FIGURE 4.1 Left ostiomeatal complex (enclosed by blue line) is bound laterally by the medial orbital wall or lamina papyracea (LP) and medially by the MT. (A) Coronal CT section outlining ostiomeatal complex boundaries. (B) Endoscopic view of the left nasal cavity with the MT being medialized. (C) Closer view of the left middle meatus. The uncinate process extends anteriorly to the anterior maxillary line (M). Its posterior free margin parallels the ethmoid bulla. The hiatus semilunaris (HS, white arrows) is a two-dimensional cleft between the posterior free edge of the uncinate and the ethmoid bulla. It is the gap through which the nasal cavity communicates with the ethmoid infundibulum (I). The infundibulum (black arrow) is a three-dimensional space between the uncinate process and lamina papyracea. This endoscopic figure shows the maxillary ball probe being passed through the linear hiatus semilunaris into the infundibulum. BE, bulla ethmoidalis; U, uncinate process. (From Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology—Head and Neck Surgery. 6th ed. Philadelphia, PA: Saunders; 2015, fig. 49-1.)
• Infundibulum: funnel-shaped three-dimensional space between the uncinate process medially and the lamina papyracea laterally
• MT
• Maxillary sinus ostium
Superior Attachment of the Uncinate Process (Fig. 4. 2)
Variable site of attachment:
• Laterally to lamina papyracea: most commonly resulting in a recessus terminalis; frontal recess drains medially to the uncinate and directly into the middle meatus
• Superiorly onto the skull base: frontal recess drains laterally into the infundibulum
• Medially to the MT: frontal recess drains laterally into the infundibulum
Middle Turbinate
• Boomerang-shaped structure
• Basal lamella is the entire MT attachment to the lateral nasal wall and skull base
• Basal lamella can be conveniently thought of in three parts from the anterior-to-posterior aspects (Fig. 4.3)
• Anterior part: oriented in the sagittal plane (vertical) and attaches to the agger nasi region anteriorly and the cribriform plate superiorly
• Middle: oriented in the coronal plane obliquely and attached to the lamina papyracea
• Posterior: oriented in the axial place (horizontal) and attached to the lateral nasal wall at the lamina papyracea, maxilla, and perpendicular process of the palatine bone
FIGURE 4.2 Coronal schematic view of the ostiomeatal complex showing the superior attachments of the uncinate process to the LP (A), the roof of the ethmoid (B), or the MT (C). If the uncinate process attaches to the roof of the ethmoid or to the MT, the frontal sinus drains into the infundibulum. If the uncinate attaches to the lamina papyracea, the frontal sinus drains medially, next to the MT. (From Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology—Head and Neck Surgery. 6th ed. Philadelphia, PA: Saunders; 2015, fig. 49-2.)
FIGURE 4.3 Schematic view of the right MT viewed from the lateral aspect illustrates the anterior vertical (1), middle oblique (2), and posterior horizontal (3) attachments. Inset, endoscopic views of the right MT show the free anterior edge (4) and the anterior (1) and posterior (3) attachments. BE, bulla ethmoidalis; U, uncinate. (From Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology—Head and Neck Surgery. 6th ed. Philadelphia, PA: Saunders; 2015, fig. 49-3.)
• Middle oblique part of the basal lamella is the only part of the MT that can be sacrificed without compromising the integrity of the turbinate: if the vertical or horizontal attachment is injured, MT will lateralize the obstructing middle meatus and posterior ethmoid complex
Ethmoid Sinuses
• The ethmoid complex is divided by the basal lamella into the anterior and posterior ethmoid cells (Fig. 4.4)
• Anterior ethmoid cells
• Drain into the middle meatus
• Ethmoid bulla: the largest and most prominent cell; it attaches laterally to the orbit
• May have a cleft behind the bulla (retrobullar recess) or above the bulla (suprabullar recess)
• Agger nasi at the attachment of the MT to the lateral wall is often pneumatized
• Agger nasi cell is the most anterior of all ethmoid cells; it is present in >98% of CT scans
• Key landmark in frontal sinus surgery
• Posterior ethmoid cells drain into the superior (or supreme) meatus
• 1-5 cells
• Ethmoid cells may pneumatize into the adjacent sinuses and affect their drainage
• Infraorbital or Haller cell into the maxillary sinus
• Frontal, suprabullar, and supraorbital cells around the frontal sinus
• Sphenoethmoid or Onodi cell over the sphenoid sinus, potentially placing the optic nerve and internal carotid artery (ICA) at risk if not recognized by surgeon
Maxillary Sinus
• Natural ostium
• Drains into the inferior aspect (usually of the infundibulum) at a 45-degree angle
• Elliptically shaped; accessory ostia are round and are present in the fontanelles in at least 10% of patients
• Halfway between the anterior and posterior walls of the sinus
• Lateral nasal wall has two areas where bone is absent between the mucosa, called fontanelles
• Anterior fontanelle is anterior to the uncinate bone
• Posterior fontanelle
Sphenoid Sinus
• Natural os opens into the sphenoethmoidal recess
• Sphenoid os halfway to two-thirds up the anterior wall of the sinus
• Medial to the posterior end of the superior turbinate in the majority (83%) of cases
• Os is average of 7 cm from the nasal spine, at an angle of 30 degrees from the floor
• Walls of the sphenoid sinus contain several critical structures such as the ICA, optic nerve, and skull base
• Septations in the sphenoid frequently attach to the ICA
Frontal Sinus
• Originates embryologically from an anterior ethmoid cell
• Outflow tract has an hourglass shape, and the narrowest part is the internal frontal ostium
• Mucocilary flow is up the intersinus septum across the frontal sinus roof laterally and then medially along the floor of the frontal sinus down to the frontal recess
• Drains through the frontal recess into the middle meatus (commonly) or into the superior aspect of the infundibulum (less commonly), depending on the uncinated attachment
• Boundaries of the frontal recess
• Medial: MT
• Lateral: lamina papyracea
• Anterior: posterior wall of the agger nasi
• Posterior: ethmoid bulla
Cells Related to the Frontal Sinus
• Frontal recess may contain anterior ethmoid cells (called frontal recess cells), which consequently narrow the frontal sinus drainage pathway (Fig. 4.5)
• Anterior to the frontal recess
• Frontal cells
• Type I: a single cell superior to the agger nasi cell
• Type II: a tier of two or more cells above the agger nasi cell
• Type III: a single cell that extends from the agger nasi cell into the frontal sinus, above the floor of the frontal sinus floor but <50% of the frontal sinus height
• Type IV: an isolated cell within the frontal sinus (Kuhn) or a single cell that extends into the frontal sinus for >50% of the frontal sinus height (Wormald)
FIGURE 4.4 The oblique, second part of the MT2 attaches to the lamina papyracea via the basal lamella, separating the anterior ethmoid (B) from the posterior ethmoid (PE) cells. This part lies in a coronal/frontal plane and is best viewed on a sagittal view CT scan. ANC, Agger nasi cell; FS, frontal sinus; IT, inferior turbinate; SS, sphenoid sinus. (From Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology—Head and Neck Surgery. 6th ed. Philadelphia, PA: Saunders; 2015, fig. 49-4.)
FIGURE 4.5 (A) The frontal sinus recess (FSR) is an hourglass-shaped space (shaded area) with the waist at the frontal sinus ostium (FSO), which is its narrowest part. In the simplest configuration, the boundaries of the frontal recess are limited by the ANC and nasal beak (NB) anteriorly, the bulla ethmoidalis (BE) and the bulla lamella (BL) posteriorly, the anterior skull base (SB) posterosuperiorly, the cribriform plate and MT medially, and the lamina papyracea laterally. (B) Frontoethmoid cells pneumatize around the frontal recess. Frontal cells lie anterior to the frontal recess; suprabullar, supraorbital ethmoid, and frontobullar cells lie posterior to the frontal recess. (From Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology—Head and Neck Surgery. 6th ed. Philadelphia, PA: Saunders; 2015, fig. 49-9.)
• Posterior to the frontal recess
• Supraorbital ethmoid cell: cells posterior to the frontal sinus, pneumatizing superiorly to the orbital roof
• Interfrontal sinus cell: pneumatizes intersinus septum and drains into one frontal sinus, medially to the frontal ostium
• Suprabullar cell: cell superior to the ethmoid bulla
• Frontal bulla cell: cell superior to the ethmoid bulla pneumatizing into the posterior frontal table (anterior skull base)
Bent and Kuhn Classification of Frontal Cells
1. Type I: a single frontal recess cell above the agger nasi
2. Type II: a tier of cells above the agger nasi projecting into the frontal recess
3. Type III: single massive cell arising above the agger nasi, pneumatizing cephalad into the frontal sinus
4. Type IV: single isolated cell within the frontal sinus
Anatomical Variants (Fig. 4.6)
• Concha bullosa: defined as aeration of the MT; cavity lines with the same epithelium as the rest of the nasal cavity
• Paradoxic MT: curvature projecting laterally; may narrow or obstruct the nasal cavity, middle meatus, and infundibulum
• Atelectatic uncinate process: free edge of the uncinate adheres to the orbital wall; associated with an occluded infundibulum and hypoplastic opacified ipsilateral maxillary sinus, possibly with a more inferior location of the orbit and increased risk of orbital complications during surgery
• Haller cell: an infraorbital ethmoid cell; pneumatizes into the maxilla
• Onodi cell: a sphenoethmoidal cell, a posterior ethmoid air cell pneumatizing over the sphenoid
Airspaces within the Paranasal Sinuses
• Suprabullar recess: air cell space left between the ethmoid bulla and the fovea ethmoidalis when the bulla does not extend up to the fovea
• Sinus lateralis/retrobullar recess: air cell space found between the posterior surface of the ethmoid bulla and the vertical portion of the basal lamella
• Sinus terminalis: uncinate process terminates in the lamina papyracea; frontal recess drains medially to the uncinate process; this sinus is essentially a superior ending of the infundibulum (blind pocket)
• Agger nasi cell: remnant of the first ethmoturbinal, found superior, lateral, and anterior to the attachment of the MT; can also refer to ethmoid cells anterior to the frontal duct
FIGURE 4.6 Ethmoid Cells.
Top row shows a CT scan with corresponding endoscopic view below. (A) The ANC is the most anterior cell seen on a coronal CT scan, anterior to the MT. Endoscopically, it is seen as a bulge on the MT attachment and may narrow the superior ethmoid infundibulum. (B) Coronal CT section shows bilateral infraorbital ethmoid cells (IOC, Haller cells) narrowing the inferior ethmoid infundibulum and attaching laterally to the infraorbital canal. The maxillary sinus opens into the inferior part of the infundibulum at a 45-degree angle. Endoscopic view of the left infundibulum after uncinectomy shows the IOC narrowing the inferior infundibulum and potentially obstructing drainage of the natural maxillary ostium (MO). The natural MO is elliptically shaped and opens into the floor of the infundibulum at a 45-degree angle, not directly into the lateral wall. Accessory ostia (AO) are usually circular and are present here in the posterior fontanelle. (C) The sphenoethmoid cell (SEC), or Onodi cell, is a posterior ethmoid cell that is lateral and superior to the SS, which is usually smaller, pushed medially and inferiorly. The figures show arrows pointing to a left SEC on coronal and sagittal CT cuts. The endoscopic image demonstrates the relationship of the SEC to the SS and shows the optic nerve (ON) and ICA lying in relation to the SEC lateral wall. (From Flint PW, Haughey BH, Lund VJ, et al. Cummings Otolaryngology—Head and Neck Surgery. 6th ed. Philadelphia, PA: Saunders; 2015, fig. 49-5.)
Anterior Skull Base
• Formed by the cribriform medially and the fovea ethmodalis laterally
• Slopes downward posteriorly
• Skull base is thinner medially (0.1 mm) along the lateral lamella of the cribriform plate
• Inverse relationship between maxillary sinus height and the height of the ethmoid cavity (ie, large maxillary sinus is related to lower-lying skull base)
Keros Classification of Lateral Lamella of Cribriform Height
1. Type 1: cribriform plate 1-3 mm below the fovea
2. Type 2: cribriform plate 4-7 mm below the fovea
3. Type 3: cribriform plate 8-16 mm below the fovea (highest risk of skull-base penetration)
Rhinitis
History and Physical
• Single most important factor in attaining a proper diagnosis is a complete history
• Symptoms: nasal discharge, congestion/blockage, change in olfaction, postnasal drainage, episodes of sneezing, nasal itching, itchy eyes, and epiphora
• Symptom frequency: intermittent or persistent?
• Medication history
• History of asthma and sensitivity to aspirin or nonsteroidal antiinflammatory drugs (NSAIDs)
• History of head trauma
• History of prior nasal/sinus surgery
• History of hay fever/allergy testing
• Other systemic disorders
• Inciting factors including weather changes, certain odors or food, time of year, occupational history, chemical exposure at work, and improvement of symptoms on weekends/holidays (away from work)
• Examination should include nasal endoscopy
Workup
• Skin testing and/or serum testing for serum-specific immunoglobulin E (IgE) antibodies to relevant allergens
• Nasal cytology; scrapings from the inferior turbinate mucosa; high-power field of 5-25 eosinophils is compatible with a diagnosis of nonallergic rhinitis with eosinophilia syndrome (NARES) with negative allergy testing
Treatment Principles
1. Avoidance of triggers
3. Consider topical nasal (and oral) antihistamines and anticholinergic sprays, depending on etiology
4. Normal saline rinses as adjunct
5. In recalcitrant cases, may consider surgery, including turbinate reduction and potentially vidian neurectomy
Causes of Rhinitis/Rhinorrhea
• Allergic rhinitis
• Churg-Strauss syndrome
• Infectious
• NARES
• Rhinitis sicca anterior
• Atrophic rhinitis
• Rhinitis medicamentosa
• Vasomotor rhinitis
• Hormonal rhinitis
• Medication-induced rhinitis
• CSF rhinorrhea
Allergic Rhinitis
• Treat with avoidance of allergens, saline irrigations, oral and nasal antihistamines, nasal steroid sprays, oral decongestants, oral antileukotrienes, and nasal mast cell stabilizers
• Consider immunotherapy
Churg-Strauss Syndrome
• Asthma, eosinophilia (>10%), allergic rhinosinusitis, pulmonary infiltrates, vasculitis, and neuritis
• Treat with oral steroids, cyclophosphamide, and management of sinonasal symptoms
Infectious Rhinitis
• Viral (supportive Rx)
• Bacterial (commonly Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, treat with antibiotics)
• Rhinoscleroma (Mikulicz cells, Russell bodies on histopathology; treat with long-term ciprofloxacin or tertracycline)
• Rhinosporidiosis (Rhinosporidium seeberi is endemic in Africa and India): painless, friable, “strawberry” lesion; pseudoepitheliomatous hyperplasia on histopathology; treat with excision, antifungals, and dapsone
Nonallergic Rhinitis with Eosinophilia Syndrome
• Nasal eosinophilia (10-20% on smear) with negative allergy testing
• Symptoms and treatment are similar to allergic rhinitis
Rhinitis Sicca Anterior
• Dry, raw nasal mucosa caused by changes in temperature/humidity, nose picking, and dust
• Symptoms include dryness, crusting, and epistaxis
• Treat with saline irrigation, topical antibiotics, and oil-based nasal ointments
Atrophic Rhinitis
• Transition from functional, ciliated respiratory epithelium to a nonfunctional lining of nonciliated squamous metaplasia, with a loss of mucociliary clearance and squamous metaplasia
• Destroyed MCT and loss of mucosal glands
• Crusting, fetor, mucosal atrophy, and widely patent nasal cavities are seen in patients who complain of nasal congestion
• Causes include aggressive turbinectomy, excessive nasal surgery, nutritional deficiencies (iron or vitamin A or D deficiency), chronic bacterial infection (eg, Klebsiella ozaenae, less common in antibiotic era), trauma, manifestations of granulomatous diseases, chronic cocaine abuse, and radiation therapy
• Symptoms include paradoxical nasal congestion/obstruction despite wide nasal cavity, nasal crusting, and odor
• Treatment options are limited: may include irrigations, humidification to provide moisture, and experimental surgical procedures
Rhinitis Medicamentosa
• Rebound congestion from decreased vasomotor tone, or increased parasympathetic activity, due of topical nasal decongestants or cocaine use
• Treat by discontinuing topical decongestants; consider short-term oral corticosteroids (for weaning)
Vasomotor Rhinitis
• Results from changes in vascular tone and permeability: stimulation of afferent sensory nerves is the most likely pathophysiologic mechanism, and it activates the parasympathetic nerves that supply the nasal mucosal glands
• Symptoms include clear watery rhinorrhea and occasionally sweating/epiphora
• More common in older adults
• Multiple triggers, including temperature change, eating (gustatory rhinitis often with hot/spicy food), and anxiety
• Treat with anticholinergic nasal sprays (ipratropium bromide); consider vidian neurectomy if refractory (risk of dry eye)
Hormonal Rhinitis
• Fluctuating hormones with menstruation and puberty
• Rhinitis of pregnancy seen in >20%
• Increased in hypothyroidism and acromegaly
Medication-Induced Rhinitis (Box 4.1)
• Aspirin and NSAIDs in patients with aspirin-exacerbated respiratory disease (AERD)
• Multiple psychotropic agents (eg, amitriptyline)
• Antihypertensives (eg, β-blockers and angiotensin-converting enzyme inhibitors)
• Hormonal replacement and oral contraceptives
Inhalant-Induced Rhinitis
• Proposed mechanism is the stimulation of chemical irritant receptors on sensory nerves (ie, C fibers) to induce neuropeptide release, which produces the vasodilation and edema associated with inflammation independent of immune-mediated responses
• Chemical exposures classifications:
• Immunologic (high molecular-weight agents, eg, wheat, latex, compounds in insecticides, adhesives, and auto-body spray paint)
• Annoyant (perfumes, exhaust fumes, cleaning agents, room deodorizers, floral fragrances, and cosmetics)
• Corrosive (ammonium chloride, hydrochloric acid, vinyl chloride, organophosphates, and acrylamide exposures causing mucosal burns and ulcerations)
Cerebrospinal Fluid Rhinorrhea
• Clear watery often unilateral rhinorrhea; worse with lowering head
• Patients will often report that the watery drainage occurs when they bend over to tie their shoes
• Treated with conservative or surgical therapy
Nasal Obstruction
Differential Diagnosis of Nasal Obstruction
• Rhinitis (inflammatory)
• Chronic sinusitis (with or without nasal polyps)
• Rhinitis medicamentosa (chronic use of nasal decongestants)
• Deviated nasal septum
• Inferior turbinate hypertrophy
• Nasal valve collapse
• Adenoid hypertrophy (children)
• Choanal atresis (infants, congenital)
• Empty-nose syndrome (prior resection of inferior turbinates is the most likely cause)
Evaluation of Nasal Obstruction
• History and physical
• Seasonal and/or daily variation of symptoms
• History of nasal trauma
• History of past nasal surgery
• History and signs of allergic or nonallergic inflammation
• Examine external and internal nasal valves (modified Cottle maneuver to assess nasal valves)
• Nasal endoscopy
• Sinus CT
• Allergy testing
Treatment Options for Nasal Obstruction
• Trial of nasal steroids and antihistamines
• Oral steroids for chronic sinusitis
• Trial of Breathe Right® nasal strips if nasal valve collapse is suspected
• Inferior turbinoplasty (submucosal resection and outfracture)
• Radiofrequency coblation
• Submucosal debridement
• Septoplasty
• Functional rhinoplasty (closed or open)
• Extracorporeal septoplasty (caudal deviations)
• Nasal valve repair
Nasal Septal Perforation
Causes of Nasal Septal Perforation
• Iatrogenic (septoplasty)
• Trauma and septal hematoma
• Drug use (cocaine, inhaled narcotics)
• Malignancy
• Granulomatous disease (granulomatosis with polyangiitis [GPA], sarcoidosis)
• Corticosteroid nasal spray (overuse)
• Infection (tertiary syphilis)
Treatment of Nasal Septal Perforation
• Nasal hygiene: increase moisture (bactroban ointment); avoid digital manipulation
• Silastic buttons
• Surgical repair
• Extending perforation posteriorly
Epistaxis
Workup of Epistaxis
• Unilateral versus bilateral
• Duration
• Frequency
• Severity (trickle vs. high flow)
• Time of day (morning vs. nighttime)
• Posterior (may be bilateral, with significant bleeding from the oropharynx/oral cavity as it runs posteriorly)
• Source (Keisselbach’s plexus, anterior ethmoid artery, posterior ethmoid artery, sphenopalatine artery, mucosal lesion, or neoplasm)
• Exacerbating factors (trauma, digital trauma, and temperature)
• Medical history (hypertension or coagulopathy)
• Family history
• Medications (aspirin, NSAIDs, and anticoagulants)
Causes of Epistaxis
• Bleeding from blood vessels in Keisselbach’s plexus is the most common cause in 90% cases (plexus in the anterior caudal septum is supplied by the anterior ethmoid artery, sphenopalatine artery, greater palatine artery, and superior labial artery)
• Mucosal trauma (digital manipulation)
• Toxic (inhaled drugs, including cocaine and heroin)
• Drugs (chemotherapy, anticoagulants, and alcoholism)
• Mucosal lesion (capillary hemangioma and telangiectasia)
• Neoplasm (juvenile nasopharyngeal angiofibroma [JNA] and malignant neoplasm)
• Congenital (hereditary hemorrhagic telangiectasias [HHT], hemophilia, and von Willebrand)
• Systemic (hypertension and coagulopathy)
Treatment Options for Epistaxis
• Nondissolvable packing (anterior pack: Kennedy Merocel vs. posterior pack)
• Dissolvable packing (hemostatic agents: surgicel Gelfoam, and Floseal)
• In-office cauterization (silver nitrate or laser)
• Cauterization under anesthesia (coblation, bipolar cautery, monopolar cautery, or laser)
• Manage underlying condition or cause (neoplasm, hypertension, and coagulopathy)
Hereditary Hemorrhagic Telangiectasias (Formerly Osler Weber Rendu)
• Diagnosis
• Autosomal dominant (at least five genes identified)
• Curacao criteria (definite if 3; suspected if 2; unlikely if <2)
• Epistaxis
• Mucosal telangiectasias (oral and sinonasal)
• Visceral lesions (pulmonary arteriovenous malformation [AVM], cerebral AVM, hepatic AVM, and spinal AVM)
• Family history (first-degree relative)
• Medical management
• Topical moisturizers (mupirocin and saline gel)
• Topical rose geranium oil
• Topical or oral estrogen agents (hormone replacement therapy and antiestrogen agents)
• Topical timolol
• Oral tranexamic acid
• Topical or intravenous (IV) bevacizumab (Avastin)
• In-office injected sclerotherapy
• Surgical management
• Cauterization (laser, bipolar, and radiofrequency)
• Injected bevacizumab (Avastin)
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