Paranasal Sinuses Sinusitis

Introduction

Pathophysiology

• Anatomical (compromised patency of ostia causes hypooxygenation and impairment of sinus drainage)

• Dysfunction of Cilia Motility

• Change in Quality of Secretions

• Immune Dysfunction

Pathogens Acute

• Viral: rhinovirus (most common)

• Bacterial: S. pneumoniae (most common bacterial agent), H. influenzae, B. catarrhalis, S. aureus, S. pyogenes

• Fulminant Fungal: Aspergillosis, Phaehyphomycosis, Mucor, Rhizopus

Chronic: anaerobes, S. aureus, H. influenzae, 1—2% fungal Complicated Sinusitis

• Cystic Fibrosis: P. aeruginosa, S. aureus

• Nosocomial: P. aeruginosa, Klebsiella, Enterobacter, Proteus

• Immunocompromised: similar to nonimmunocompromised patients, however also susceptible to Aspergillus, Rhizopus, Fusarium, P. aeruginosa, S. aureus

Evaluation

Symptoms and Physical Exam Findings

• Acute Sinusitis Symptoms: facial pain and tenderness worse with straining of bending over, pressure headache (frontal, occipital headaches may arise from sphenoid sinusitis), nasal congestion, postnasal drip, nasal obstruction, nasal discharge (mucopurulent, serous, mucoid), cough and halitosis (especially in pediatric patients)

• Chronic Sinusitis Symptoms: presents with more subtle symptoms of nasal obstruction, less fever and pain complaints

• Associated Symptoms: anosmia, loss of taste (chronic sinusitis), allergic components (sneezing, watery eyes), fever, malaise, lethargy, cough, eustachian tube dysfunction, anosmia/hyposmia

• Physical Exam: rhinoscopy/nasopharyngoscopy (osteomeatal unit obstruction, nasal masses and obstruction, purulence, hypertrophied adenoid tissue); decreased sinus transillumination (not reliable); frontal and maxillary tenderness (acute sinusitis); polyps and edema (chronic sinusitis)

• DDx of Facial Pain: rhinogenic, migraines and other headaches, dental disease, neuralgias, temporomandibular joint disease, ocular disease, tonsillitis, pharyngitis, otogenic disease, intracranial pathologies, hypertension, temporal arteritis

Evaluate for Causes and Risk Factors

• Anatomical: deviated septum, mucosal edema (rhinitis, allergic), hypertrophic adenoids, nasal masses, nasal foreign bodies, nasogastric tubes, nasal packing, facial fractures, concha bullosa, lateral deviated uncinate process, paradoxical middle turbinate, uncinate hypoplasia, nasal polyposis

• Ciliary Dysfunction: (see below)

• Medical Condition: immunocompromised (HIV, diabetes, malnutrition), cystic fibrosis, smoker, elderly

• Local Causes: apical dental infection, trauma, barotrauma

Imaging Studies

Plain Radiography

• Indications: screening study for acute sinusitis

• evaluates presence of air-fluid levels, opacification, and bone destruction

• high rate of false positives and false negatives to evaluate for chronic sinusitis

CT of Paranasal Sinuses

• Indications: severe acute sinusitis, medical failure of chronic sinusitis, diagnosis of epistaxis, nasal or sinus tumors, nasal polyps, CSF leak, trauma, preoperative films

• Evaluation

1. examine distribution of mucosal disease (mucosal thickening, air-fluid levels suggest acute inflammatory process)

2. inspect development of sinus (symmetry, aeration of sinus cavities)

3. examine nasal structures, airway, and access

4. evaluate for underlying causes of disease (OMC patency, paradoxical turbinates, nasal septal defects, concha bullosas)

5. examine for anatomical variations and landmarks (cribiform plate, posterior ethmoidal height, thickness of skull base, optic nerve, orbital dehiscence, carotid artery)

MRI of Paranasal Sinuses

• improved soft tissue detail, poor bone resolution

• Indications: complicated sinusitis (intracranial and intraorbital extension), evaluation of soft tissue masses (neoplasms), fungal sinusitis (hypodensity in T2—weighted sequences from the presence of metallic proteinaceous material, magnesium, iron, and calcium)

Ancillary studies

• sinus cultures (may be obtained through an anterior maxillary puncture or from an endoscope) indicated for failed medical management, complicated sinusitis (sepsis, orbital infection, intracranial extension), immunocompromised patients

• immunological profile (qualitative immunoglobulins including IgG subclasses)

• ciliary biopsy

• allergy testing

Management

Acute Sinusitis (<1 month)

• Antibiotics: may treat empirically with first-line oral antibiotics with gram positive and gram negative coverage (amoxicillin, amoxicillin-clavulanate, trimethoprim-sulfate, cefuroxime, or azithromyocin) for 10—14 days, consider changing antibiotics if no improvement after 2—3 days, if no improvement after 1 week may consider sinus lavage for culture and sensitivity

• Improve Nasal Clearance: nasal saline irrigations, oral and topical decongestants, mucolytic agents, humidity

• Symptomatic Medications: analgesics, antipyretics

• Address Risk Factors: smoking cessation, septoplasty, remove nasogastric tube, antireflux regimen, etc

Acute Frontal Sinusitis

• frontal sinusitis is treated more aggressively to avoid intracranial complications

• identified by frontal pain and tenderness and frontal sinus air-fluid levels on x-ray

• parenteral antibiotics, observation for intracranial involvement (select patients may be followed with close follow-up on an outpatient basis)

• consider surgical management if no improvement after 24—48 hours of aggressive medical management

Chronic Sinusitis: persistent sinus infection greater than 6 weeks

• Antibiotics: 3—6 weeks regimen with broad spectrum agents (eg, amoxicillin-clavulanate, cefuroxime, ciprofloxacin, clarithromycin, cefpodoxime, cefprozil)

• nasal corticosteroid sprays are useful for chronic sinusitis

• nasal hypertonic saline irrigations, oral decongestants, and mucolytic agents

• medical management often fails with chronic sinus disease, surgical management is frequently required

• allergy management (see above)

Surgical Management: see below for indications and techniques Pediatric Sinusitis

• usually involves the maxillary sinus and anterior ethmoids (the sphenoid and frontal sinuses are less developed)

• Most Common Pathogens: Streptococcus, S. aureus, S. pneumoniae, M. catarrhalis, H. influenzae

• SSx: similar presentations to URI, however tend to have cough, halitosis, persistent nasal obstruction, rhinorrhea, and fever

• W/U: similar to adults, however for persistent sinusitis must consider adenoid hypertrophy, cystic fibrosis, and immunodeficiencies

Management

• Antibiotics: antibiotics are the primary therapeutic agent in pediatric sinusitis, agents used are similar to adults

• Adjunctive Medical Agents: saline irrigations, nasal corticosteroids, oral decongestants, mucolytics

• Endoscopic Sinus Surgery: indicated for select patients who fail extensive medical management and have significant effect on quality of life

• Adenoidectomy: controversial relationship with sinusitis (may harbor pathogens and block drainage), may be considered as an adjunctive therapeutic option

• Antral Lavage: controversial efficacy, addresses only the maxillary sinus, typically require multiple lavages

Complicated Sinusitis

Fungal Sinusitis Fungus Ball

• Pathophysiology: noninvasive fungal infection (most commonly Aspergillus)

• SSx: unilateral chronic or recurrent sinusitis, unilateral proptosis, facial hypesthesia

• Dx: CT/MRI of paranasal sinus, biopsy with culture

• Aspergillosis Histology: septated 45 degree, Y-shaped (Sabouraud's agar stain)

• Rx: adequate surgical debridement, consider adjuvant less toxic antifungal medications

Allergic Fungal Sinusitis

• Pathophysiology: fungal infection, most commonly Aspergillus or demitaceous molds (Alternaria, Bipolaris, Curvularia, Exophilia), becomes the antigen for an allergic response

• Risks: atopic disease, young asthmatics

• SSx: sinusitis symptomatology with allergic component (sneezing, watery eyes, periorbital edema, etc.)

• Dx: allergic evaluation for fungal elements (RAST, skin testing, nasal eosinophilia), tissue stains reveal presence of allergic mucosa with fungal hyphae, CT/MRI of paranasal sinus

• Rx: surgical debridement with complete sphenoethmoidectomy, topical and oral corticosteroids, consider adjuvant antifungal medications or immunotherapy

Chronic Invasive Fungal Sinusitis

• Pathophysiology: pathogen invades soft tissue

• Pathogens: Aspergillosis, Saprophytics (Mucor, Rhizopus, Absida)

• SSx: chronic sinusitis with or without symptoms of local invasion (eg, blindness, cerebritis)

• Dx: biopsy and culture, MRI of paranasal sinus (image of choice, enhancement in T2-weighted images from fungal elements), CT of paranasal sinus

• Rx: surgical debridement and long-term amphotericin B and itraconazole (1 year)

Fulminant Fungal Sinusitis and Mucormycosis (Rhinocerebral Phycomycosis)

• Pathophysiology: pathogen invades soft tissue; in mucormycosis pathogen invades vessel walls causing local vascular occlusion, thrombosis, infarction, and tissue necrosis

• Pathogens: Aspergillosis (most common), Saprophytics (Mucor, Rhizopus, Absida)

• Risks: manifests almost exclusively in immunocompromised host (diabetic ketoacidosis, chemotherapy, HIV, bone marrow transplant)

• SSx: in mucormycosis may present with necrotic black turbinates and soft palate, epistaxis, cranial nerve involvement, progresses rapidly into obtundation and death

• Dx: biopsy and culture, MRI of paranasal sinus (image of choice, enhancement in T2-weighted images from fungal elements), CT of paranasal sinus

• Mucormycosis Histology: nonseptated, 90 degree broad branching hyphae

• Rx: urgent surgical debridement and long-term amphotericin B, address underlying derangements (eg, correct ketoacidosis)

Sinobronchial Syndrome

• association of chronic sinusitis with asthma, bronchiectasis, recurrent pneumonia, and chronic bronchitis

• Pathophysiology: controversial: may be from two separate manifestations with same underlying entity or postnasal drip with bronchial seeding which may result in bronchospasm

• Dx: clinical history and exam

• Rx: aggressive management of sinusitis may better control asthma

The HIV Patient with Sinusitis

• 75% of HIV patients develop sinusitis

• Pathophysiology: increased risk of sinusitis secondary to impaired immunity, mucociliary dysfunction, and atopy

• Pathogens: similar to nonimmunocompromised patients for CD4 count >200, however for CD4 count <200 high incidence of unusually and more virulent organisms (fungal, CMV, Pseudomonas, Myobacterium)

• Management of Sinusitis for CD4 count <200 (CD4 count >200 managed similar to a nonimmunocompromised patient)

1. may consider initially one course of empiric therapy (broad spectrum antibiotics) and sinus regimen (decongestants, hypertonic saline irrigations, mucolytics, etc)

2. aggressive early work-up (CT/MRI of paranasal sinuses, nasal endoscopy)

3. low threshold for sinus aspirate for culture and sensitivity to avoid empiric therapy

4. early surgical management

Cystic Fibrosis and Sinusitis

• Cystic Fibrosis (CF): autosomal recessive multisystem disorder characterized by abnormal exocrine gland function (chronic progressive pulmonary disorder with associated pancreatic, hepatobiliary, and genitourinary manifestations)

• universally develop chronic sinusitis

• 10% associated obstructive nasal polyps

• Dx: sweat chloride test >60—90 mmol per liter, genetic screening

• Pathogens: higher risk for pseudomonal infections (Burkholderia capacia) and methicillin resistant S. aureus (MRSA)

• Management of Sinusitis

1. attempt initial conservative medical management with mucolytics, topical corticosteroids, and hypertonic saline irrigations

2. avoid antibiotics (may develop resistant pathogens)

3. avoid surgical management (high recurrence rate, increases nasal scarring, patients do not tolerate long-term general anesthesia due to retained pulmonary secretions)

4. surgery may be considered for uncontrolled pain, nasal obstruction, mucocele, unresolved fevers, and fungal infections

Mucoceles

• Mucocele: obstructed sinus that undergoes expansion from mucous secretion

• frontal sinus most commonly involved

1. Primary: arises de novo, mucous retention cyst (see below)

2. Secondary: arises secondary to surgery, trauma, or tumor (or other nasal mass)

• Causes: trauma, chronic sinusitis, polyposis, sinus surgery, allergy, osteoma, hyperaeration of ethmoid

• SSx: asymptomatic, dull headache that localizes to involved sinus, periorbital swelling, ocular symptoms (proptosis, diplopia)

• Dx: CT of paranasal sinus reveals expansion of sinus with opacification, rounded process of a sinus cavity or air cell, bone remodeling (thinned sinus walls)

• Complications: pyoceles, may rupture (bacteremia), orbital and intracranial involvement, pituitary abnormalities, cosmetic deformity

• Rx: endoscopic sinus surgery, open procedures reserved for failed endoscopic approaches or rare lateral lesions in frontal sinus

Mucous Retention Cysts

• Pathophysiology: serous or mucinous submucosal collection of fluid secondary to blocked glands, may be infectious or allergic in origin

• SSx: typically asymptomatic, larger cysts may cause dental pain or symptoms from sinus obstruction

• Dx: CT of paranasal sinus, sinus films (10% incidental findings), most commonly found on floor of maxillary sinus

• DDx: dental radicular or follicular cysts

• Rx: observation if asymptomatic or nonobstructing, otherwise may consider surgical management

Kartagener's Syndrome

• Pathophysiology: deficient outer dynein arm results in primary ciliary dyskinesis

1. chronic rhinitis/sinusitis/otitis media

2. bronchiectasis

3. situs inversus

• SSx: recurrent sinusitis, otitis media, and rhinitis; male infertility (sperm dysmotility)

• Dx: ciliary biopsy with phase contrast microscopy or electronmicroscopy

• Management of Sinusitis

1. aggressive antimicrobial therapy, consider prophylactic antibiotics

2. mucolytics

3. avoid surgical management with "standard functional" antrostomies (do not work since there is no normal mucociliary clearance)

4. consider "gravity dependent" surgical inferior antrostomies for refractory sinus disease

Polyposis (see p. 17)

Complications of Sinusitis

Orbital Complications

• Intraorbital Pathways: direct extension (especially though thin walled lamina papyracea), thrombophlebitis (valveless veins), congenital dehiscence, trauma, direct lymphatics

• Dx: CT of paranasal sinus with contrast or MRI of paranasal sinus with gadolinium

• ophthalmology consultation should be obtained with any orbital complication from sinusitis

• urgent surgical intervention should be considered for orbital abscesses (or orbital cellulitis), changes in vision, progressive involvement of symptoms despite appropriate medical therapy, relapses, involvement of opposite eye

• concurrent aggressive sinusitis regimen (parenteral antibiotics, decongestants, mucolytics, saline nasal irrigations) is indicated for any complication of sinusitis

Stages of Orbital Complications

1. Periorbital (Preseptal) Cellulitis: eyelid edema, erythema, tenderness; no vision changes, chemosis, proptosis, or restriction of ocular muscles; Rx: parenteral antibiotics and concurrent aggressive sinusitis regimen (decongestants, mucolytics, saline nasal irrigations)

2. Orbital Cellulitis: proptosis, chemosis, may cause vision changes (anterior pupillary defect), may limit extraocular muscles; Rx: endoscopic sinus surgery to drain sinuses in all cases (controversial), parenteral antibiotics, vision acuity checks, aggressive sinusitis regimen (decongestants, mucolytics, saline nasal irrigations)

3. Subperiosteal Abscess: collection of pus between bone and periosteum, chemosis, may displace globe (proptosis), restrict extraocular motion, and affect vision; Rx: urgent surgical decompression

4. Orbital Abscess: collection of pus in orbital soft tissue, proptosis, chemosis, restricted extraocular motion, may have no light perception (may be reversible); Rx: urgent surgical decompression

5. Cavernous Sinus Thrombosis (see below))

Cavernous Sinus and Venous Sinus Thrombophlebitis

• Pathophysiology: perinasal sinus infection — orbital extension — mural thrombus forms in vessel wall (thrombophlebitis) — propagates distally as clot softens and begins to seed

• Pathogens: S. aureus (most common), hemolytic Streptococcus and Type III Pneumococcus

• SSx: "picket fence" spiking fevers, toxemia, papilledema, paralysis of extraocular muscles (CN III, IV, and V), proptosis, chemosis, eyelid edema

• Dx: CT/MRI may show intraluminal enhancement, positive blood cultures, Tobey-Ayer or Queckenstedt's Test (tests for obstruction;

external compression of jugular vein does not cause an increase in CSF pressure but compression on nonobstructed side does increase CSF pressure), CSF may reveal high cell and protein count

• Complications: meningitis, septic metastasis (pulmonary, blood)

• Rx: parenteral antibiotics, may require ligation of internal jugular vein if septic emboli suspected, anticoagulants (controversial), bed rest, sinus surgery once patient is stable

Intracranial Complications

• Intracranial Pathways: congenital dehiscence, trauma, direct extension (osteomyelitis), lymphatics, olfactory nerve sheath, venous system, foramina of Breschet

• Dx: initial CT of brain with contrast or MRI of brain with gadolinium (evaluate for mass effects that may risk herniation with a lumbar puncture), lumbar puncture for cells and culture

Epidural Abscess

• pus collection between skull and dura

• higher risk from frontal osteomyelitis (direct extension)

• Pathogens: S. aureus, E. coli, Streptococcus, Pseudomonas, Proteus

• SSx: headaches, low grade to spiking fevers, malaise, mental status changes (may be asymptomatic)

• Rx: parenteral antibiotics, neurosurgical consultation for possible drainage procedure, sinus drainage or obliteration procedure with wide exposure of dura until healthy tissue is exposed on all sides

Subdural Abscess

• pus collection between dura and arachnoid membrane (less resistance to spread, crescent shaped enhancement on CT/MRI, does not cross midline)

• Pathogens: similar to epidural abscess

• SSx: more neurological sequellae than extradural infections (seizures, delirium, hemiplegia, aphasia), mild increase in intracranial pressure (ICP) depending on the size

• Rx: high-dose parenteral antibiotics, neurosurgical consultation for possible drainage procedure

Brain Abscess

• Pathogens: Streptococcus, Staphylococcus, anaerobes

1. Encephalitis: (initial invasion) fevers, headache, nuchal rigidity

2. Latency: (organization of abscess, liquification necrosis) minimal symptoms, may last weeks

3. Expanding abscess: intracranial hypertension, seizures, paralysis

4. Termination: rupture of abscess, often fatal

• Rx: parenteral antibiotics, neurosurgical consultation for possible drainage procedure, concurrent sinus surgery

Meningitis

• most common form of intracranial complication from sinusitis

• highest risk from sphenoid sinusitis

• Pathogens: H. influenzae (type B), Pneumococcus, hemolytic Streptococcus

• SSx: headache, lethargy, nuchal rigidity, fever, Kernig's sign (with hip in flexion, pain is elicited with leg extension), Brudzinski's sign (flexion at neck causes a reflexive flexion of the legs), seizures, photophobia

• Dx: initial CT/MRI with contrast or gadolinium (evaluate for mass effects that may risk herniation with a lumbar puncture), lumbar puncture for cells and culture

• Rx: parenteral antibiotics, sinus surgery with exposure of diseased dura (if present)

Other Complications

• Osteitis: diagnose initially with technetium bone scan (osteoblastic activity) and gallium bone scan (inflammation), follow with gallium scans; Rx: parenteral antibiotics, surgical debridement, sinus surgery

• Pot's Puffy Tumor: frontal bone osteomyelitis, soft doughy swelling of forehead, high risk of intracranial extension; Rx: parenteral antibiotics, trephination, may require surgical debridement

• Superior Orbital Fissure Syndrome: fixed globe, dilated pupil (CN III, IV, VI), ptosis, hypesthesia of upper eyelid (CN V1); Rx: urgent surgical decompression

• Orbital Apex Syndrome: similar to Superior Orbital Fissure Syndrome with added involvement of optic nerve (papilledema, vision changes)

• Sinocutaneous Fistula: usually begins as a frontal osteomyelitis

Sinus Surgery

Functional Endoscopic Sinus Surgery (FESS)

• Advantages: superior visualization, better precision, preserves function (recognizes normal mucociliary flow pattern at the osteomeatal complex), completeness, no external scar

• Disadvantages: requires one-handed technique, monocular vision (difficulty with depth perception)

• Contraindications: osteomyelitis, no evidence of paranasal disease on CT, inaccessible lateral frontal sinus disease

• Steps of a FESS for Sinusitis: medialize middle turbinate, excise uncinate process, anterior then posterior ethmoidectomies, sphenoidotomy, frontal recess sinusectomy, create maxillary antrostomy

• Postoperative Care: sinus packing (2—6 days), oral antibiotics for a minimum of 2 weeks, aggressive nasal hygiene to prevent adhesions (saline irrigations), nasal steroids, nasal debridement at 1, 3, and 6

weeks

Indications for Endoscopic Sinus Surgery

• chronic sinusitis, complicated sinusitis, recurrent acute sinusitis, failed medical management of acute sinusitis, fungal sinusitis

• obstructive nasal polyposis

• sinus mucoceles

• remove foreign bodies

• tumor excision, transsphenoidal hypophysectomy

• orbital decompression, dacryocystorhinotomy, orbital nerve decompression, Grave's ophthalmopathy

• choanal atresia repair

• control epistaxis

• septoplasty, turbinectomy

Ethmoid and Maxillary Open Sinus Procedures Caldwell-Liw

• intraoral approach to anterior maxillary wall from canine fossa above gum line, the diseased mucosa is removed from the maxillary sinus, also allows for a middle meatal antrostomy, and ethmoidectomy (transantral ethmoidectomy)

• Indications: sinus disease not obtainable by endoscopic sinus surgery, inspissated secretions, neo-ossification, cystic fibrosis

• Advantages: allows adequate exposure of inside of maxillary sinus, favorable intraoral incision

• Disadvantages: nonfunctional, damages mucosa (decreased cilia count, increased fibrosis and bone growth), risk of infraorbital nerve and dental injury (hypoesthesia to teeth and lip), transantral ethmoidectomy does not allow exposure anterior to the ethmoidal bulla

Intranasal Ethmoidectomy (without Endoscopy)

• requires medialization of middle turbinate to gain access to the ethmoid cells, diseased mucosa is removed by piecemeal forceps dissection

• Indications: largely been replaced by endoscopic sinus surgery

• Advantages: no external scar

• Disadvantages: poor visualization (increased risk of bleeding and CSF leak), poor precision, excess mucosal damage, no visualization of frontal sinus recess or inside maxillary sinus

External Ethmoidectomy

• requires ligation of angular and anterior ethmoid arteries, access gained through lamina papyracea and lacrimal fossa

• Indications: inability to obtain transnasal exposure, subperiosteal abscess or orbital abscess

• Advantages: can access ethmoid sinus in all cases

• Disadvantages: poor visualization (especially anteriorly), poor precision, excess mucosal injury, external scar

Frontal Sinus Surgery

• Frontal Sinus Trephination: useful to relieve pain and obtain cultures for acute frontal sinusitis, may be used as an adjunctive procedure with endoscopic sinus surgery

• Lynch Procedure (Fronto-ethmoidectomy): consists of removal of the frontal sinus floor, middle turbinate, and anterior ethmoids, easiest and quickest technique, risk of recurrent mucocele formation from stenosis of nasofrontal duct

• Riedel Method: consists of removal of the frontal sinus floor and anterior wall (disfiguring), allows for complete obliteration

• Killian Method: modification of the Riedel by preserving a bridge at the supraorbital rim to reduce deformity

• Lothrop Method: creates a large drainage opening into the nasal cavity by removing bilateral anterior ethmoids, middle turbinate, and frontal septum

Osteoplastic Flap with Frontal Sinus Obliteration

• Technique: bicoronal flap for exposure, "trapdoor" access to the frontal sinus via a periosteal and bone flap (requires a template patterned from a Caldwell view film), remove mucosa, obliterate cavity and occlude frontonasal recess (may use fat, muscle, or bone)

• Indications: chronic or recurrent sinusitis, mucoceles (pyoceles), frontal bone osteomyelitis, benign tumors, frontal sinus fractures, orbital or intracranial complications

• Advantages: best view of entire frontal sinus and anterior base of skull, minimal deformity, direct approach, fail-safe method to eradicate frontal sinus disease (permanent and complete removal of diseased mucosa)

• Disadvantages: technically more difficult, time consuming, requires hospitalization, risk of mucocele formation and chronic pain

• Contraindicated: aplastic frontal sinus

Approaches to the Sphenoid

• Transseptal Approaches are useful for pituitary tumors and CSF leaks (transsphenoidal hypophysectomy)

• external transethmoidal and transantral routes are less popular approaches to the sphenoid sinus

Sublabial Transseptal Approach

• Indications: most common access for transphenoidal hypophysectomy (tumors), sinusitis, and mucoceles

• Advantages: wide midline exposure, no external scar

• Disadvantages: soft tissue trauma, sensory disturbances, difficult to displace distal lateral nasal mucosa with speculum, oral contamination

Transcolumellar Transseptal Approach (External Rhinoplasty)

• Indications: transsphenoidal hypophysectomy (tumors), sinusitis, and mucoceles

• Advantages: wide midline exposure, shorter access distance, no manipulation of upper lip (shorter recovery time)

• Disadvantages: small external scar, disrupts medial crura (major tip support), narrower exposure

Endonasal Approach

• Indications: transsphenoidal hypophysectomy (tumors), sinusitis, and mucoceles

• Advantages: limited septal incisions

• Disadvantages: compromised three-dimensional exposure

Endoscopic Approaches (Transnasal, Transethmoidal)

• Transnasal Indications: hypophysectomy or biopsy (tumors), sinusitis, and mucoceles

• Transethmoidal Indications: sinusitis, mucoceles, CSF leaks, biopsy, optic nerve decompression

• Advantages: limited septal incisions, visualization, better lateral exposure

• Disadvantages: one-handed surgery, difficulty with depth perception

Complications of Sinus Surgery

Ocular and Orbital Complications

• Blindness: may be secondary to an indirect injury (eg, retrobulbar hematoma, see below) or direct injury to the optic nerve

• Intraoperative Orbital Fat Penetration: increases risk of retrobulbar hematoma; Rx: recognize orbital fat (orbital fat floats); avoid further trauma; may complete the FESS; avoid tight nasal packing; observe for vision changes, proptosis, or restricted ocular gaze

• Diplopia: orbital muscle injury, most commonly from medial rectus and superior oblique muscles

• Epiphora: injury to lacrimal duct system, avoid operating anterior to the attachment of the uncinate; Rx: observation initially, if no resolution then dacryocystorhinostomy

Retrobulbar Hematoma

• Pathophysiology: most commonly from retraction injury of the anterior ethmoid artery which causes increased orbital pressure that compresses the vascular supply to the optic nerve, also may occur from venous injury near the lamina papyracea

• Avoidance: maintain orientation and operate under direct vision, examine CT for dehiscence, correct coagulopathies

• SSx: ecchymosis, proptosis, conjunctival changes (chemosis), pupillary changes (afferent pupillary defect)

1. if noticed intraoperatively terminate case

2. Ophthalmology consult

3. Mannitol (1—2 g/kg), consider high-dose steroids

4. orbital massage and place ice pack

5. lateral canthotomy, medial external (Lynch) procedure, or orbital decompression

6. control hemorrhage

Intracranial Complications

• CSF leak: occurs near the frontal recess, anterior ethmoid artery, cribiform plate, and posterior ethmoid sinus; Rx: recognize leak (clear or swirling fluid), prepare site of leak, apply graft (mucosa, fascia, or muscle flap), stabilize graft (Gelfoam), consider neurosurgical consult, consider lumbar puncture, bed rest, avoid straining

• Intracranial Infections: meningitis, brain abscess

• Intracranial Hemorrhage: uncommon

Neural and Vascular Injury

• Anosmia: injury to the olfactory epithelium

• Hemorrhage: injury to sphenopalatine, carotid, and ethmoid arteries, carotid-cavernous fistulas; Rx: control bleeding with electrocoagulation or packing, consider embolization for carotid injuries

• Paresthesias: injury to infraorbital, supraorbital, supratrochlear nerves

Synechia

• most common complication of endoscopic sinus surgery

• scarring most commonly occurs between middle turbinates and nasal wall

• Rx: lysis of adhesions (endoscopic approach), may consider spacers (Telfa, Merocel, Gelfilm); prevent by minimizing trauma, reduce concha bullosas and symptomatic polypoidal middle turbinates, and good postoperative care (nasal hygiene, endoscopic debridements)

Other Complications

• residual disease

• hematomas and seromas (abdominal fat graft complication of osteoplastic flap surgery)

• facial edema (especially from Caldwell-Luc procedures)

• aspiration of packing material

• toxic shock syndrome

• osteomyelitis

• tooth numbness and pain (Caldwell-Luc)

• embossment (frontal sinus obliteration)

IMMUNOLOGY Introduction

Cell-Mediated Immunity

• Antigen Presenting Cells (macrophages, dendritic cells, Langerhans' cells) phagocytize antigens then present a fragment of the antigen to the surface via Major Histocompatibility Complex (MHC) Type II receptor and secretes IL-1

• Helper T-cells recognize the antigen presented by the MHC Type II receptor complex and are activated by IL-1, resulting in secretion of IL-2 (IL-2 up-regulates other T-cells including killer T-cells, macrophages, and natural-killer cells)

• Killer T-cells attack the body's own cells that have been transformed from infection or malignancy via the MHC Type I receptor_

• Major Histocompatibility Complex (MHC): surface receptors for antigenic determinants of foreign molecules

1. Type I: found on all nucleated cells; encoded by gene complex, Human Leukocyte Antigen (HLA) A, B, and C

2. Type II: found on antigen presenting cells and B-cells; encoded by gene complex HLA DR, DQ, and DP

• Common Clusters of Differentiation (CD) Markers

1. CD2 and CD3: all T-cells

2. CD4: helper T-cells, associated with MHC Type II response, receptor for HIV

3. CD8: killer T-cells, associated with MHC Type I response

4. CD56 and CD16: natural killer cells

Humoral Immunity

• B-cells are produced in bone marrow, migrate to lymph nodes and spleen, bare multiple receptors similar to the immunoglobulins they secrete

• B-cells are positive for CD19, 20, and 22, and carry MHC class I on their surface

• B-Cell Activation Types

1. T-cell Dependent Activation: B-cell receptors internalize antigen, fraction of antigen presents on surface via MHC Type II receptor which recognizes helper T-cells, T-cell then stimulates B-cell (via IL-2 and IL-4) to mature to plasma cells which secrete immunoglobulins

2. T-cell Independent Activation: large antigens (eg, carbohydrates on bacterial cell walls) bridge immunoglobulins on B-cell surfaces that activates the B-cell

Immunoglobulins

• glycoproteins produced by plasma cells that participate in antigen recognition, complement fixation, opsonization, and promotion of phagocytosis

• composed of two heavy chains (determines class: 7, a, e, 8) and two light chains (k and X), both heavy and light chains have a variable and a constant region

• antigen binds to the variable portion of heavy and light chains

• Fab Fragment: antigen binding portion of the immunoglobulin

• Fc Fragment: crystalizable fragment portion of the immunoglobulin that initiates other functions such as complement fixation

• kills bacterium by complement fixation via C1q (IgG and IgM) or antibody-dependent cellular cytotoxicity (ADCC) which attaches Fc to a cytotoxic cell

1. IgG (7): most abundant, involved in complement fixation and ADCC, may cross the placenta (provides protection in the newborn), divided into four subclasses (G1—4)

2. IgA (a): predominantly found in external secretions, associated with dimeric "secretory piece" and a "J" chain

3. IgD (8): initial type of immunoglobulin secreted, trace amounts in serum

4. IgM (^): predominant antibody in early response phase (declines rapidly and replaced with IgG of same specificity), binds complement, pentamer arrangement

5. IgE (e): major contributor in allergy (Type I hypersensitivity), Fc fragment binds to mast cells and basophils

Nonspecific Immunity

• Natural Killer Cells: granular lymphocytes that participate in killing tumor cells and viral infected cells, do not depend on prior immunization, activated by interferon

• Complement System: system of plasma proteins that act with each other that causes lysis of cells and bacteria, stimulation of chemotaxis and cell activation, and opsonization

• Monocytes and Macrophages: produced in bone marrow, recognize and ingest foreign and damaged material

• Polymorphonuclear Cells (PMNs): granulocyte that accumulates in acute infections and participates in phagocytosis

• Eosinophils: granulocyte, active in allergic response and parasitic infections

• Basophils and Mast Cells: granulocytes that release histamine and other substances released with exposure to an allergen, IgE presents on cell surface

• Others: skin and mucosal lining, lysozymes, saliva, gastric acid, etc

Cytokines

• immunomodulatory peptides produced by mononuclear inflammatory cells that participate in paracrine cellular modulation

• see Table 1—5 for cytokines and their actions

Immunodeficiency

B-cell Disorders

• SSx: recurrent sinonasal and pulmonary infections, conjunctivitis, dermatitis, malabsorption, pyogenic bacterial infections

• Dx: quantitative immunoglobulins and subclasses, Schick test, serum protein, immunoelectrophoresis, in vitro specific antibody responses

TABLE 1-5.

Cytokines and Their Actions

Cytokines

Source

Primary Action

IL-1

M^ and any nucleated cells, usually from stimulation by antigen MHC class II

activates other cells and stimulates IL-2 secretion, pyrogen

IL-2

activated T-cells

essential to stimulate T-cells, B-cells, and NK cells

IL-3

T-cells

proliferation of early hematopoietic cells

IL-4

T-cells

stimulates B-cells

IL-5

T-cells, mast cells

eosinophil proliferation, IgA production

TNF-a & ß

lymphocytes, M^, endothelium, keratinocytes

same as IL-1 but may be more cytotoxic to tumors

TGF-ß

lymphocytes, M^, platelets

inhibits cells (immunosuppressive)

IFN-a

leukocytes

anti-viral and anti-tumor effects, increases MHC cell surface proteins

IFN-ß

fibroblasts, epithelial cells

similar to IFN-a

IFN-7

T-cells, NK cells

direct cytotoxic effects

• Hypogammaglobulinemia of Burton: X-linked disorder causing a defect in tyrosine kinase, prevents pre-B cells maturation to B-cells (does not affect T-cells), does not manifest until 6 months of age (after maternal antibodies are gone)

• Common Variable Immunodeficiency: failure of B-cell maturation, associated with T-cell deficiencies and other autoimmune disorders, manifests in early adulthood; Rx: IVIgG

• Isolated IgA Deficiency: most common inherited B-cell defect, selective IgA B-cells do not mature to plasma cells, may be asymptomatic, associated with allergies, transfusion anaphylaxis, autoimmune disorders, and IgG subclass deficiency

• Selective IgG Hypogammaglobulinemia: may affect one or more than one subtype (G14)

1. IgG3: most common hypogammaglobulin deficiency in adults

2. IgG2: most common hypogammaglobulin deficiency in pediatrics

T-cell Disorders

• SSx: increased viral, fungal, protozoal, and bacterial infections, atrophic lymphoid tissue

• Dx: total lymphocyte count, T-cell count, skin tests (candidal, mumps controls, PPD), functional tests (proliferation to mitogens, alloantigens helper/suppresser function)

• DiGeorge Syndrome: disorder of third and fourth branchial arch development, thymic hypoplasia, also associated with hypoplastic parathyroids (hypocalcemia, tetany), aortic arch and facial abnormalities

• Severe Combined Immunodeficiency Disease: multiple genetic forms resulting in lack of T- and B-cell immunity, severe infections (pneumonia, diarrhea, thrush), higher risk of malignancy, variant associated with adenosine deaminase (ADA) deficiency (accumulation of deoxyadenosine, toxic to lymphocytes); Rx: bone marrow transplant

• Wiskott-Aldrich Syndrome: associated with thrombocytopenia (bleeding), eczema, and recurrent infections secondary to poor functional antibody response to polysaccharides (otitis media, pneumonia, and pyogenic organisms), increased risk of malignancy

Atopic Disease

• Pathophysiology: exaggerated immediate hypersensitivity response

• clinical features of asthma, urticaria, hay fever, eczema

• strong genetic disposition

• SSx: immediate wheal and flare skin reaction to common allergens

Human Immunodeficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS)

• see Table 1-6: Head and Neck Manifestations of HIV by Anatomical Location

• Human Immunodeficiency Virus (HIV) infection results from inoculation of infected body fluid (blood, semen, saliva, etc)

• HIV is a retrovirus that attaches to the CD4+ cell marker of T-helper cells, macrophages, and other immunological cells; proviral DNA is synthesized from reverse transcriptase which integrates into host DNA

• HIV results in a decrease in T-helper lymphocytes and impaired function of macrophages, neutrophils, B-lymphocytes, and complement activation

• HIV is also associated with abnormal immune regulation, atopy, and increased autoimmune disease

• Acquired Immune Deficiency Syndrome (AIDS) is defined when an HIV patient develops an AIDS-defining illness (candidiasis, cytomegalovirus disease, Kaposi's sarcoma, Pneumocystis carinii, others) or CD4+ count <200 cells/^l

• the cause of death for most AIDS patients is from sepsis or disseminated neoplasms

• Risks: homosexuals, multiple sex partners, IV drug abuse, previous blood transfusions, health care workers (rare)

• Dx: anti-HIV antibodies detected by enzyme-linked immunosorbent assay (ELISA) and Western Block, polymerase chain reaction of viral genes, CD4+ Count, CD4+/CD8+ Ratio

Other Immunological Disorders

• Complement Disorders: associated with autoimmune diseases, abnormal opsonization, and capsular organism infections

• Chronic Granulomatous Disease: multiple genetic forms results in dysfunction of intracellular hydrogen peroxide production (does not allow intracellular killing of organisms), susceptible to infection of catalase-positive organisms (S. aureus, Aspergillus, Candida, Serratia)

TABLE 1-6. Head and Neck Manifestations of HIV by Anatomical Location

Oral and Pharynx

• Oral Candidiasis

• Oral Hairy Leukoplakia

• Herpes Stomatitis

• Thrombocytopenic Purpura

• Recurrent Aphthous Ulcers

• Bone Loss (Bacillary Angiomatosis)

• Gingivitis (Acute Necrotizing Ulcerative Gingivitis, Necrotizing Stomatitis)

• Kaposi's Sarcoma, Non-Hodgkin's Lymphoma, Squamous Cell Carcinoma

Larynx

• Epiglottitis

• Kaposi's Sarcoma, Non-Hodgkin's Lymphoma

• Laryngitis (Mycobacterium, fungal, cytomegalovirus, Epstein-Barr virus, bacterial)

Neck

• Deep-space Neck Abscess

• Infectious Lymphadenopathy (Mycobacterium, Pneumocystis, cytomegalovirus, Epstein-Barr virus, Toxoplasmosis, Cat-scratch disease, bacterial)

• Neoplastic Lymphadenopathy (Hodgkin's and Non-Hodgkin's Lymphoma, Metastatic disease, Thyroid tumors)

• Persistent Generalized Adenopathy

Salivary Glands

• Lymphoepithelial Cysts of the Parotid Gland

• Salivary Gland Neoplasms

Otologic

• Acute and Chronic Otitis Media, Otitis Externa, Mastoiditis (invasive Aspergillosis, Pneumocystis, Mycobacterium)

• Malignant Otitis

• Sensorineural Hearing Loss (Cryptococcal or Mycobacterial meningitis, Otosyphilis, Toxoplasmosis, autoimmune demyelination of the cochlear nerve, cerebellopontine angle tumors)

• Tympanic Membrane Perforations

• Facial Nerve Paralysis (Herpes Zoster, Cytomegalovirus, Epstein-Barr, HIV, autoimmune demyelination, malignant otitis externa, meningitis and encephalitis)

• Temporal Bone Neoplasms (Hodgkin's and Non-Hodgkin's Lymphoma, Kaposi's sarcoma)

Paranasal Sinus

• Rhinosinusitis (Mucor, Aspergillosis, Pseudomonas)

• Nasal Tumors (Kaposi's Sarcoma, Nasal Lymphomas)

CHAPTER

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