) rhinitis,
- rhinitis -associated with medication use (rhinitis medicamentosa)
- secondary atrophic rhinitis (ie, “empty nose syndrome”)
Maxillary Sinus Hypoplasia Types
I: normal uncinate process, a well-defined infundibular passage, and mild sinus hypoplasia 7%
II: absence or hypoplasia of the uncinate process, an ill-defined infundibular passage, and soft-tissue density opacification of a significantly hypoplastic sinus. 3%
III: absence of the uncinate process and a profoundly hypoplastic, cleft-like sinus. 0.5%
CRS warning signs
Ocular symp: Diplopia, proptosis, Ophthalmoplegia Periorbital edema Fever>102 Severe headache/meningeal signs Significant/recurrent epistaxis
Types of CRS
- w/ Nasal polyposis
- w/o nasal polyposis (most common)
- allergic fungal (more common in south)
CRS time duration
> 12 weeks
ABRS vs ARS
ABRS >10d or if symptoms beginning to improve and then worsen
Sinus disease: evaluation history
4 cardinal symp duration Exacerbating conditions prior tx prior imaging prior surgery exposure to environmental allergies
Exacerbating conditions of CRS
- Allergic rhinitis
- Environmental irritants
- Immunodeficiencies
- Mucociliary clearance (CF; PCD)
- Recurrent URIs
- GPA, churg-strauss, sarcoid
- Anatomic abnormality
- Iatrogenic
Demonstration of mucosal disease
requirement of CRS dx
- purulent mucus/edema
- polyp
- radiographic imaging demonstrating mucosal thickening or opacifications of sinus
Nasal endoscopy normally can visualize what:
In virgin nose
sphenoethmoidal recess,
sphenoid and posterior ethmoid ostia,
and middle meatus
Haller air cells
Infraorbital ethmoidal air cells
Clinically significant when: infected–> extension into orbit
Narrowing of ostiomeatal complex–> maxillary obstruction
Inadvertent entry into orbit during FESS
Agger Nasi air cells
Most anterior ethmoidal air cells
Lie anterolat and inf to frontoethmoidal recess
Anterior above attachment of middle turb
Basal Lamellae
Divides ethmoidal air cells into anterior and posterior groups w/ different drainage patterns
Ant ethmoid drainage
Hiatus semilunaris and middle meatus
Post ethmoid drainage
Sphenoethmoidal recess
Nasolacrimal duct empties where?
Into the inferior meatus
Ostiomeatal complex
Uncinate process
Hiatus semilunaris
Ethmoid bulla
Ostium of maxillary sinus
Located in middle meatus
Samter’s triad sensitivity
NSAID sensitivity results in large spectrum of symp
Mild–> congestion
Severe: wheezing/coughing even anaphylaxis
Samter Triad Pathophys
Anomaly of archidonic acid metabolism
Increased leukotrienes
COX-1 blockage stops anti-inflam proteins like prostaglandins
Surgical mgmt of chronic maxillary sinusitis
Endoscopic uncinectomy w/ or w/o max antrostomy
Caldwell-Luc procedure
Inferior antrostomy
Tx differences in CRS w/ and w/o nasal polyps
In CRS w/ polyps–> relieve obstruction w/ intranasal and/or systemic glucocorticoids
Common pathogens of ABRS
S. pneumo
H. influ
M. catarrhalis
Hiatus semilunaris
Crescent groove in lateral wall.
Inf to ethmoidal bulla
Location where frontal, maxillary and ant ethmoid sinuses drain
Bounded inferiorly and anteriorly by uncinate process of ethmoid
Uncinate process
Ethmoid bone, outcropping just anterior to hiatus semilunaris and where the frontal, ant eth and max drain
House-Brackman grading
Originally used for Bell’s palsy
I: normal
VI: completely paralyzed
House Brackman grade II
Slight weakness, slight synkinesis
At rest: normal tone/symmetry
Eyelid closes
Mouth: slight asymmetry
House Brackman grade III
Obvious but not disfiguiring difference
Noticeable (not severe) synkinesis, contracture, or hemifacial spasm
At rest: normal tone/symmetry
Eye: complete closure w/ effort
Mouth: Slightly weak w/ max effort
Forehead: slight to moderate movement
House Brackman grade IV
Mod-severe dysfx
At rest: normal tone/symmetry
No forehead
Eye: Incomplete clsoure
Mouth: Asym w/ max effort
House Brackman grade V
Severe
At rest: asymmetry
Barely perceptible motion
Best House brackman grade post-nerve graft
Grade III
takes 4-6 months to see
Silent sinus syndrome
can be 2/2 Maxillary hypoplasia
Infraorbit bone destruction leading to enophthalmosis
Acute suppurative sialadenitis pathophys and organisms
bacterial infxn
causes: salivary stasis, reduced flow, obsruction, xerostomia
S. aureus**, anaerobes, S. pneumo, E. coli, H. influ
Acute suppurative sialadenitis: presentation
Acute swelling, pain, tenderness of gland. Gland massage may result in pus. Gland may be firm.
Fevers, chills, trismus, even dysphagia
MC in parotid gland
Acute suppurative sialadenitis: TX
Massage, hot compresses, sialogogues,
Antibiotics: IV nafcillin+ clinda or flagyl as in patient. Can substitute nafcillin for vanc
If no improvement in 2 days consider imaging for possible abscess requiring surgical drainage (modified blair incision)
Acute suppurative sialadenitis complications
massive swelling of neck
respiratory obstruction
septicemia
Parapharyngeal space infection w/ potential for Lemierre’s syndrome (septic jugular thrombophlebitis)
Viral causes of sialadenitis
CMB, EBV, coxsackie, echovirus, HIV
Often bl instead of unilateral
No pus
Less toxic appearing
Symptomatic treatment
Mycobacterial Sialadenitis
Granulomatous Rare, seen more in adults ♣ MC in parotid w/ primary TB ♣ MC in Submandibular w/ Disseminated TB ♣ Looks like neoplasm on imaging ♣ Can mimic Acute suppurative sialadenitis ♣ TX: like TB infection
Mycobacterial infection of cervical LNs
Non-TB mycobacteria • Common in soil, water, food • MC in kids <5 yo • Fail Abx therapy • Violaceous hue characteristic • FNA has risk of fistula formation and cultures often negative • TX: Clarithromycin
Bartonella in Sialadenitis
♣ Cat scratch disease
♣ Local infection of scratch followed 1-2 weeks later by LAD
• LAD can progress over 1-2 weeks and last 2-3 months
• Watch for abscess
TX: OBs unless severe. Rifampin, erythromycin, gentamycin, Cipro all options
Sarcoidosis and salivary gland involvement
6-30% have parotid involvement
swelling can last for years but eventually resolves on its own
- sub category Heerfordt syndrome
Heerfordt syndrome characteristics
Uveitis
Parotid enlargement
Facial paralysis
-Corticosteroids effective acutely, esp for facial paralysis
Sjogren’s: general features
♣ Xerostomia, dry eyes, salivary gland enlargement
♣ ~1million people in US dx w/ 2-4x affected. Male:Female 9:1
♣ B- and T- cell mediated damaging exocrine glands
• Histo: focal dense lymphocytic infiltration. T cells dominate
• 44x higher risk of lymphoma
Primary vs secondary Sjogrens
♣ 1’ affects exocrine glands alone
♣ 2’ has superimposed autoimmune d/o
Sjogren’s treatment
♣ Tx: symptomatic w/ sialogogues and prevention of dental problems
• Sialologues
♦ Lemon juice
♦ Pilocarpine (muscarinic-cholinergic agonist)
♦ Cevimeline
• Artificial saliva
• Fluoride tx
Sjogren’s Dx
SSA/Ro, SSB/La. La antibody much more specific
These are not always positive
Other tests for dx
Schirmer’s tear test
Salivary flow rate
Lip biopsy of minor salivary gland looking for lymphocytic invasion
Chronic Sialadenitis: features
♣ Parotid MC involved
♣ Destroys the duct
♣ Symp often exacerbated by eating
Precipitating events: stasis, obstruction, decreased flow
Chronic sialadenitis: Presentation
• Recurrent painful swelling of gland(s)
• Asymmetric, firm, occasionally tender glands
• Gland massage typically reveals decreased output
Saliva Consistency may be more tenacious
Worsen with eating
Chronic sialadenitis: TX
• Treat cause if possible • Symptomatically • Abx during acute flares • If these fail ♦ Papillary dilation +/- sialodochoplasty ♦ Steroid injection ♦ Dilation of ductal strictures ♦ Ductal ligation to promote gland atrophy ♦ Surgical excision ♦ Sialoendoscopy
Juvenile Recurrent Parotitis features
¬ 2nd MC salivary gland disorder in kids
¬ Recurrent, nonobstructive, nonsuppurative swelling of unilateral or BL parotid glands
¬ Seen in infancy-12 y/o, most cases stop after puberty
¬ Flare ups require
♣ Intense antibiotics, analgesics and hospital admissions
♣ Unpredictable disease pattern
Idiopathic