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199 Cards in this Set
Describe the embryologic derivations of the Ethmoturbinals (appear in 8th week gestation)
A: 1st ethmoturbinal, Ascending portion – Agger nasiA: 1st ethmoturbinal, Descending portion – Uncinate processA: 2nd ethmoturbinal – Bulla ethmoidalisA: 3rd ethmoturbinal – Middle turbinateA: 4th ethmoturbinal – Superior turbinateA: 5-6th ET: Usually fuse and degenerate, but occasionally can form a Supreme turbinate3: Maxilloturbinal – Arise inferiorly, eventually becomes theInferior turbinate
Development of the Maxillary sinus
A: Begins at the 10th week of gestation, along with the hiatus semilunarisA: Present at birth, conspicuous growth by 3 years, second sinus to fully developA: Inferior expansion starts with permanent dentition (7-8 years, overlies the 2nd bicuspid to 2nd molar)A: Reaches adult si volume up to 15 cc3: Remember “10 = 3 + 7”
Development of the Ethmoids sinus
A: Begins at the 14th week of gestationA: Present at birth, first sinus to fully developA: Pneumatization begins significantly at 3-7 years, reaches adult form by 12-14 years, with ~14 cells (2-3 cc)3: Remember “14”
Development of the Sphenoid sinus
A: Begins during the 3rd monthA: Later becomes the Ossiculum of B third sinus to fully developA: Does not pneumatize and become clinically significant until 4-5 yearsA: Growth complete by midadolescence, variable pneumatization3: Remember “3-4-5”
Development of the Frontal sinus
A: Last sinus to fully developA: Not present at birth, begins growth in the 3rd-5th year, and continues into adolescenceA: Pneumatiza volume up to 7 5-10% are atretic3: Remember “3-5 years”
Name the Plain Film projections useful for each Sinus
A: Frontal – Lateral and CaldwellA: Ethmoid – Lateral and CaldwellA: Maxillary – WatersA: Sphenoid – Lateral and Submentovertex
Describe the Mucociliary flow in the frontal sinus
A: Medial to the ostium – Flows superiorly then laterally along the roofA: Lateral to the ostium – Flow medially and inferiorly toward the ostium
Six bones of the Nasal Septum
A: Perpendicular plate of EthmoidA: VomerA: Maxilla – Anterior nasal spine and Maxillary crestA: Palatine bone – Maxillary crestA: SphenoidA: Nasal bones (included in Schuenke)
Define Agger nasi cell
A: Product of 1st ethmoturbinal, found superior, lateral & anterior to attachment of
can also refer to the anteriormost ethmoid cell, anterior to the frontal recessA: Boundaries are frontal process of maxilla anteriorly, nasal bones anterolaterally, frontal recess superiorly, lacrimal bone inferolaterally, uncinate process inferomedially
Define Suprabullar recess
A: Air cell space left between the ethmoid bulla and the fovea ethmoidalis when the bulla does not extend up to the fovea
Define Sinus Lateralis/Retrobullar Recess
A: Variable air space found posterior and superior to the ethmoid bulla, in the anterior ethmoid regionA: Boundaries are the ethmoid roof superiorly, lamina papyracea laterally, vertical portion of the basal lamella posteriorly
Define Terminal Sinus/Recessus Terminalis
A: Superior boundary of the ethmoid infundibulum when the uncinate process terminates in the lamina papyracea (80%); the frontal recess drains medial to the uncinate process in this instance
Define Haller cell
A: An infraorbital ethmoid cell, pneumatizes into the maxilla
Define Onodi cell
A: A sphenoethmoidal cell, a posterior ethmoid air cell pneumatizing into the sphenoid
Keros classification of lateral cribriform plate lamella length/olfactory fossa depth
A: Type 1 – Cribriform plate 1-3 mm below foveaA: Type 2 – Cribriform plate 4-7 mm below foveaA: Type 3 – Cribriform plate 8-16 mm below fovea (greatest risk of intraoperative CSF leak)A: Type 4 – Asymmetrical
Describe the Kuhn classification of frontal cells
A: Definition – An anterior ethmoid cell above the agger nasi that can obstruct the frontal recess or the frontal sinusA: Type I – Single frontal recess cell above agger nasi but below the floor of the frontal sinusA: Type II – Multiple cells (tier) in frontal recess above agger nasi but below floor of frontal sinusA: Type III – Single cell pneumatizing cephalad into frontal sinusA: Type IV – Single isolated cell completely within the frontal sinus, not located within the frontal recess
What are the six cell types found in olfactory epithelium?
A: Ciliated Bipolar receptor cells – Increase surface area, lack dynein arms and do not beatA: Sustentacular cells – Microvilli, insulate bipolar cells, deactivate odorants, protect epithelium from foreign agents, regulate mucus compositionA: Microvillar cells – 1/10th as frequent as bipolar cells, may have a receptor function (unknown currently)A: Lining epithelium of Bowman’s glands & ductsA: Globose (light) Basal cellsA: Horizontal (dark) Basal cells3: “Be My Big Sister HoBo!”
Olfactory neuroepithelium histology
A: Pseudostratified columnar epithelium
Describe the histology of the Olfactory Bulb
A: Two layers – Internal and External Plexiform layersA: Synapses form aggregates called GlomeruliA: Three cell types – Mitral, Tufted, and Granular cellsA: Synapses are mostly GABAergic and Dopaminergic3: “My Tough Granny lives in the olfactory bulb, Dopi Grama!”
List the central olfactory connections
A: Olfactory tubercleA: Prepyriform cortexA: Lateral Entorhinal cortexA: Periamygdaloid cortexA: Amygdaloid nucleusA: Nucleus of the Terminal StriaA: Dentate and Semilunate gyri
Describe the olfactory transduction mechanism
A: Odorants are solubilized in mucus, or hydrophobic odorants by Odorant Binding Protein (OBP)A: G-Protein coupled receptors (~1000, 1% of expressed genes)A: Second messenger = cAMP
Three differences between Olfactory and Respiratory epithelium
A: Olfactory epithelium is thicker (60-70 nm) than respiratory epithelium (20-30 nm)A: Olfactory epithelium has cilia that lack dynein armsA: At physiologic flow rates olfactory epithelium gets ~15% of nasal airflow, 50% flows through middle & inferior meati
Describe Foster Kennedy syndrome
A: Ipsilateral anosmia/hyposmiaA: Ipsilateral optic atrophyA: Central/contralateral papilledema3: Due to tumors of the olfactory groove or sphenoid ridge (e.g. meningiomas)
Define Kallmann’s syndrome
A: Transmitted X-linked (Cummings)A: Endocrine anomalies – D Hypogonadotropic hypogonadism (deficiency of hypothalamic GnRH secretion)A: Genito-urinary anomalies – Micropenis, Cryptorchidism,Unilateral renal agenesisA: Anosmia - Agenesis of the olfactory bulbsA: DeafnessA: Midline facial deformities
Define Anosmia
A: Loss of ability to smellA: Can be specific, partial, or total depending on whether certain odors or no odor can be detected, uni or bilateral
Define Hyposmia/Microsmia and Hyperosmia
A: Decreased ability to smell and hypersensitivity to odors, respectively
Define Dysosmia
A: Distorted or perverted smell perception3: Causes (Bailey’s): degenerative-regenerative process (post trauma, URTI), psychosis, aura-like hallucinations from central dysfunction, foul odors (purulence in CRS)
Define Parosmia/Cacosmia
A: Change in the quality of the olfactory cue, particularly of putrefactive odor
Define Phantosmia
A: Odor sensation in the absence of an olfactory stimulus (olfactory hallucination)
Define Olfactory Agnosia
A: Inability to recognize an odor
Two surgical treatment options for Parosmia/Phantosmia
A: Olfactory bulbectomyA: Endoscopic removal of olfactory neuroepithelium
Six Methods of olfactory testing
A: Subjective odorant testing/Detection threshold – Sniffing sticks, 1 minute smell testA: Standardized psychophysical tests – OCM = Odorant Confusion M UPSIT = University of Pennsylvania Smell Identification Test, highly reliableA: Electrophysiologic tests –
OERP = Odor event-related potentials, experimental, identifies brain EEG activity aft far field potentials, cannot loc
“EOG” = Electoolfactogram, electrode placed on olfactory epithelium identifies summated generator potentials of olfact no local anesthe Flase positives in Kallman’s and schizophrenia
Five factors affecting olfactory testing (MASSAM)
A: Mental StateA: Age A: Satiety A: Sex A: Adaptation/Cross-adaptationA: Masking
Classification of Hyposmia/Anosmia (3)
A: Access of odorant changed – ConductiveA: Damage to olfactory nerve & receptors – SensoryA: Damage to central olfactory pathways – Neural
Ddx of Olfactory dysfunction
A: Congenital – Kallman’s, Familial anosmia (AD, premature baldness, vascular headaches)A: Obstructive nasal disease (23%) – Polyps, edema, tumors, nasal deformityA: Idiopathic (21%)A: Postinfectious (19%) – Viral injury to olfactory neuronsA: Head Trauma (15%) – Shearing of filaments, olfactory bulb contusion, CN I is the most commonly damaged CN, followed by VIII, X, and VII ?VIA: Neurologic – Parkinson’s, Alzheimer’s, Multiple SclerosisA: Psychogenic (schizophrenia)A: Toxins/medications (3%) – Smoking, FormalinA: AgingA: Neoplastic – Foster-Kennedy syndromeA: Other
Three reasons for Age-related olfactory changes
A: Cumulative damage to the olfactory epithelium from viral and other insultsA: Ossification/closure of the foramina of the cribriform plateA: Pathologies such as Alzheimer’s and Parkinson’s
Name the 3 main functions, and 6 subfunctions, of the nasal airway
A: Respiration – Warming (37 C), Humidification (85%), and Nasal airflow (which can be altered through airway resistence by congestion & decongestion of the mucosa)A: Protection – Filtration, Mucocilliary clearance, and Immune protectionA: Olfaction – To sense the environment through the specialized & general sensory nerves (olfactory & trigeminal)
Name four mechanisms of Innate immunity in the nose
A: Barrier – Epithelial tight junctionsA: Enzymes/Peptide antibiotics – LocalLactoferrin, Lysozyme, IgAA: Phagocytes – Neutrophils and macrophagesA: PAMP Receptors – Expressed on epithelium and phagocytes, detect Pathogen Associated Molecular Patterns, cause secretion of immune mediators
Describe the Sympathetics Autonomic supply to the nasal mucosa
A: Vasoconstrictor toneA: Preganglionics from sympathetic chain synapse in the Superior Cervical GanglionA: Postganglionics travel with ICA, split off as deep petrosal nerve and joins with greater superficial petrosal nerve to form the vidian nerveA: Pass through the sphenopalatine ganglion without synapsing, into the sphenopalatine nerve, through the foramen and into the nasal cavity
Describe the Parasympathetics Autonomic supply to the nasal mucosa
A: Vasodilation of capacitance & resistance vessels, also mediate nasal secretionA: Preganglionics arise in Superior Salivatory Nucleus, travel in nervus intermedius and branches off a t the geniculate ganglion as the greater superficial petrosal nerve and becomes the vidian nerve, synapses at the Pterygopalatine GanglionA: Postganglionics distributed with sympathetics throughMaxillary trigeminal branches to the nose
Internal Nasal valve & Cross sectional area
A: Extends from caudal end of upper lateral cartilages to anterior end of inferior turbinatesA: Influenced by nasal septum, upper lateral cartilage, pyriform aperture, anterior inferior turbinateA: Cross sectional area 0.73 cm2; 10-15 degrees caucasians3: Nasal valve competency tested with the Cottle maneuver
Discuss Rhinomanometry
A: Measures the resistance to airflow in the nose (transnasal pressure and air flow), but cannot identify specific
3 typesA: Anterior Rhinomanometry – Occlusion of one nostril with an inflatable cuffed pressure sensor at the nasal orifice measures nas nonphysiologic, as all airflow happens through the other unoccluded nostrilA: Posterior Rhinomanometry – Placement of pressure catheter in mouth which can accurately measure nas more physiologic measure of nasal resistance through both nostrils simultaneouslyA: Postnasal (Pernasal) Rhinomanometry – Tube is placed in the posterior nose through one of the nostrils3: Total nasal resistance &0.3 Pa/cm2 usually is symptomatic3: &35% reduction in resistance after decongestion in &35% reduction in resistance infers a structural cause
Discuss Acoustic Rhinometry
A: Analyzes 10 msec sound pulses reflected from the airway, can accurately identify the minimal cross-sectional area (MCA), the location of the MCA, and the cross-sectional area at various distances from the nostrilsA: I-Notch – Isthmus of the internal nasal valve, within 2 cm of nostril, usually narrowest = 0.73 cm2A: C-Notch – anterior inferior Concha, ~3.3 cm from nostrilA: Does not rely on nasal airflow, but cannot measure the effects of narrow regions on airflow dynamics or resistance3: Three areas of nasal resistance – Vestibule (1/3), Valve (1/2-2/3), Turbinated cavity is the rest
Five factors controlling nasal airflow
A: Vasomotor control/Nasal cycleA: Exercise – EpinephrineA: Sex Hormones – Puberty, Menstruation, PregnancyA: Nitric Oxide – Affects Nasal AND Pulmonary blood flow, Ciliary beat frequencyA: Head & body Position
Ten complications of Septoplasty
A: Failure/persistent obstructionA: CSF leakA: SynechiaA: AnosmiaA: HemorrageA: Septal Hematoma/AbscessA: PerforationA: Saddle nose deformityA: Toxic-shock syndromeA: Aspiration
Surgical options for Nasal Valve Obstruction
A: Spreader graftsA: Baten graftsA: Nasal-orbital suspensionA: Valvuloplasty with composite graftA: Columellar strut graft (Bailey p. 331)A: Address other components of the valve – Septum, Turbinate3: Others: Flaring sutures, overlay grafts, lateral suture suspension
Five foramina of maxilla
A: InfraorbitalA: Superior alveolar canal(s)A: Incisive canalA: Maxillary ostiumA: Accessory maxillary ostium
Four broad categories of Rhinitis
A: AllergicA: InfectiousA: StructuralA: Other3: “All Other Infra-Structures”
Name the 13 etiologies of “Other” rhinitis (non-Structural, non-Inflammatory, non-Allergic causes)
A: Compensatory hypertrophic rhinitisA: Non-Airflow rhinitis – Postlaryngectomy, choanal atresia, adenoid hyperplasiaA: Temperature mediatedA: Environmental/Irritative rhinitisA: Gustatory rhinitisA: Endstage vascular atony of chronic allergic or inflammatory rhinitisA: Hormonal – OCP, Puberty, Pregnancy (estrogen effect in 2nd trimester), Menopause, Hypothyroidism, AcromegalyA: Drugs – Antihypertensives, Topicals (cocaine & nasal spray abuse), NSAIDs, ASA, PsychotropicsA: Non-Allergic Rhinitis with Eosinophilia Syndrome (NARES), or Basophilia – Similar to perennial allergic rhinitis, lacks the IgE mediated immunopathologic events, AND &20% eosinophils on nasal smearA: Recumbency rhinitisA: Paradoxic nasal obstruction and nasal cycleA: Emotional causesA: Idiopathic3: “Compensating for Non Temperate Environments by Gustating Endstage Hormonal Drugs through my Nares Renders me a Paradoxically Emotional Idiot!”
Etiology of vasomotor Rhinitis during Pregnancy
A: 20% of pregnancies, usually starts in 2nd trimestersA: Increased Estrogen levels inhibits Acetylcholinesterase activity, leads to increased ACh in parasympathetic ganglia, causes swelling & edema of nasal mucosaA: Treatment – Conservative, saline spray, possible use ofBudesonide (Rhinocort) spray, C no use of decongestants
Define Atrophic Rhinitis
A: Classified as a transformation of the respiratory pseudostratified columnar epithelium to a keritanized squamous epithelium that sloughs off
Ten Granulomatous diseases of the Sinonasal tract
A: Systemic (3) and Infectious (8)A: SporotrichosisA: Blastomycosis (dermatiditis)A: Coccidiomycosis (immitis)A: RhinoscleromaA: Rhinosporidiosis (seeberi)A: TBA: LeprosyA: SyphilisA: SarcoidosisA: Wegener’sA: Histiocytosis X3: “Sporo Blasto Cocci Rhino-Rhino, TB Lepy Syphi, Sarcoid,Wegener’s & Histio”
How to detect Eosinophilia on nasal smears
A: Acquire sample of nasal mucus (wax paper or swab), smear on slideA: Stain with Hansel stain (Eosin & Methylene Blue)A: Positive criteria = &20% eosinophil content, or if Eosinophils,Mast cells & Goblet cells (EMG) are present
Describe the Gell and Coombs Type Hypersensitivity Reactions (ACID)
A: Type I – Immediate IgE (Allergic rhinitis, anaphylaxis, asthma)A: Type II – Cytotoxic IgG or IgM antibody mediatedA: Type III – Immune complex mediated, Ag-Ab-Complement (serum sickness, Arthus reaction)A: Type IV – Delayed type hypersensitivity, T-cell mediated
Discuss the Methods of testing for Atopy
A: Skin tests –
Detect presence of IgE- takes little time to do (~1 hr), but uncomfortable,
generally classified as Epicutaneous (scratch tests and prick puncture tests) or Intracutaneous (single-dilution and multiple dilution intradermal tests);
Negative control is GLYCEROL/saline, and
Positive control is Histamine
Scratch tests – Neither sensitive nor reproducible
Prick tests – Not sensitive for low levels of atopy
Intradermal testing – More sensitive & reproducible
Serial Dilution Endpoint testing/ Skin Endpoint Titration – Intradermal test, determines more specific levels of atopy, used to determine immunotherapy concentrationsA: Direct measurement of Allergen-specific IgE serumincubated with known A excess serum washed off, and residual complexes incubated with anti-IgE More specific but less sensitive cf. skin tests, takes longer to do (days) RadioAllergoSorbent Test (RAST) – Radioactive marker Enzyme-Linked ImmunoAssay (ELISA) – Fluorescent marker
Describe the ARIA Classification of Allergic Rhinitis
A: Intermittent – &4 days/week OR &4 weeks/yearA: Persistent – &4 days/week AND &4 weeks/yearA: Mild – Normal sleep, no impairment in ADLs/Work/School, and no troublesome SymptomsA: Moderate-Severe – Any of Abnormal sleep, impairment inADLs/Work/School, or troublesome Symptoms
Three approaches to Treatment of Allergy
A: Avoidance – Mattress/pillow covers are be removing carpets also usefulA: Pharmacotherapy –Nasal Steroid (1st line therapy, spray or inferior turbinate injections), Antihistamines, LeukotrieneReceptor Antagonists, Cromolyn (topical mast cell stabilizer, decreases influx of calcium), Decongestants (topical or systemic),Systemic steroids (short course)A: Immunotherapy
List 3 First generation H1 Antihistamines
A: Diphenhydramine/BenadrylA: Hydroxizine/AtaraxA: Chlorpheneramine/Chlortripolon3: S “Diphen-Hydroxy-Chlorphen”
List 4 Second generation H1 Antihistamines
A: Loratidine/ClaritinA: Desloratidine/Aerius (3rd gen?)A: Certirizine/ReactineA: Fexofenadine/Allegra (3rd gen?)3: “Lora-Deslora-Certri-Fexo”
Six effects of corticosteroids in Allergic Rhinosinusitis
A: Decreased Arachidonic Acid metabolism (PG/LT/TX) A: Decreased secretion of Mediators of inflammatory cellProliferationA: Decreased Influx of Eosinophils, Basophils & T-lymphocytes into the nasal epitheliumA: Decreased Capillary Permeability and promotesVasoconstrictionA: Decreased glandular response to ACTH,Decreases Mucus productionA: Stabilize Lysosomal membranesA: decreased Migratory inhibitory factor
List 4 Intranasal corticosteroids
A: Mometasome/NasonexA: Fluticasone/Flonase AND AvamysA: Triamcinolone/NasacortA: Budesonide/Rhinocort AND PulmicortA: Omnaris/ciclesonide
Ten Complications and Contraindications of Steroid sprays
A: HypersensitivityA: Atrophic rhinitisA: EpistaxisA: Septal perforationA: GlaucomaA: CataractsA: Ocular herpesA: Systemic fungal infectionsA: TBA: Adrenal suppression
Describe the Mygind, Ragan & Moffett positionsNasal drop bioavailablity is enhanced by head position
A: Improves efficacy of nasal steroid application (controversial)A: Mygind’s position (a)
- Administration of nasal drops in a head back supine position, followed by a series of head turnsA: Ragan position (b)- Involves the patient lying on one side with the head touching the bed or floor surface, while the drops are instilled in the inferior nostrilA: Moffett position (Mecca) (c)- The patient kneels and leans forward with forehead to the ground and administers drops in nostrils
Ten causes of Septal Perforation
A: TraumaA: SurgeryA: Cocaine abuseA: Septal hematoma/abscessA: HHTA: Wegener’sA: LymphomaA: SyphilisA: TBA: Chrome workersA: Bilateral AgNO3 cauterization
Ten indications for Immunotherapy in allergic rhinitis include symptoms of allergy after natural exposure to aeroallergens and evidence of clinically relevant specific IgE, AND…
A: Poor response to Avoidance measuresA: Allergens not easily avoidedA: Poor response to PharmacotherapyA: Unacceptable Adverse Effects of medicationsA: Severe symptomatology, persisting for &1 seasonA: Coexisting allergic rhinitis and asthmaA: Possible Prevention of asthma in childrenA: Patient Wishes to reduce/avoid long-term pharmacotherapy and costA: Motivated patients willing to undergo a program that may last up to 5 years
Administration & Mechanism of Action of Immunotherapy
A: Parenteral administration of antigens identified on appropriate in vivo or in vitro testsA: Stimulate formation of allergen-specific IgG4 blocking antibodies which will compete with IgE for binding sites on Mast cells or BasophilsA: Decreases IgE and reduces the seasonal rise of IgEA: Changes CD4+ cells from Th2 to Th1 phenotypeA: Typically twice a week until a response is noted, then q1 week x 1 year, q2 weeks x 2 years, q3 weekly x 3 years
Describe the Skin Endpoint Titration technique and results
A: 0.01 mL injected – Wheel response of 5 mm normal with controlA: Induration (not erythema) is measured, serial increase by 2 mm is the endpoint titration. Recall that need a confirmatory wheel of greater than 2 mm to confirm previous wheel (which also grew by at least 2 mm)
Three abnormal wheeling patterns on Skin Endpoint Titration
A: FlashDay 1 – 5-5-5-13-18-21Day 2 – 5-5-5-5-7-9-11A: Plateau – 7-7-9-9-11-11Confirmatory here is fifth injection with fourth injection the SETA: Hourglass – 9-7-5-5-7-9-11
Six factors influencing Skin Endpoint Titration
A: AgeA: AntihistaminesA: Skin reactivity (eg to trauma, Dermatographia)A: Food allergensA: Increased Allergen exposure – Greater response during allergic seasonA: Volume injected
Condition of positive Skin Endpoint Titration with negative control solution
A: Dermatographia3: Can do RAST testing for these patients (not affected by antihistamines)
The 3 Pollen seasons for seasonal allergens
A: Trees – SpringA: Grass – summerA: Weeds – Fall
List the 4 types of Perennial Allergens
A: Animal DanderA: Dust mite (#1)A: Cockroach allergensA: Mold (notes say only outdoor, not black mold?)
Most common pollen, mold, and perennial allergens
A: Pollen – Short RagweedA: Mold – AlternariaA: Perennial –Dust Mite (Dermatophagoides spp)
indications for use of in-vitro allergy testing include
A: Impracticality of skin testing due to Skin disorder, Drug inhibition or Uncooperative patientsA: Clarification of Bizarre or Borderline results from skin testingA: Prevention of systemic reactions in patients with a prior history of or suspected Anaphylactic reactions, Asthma, or when testing for Stinging hypersensitivityA: Convenience of in vitro testing3: “Impractical Clarifications Prevent Convenience”
Three differences between mucosa of nose and sinuses
A: Ciliated cells more concentrated at the ostiaA: Increased number of goblet cells present in the noseA: (No olfactory neuroepithelium in the sinuses)
Seven etiologic factors for Nasal Polyps
A: Chronic infectionA: Allergy, including FungalA: Samter’s triadA: Cystic fibrosisA: Nasal mastocytosis (increased mast cells in nasal mucosa)A: Kartegener’s syndromeA: Young’s syndrome (bronchiectasis, rhinosinusitis and reduced fertility)
Define Samter’s triad
A: Nasal polyposis, asthma, and ASA sensitivityA: Thought to block oxida anti-inflammatory actions due to blockage of c polyp formation influenced by stimulation of 5-lipoxygenase, which causes leukotriene overproduction
Not including polyps, what are the 4 most common benign nasal cavity lesions in order of frequency? (OHPA!)
A: Osteoma (most commonly in the frontal sinus)A: HemangiomaA: PapillomaA: Angiofibroma
Discuss Osteoma
A: Most common tumor of the paranasal sinusesA: Clinical – Males affected 3:1; R/O Gardner’s syndrome (with soft tissue tumors/cysts, and colonic polyps) because 100% risk of colorectal cancer by age 40A: Causes – Developmental (at the junction of membranous frontal bone and endochondral ethmoid bone), but can also be Tramatic, or Infectious (osteitis)A: Histopathology – Eburnated (dense), Mature (cancellous), orMixedA: Types (FEMS) – Frontoethmoidal (95%) & Frontal (80%) &Ethmoid (25%) & Maxillary & SphenoidA: Complications – Sinusitis (28%), Orbital, or IntracranialA: Treatment – Complete removal, only if symptomatic
Discuss Ossifying Fibroma
A: Can be aggressive & locally destructiveA: Osteoid rimmed by osteoblasts forming lamellar boneA: Round or oval, eggshell rims, central translucencyA: Treatment – Complete removal
Discuss Schneiderian papilloma
A: Definition – Proliferation of squamous epithelium through fingerlike projections into underlying stromaA: Ddx – Benign vs. Malignant, Epithelial vs. Non-epithelial tumorsA: Diagnosis – BiopsyA: Causes – HPV 6 & 11 suspected (inhibit p53)A: Clinical – White, males 3:1, 5th-7 Nasal obstruction(87%), rhinorrhea, facial pain/pressure, epistaxis, frontal headaches, Exophytic, fleshy, sessile vs. pedunculated, bony destruction/erosion common, tendency to recurA: Complications – Recurrence, Malignant change (~10%, lateral wall & septal)A: Types – Inverting (50%, lateral wall), Fungiform (47%, septal), Cylindrical/Oncocytic (3%)A: Tests – FOB scope, CT, MRI (iso/hypo on T1, enhance with gad, hyperintense on T2, convoluted cerebriform pattern), BiopsyA: Treatment – Total surgical removal with medial maxillectomy, either via Lateral rhinotomy or Transnasal/ESS approach
Krause staging for Schneiderian inverting papilloma
A: T1 – Limited to nasal cavityA: T2 – Extension ethmoids and/or to medial wall of maxillary sinusA: T3 – Extension to sup/lat/inf/ant/posterior wall of maxillary sinus and/or frontal or sphenoid sinusA: T4 – Extension outside the nasal cavity and sinuses and/or malignancy
Eleven limits of Endoscopic Resection of Sinonasal tumors
A: Massive Dural/Intradural extensionA: Massive Skull Base erosionA: Frontal sinus extensionA: Nasal pyramid extensionA: Intraorbital extensionA: Lacrimal tract extensionA: Maxillary wall involvement (except medial)A: Nasopharyngeal extensionA: Hard palate extensionA: Abundant scar tissue from previous surgeryA: Associated Squamous cell carcinoma3: Contraindications to exclusive endoscopic technique in Sinonasal benign tumors (Nicolai & Castelnuovo):(1) Massive involvement of the frontal sinus and/or of a supraorbital cell(2) Intradural extension or orbital extension(3) Concomitant presence of a malignancy involving critical areas(4) Presence of abundant scar tissue from previous surgery.
Five types of nasopharyngeal cysts
A: Rathke’s pouch cyst – Remnant of invaginated ectoderm that forms the anterior pituitary gland, anterior to located high in nasopharynx near sp ciliated respiratory epitheliumA: Tornwaldt’s cyst – Remnant of notochord, inferior to Rathke’ filled wit ciliated respiratory epithelium (high signal intensity on both T1- and T2-weighted images)A: Dermoid cyst – Benign developmental cyst derived from e stratified squamous epithelium with adnexal structuresA: Intraadenoidal – From median pharyngeal recess, opens onto adenoid bedA: Extraadenoidal – Deep within pharyngobasilar fascia, remnant of
usual findings are a cuff of granulation tissue rostral to the pharyngeal tubercle
Describe the 4 cell types making up the nasal epithelium
A: Pseudostratified Ciliated Columnar epithelium – ~50 cilia per cell beating, ~12/second at physiologic temperature, moves mucus 3-25 mm/minuteA: Pseudostratified Nonciliated Columnar epithelium – Possess microvilli that expand the surface area of the epitheliumA: Goblet cellsA: Basal cells3: Other cell types – Stratified squamous epithelium in nasal vestibule, and olfactory epithelium found along roof of nose
Two Mucous layers in upper resp tract, and function of each
A: Sol layer – Thin periciliary layer which allow produced by microvilliA: Gel layer – Thick layer of mucoglycoproteins in which ci produced by goblet cells and submucosal glands, propelled by (antibacterial and clearance of foreign particles?)
Three stages of sphenoid sinus pneumatization
A: Sellar (86%)A: Presellar (11%)A: Conchal (3%)3: Pneumatization starts between 5 & 7 years of age, complete by20-25 years
Incidental findings of sphenoid sinusitis on imaging – what should you consider?
A: Optic complications – 25% of patients with sphenoid sinusitis have neurophthalmic dysfunction
Five factors present in nasal secretions which fight infection
A: IgAA: IgGA: LysozymeA: LactoferrinA: Interferon
What 10 local factors influence nasal ciliary motility?
A: AllergyA: Rhinitis medicamentosa (chronic abuse)A: Infection (viral, bacterial)A: Primary ciliary abnormalitiesA: Temperatures &18 CA: Humidity &50%A: Hypertonic or hypotonic solutionsA: DehydrationA: Excessive acidic or basic environment (optimal ciliary function @ pH 7.0)A: Mucosal to mucosal surface contact (coapting)
Five clinical features of Kartagener’s (immotile cilia) syndrome, abnormalities in cilia?
A: SinusitisA: Bronchiectasis (chronic cough)A: Situs inversus & dextrocardiaA: Otitis mediaA: Male Infertility (immotile sperm)3: Autosomal recessive inherited lack of Dynein arms in A-tubules (9+2 microtubule structure)
Six possible findings in Immotile cilia
A: Lack of Dynein armsA: Lack of central core structuresA: Radial spoke defectA: Microtubule translocationA: Microtubule altered in lengthA: Ciliary aplasia * Left, Normal cilium, Right, the absence of outer and inner dynein arms in a patient with primary ciliary dyskinesia
What are the associations between CRS, Polyps (NP), and Asthma?
A: 20% of CRS have NPA: 20% of CRS have AsthmaA: 40% of FESS have AsthmaA: 50% of NP have Asthma (35% of which have Samter’s triad)A: 10% of NP have Samter’s triad
Seven areas to evaluate in preoperative CT scan
A: Frontal sinus/recess and Agger nasiA: Skull base (Keros classification)A: Anterior ethmoid arteryA: Lamina papyracea/Uncinate processA: Maxillary sinuses (Haller cells)A: Vertical height of the posterior ethmoidA: Sphenoid sinus (Onodi cells, ON, ICA)
General method of subclassifying Complications in Rhinology
A: VascularA: Nerve damageA: Facial swelling or ecchymosisA: OrbitalA: IntracranialA: Packing related3: “Very Nice Face or Brain Please!”
Six risk factors for complications in FESS
A: General anesthesia – lack of patient feedbackA: Extent of diseaseA: Amount of BleedingA: Left orbit for a right-handed surgeonA: Revision FESSA: Expertise of the surgeon3: “this General Extent of Bleeding is Right for a Revision Expert”
Major FESS complications
A: Intracranial (7) – CSF leak, Tension pneumocephalus,Meningitis, Abscess, Hemorrhage, Encephalocele, Direct brain injuryA: Orbital (5) – NLD injury, Enophthalmos, Diplopia (medial rectus injury), Hematoma, Blindness (optic nerve injury)A: Bleeding (4) – Damage to Anterior ethmoidal, Sphenopalatine, or Inter any requirement of a transfusionA: Other – Anosmia, Asthma exacerbation, Toxic Shock, Death
Minor FESS complications
A: Intracranial – CSF leakA: Orbital – Emphysema, Fat herniation, EcchymosisA: Bleeding – Small amount, not requiring transfusionA: Other – Hyposmia, mild Asthma exacerbation, MRSA infection, Hypesthesia of the infraorbital nerve or teeth, Synechiae, Atrophic rhinitis, Osteitis
Seven predictors of poor FESS outcome
A: Smoking!A: AsthmaA: PolypsA: ASA sensitivityA: Fungal diseaseA: Extensive disease (CT)A: Previous surgery
Seven Indications for Image Guided Surgery according to the AAO-HNS
A: Revision surgeryA: Distorted anatomyA: Extensive NPA: Disease in Frontal, Posterior Ethmoid, or SphenoidA: Disease abutting the Skull base, Orbit, Optic nerve or carotidA: CSF rhinorrhea or skull base defectA: Benign and malignant sino-nasal neoplasms
Define Myospherulosis
A: Foreign body reaction to the petroleum ointment used in packing
Define the Holman-Miller sign
A: Anterior bowing of posterior maxillary sinus wallA: Indicates JNA invasion of pterygopalatine fossa
Biopsy of which 4 nasal masses are at significant risk of hemorrhage?
A: JNAA: HemangiomaA: HemangiopericytomaA: AV malformations
Potential complications of radiotherapy for management of JNA?
A: Failure of treatmentA: Induction of malignancyA: Failure of facial growth centersA: Cataract formation3: Radiotherapy used in past successfully for primary therapy, recurrences, inoperable tumors
Difference between a Mucocele and a Mucus Retention Cyst
A: Mucocele – A chronic, cystic lesion of the paranasal sinuseslined with pseudostratified or low columnar epithelium, containing occ presents radiologically with complete sinus opacification, with rounded thin blocked sinusA: Mucus retention cyst – Retained mucus within a blocked goblet cell, lined by sinus mucosa rather than a true epithelium3: These definitions do not apply to salivary pathology, where only the mucus retention cyst is the true cyst, and mucocele refers to mucus extravasation
Ddx of small round cells on nasal biopsy (MRS SLEEPI)
A: MelanomaA: RhabdomyosarcomaA: Small cell neuroendocrine tumor (Carcinoid?)A: Sinonasal undifferentiated carcinoma (SNUC)A: LymphomaA: EsthesioneuroblastomaA: Ewing’s sarcoma/PNET (Carcinoid?)A: PlasmacytomaA: Immature teratoma
60 year old female with blocked nose, and nasopharyngeal mass. Biopsy is LCA positive and cytokeratin negative. What is this? What is ruled out?
A: LymphomaA: SCC (NPC) ruled out by negativity of Cytokeratin
Four histologic and clinical differences of T-cell lymphoma and Wegener’s granulomatosis of the nose
A: Wegener’s has diffu Lymphoma lesions are Focal, localized & explosiveA: Wegener’s has a Small & Medium vessel V Lymphoma has a polymorphic lymphoid infiltrate with Angiocentric & Angioinvasive featuresA: Wegener’s has an inflamma Lymphoma has am primarily lymphocytic infiltrateA: Otologic, Tracheal, Renal involvement rare in lymphoma
Ddx of Fibroosseous nasal lesions (4)
A: OsteomaA: OsteochondromaA: Ossifying fibromaA: Fibrous dysplasia
Discuss Hemangiopericytoma* Staghorn-shaped capillary spaces lined by plump pericytes (arrows)
A: Originates from the capillary Pericyte of ZimmermannA: Occurs wherever t MSK and Skin predilectionA: Histologically consist of packed ovoid/spindle cells, and staghorn vessels displaying perivascular hyalinizationA: Unpredictable, considered Malignant & infiltrativeA: Treatment – Wide surgical excision, may require preo Radiotherapy generally for palliative cases, although adjuvant XRT has been recommended for high-grade features Neck dissection not necessary as lymp 5-year survival rate near 70%, and distant metastases usually portend recurrence at the primary site
Two Absolute Contraindications to IV iodinated contrast for CT
A: Previous adverse reactionA: Severe renal insufficiency (esp. in Multiple Myeloma, DM,Nephrotoxic meds)
Seven Relative Contraindications to IV iodinated contrast for CT
A: Advanced ageA: AsthmaA: AtopyA: Beta-blockersA: Cardiac diseaseA: DehydrationA: Mild renal insufficiencyA: Planned thyroid radio-ablation
Precautions for patients on Metformin receiving IV contrast
A: Stop Metformin for 48 hrs post-CTA: Check renal function prior to resumption3: Causes ARF with lactic acidosis
Four benefits of MRI for sinuses
A: Differentiation of soft tissue involvementA: Differentiation of soft tissue from fluidsA: Multiplanar capabilities with minimal patient movementA: No exposure to radiation
Three limitations of MRI for sinuses
A: Poor visualization of bony involvementA: Increased cost compared to CT scanA: Limitations due to metal
Five general Advantages of MRI
A: Better soft tissue definition than CTA: Multiplanar capabilityA: Clear delineation of arteries, veins, major cranial nervesA: Absence of ionizing radiationA: Absence of beam-hardening artifacts from dental implants
Six General Disadvantages of MRI
A: Prolonged data collection timesA: Higher sensitivity to patient motionA: Contraindications – Pacemakers, certain Implants, Metallic foreign bodiesA: Inferior bony detailA: Claustrophobia may prohibit examinationA: Higher equipment cost & exam cost
List 5 absolute and 4 relative Contraindications to MRI
A: Pacemakers (most common) and Pacer-wiresA: Swan-Gantz catheterA: Cochlear or Brainstem ImplantsA: Ocular (do xray) or Metallic foreign bodiesA: Certain aneurysm clipsA: Cardiac valve (relative, usually safe)A: Vascular clips (relative, usually safe)A: Orthopedic prosthesis (relative, usually safe)A: Claustrophobia (relative, premedicate)
CT & MRI findings for Mycetoma
A: Heterogeneous (double density) on CTA: Hypointense on T1/T2
CT & MRI findings for Allergic Mucin
A: Hyperintense/heterogenous on CTA: Hypointense on T1/T2 – lack of water
CT & MRI findings for Polyps
A: Low density on CTA: Hypointense on T1, Hyperintense on T2
CT & MRI findings for Mucocele
A: Typically hypointense on CTA: Variable pattern,
Hyperintense on T1 (when dehydrated), Hyperintense secretions on T2 with hypointense central areaA: T1 w GAD: Generally does NOT enhance, but if enhancing will do so at periphery3: Som and Curtin patterns of MRI signal intensity of mucous in CRS (Cummings): (1) Protein concentration & 9% → Hypointense on T1 and hyperintense on T2(2) Protein concentration of 20-25% → Hyperintense on T1 and hyperintense on T2(3) Protein concentration of 25-30% → Hyperintense on T1 and hypointense on T2(4) Protein concentration & 30% → Hypointense on T1 and T2
CT & MRI findings for Fibrous Dysplasia
A: Featureless trabecular (ground glass) pattern on CTA: Hypo to Hyperintense on T1, T2 homogenous (like air)3: Histology: Marrow-space replaced by irregular spindle-shaped mesenchymal cells forming whorled patterns and poorly developed bony trabecular with lack of osteoblastic rimming.
Describe the 6 structures involved in the Ostiomeatal Unit
A: Uncinate processA: Ethmoid Bulla and anterior ethmoid ostiaA: Ethmoid InfundibulumA: Maxillary sinus ostiumA: Frontal recessA: Middle turbinate
Etiologic factors for the development of sinusitis, classified into 3 main categories
A: Infectious – Viral, Bacterial, FungalA: Immune – Congenital, Acquired, AllergicA: Local – Craniofacial anomalies (Choanal atresia, VPI, Cleft palate), Trauma, Surgery, Dental, Ciliary, Anatomic
Seven Anatomic variations influencing incidence of sinusitis
A: Septal deviation and spurA: Conchal bullosaA: Paradoxical middle turbinate (Lateral convexity)A: Prominent ethmoidal bullaA: Pneumatization or deviation of the uncinate plateA: Prominent agger nasi cellsA: Haller cells (Infraorbital ethmoids)
Eight Congenital immune deficienciesA: Selective antibody deficiencies – IgA, IgG (IgG3 most common in RARS)
A: Common Variable ImmunodeficiencyA: Severe Combined ImmunodeficiencyA: X-linked AgammaglobulinemiaA: Complement deficiencyA: Hyper IgMA: Hyper IgE/Job syndromeA: Ataxia-TelangiectasiaA: Wiskott-Aldrich syndromeA: Digeorge syndrome
Eight circumstances in which to screen for primary immunodeficiency
A: &8 new ear infections per yearA: &2 serious sinusitis per yearA: &2 pneumonias per year, or bonchiectasisA: &2 months on antibiotics without improvement, or patient not responding to treatment as expectedA: Recurrent deep skin or organ abscessesA: Persistent thrush after age 1A: Failure to thriveA: Family history of PIDA: Any patient with recurrent, unusual, severe infections
Primary immunodeficiency screening workup (10)
A: CBC and DifferentialA: T and B cell subsetsA: T-cell stimulation tests – for candidaA: IgM/A/G/E, with albumin & TPA: IgG subsetsA: Specific antibodies – if titers low, Vaccine responseA: C3, C4, CH50A: Special tests – Phagocytic tests for CGD
Three important factors for normal nasal function
A: Ostial patencyA: Mucociliary functionA: Quantity/quality of nasal secretions
Timeframe of Rhinosinusitis
A: Acute – 7-10d →&4 weeks (symptom-free interval if Recurrent)A: Subacute – 4-12 weeks (not used much anymore, can be grouped with acute or recurrent acute)A: Chronic – &8-12 weeks
Six Major signs/symptoms of Rhinosinusitis
A: Nasal obstructionA: Nasal discharge/PNDA: Facial pain/pressureA: Hyposmia/AnosmiaA: Purulence on examinationA: Fever (only in ARS)
Seven Minor signs/symptoms of Rhinosinusitis (ABCDEFF)
A: headAcheA: Bad breath (Halitosis)A: CoughA: Dental painA: Ear pain/pressure/fullnessA: FatigueA: Fever
EPOS 2007 guidelines for diagnosis of Rhinosinusitis
A: Inflammation of the nose and sinuses with 2 or more symptoms, one of which is either nasal congestion, obstruction, or anterior or posterior nasal discharge, AND +/-A: Facial pressure/painA: Hyposmia/AnosmiaAND EITHERA: Endoscopic finding of polyps, middle meatal edema, mucosal obstructionA: CT evidence of mucosal changes in the OMC or sinuses
The 2003 Task Force criteria for the Diagnosis of Chronic Rhinosinusitis
A: Duration &12 weeks AND EITHER OF…A: Discolored discharge, polyp, polypoid swelling on anterior rhinoscopy or endoscopyA: Edema/erythema of the MM on endoscopyA: Edema/erythema/granulation in the nasal cavity, but if somewhere else than the MM, imaging is requiredA: Imaging confirmation (plain films or CT)
Describe the Lund-Mackay CT Staging system
A: Frontal sinus R & LA: Maxillary sinus R & LA: Anterior Ethmoid R & LA: Posterior Ethmoid R & LA: Sphenoid sinus R & LA: OMC R & L3: Scoring is 0 = clear, 1 = partial opacification, and 2 = except for the OMC which is 0 = clear, and 2 = occluded, total score is 24.
Six types of Fungal sinusitis classification
A: Invasive:
Acute/Fulminant invasive
Immunocompromised pts
Fungi: Mucorales order (Rhizopus, Rhizomucor, Absidia, Mucor) , Aspergillus fumigatus
Tx: IV ampho b 1mg/kg/day (lipid based is more expensive, less nephrotoxic, can maintain higher doses), voriconazole or itraconazole if not mucor + ampho b nasal rises + aggressive surgical debridement + optimize immune status
Chronic/Indolent invasive
Limited or no immunocompromise
Fungi same as acute but Aspergillus fumigatus more common (sources vary)
Granulomatous invasive
Limited or no immunocompromise
Aspergillus flavus
In Sudan areaA: Non-invasive:
Allergic fungal – CRS with eosinophilic polyps can be divided into AFRS/EFS/EMRS/ECRS based on fungal cultures and IgE status (see below)
Mycetoma – Fungal ball, Aspergillus fumigatus and dematiaceous fungi most common
Saprophytic fungal infestation: fungus grows on crust and doesn’t involve mucosa* AFRS; allergic fungal RS, EFRS; eosinophilic fungal RS, EMRS; eosinophilic mucin RS, ECRS; eosinophilic CRS
5 major diagnostic criteria for Allergic Fungal Sinusitis (Bent & Kuhn)
A: Testing or history positive for fungal atopy (type I hypersensitivity)A: Nasal polypsA: Eosinophilic mucin with Noninvasive fungal hyphaeA: Positive fungal smearA: CT scan with hyperdense material in sinus cavity and possible sinus wall erosion or expansion of the sinus cavity3: Minor criteria:(1) Asthma(2) Unilateral predominance(3) Radiographic bone erosion(4) Positive fungal culture(5) Charcot Leyden crystals(6) Serum eosinophilia
Four histopathologic findings of Eosinophilic Mucin in fungal sinusitis?
A: EosinophilsA: Charcot-Leyden crystals (byproduct of eosinophil degranulation)A: Fungal elements & HyphaeA: Necrotic inflammatory cellular debris
Kupferberg mucosal staging system for AFS
A: Stage 0 – No edema or Allergic MucinA: Stage I – EdemaA: Stage II – Polypoid edemaA: Stage III – Polyps3: Suffix A – Without Allergic M Suffix B – With AllergicMucin
Two histological findings with Allergic Rhinitis (from inferior turbinate)
A: Increased ratio of columnar epithelium to goblet cellsA: Increased number of eosinophils (&20% of granulocytes is suggestive of inhalant allergy)
What fungi are most commonly seen in allergic fungal sinusitis?
A: AspergillusA: Demitaceous species (ABC) – Alternaria, Bipolaris, Curvularia, Cladosporium, Dreshleria, Exophilia, Fusarium3: UT Southwestern Medical Center in Dallas, Texas study showed Bipolaris is the most common pathogens present, followed by Curvularia, Aspergillus then Alternaria
Characteristics of Fungal Hyphae in Invasive fungal sinusitis
A: Mucor – Broad & ribbonlike (10-15 um), irregular/90 degree branching, order Mucorales in Zygomycetes class, most virulent and common is R more commonly seen in diabetic ketoacidotic patientsA: Aspergillus – Narrow hyphae, regular septations, 45 most virulent & frequent species found in those with invas typically A. fumigatus in North A more commonly seen in immune compromised patients with neutropenia * Aspergillus on Lt, Mucor on Rt
Diabetic patient with poor glycemic control, acute onset sharp R facial pain, opacification of right maxillary sinus w what is dx and what would you see on anterior rhinoscopy?
A: MucormycosisA: Necrosis of nasal mucosa, ischemic infarction, granular seros fungal hyphae may be seenA: Stains – Gomori methenamine silver (GMS), KOH, and PAS
Name 4 genera of Mucormycosis
A: MucorA: RhizomucorA: RhizopusA: Absidia
Etiologic agents in Acute Sinusitis
A: Streptococcus pneumoniaA: Hemophylous influenzaeA: Moraxella catarhallisA: Streptococcus pyogenesA: PeptostreptococcusA: FusobacteriumA: Bacteroides
Etiologic agents in Chronic Sinusitis (CCPG 2011)
A: Main pathogens: S. aureus, Pseudomonas & EnterobacteriaceaeA: Less common: Pneumococcus, H. influenzae, Beta hemolytic streptococci, Coagulase-negative StaphylococciA: Greatly increased role of anaerobes – Peptococcus, Bacteroides,
Peptostreptococcus
Treatment of Acute Rhinosinusitis
A: Watchful waiting for 7 day IF Non-severe/mild pain, fever&38.3 C, followup ensured, able to re-evaluat 5 adjunctive treatments:A: Double dose Mometasone sprayA: Saline irrigations – No iodinated table salt as it inhibits ciliary actionA: Mucolytics – Guaifenesin 1200 mg bid, or N-Acetyl Cysteine600 mg bidA: DecongestantsA: Analgesics3: CPG 2011: Diagnosis requires the presence of ≥ 2 PODS, one of which must be O or D, and- Symptom duration of & 7 days without improvement- Biphasic worsening (better then worse between 5-7 days) or- Purulence for 3-4 days with high fever
Antibiotic therapy for community-acquired bacterial sinusitis (CCPG 2011)
A: Abx + INCS used if: Severe symptoms, mild-mod symptoms with no improvement on INCS in 72 hrsA: First-line:
Amoxicillin
In beta-lactam allergy: TMP/SMX or macrolideA: Second-line:
Amoxicillin/clavulanic acid combination, or quinolones with enhanced gram-positive activity (ie, levofloxacin, moxifloxacin)
For use if
First-line therapy failed (defined as no clinical response within72 hours)
Risk of bacterial resistance is high or
Where consequences of therapy failure are greatest (ie, because of underlying systemic disease)A:
High likelihood of resistance: exposure to antibiotics in the prior 3 months, exposure to daycare, and chronic symptoms.A: Duration of treatment should be 5 to 10 days as recommended by product monographs
Indications for referral of ABRS cases as per CCPG 2011?
o Persistent symptoms of ABRS despite appropriate therapy, or severe ABRS o Treatment failure after extended course of antibiotics o Frequent recurrence (≥4 per year) o Immunocompromised host o Evaluation for immunotherapy of allergic rhinitis o Anatomic defects causing obstruction o Nosocomial infections o Biopsy to rule out fungal infections, granulomatous disease, neoplasms. 3: IN CRS: Referral to a specialist is warranted when a patient Fails ≥ 1 course of maximal medical therapy or
Has ≥ 4 sinus infections/year URGENT consultation w/otolaryngologist is required when a patient: Has severe symptoms of pain/swelling of the sinus areas, or
Is immunosuppressed, or Suspect invasive fungal sinusitis
What if the half-life of azithromycin?
A: 68 hours
Six Indications for Surgical intervention in acute bacterial sinusitis
A: Severe painA: ToxicA: Impending complications of sinusitisA: Nonresponse to medical therapyA: Immunocompromised patientA: &4 infections per year
Five groups of mediators important in CRS and asthma
A: Cells – Eosinophils, Th2 LymphocytesA: Cytokines – Interleukins (IL-1B predominant, also -4, -5, -13),PAF, TNFA: Prostaglandins & Cysteinyl LeukotrienesA: Chemokines – RANTES, EotaxinA: Adhesion Molecules – VCAM, ICAM, ELAM
Seven Histopathologic findings in CRS
A: Eosinophilic and Lymphocytic infiltrationA: Major Basic Protein depositionA: Basement membrane thickeningA: Subepithelial edema/fibrosisA: Goblet cell hyperplasiaA: Mucous hypersecretionA: Submucosal gland formation
What is the management of a frontal sinusitis and brain abscess in 10 year old?
A: CTA: Neurosurgical consultA: Surgical debridement of sinusesA: IV antibiotics with good CSF penetration
What are the frontal veins of Breschet in the frontal bone and what is their significance?
A: Perforating veins connecting the intracranial and extracranial venous draining systemsA: A potential pathway of hematologic spread of infectionA: If not cleared in frontal sinus obliteration, can harbor mucosa and cause mucopyocele formation
Sinusitis pathways of spread
A: Hematogenous spread – Retrograde thrombophlebitis through valveless veins (veins of Breschet)A: Direct extension – Preformed pathways (eg. natural dehiscence of lamina)A: Direct extension – Traumatic/surgical pathways (eg. Traumatic dehiscence of lamina papyracea)A: Direct extension – Osteomyelitis (Pott’s puffy tumor)
Describe Chandler classification of orbital complications in sinusitis
A: Preseptal cellulitisA: Orbital cellulitisA: Subperiosteal abscessA: Orbital abscessA: Cavernous sinus thrombosis
Organisms seen in orbital/periorbital cellulitis
A: H. influenzaeA: S. aureusA: S. pneumoniaeA: S. pyogenesA: Bacteroides speciesA: PeptostreptococcusA: Veionella
Nine indications of the Caldwell Luc procedure
A: Chronic maxillary Sinusitis, or disease refractory to endoscopic surgeryA: Maxillary sinus foreign body, Tumor, Mycetoma, Multi septate Mucocele, or Antrochoanal polypA: Approaches to Pterygomaxillary space (Imax ligation, Vidian neurectomy, biopsy of skull base lesions)A: Repair of Oroantral FistulaA: Repair of TraumaA: Orbital Decompression of Grave’s ophthalmopathy
Six complications of the Caldwell Luc procedure
A: Cheek edema & ecchymosisA: Dysesthesia of infraorbital n. distributionA: EpiphoraA: Oroantral fistulaA: Antral scarringA: Bone thickening
Six indications of External Frontoethmoidectomy
A: Frontoethmoidal mucopyoceleA: Orbital complication of sinusitisA: Revision surgery with absent or distorted landmarksA: CSF leak repairA: Biopsy of Anterior skull base lesion – Frontal, orbital, or ethmoid lesionA: Access to the anterior ethmoid artery
Twelve complications of External Frontoethmoidectomy
A: CSF leakA: Intracranial hemorrhageA: Bleeding/crustingA: Orbital hemorrhageA: Diplopia or blindnessA: TelecanthusA: EpiphoraA: Persistent or Recurrent diseaseA: MucoceleA: Stenosis/Synechiae of Frontal Recess with Frontal sinusitisA: Scarring/Keloid formationA: Forehead dysesthesia
Medial Maxillectomy is the En-bloc resection of what 5 structures?
A: Medial Maxillary sinus wall (middle/inf turbinates)A: Ethmoid sinusesA: Lamina papyraceaA: Medial Orbital floorA: Lacrimal bone
Indication and 4 Contraindications for Medial Maxillectomy
A: Indication – Benign or low grade malignant tumors confined to the lateral nasal wall, maxillary antrum, and/or ethmoid sinusA: Contraindications – Invasive malignancies extending intracranial, to the pterygoid plates, palate, or extensively into the orbit
Six complications of Medial Maxillectomy
A: Facial neuralgia/DysesthesiaA: Epiphora/DacryocystitisA: TelecanthusA: Diplopia (may be transient)A: Nasal collapseA: Mucocele
Major landmarks along the medial orbital wall
A: Blood vessels found along the frontoethmoidal suture, which divides the ACF from the ethmoid sinusesA: Anterior Ethmoid artery ~16 (14-22) mm posterior to the anterior lacrimal crest (maxillolacrimal suture)A: Posterior Ethmoid artery ~10 (10-12) mm posterior to the anterior ethmoid arteryA: Optic nerve ~6 (4-7) mm posterior to the posterior ethmoid artery
Three approaches to a frontal mucocele, advantages & disadvantages of each
A: Lynch frontoethmoidectomy – Ethmoidectomy plus removal of entire frontal sinus floorA: Osteoplastic flap – Advantage = Eradication o Disadvantage = requires coronal or mid-forehead approach, disfiguring, high rate of mucocele recurrenceA: Endoscopic – Advantage = A Disadvantage =Cannot access sinuses to eradicate mucosa, limited access laterally
Six indications for Osteoplastic Flap of the frontal sinus
A: Chronic frontal sinusitis with persistent intractable symptoms, sepsis, or other complications despite previous interventionA: Mucocele with Orbital or Intracranial extensionA: OsteomyelitisA: Frontal sinus tumorA: Frontal sinus fracture with comminuted anterior table or displaced posterior tableA: CSF leak
Four contraindications for Osteoplastic Flap Obliteration of the frontal sinus
A: Hyperpneumatized supraorbital ethmoid cellsA: Fungal sinusitisA: Inverting papilloma or other frontal sinus tumorA: Posterior frontal table or orbital roof dehiscence
Five historical open frontal sinus procedures
A: Reidel – Removal entire floor & anterior w significant cosmetic deformityA: Killian – Combination of Reidel and L removal of floor and anterior wall, retain frontal barA: Lynch – Ethmoidectomy plus removal of entire frontal sinus floor, and part of the lamina papyraceaA: Lothrop/Chaput-Mayer – Superior nasal septum and inner sinus septum taken downA: Osteoplastic Flap – Anterior wall frontal sinus based inferiorly retracted and replaced with periosteum intact
Describe the Draff classification for endoscopic frontal sinus drillout procedures
A: Type I – Removal of obstructing disease inferior to frontal ostium, includes removal of anterosuperior ethmoid cells without indicated for minor pathology, in patient without adverse prognostic risk factors (ASA intolerance, asthma, NP, etc.)A: Type IIa – Extended drainage with ethmoidectomy and resection of the floor of the frontal sinus between the lamina papyracea and
uncapping the eggA: Type IIb – Extended drainage with ethmoidectomy and resection of the floor of the frontal sinus between the lamina papyracea and the nasal septum, anterior to the ventral margin of the olfactory fossaA: Type III – Endonasal median drainage, the extended IIb opening is enlarged by resecting portions of the superior nasal septum in the neighborhood of the frontal sinus floor (diameter should be ~1.5 cm), followed by resection of the
this results in an opening from lamina papyracea to contralateral lamina papyracea3: The AP diameter of the frontal sinus should be ≥8 mm to undergo a Draff III, otherwise an osteoplastic flap should be considered
Ten Surgical approaches to the sphenoid sinus
A: TransantralA: Transpalatal – Ideal for tumors involving the nasopharynx, posterior pharyngeal wall, and choanaeA: Transseptal – Sublabial, Intranasal, External rhinoplastyA: Transethmoidal – Internal, ExternalA: Endoscopic – Transnasal, Transethmoidal, Transantral
Four anterior to posterior bony lamina encountered in ESS
A: Uncinate processA: Ethmoid bullaA: Vertical portion of the basal lamella of the middle turbinateA: Lamella of the Superior turbinate3: Additional answers may include the Supreme turbinate, andAnterior wall of sphenoid sinus
Four bony components of the Medial Orbital Wall
A: Frontal process of the MaxillaA: Lacrimal boneA: Lamina papyracea of the EthmoidA: Sphenoid bone (just anterior to the optic canal)3: Orbital process of palatine bone is also near the apex (more inferior than lateral?)
Which anatomic sinus variation is more common in Asians
A: Sphenoethmoidal/Onodi cells
What are the four sides of Bolger’s parallelogram?
A: Lamina papyraceaA: Skull baseA: Superior turbinateA: Basal lamella of SUPERIOR turbinate
Your postop ESS patient develops a postoperative orbital hematoma. What are your management considerations?
A: Fast (arterial) (15-30 min) vs. slow (venous) hematoma formation (60-90 min); Proptosis, pupil changes, vision loss indications for immediate surgical interventionA: Medical treatment (5)
Urgent Ophthalmology consultation and assess vision
Remove packing and suction at bleeding site
Mannitol 1-2 g/kg in 20% IV infusion (100 g in 500 cc bag) over 20 minutes
Acetazolamide 500 mg IV q4h prn
Timolol 0.5% ophthalmic drops (only if slow bleed)
Steroids (controversial)
Orbital massage (controversial)A: Surgical treatment (4)
Lateral canthotomy/cantholysis
Medial external (Lynch) decompression
Endoscopic decompression3: If anterior or posterior Ethmoid artery is suspected, Kennedy recommends postop CT sinus to R/O concomitant skull base injury
Describe the 7 features of superior orbital fissure syndrome
A: Orbital painA: PhotophobiaA: ProptosisA: OphthalmoplegiaA: Failure of accommodationA: Upper eyelid paralysisA: Forehead paresthesia/hypoesthesia3: Caused by sphenoid sinusitis, neoplasm, Involves CNIII, IV, V1, VI; Differs from Orbital apex syndrome in that CN II usually not involved as it is in its own canal
Discuss Cavernous Sinus Syndrome
A: Cause – Ethmoiditis, 80% mortality rateA: Symptoms – Orbital pain (V1), Proptosis, Photophobia, Ophthalmoplegia (CN III, IV, VI involvement), venous congestion of retina, lids, conjunctivaA: Treatment – Antibiotics, Anticoagulation3: Similar to superior orbital fissure syndrome, except for additional involvement of venous system
Name the 4 structures visible on the walls of the sphenoid sinus (top to bottom)?
A: Optic nerve – Projects into sinus less commonly, ~50%; bone dehiscent in ~4-6%A: Optico-carotid recessA: Internal carotid artery – Medial deflection into lateral wall called the carotid sulcus, present 65-98% bone dehiscent in ~7-22%A: V2A: lateral recess between V2 and vidianA: vidian nerve
Six anatomic relationships of the Sphenoid Ostium
A: 7 cm from the Anterior Nasal SpineA: 30o angle from the floor of the nose (Pasha: most reliable)A: 1-1.5 cm above the upper limit of the choanaA: 1/3 up from the choana to the skull baseA: Adjacent the posterior border of the nasal Septum (2-3 mm)A: Inferomedial to the posterior attachment of the Superior Turbinate on sphenoid face (Parson’s ridge)
Six useful landmarks for Revision ESS
A: Skull baseA: Superior attachment of Middle TurbinateA: Sphenoid sinus ostiumA: Maxillary ostiumA: Roof of maxillary sinusA: Lamina papyracea
Internal carotid artery branches supplying the internal nose
A: Anterior Ethmoid arteryA: Posterior Ethmoid artery3: Branches off the ophthalmic artery, each divides into a medical branch (Little’s area & septum) and a lateral branch (superior & middle turbinates)
External carotid artery branches supplying the internal nose
A: Sphenopalatine artery – Lateral posterior nasal artery (supplies lateral nasal wall), and Septal posterior nasal artery (across anterior sphenoid and along septum up to Little’s area)A: Descending Palatine artery – Splits into lesser and GreaterPalatine arteries (the latter supplies Little’s area in the septum & floor of nose through the Incisive branch)A: Septal branch of Superior Labial artery – Supplies the Septum and AlaA: Pharyngeal branch – Supplies posterior nose & nasopharynx3: All are terminal branches of the internal maxillary artery except the superior labial artery, which is a branch off the facial artery
Describe the Venous drainage of the nose
A: Greater Palatine vein – Posterior Facial vein, into ExternalJugular veinA: Septal and Angular veins – Anterior Facial vein, into InternalJugular veinA: Anterior and Posterior Ethmoidal veins – Ophthalmic vein, toCavernous sinus, into Internal Jugular veinA: Sphenopalatine vein – Maxillary vein, to Cavernous sinus, into Internal Jugular vein
Describe the two nasal vascular arterial plexuses and their blood supply
A: Kiesselbach’s plexus – Little’s area, found on the anterior septum (Anterior ethmoid, Sphenopalatine, Greater palatine, andSuperior labial arteries)A: Woodruff’s plexus (naso-nasopharyngeal plexus) – Venous, located in the posterior lateral nasal wall inferior to the InferiorTurbinate
Management of Epistaxis
A: Non-surgical (5)
Topical decongestion
Cauterization – silver nitrate, electrocautery
Packing – Absorbable vs. nonabsorbable, anterior, posterior, combined, balloon packs
Greater palatine canal injection
Radiologic Embolization of internal maxillary & facial arteriesA: Surgical (4)
Sphenopalatine artery ligation – Transantral vs. Endoscopic
Ethmoid artery ligation – Lynch frontoethmoidectomy approach vs. Endoscopic
Maxillary artery ligation – Transantral
External carotid artery ligation
Name the most important landmark for performing and Endoscopic Sphenopalatine artery ligation
A: The Crista Ethmoidalis, part of the perpendicular process of the Palatine bone
What 2 vessels must be ligated in a transantral maxillary artery ligation to prevent recurrent epistaxis from collaterals?
A: Sphenopalatine arteryA: Descending palatine artery
Complications of posterior nasal packing
A: Airway obstruction & exacerbation of OSAA: DyspneaA: Nasopulmonary reflex – Bronchoconstriction, hypoxemia, apnea, and cardiac dysrhythmiaA: SinusitisA: Otitis mediaA: Toxic shock syndromeA: Septal or alar necrosis
Discuss Osler Weber Rendu syndrome/Hereditary Hemorrhagic Telangiectasia
A: Definition – Autosomal dominant disorder characterized by ectatic vessels of the skin, mucous membranes, and visceraA: Diagnosis – The Curacao criteria, published in 2000, remain the mainstay of HHT clinical diagnosis:
Recurrent, spontaneous nosebleeds
Mucocutaneous telangiectases at characteristic sites (fingertips, lips, oral mucosa, tongue)
Visceral AVMs (gastrointestinal, pulmonary, hepatic, cerebral, or spinal)
Family history (first-degree affected relative)Definite HHT = 3 or 4 criteriaPossible HHT = 2 criteriaUnlikely HHT = 0 or 1 criteriaA: Cause – Mutation in the Endoglin protein, a receptor for TGF beta, which has a role in tissue repair and angiogenesis, leading to the development of abnormal vasculature, chromosome 9A: Clinical – Triad of Telangiectasias, recurrent Epistaxis, and a positive Family Hist may also have pulmonary, GI & CNS bleedsA: Complications – Morbidity and mortality due to multiorgan arteriovenous malformations, and associated hemorrhagesA: Treatment – Manage anemia/ septal dermoplasty for epistaxis, laser, Young’s procedure, septectomy?
CSF leak anterior skull base – Size of defect that is suitable for a) mucosa only coverage and b) composite (multilayer) coverage
A: &3 or 5? mm mucosal defectA: &3 or 5? mm mucosal or &2 cm bony defect
Ddx of CSF rhinorrhea
A: IatrogenicA: Blunt trauma (closed HI or skull fractures)A: Increased ICP – Tumors, Post-infectious, Post-trauma,HydrocephalusA: Arachnoid granulationsA: EncephaloceleA: CSF otorrhea via ET3: Consult Neurosurgery for all cases of spontaneous CSF leak in order to R/O elevated Intracranial Pressure
Diagnostic tests for CSF leak
A: Clinical – Halo signA: Chemistry – Glucose (≥5 mg/dl), beta-2 transferrin, beta-trace proteinA: Endoscopy +/- ValsalvaA: High resolution CT with coronal and sagittal reconstructionsA: CT or MR CisternographyA: Intraoperative intrathecal fluorescein – 0.1 cc of 10% fluorescein in 10 cc of CSF, slowly infusedA: Radionucleotide scanning or scintiphotography
List 5 Complications of intrathecal fluorescein
A: Generalized SeizuresA: Opisthotonus (hyperextension and spasticity)A: Lower limb weakness/paresthesiasA: HeadacheA: Cranial nerve deficits
Three approaches for CSF leak repair
A: IntracranialA: Extracranial externalA: Endoscopic3: Can be Overlay or Underlay (&5 mm)3: Postop care = 24 hrs bed rest, HOB elevated, lumbar drain, no nose blowing, no straining, stool softeners at 10 cc/h for 24-48 hrs may be used
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