Evaluation Of Nasal Obstruction History and Physical Exam

History

• Character of Nasal Obstruction: onset and duration, constant versus intermittent, unilateral (tumors, normal nasal cycle) versus bilateral obstruction, associated mouth breathing, snoring, anosmia/hyposmia/taste disturbances, tearing (nasolacrimal duct obstruction or allergy)

• Contributing Factors: potential toxin and allergen exposure, known drug allergies, medications (see Table 1—1), history of immunodeficiency, asthma, sinusitis, otitis media, allergy, sleep disturbances, facial trauma or surgery

• Associated Symptoms: allergic component (sneezing, itchy and watery eyes, clear rhinorrhea), sinus involvement (facial pain,

TABLE 1—1. Common Classifications of Drugs that Cause Rhinorrhea and Nasal Congestion

Antihypertensives

• Psychotropic Medications

• Oral Contraceptives

• Chronic Nasal Decongestants: rhinitis medicamentosa

• Cocaine: local vasoconstriction

• Tobacco: irritates mucosa and impairs ciliary clearance

• Antithyroid Medication

• Aspirin: activates peripheral chemoreceptors

Marijuana headaches), acute infection (fevers, malaise, purulent or odorous nasal discharge, pain)

• Other Head and Neck (H&N) Symptoms: sore throat, postnasal drip, cough, ear complaints, halitosis, ocular pain, hoarseness

• Think "KITTENS" for differential diagnosis (see Table 1-2)

Physical Exam

• External Nasal Exam: external deformities (firmness, tenderness on palpation), nasal flaring, nasal airflow

• Anterior Rhinoscopy/Nasal Endoscopy: examine twice (with and without topical decongestion), quality of turbinates (hypertrophic, pale, blue), quality of nasal mucosa, nasal septum, osteomeatal complex obstruction, foreign bodies, nasal masses, choanal opening

• Quality of Nasal Secretions: purulent or thick (infectious), watery and clear (vasomotor rhinitis, allergy), salty and clear (CSF leak)

• H&N Exam: facial tenderness, tonsil and adenoid hypertrophy, cobblestoned posterior pharynx, cervical adenopathy, otologic exam

Ancillary Tests

• Allergy Evaluation: (see below)

• Paranasal Plain Films: may be considered for screening, largely been replaced by CT/MRI

• CT/MRI of Paranasal Sinus: indicated if obstruction may be secondary to nasal masses, polyps, or complicated sinusitis

TABLE 1-2. Differential Diagnosis of Nasal Obstruction: KITTENS Method

Infectious &

Toxins &

Tumor

(K) Congenital

Idiopathic

Trauma

(Neoplasia)

Neurogenic

Infectious

Nasal and septal

Papillomas

tumors

rhinitis

fractures

Nasal Polyps

Congenital

Rhinoscleroma

Medication side

Hemangiomas

nasopharyngeal

Chronic sinusitis

effects (rhinitis

cysts

medicamentosa)

Pyogenic

Teratoma

Adenoid

Synechia

granulomas

Choanal atresia

hyperplasia

Environmental

Juvenile

irritants

nasopharyngeal

Naso septal

angiofibromas

deformities

Septal hematomas

Malignancy

Foreign bodies

Endocrine Neurologic Systemic

Diabetes

Hypothyroidism

Pregnancy

Vasomotor rhinitis

Granulomatous diseases

Vasculitis

Allergy

Cystic fibrosis

• Biopsy: indicated for any mass suspect for malignancy, avoid biopsy of vascular neoplasms (juvenile nasopharyngeal angiofibroma, sarcomas) or encephaloceles

• Rhinomanometry: provides an objective measurement of airway resistance, largely not utilized in clinical practice since highly time consuming, not cost effective, and inaccurate

• Ciliary Biopsy and Mucociliary Clearance Tests: electronmicroscopy and ciliary motility studies for ciliary defects

• Nasal Secretion Protein and Glucose: evaluate for CSF leak if suspected

• Culture and Sensitivity: surgically obtained cultures usually indicated for complicated acute rhinosinusitis and resistant chronic sinusitis

• Pulmonary Function Tests: suspect reactive airway disease component

• Olfactometry: qualitative and quantitative testing of olfactory substances

NASAL DISEASES Congenital Nasal Disorders

Neurogenic Tumors

• Fronticulus Frontalis: embryologic space that normally fuses in the development of the frontal bones

• Prenasal Space: embryologic space between the nasal bone and nasal cartilage

• Pathophysiology: dura projects through the foramen cecum, through the fronticulus frontalis (intranasally), through the prenasal space into skin (extranasally) with failure of closure of neuropore

• Dx: MRI/CT to evaluate intracranial extension, do not biopsy

Encephalocele

• Pathophysiology: failed closure of neuropore or failed migration of neural crest cells results in ependymal-lined meninges herniation though the base of skull; communicates with subarachnoid space (CSF filled)

• more common in lumbar-sacral region

• Types by Contents

1. Meningocele: contains meninges only

2. Meningoencephalocele: contains meninges and brain elements

3. Meningoencephalocytocele: contains meninges, brain, and a part of the ventricular system

• Types by Location

1. Occipital: defect occurs over the occiput, most common

2. Sincipital (Frontoethmoid): defect occurs between frontal and ethmoid bones at the foramen cecum; Nasofrontal (glabellar lesion), Nasoethmoidal (lateral nose lesion), and Naso-orbital (medial orbital wall lesion) subtypes

3. Basal: transethmoidal, sphenoethmoidal, transsphenoidal, and sphenomaxillary subtypes

• SSx: soft, compressible masses that change with straining and crying, transilluminates, intranasal encephaloceles are often confused with nasal polyps

• Dx: CT or MRI reveals a bony defect, Furstenburg test (compression of the jugular vein causes increase in the size of the mass from increased CSF pressure)

• Complications: meningitis, nasal obstruction, cosmetic deformity, hydrocephalus

• Rx: surgical excision similar to gliomas, must also close the dural defect to prevent CSF leak and brain herniation (neurosurgical consultation)

Nasal Gliomas

• Pathophysiology: sequestered glial tissue or "pinched-off encephaloceles" results in unencapsulated collection of heterotrophic glial cells

• 60% extranasal, 30% intranasal

• SSx: intranasal or extranasal firm, nonpulsatile mass (typically not midline), skin covered, does not change in size with straining, may present as an intranasal polyp, broad nasal dorsum

• Dx: CT or MRI to evaluate for intracranial extension

• Complications: meningitis, nasal obstruction, cosmetic deformity

• Rx: surgical excision (intranasal approach for small tumors, extranasal approach for larger tumors), may require craniotomy for intracranial involvement (neurosurgical consultation)

Dermoids (Ectodermal Cysts, Nasal Dermal Sinus Cysts)

• Pathophysiology: defective obliteration of dural tissue in prenasal space or fronticulus frontalis, forms an epithelial lined cyst (may contain other ectodermal components including hair follicles and adnexal tissue)

• SSx: presents at birth; forms a fistulous tract, pit, or cyst on midline or off-midline of nasal dorsum or septum; tuft of hair may protrude from pit

• Dx: CT or MRI to evaluate for intracranial extension

• Complications: meningitis, CSF leak, infection, cosmetic deformity

• Rx: meticulous excision, must excise complete tract (usually subcutaneous although may dive deep into nasal bone or intracranially)

Rathke's Pouch Cyst

• Pathophysiology: persistent craniopharyngeal canal from failure of the obliteration of Rathke's pouch (a diverticulum of ectoderm which invaginates to form the anterior lobe of the hypophysis and pars intermedius)

• Location: nasopharynx

• SSx: typically asymptomatic, smooth mass in nasopharynx

• Rx: antibiotics with marsupialization or excision for infected lesions

Nasolacrimal Duct Cyst

• Pathophysiology: failure of opening of the distal lacrimal duct

• Location: nasolacrimal duct

• SSx: usually asymptomatic, epiphora

• most spontaneously resolve

• Dx: MRI of paranasal sinus

• Rx: marsupialization for symptomatic cysts or antibiotics with excision for infected lesions

Thorwaldt's Cyst

• Pathophysiology: arises from a pharyngeal notochord remnant (pharyngeal bursa or pouch of Luschka)

• Location: nasopharynx (midline, surrounded by adenoid tissue)

• SSx: asymptomatic, smooth mass found in nasopharynx

• Rx: observation, antibiotics with marsupialization or excision for infected lesions

Choanal Atresia

• Pathophysiology: persistence of the bucconasal membrane resulting in a complete or incomplete bony (90%) or membranous (10%) defect

• more common in females

• unilateral more common than bilateral atresia

• SSx: rhinorrhea, anosmia, nasal obstruction; bilateral involvement presents within first days of life with cycles of apnea and cyanosis followed by crying due to obligate nasal respiration in neonates

• Dx: passage of a 6F catheter, nasal endoscopy, CT of paranasal sinus

• CHARGE Syndrome: most common concurrent syndrome; Coloboma (iris keyhole defect), Heart disease, Atresia (choanal), Retardation (CNS), Genital hypoplasia, Ear abnormalities

• also associated with Apert, Treacher Collins, Trisomy D syndromes

• Rx: unilateral atresia may be managed on an elective basis via a transnasal approach for membranous defects or a transantral, transseptal, or transpalatal approach for bony defects; bilateral atresia must be addressed during first weeks of life (McGovern's nipple may be required for feeding initially for bilateral choanal atresia)

Inflammatory Nasal Masses

Nasal Folliculitis and Furuncles

• Pathogenesis: a pyodermia secondary to Staphylococcus aureus or Streptococcus bacterium, typically arises from a hair follicle (folliculitis), may organize to form pus with a central core (faruncle)

• SSx: intranasal tenderness, reddening and edema of nasal vestibule, sensation of tension at tip of nose, fever

• Complications: septal abscess, septal chondritis, saddle-nose deformity, cavernous sinus thrombosis

• Rx: antibiotic ointment may be utilized initially for folliculitis, avoid manipulation, oral antibiotics with local antibiotic ointment for faruncles, incision and drainage for abscess formation

Septal Abscess

• Pathophysiology: commonly secondary to trauma (septal hematoma) or a faruncle

• SSx: widened septum, nasal obstruction, fever, erythema in nasal vestibule

• Complications: intracranial extension (cavernous sinus thrombosis, meningitis), septal chondritis, saddle-nose deformity

• Rx: aggressive management with incision and drainage and intravenous antibiotics

Rhinophyma

• Pathophysiology: massive hypertrophy of sebaceous glands (form of acne rosacea), associated with Demodex folliculorum

• SSx: begins with coarsening of nasal skin over cartilaginous portion of the nose, develops into a large protuberant lobular swelling of the nasal tip, nasal obstruction

• Rx: surgical full thickness excision (laser, cold scalpel, or dermabrasion) until normal nasal contour, may require STSG

Rhinoliths/Nasal Foreign Bodies

• Pathophysiology: concretions secondary to encrustation of foreign body or longstanding nasal crusting may form rhinoliths

• SSx: unilateral, purulent rhinorrhea, pain, epistaxis

• Dx: anterior rhinoscopy, plain films, or nasal endoscopy

• Complications: secondary infection

• Rx: removal (may require general anesthetic, may trigger epistaxis)

Nasal (Sinonasal) Polyposis

• Pathophysiology: unclear, may be secondary to abnormal cellular homeostasis from chronic inflammation resulting in polypoidal degeneration, typically arises from lateral nasal wall

• associated with chronic sinusitis (approximately 50%), ASA intolerance, and asthma (Samter's Triad), allergy, fungal sinus infection, cystic fibrosis, trauma, and metabolic diseases

• SSx: smooth, pale, intranasal clustered grape-like masses (usually bilateral), nasal obstruction, anosmia, postnasal drip, rhinorrhea, hyposomia

• Dx: anterior rhinoscopy, nasal endoscopy, CT of paranasal sinus (nonenhancing nasal mass with partial or complete sinus opacification may reveal expansion of superior nasal fossa and ethmoid air cells in advanced cases, also required to evaluate for potential encephalocele, gliomas, or inverting papillomas)

• Histopathology Types: edematous (few inflammatory cells with edematous stroma), inflammatory (predominantly inflammatory cells), fibrous (collagen stoma)

• Complications: proptosis, diplopia, bone erosion, osteitis, meningitis

Management

• Medical Management: allergy desensitization, avoidance of aspirin or other allergens, nasal corticosteroid sprays or oral corticosteroids, hypertonic saline irrigations

• Polypectomy: effective in short term (high rate of recurrence), provides a biopsy specimen

• Endoscopic Sinus Surgery: treatment of choice, includes polypectomy, complete sphenoethmoidectomy, antrostomy for ventilation and drainage, polypoid specimen should be sent as specimen to evaluate for potential underlying tumor, recurrence common

• consider lipoxygenase pathway inhibitors

Neoplasms

Keratotic Papilloma (Benign Squamous Papilloma, Vestibular Wart)

• Pathophysiology: benign lesions arise from squamous or schneiderian epithelium (associated most commonly with Human Papilloma Virus 6 and 11)

• low malignant potential

• SSx: verrucous lesion, commonly on nasal vestibule, painless

• Dx: anterior rhinoscopy, nasal endoscopy

• Rx: simple excision or laser ablation; for septal keratotic papillomas a cuff of normal mucoperichondrium should be taken with lesion to avoid recurrence

Inverted Papilloma

• Pathophysiology: arise from proliferation of reserve cells in schneiderian mucosa (associated with human papilloma virus)

• more common in males

• often misdiagnosed as a nasal polyp (polyps are more translucent, bilateral, and bleed less)

• SSx: unilateral obstruction, sinusitis, epistaxis, rhinorrhea, diplopia, typically presents on the lateral nasal wall (rarely on the nasal septum), may be associated with a benign nasal polyp

• Dx: CT of paranasal sinus reveals erosion into lateral nasal wall or extension into maxillary sinus, may reveal calcifications; MRI may be considered for extensive involvement or for recurrence

• Histopathology: cristae-laden senescent mitochondria, inflammatory cells throughout epithelium, endophytic growth of epithelium

• Complications: 10% malignant degeneration from lateral wall lesions (rare from nasal septum), extension into sinuses, orbit (blindness, diplopia, proptosis), or intracranial and skull base

• Rx: adequate en bloc excision typically requires a medial maxillectomy, may require an ethmoidectomy or craniofacial resection, endoscopic excision may be considered for select lesions (recurrence rate up to 20%)

Juvenile Nasopharyngeal Angiofibroma (JNA)

• most common vascular mass in nose

• exclusive to adolescent males

• Pathophysiology: benign vascular tumor, etiology unknown

• slowly growing, locally invasive, may spread intracranially, does not metastasize

• SSx: smooth purplish lobulated mass in nasopharynx or lateral nasal wall (posterior aspect of the middle turbinate), recurrent unilateral epistaxis (may be bilateral), rhinorrhea, nasal obstruction, anosmia

• Dx: CT/MRI/MRA (magnetic resonance arteriography) of paranasal sinuses (mass with extension into pterygomaxillary fissure), carotid angiography, avoid biopsy

• Complications: extension into sinuses, orbit (blindness, diplopia, proptosis), or intracranial and skull base

• Rx: surgical excision; consider preoperative embolization; radiation therapy reserved for residual tumors, intracranial extension, or inoperable candidates

Other Benign Tumors

• Benign Salivary Gland Tumors: rare, pleomorphic adenoma most common

• Hemangiomas: most often present at Little's area or inferior turbinate; Rx: excision with cuff of normal mucoperichondrium, may consider preoperative embolization

• Pyogenic Granulomas: friable polypoid lesion (usually on septum, may be secondary to trauma), difficult to distinguish from hemangiomas, presents with epistaxis and unilateral obstruction, may present during pregnancy ("pregnancy tumor"); Rx: excision although most resolve

• Hemangiopericytomas: arise from the pericyte, 10% malignant degeneration; Rx: excision, 50% recur

• Osteomas: common benign tumor, slow growing, usually asymptomatic, multiple lesions associated with Gardner syndrome (malignant degeneration of intestinal polyps); Rx: excision for symptomatic lesions otherwise may observe with serial radiographs

• Chordomas: arise from notochord of nasopharynx, may produce obstructive symptoms or involve cranial nerves; Rx: excision

Malignancy (see p. 259)

Systemic Diseases Affecting The Nose

Granulomatous Diseases (see also pp. 205—212)

Sarcoidosis: cobblestoning of sinonasal mucosa from granulomatous inflammation, dryness, crusting, epistaxis, or septal perforation

• Histocytosis X: nasal mass, epistaxis, or septal perforation

• Lethal Midline Granulomas: clear to purulent rhinorrhea, septal perforation, epistaxis, facial destructive lesions

Vasculitic Diseases (see also p. 214)

• Wegener's Granulomatosis: inflamed friable mucosa, ulcerative septal perforation, saddle nose deformity, epistaxis

• Periarteritis Nodosa: nasal mucosal lesions

Lupus Erythematosis: ulcerated nasal septum (nasal perforation)

Nasal Anatomical Abnormalities

Valvular Collapse

• Pathophysiology: weak structural support of nasal valve results in inspiratory obstruction

• Causes: congenital, trauma, iatrogenic (excessive cartilage removal at intercartilaginous junction), aging

• SSx: nasal airway obstruction on inspiration

• Dx: Cottle maneuver (demonstrates decreased nasal resistance by pulling superiorly on medial maxilla skin to open valve)

• Rx: mechanical cartilaginous spreader grafts, battons placed over the valve, traction sutures, or may consider nasal stent apparatus at night

Septal Deviations

• Types: traumatic and congenital

• Common Defects: spurs, crests, dislocation of quadrangular septal cartilage, buckling

• SSx: unilateral nasal obstruction (may be bilateral), hyposmia, epistaxis, recurrent sinusitis

• Dx: anterior rhinoscopy

Surgical Management

• Submucous Resection: obstructing cartilaginous and bony portion of the nasal septum is removed

• Septoplasty: removal of deviated cartilaginous and bony septum with reinsertion after remodeling and repositioning (preserves support system, less risk of perforation)

• Indications: nasal obstruction (deviated nasal septum), epistaxis, chronic sinusitis (when septum is obstructing), access for transseptal sphenoidotomy, headache from an impacted spur, septal neoplasia (rare)

• Complications: perforation, saddle nose deformity (over resecting cartilage anteriorly), cribriform plate fracture, septal hematomas, anosmia, septal abscess, bleeding

Septal Perforations

• Causes: septoplasties (most common cause, >50%), infections (tertiary syphilis), trauma (nose picking), neoplasms, granulomatous disease, vasculitis, cocaine abuse, corticosteroid nasal spray

• Dx: anterior rhinoscopy, consider biopsy of granulation tissue or abnormal mucosa to evaluate for malignancy, sarcoidosis, tuberculosis, and other granulomatous diseases

• SSx: crusting, epistaxis, whistling, obstructive sensation from turbulent flow, may be asymptomatic

1. saline irrigation, emollients

2. consider sliding or rotating mucoperichondrial flaps with or without a fascial graft; contraindicated for large perforations (approximately >2 cm of vertical height), cocaine abusers, malignancy, granulomatous or vascular diseases

3. silastic button

Septal Hematomas

• Pathophysiology: hemorrhage (usually from trauma) collects beneath mucoperichondrium and mucoperiosteum resulting in elevation of the mucosa off the cartilaginous septum (loss of vascular supply)

• SSx: unilateral obstruction (may be bilateral), septal swelling

• Complications: septal abscess, cavernous sinus thrombosis, saddle nose deformity

• Rx: immediate evacuation of hematoma, nasal packing, and antibiotic prophylaxis

Olfactory Dysfunction

Evaluation

History and Physical Exam

• Quality of Olfactory Dysfunction: anosmia, hyposmia (decreased olfactory acuity as seen in smokers, postmenopausal, elderly), phantosmia (sense odors that are not present), versus hyperosmia (heightened sense of smell as in hunger, as seen in cystic fibrosis, Addison disease), single-sided (obstructing, traumatic, infectious) versus bilateral olfactory loss

• Contributing Factors: history of upper respiratory infections, sinusitis, allergy, trauma, toxins, medications

• Associated Symptoms: changes in sense of taste (80% of flavor is appreciated from olfaction), other cranial nerve involvement (diplopia, hearing loss, hoarseness, etc.)

• Physical Exam: sinus and rhinology evaluation including nasal endoscopy to evaluate for obstruction, otologic examination to evaluate potential injury to the chorda tympani, full neurological work-up to determine other possible coexisting defects

Diagnostic Tests

• CT of paranasal sinuses: mainstay for complicated olfaction disorders or unclear etiology

• MRI: examine olfactory bulb and tracts

• Olfactory Tests: includes scratch and sniff identification tests, odor vials (including ammonia)

• Taste Testing

Causes

Obstructive Nasal and Paranasal Disease

• most common etiology of anosmia

• Pathophysiology: obstruction may compromise airflow to olfactory bulb

• Common Causes: mucosal edema, tumors, nasoseptal deformities, polyps

• Rx: address underlying cause, relieve obstruction

Upper Respiratory Infection

• second most common etiology of anosmia

• may cause parosmia (distorted perception of smell)

• Pathophysiology: may be secondary to viral-induced neuronal injury (Essential Anosmia), epithelial damage, or obstruction

• Rx: no effective treatment

Head Trauma

• third most common etiology of anosmia

• Pathophysiology: shearing forces injure the axons of olfactory neurons at cribiform plate (more common in occipital injuries)

• Rx: no effective treatment

Other Causes

• Congenital: familial dysautonomia, Kallmann's syndrome (autosomal dominant, hypogonadotrophic, anosmia secondary to incomplete olfactory bulb and stalk, hypothalamus, or olfactory epithelium)

• Tumors: frontal or temporal lobe lesions, esthesioneuroblastoma, meningiomas, pituitary adenomas

• Aging Effects: Parkinson's, Alzheimer's (typically causes parosmias)

• Medications and Toxins: smoke, sulfur dioxide, putrid gases, cocaine, cadmium, heavy metals, radiation, chemotherapy

Epistaxis

Introduction

• trauma (including nose picking and vigorous nose blowing) and mucosal dehydration are the most common cause of epistaxis

hypertension, aspirin (and other platelet inhibiting medications), and alcohol abuse account for the most common causes of refractory epistaxis

• colder temperatures and dryness (winter seasons) increase risk of vascular injury

• nasoseptal deformities may result in epistaxis secondary to the drying effects of turbulent airflow

Kiesselbach's Plexus (Little's area)

• confluence of arterial vessels at the anterior nasal septum

• susceptible to bleeding due to the fragile mucosa and tightly adherent to underlying mucosa affording little resistance to mechanical stress

• Contributing Vessels: anterior ethmoidal, superior labial, greater palatine, and sphenopalatine arteries

Osler-Weber-Rendu Syndrome (Hereditary Hemorrhagic Telangiectasia)

• Pathophysiology: autosomal dominant ^ defect in contractile elements (elastic and muscular layers) of vessels, results in arteriovenous malformations

• SSx: friable mucosa, visceral and mucosal telangiectasia (tongue, oral mucosa, colon, lung), intermittent epistaxis, intracranial hemorrhage (neurological symptoms), hematemesis

• Rx: septoplasty or septodermoplasty (requires STSG, amniotic, or myocutaneous grafts for coverage after removing telangiectatic area), embolization, laser ablation

Evaluation and Management History and Physical Exam

• after evaluating the ABCs (airway, breathing, intravenous access), ideally should perform a systematic evaluation of the patient prior to controlling the bleeding (may not be possible for heavy bleeding, may consider neosynephrine soaked cotton pledgets as a temporizing procedure)

• Characterize Epistaxis: estimate amount of blood loss, length of time of epistaxis, intermittent versus continuous bleeding, and side of bleeding; previous episodes, hospitalizations, packing, or other management for epistaxis

• Medical History and Blood Dyscrasias: hypertension, arteriosclerosis, leukemia, idiopathic thrombocytopenic purpura, von Willebrand's disease, renal and hepatic failure, anemia, hemophilia (higher risk of arterial, pulsatile bleeding)

• Medications: antiplatelet medications (ASA), anticoagulants (coumadin, heparin)

• Social History: cocaine abuse, alcoholism, smoking

• Toxin Exposure: ammonia, sulfuric acid, gasoline, phosphorus (associated with nasal dryness and crusting)

• Other Contributing Factors: previous septal or nasal surgery, recent trauma to nasal bone or septum, facial skeleton, dry environment, high altitude living (home CPAP ventilators or oxygen), symptoms of allergy, sinusitis, rhinitis, URI (typically short-lived bleeding)

• Think "KITTENS" for differential diagnosis (see Table 1-3)

TABLE 1-3. Differential Diagnosis of Epistaxis: KITTENS Method*

Infectious &

Toxins &

Tumor

(K) Congenital

Idiopathic

Trauma

(Neoplasia)

Endocrine

Systemic

Nasoseptal deformities

Infectious rhinitis/sinusitis

Nasal and septal fractures

Juvenile nasopharyngeal

Pheochromocytomas (hypertensive

Granulomatous diseases

Osler-Weber-Rendu

Mucosal

Foreign bodies

angiofibromas

crisis)

Vasculitis

Escaped blood from gastrointestinal bleeding, hemoptysis, etc...

Medication

Environmental toxic agents

Iatrogenic

Nasal picking

Other benign or malignant sinonasal tumors

Blood dyscrasia (hemophilia, aspirin abuse, chronic renal failure)

Hypertension

*No Neurological causes of epistaxis

*No Neurological causes of epistaxis

Physical Exam and Initial Ancillary Tests

• patient should sit up with body tilted forward to allow blood to be spit out and not swallowed

• initial attempt to stop bleeding by applying pressure to nasal alae for several minutes

• apply decongestant/anesthetic agents (4% cocaine or 0.25% phenylephrine HCL)

• acquire adequate lighting (head lamp), nasal speculum, bayonet forceps, frazier and Yankhauer suctions available to suction clot and attempt to localize active bleeding (examine for escoriations, foreign bodies, masses, nasoseptal deformities, etc.)

• for chronic or recurrent epistaxis without an obvious bleeding source patient should undergo an endoscopic exam

• Lab Tests: PT/PTT, bleeding time, liver function tests, creatinine, CBC, type and cross

Medical Management

• Acute Management: may need to correct hypovolemia (3:1 Rule: for every 100 cc of blood loss, replace with 300 cc of crystalloid fluid), hypertension (antihypertensive agents), or coagulopathy (fresh frozen plasma, platelets, cryoprecipitate)

• Chronic Management: hypertonic nasal spray and humidification; long-term medical management of hypertension; antimicrobial ointment to excoriated lesions; avoid excess straining, nose blowing, and digital manipulation

Cauterzation

• may use silver nitrate, chromic acid pearls, electrocautery (for deeper penetration and posterior bleeding), cryotherapy

• laser cauterization may be considered for vascular malformations

• endoscopic instrumentation may be used for posterior and difficult to visualize bleeding

• Indications: minor bleeding, single bleeding points, easily visualized regions (Kiesselbach's plexus)

• Advantages: simple, quick, minimal tissue damage, no packing required

• Disadvantages: allows for coagulation of superficial vessel only, risk of perichondrial exposure, septal perforation (avoid cauterization of both sides of the septum at similar points), cartilage injury

Anterior Nasal Packing

• Gelfoam, Cellulose, or Microfibrillar Collagen Packing: provides a procoagulant effect, gentler packing, useful for coagulopathies, dissolves (does not require removal), may be placed after initial coagulation

• Nasal Tampons and Expandable Sponges: expand with instillation of water to provide pressure against the nasal mucosa

• Vaseline Strip-Gauze: formal anterior packing placed to posterior choanae, controls most posterior bleeding

• keep packing in place for 3—5 days to allow vessel to develop a mature thrombus

• may supplement with thrombin, oxycellulose, or fibrin

• Indications: acute or recurrent epistaxis after failed medical management or cauterization

• Advantages: simple, proper formal strip-gauze pack controls most posterior bleeding, does not require inpatient monitoring

• Disadvantages: results in nasal obstruction, risk of pressure necrosis (nasal and septal cartilage), hypoxia, sinusitis, bacteremia, and epiphora; requires prophylactic antibiotics to reduce risk of otitis media, sinusitis, and toxic shock syndrome

Posterior Nasal Packing

• gauze, sponge pack, Foley catheter, pneumatic nasal catheters, or tonsillar packing is placed to close off the choana to prevent escape of bleeding into the nasopharynx

• requires a formal anterior pack for stability

• Nasal Balloons: catheter with two balloons (one placed in the nasopharynx and the other in the nasal cavity), designed for easier placement of a posterior pack, provides less trauma and is simple to adjust pressure

• Indications: failed anterior packing, skull base trauma, hemorrhage from a major branch of the sphenopalatine artery

• Advantages: may be inserted for severe bleed in the emergency room or office

• Disadvantages: risk of airway compromise (requires hospital monitoring), requires patient cooperation (painful), may require intubation or general anesthesia, eustachian tube dysfunction (hearing loss), other risks similar to anterior nasal packing

Embolization

• Indications: intractable nasal hemorrhage, surgically inaccessible sites, inoperable candidates

• Advantages: diagnostic (defines bleeding site) and therapeutic, may be repeated, can be done under local anesthesia

• Disadvantages: risk of embolic event (pulmonary emboli, stroke), requires active bleeding, facial pain

Vascular Ligation

• Indications: uncontrolled epistaxis (typically posterior bleeding), identifiable bleeding site

• Techniques

1. Anterior and Posterior Ethmoidal Artery Ligation: approach from a Lynch incision, anterior ethmoid artery is located 14—18 mm posterior to frontoethmoid suture line, posterior ethmoid artery is located 10 mm posterior to anterior ethmoid foramen, the optic nerve is located 4—5 mm posterior to the posterior ethmoid foramen

2. Maxillary Artery or Sphenopalatine Artery Ligation: may be approached transantrally, transorally, or endoscopically

3. External Carotid Artery Ligation: severe uncontrolled, life-threatening bleeding, ligate above the origin of the lingual artery

• Advantages: decreases pressure gradient in nasal vessels to allow clotting

• Disadvantages: periorbital ecchymosis, possible recurrence from collateral circulation, risk of retrobulbar hematoma, hemorrhage, optic nerve and infraorbital nerve injury, clip dislodging

Septoplasty/Submucous Resection

• Use: septal defects (unable to pack), Osler-Weber-Rendu Syndrome

• Advantages: removes diseased mucosa and replaces with STSG (Saunder's Dermoplasty), reduces drying effect by decreasing turbulent airflow

• Disadvantages: risk of septal perforation

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