Acute and chronic diseases of the nose. Trauma of the nose. lpistaxis. Anterior and posterior tamponade. Hematoma and abscess of the nasal septum

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Diseases of the Nose, Nasal Trauma, and Epistaxis

1. Acute and Chronic Diseases of the Nose

Acute Rhinitis (Common Cold)

Acute rhinitis is an inflammatory condition of the nasal mucosa lasting less than 4 weeks. It is most commonly viral in origin (rhinovirus, coronavirus, adenovirus) and presents with:

Nasal congestion, rhinorrhea (initially clear, may become mucopurulent)
Sneezing, mild fever, malaise
Onset in winter, associated with dry air that desiccates nasal mucosa

Management: Symptomatic — nasal decongestants (oxymetazoline for ≤3 days to avoid rebound rhinitis), saline irrigation, antihistamines for sneezing. Antibiotics are NOT indicated for uncomplicated viral rhinitis.

Acute rhinitis and sinusitis, together with allergic rhinitis, comprise the vast majority of upper respiratory complaints and represent an enormous socioeconomic burden in terms of missed workdays. — Textbook of Family Medicine 9e

Allergic Rhinitis

A type I hypersensitivity (IgE-mediated) reaction to inhaled allergens (pollens, dust mites, pet dander). Classified as:

Seasonal (hay fever): triggered by pollens
Perennial: triggered by year-round allergens

Clinical features: Sneezing, watery rhinorrhea, nasal/palatal/ocular pruritus, nasal congestion, "allergic salute" (transverse nasal crease from repeated upward nose wiping), pale boggy turbinates.

Treatment: Intranasal corticosteroids (first-line), antihistamines (oral or intranasal), leukotriene receptor antagonists, allergen immunotherapy.

Chronic Rhinitis / Rhinosinusitis

Chronic rhinitis/sinusitis persists for more than 12 weeks. Forms include:

Chronic hypertrophic rhinitis: persistent mucosal thickening, inferior turbinate hypertrophy, nasal obstruction
Atrophic rhinitis (ozena): mucosal atrophy, crusting, foul odor (Klebsiella ozaenae), loss of smell
Chronic rhinosinusitis (CRS): persistent inflammation of nasal and paranasal sinus mucosa; may be with or without nasal polyps

Nasal polyps: Semi-translucent, pale grape-like masses arising from edematous ethmoid mucosa; associated with allergy, CRS, aspirin sensitivity (Samter's triad: polyps + asthma + aspirin intolerance). May cause progressive nasal obstruction and anosmia.

2. Trauma of the Nose

Nasal Fracture

The nasal bones are the most commonly fractured bones in the face. Forces may be lateral (causing displacement) or anterior (causing comminution/"saddle nose").

Clinical features:

Swelling, epistaxis, periorbital ecchymosis ("raccoon eyes")
Nasal deviation, crepitus, nasal obstruction
Tenderness over nasal bones

Assessment priorities:

Rule out septal hematoma (urgent) — look for a unilateral bluish, fluctuant swelling of the nasal septum
Rule out CSF rhinorrhea (halo sign, β-2 transferrin)
Assess for associated orbital wall or ethmoid fractures
Nasal radiographs are NOT routinely needed — they will not alter treatment — Roberts and Hedges' Clinical Procedures in Emergency Medicine

Timing of reduction:

Immediate reduction (<3 hours from injury) if minimal edema and simple fracture
Delayed reduction 3–10 days post-injury in children, 6–10 days in adults, once edema resolves but before fracture consolidation
Fractures >3 weeks old should not be reduced in the ED

ED reduction indications: Simple nasal bone fractures, nasal-septal complex fractures with deviation <½ nasal bridge width, nasal obstruction from deviated septum.

Contraindications to ED reduction: Severe comminution, orbital/ethmoid involvement, deviation >½ nasal bridge width, caudal septal fracture-dislocation, open septal fractures, fractures >3 weeks old.

Technique: Closed reduction using elevators (Goldman, Boies), Walsham forceps for nasal bones, Asch forceps for the septum. After reduction, apply an external nasal splint. Refer to otolaryngologist/plastic surgeon within 10 days.

3. Epistaxis

Epidemiology and Anatomy

Epistaxis is one of the most common otolaryngologic emergencies, with a bimodal age distribution — peaks in children and in adults aged 70–79. Incidence is highest in winter months due to dry, heated indoor air that desiccates nasal mucosa.

Blood supply to the nasal cavity (three main arteries with anastomoses): — Rosen's Emergency Medicine

Sphenopalatine artery (from external carotid via internal maxillary): supplies turbinates, posterior/inferior septum — most commonly implicated in posterior epistaxis
Anterior and posterior ethmoidal arteries (from ophthalmic branch of internal carotid): supply superior mucosa
Superior labial branch of facial artery (external carotid): supplies anterior mucosal septum

Kiesselbach's plexus (Little's area): The confluence of multiple vessels on the anteroinferior nasal septum — the site of 90% of all nosebleeds (anterior epistaxis). It is accessible, usually self-limited, and amenable to direct pressure and cautery.

Posterior epistaxis (~10%): Arises more posteriorly (sphenopalatine territory), predominantly in older adults with hypertension or coagulopathy. More severe, less accessible, higher risk of significant blood loss.

Causes / Risk Factors

Category	Examples
Local	Trauma (nose-picking, blunt), dry air, foreign body, septal deviation, cocaine use
Systemic	Anticoagulants (warfarin, NOACs), antiplatelets (aspirin, clopidogrel), hypertension, coagulopathies, thrombocytopenia, HHT
Neoplastic	Nasopharyngeal angiofibroma, inverted papilloma, carcinoma
Vascular	Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu disease) — spontaneous rupture of telangiectasias causes recurrent serious epistaxis — Robbins Pathology

Note on hypertension: Studies have NOT established a direct causal relationship between hypertension and epistaxis. Elevated BP seen with epistaxis is most often a stress response. Antihypertensive treatment is only urgent if there are signs of a true hypertensive emergency. — Roberts and Hedges'

Initial Assessment

Hemodynamic stability: vital signs, orthostatic symptoms, estimate blood loss
Start IV access and fluid if significant hemorrhage
CBC, coagulation studies (only if on anticoagulants, known coagulopathy, or recurrent/prolonged epistaxis)
Identify bleeding source: anterior vs. posterior (history + nasal speculum exam)
Topical anesthesia + vasoconstrictor (e.g., oxymetazoline, cocaine 4%, or lidocaine + phenylephrine) before procedures

4. Anterior Tamponade (Anterior Nasal Packing)

Indication: Anterior epistaxis not controlled by direct pressure or chemical cautery.

Step-by-step Approach

First-line: Direct compression — squeeze the soft lower third of the nose (not the nasal bones) for 10–20 minutes.

Chemical cautery (if bleeding source is visible): Silver nitrate sticks applied to the visible bleeding point. Never cauterize both sides of the septum simultaneously (risk of septal perforation).

Anterior packing options:

Merocel sponge (nasal tampon): Insert dry, along the floor of the nasal cavity parallel to the hard palate. Expand with 5–10 mL of saline. If it has a drawstring, tie around a gauze to prevent posterior displacement.
Rapid Rhino device: Soak in sterile water (NOT saline — saline inhibits its hydrocolloid gelling) for 30 seconds. Insert along the floor parallel to the hard palate. Inflate with air only (not saline/water) until the pilot cuff is rounded and firm.
Traditional petroleum gauze packing: Layer accordion-style into the nasal cavity from floor to roof using bayonet forceps.

Duration: Packs are left in place for 3–5 days. Premature removal risks rebleeding.

Antibiotics: Oral antibiotics (cephalexin, amoxicillin, or TMP-SMX) may be prescribed to reduce the minimal risk of sinusitis and toxic shock syndrome (TSS), though necessity is unproven for short-term anterior packing.

Complications: Sinusitis, nasolacrimal duct obstruction (blood may appear to exit from the eye — benign), mucosal pressure necrosis, aspiration of packing, rare pneumocephalus (ethmoid plate fracture). — Roberts and Hedges'

5. Posterior Tamponade (Posterior Nasal Packing)

Indication: Posterior epistaxis — when no anterior bleeding source is identified and blood flows down the posterior pharynx. Anterior packing alone does NOT control posterior bleeding because it does not compress the sphenopalatine artery region.

Posterior Gauze Pack (Classic Method)

Anesthetize the nares and posterior pharynx with topical anesthetic.
Prepare a rolled gauze with two silk ties (2-0) — one pair to pull through the nose, one to remain oral for removal.
Pass a No. 10 red rubber catheter through the bleeding nostril; retrieve it from the oropharynx with forceps.
Attach catheter to the silk ties on the gauze pack; retract catheter to carry the pack into the nasopharynx.
Guide the pack manually into position. Attach the oral silk tie to the cheek.
Place anterior packing in addition.
Secure nasal silk ties over a gauze pad/dental roll to maintain posterior pack position.

Inflatable Balloon Packs (Preferred — Easier, Better Tolerated)

Foley catheter technique:

Insert 12-Fr Foley catheter through the bleeding naris into the nasopharynx
Inflate balloon halfway with 5–7 mL saline, then pull forward to seat against the posterior choana
Finish inflating, then place anterior packing to prevent forward migration

Commercial double-balloon devices (e.g., Rapid Rhino posterior, Brighton Epistaxis Balloon):

Posterior balloon inflated first to tamponade the nasopharynx
Anterior balloon then inflated to compress the nasal cavity
Easier to use than gauze, less distressing to patients

Admission: Patients with posterior packing traditionally require hospital admission for monitoring, humidified oxygen, hemodynamics, and pulse oximetry — posterior packs can cause hypoxia (nasopulmonary reflex), cardiac arrhythmias, and are particularly poorly tolerated in the elderly. — Cummings Otolaryngology

Definitive management for refractory posterior epistaxis: Endoscopic sphenopalatine artery ligation or embolization of the internal maxillary and facial arteries via superselective catheterization. Success rates of 91–97%. — Cummings Otolaryngology

6. Septal Hematoma

Definition: Accumulation of blood in the submucoperichondrial space (between the septal cartilage and its perichondrium), stripping the cartilage of its blood supply.

Mechanism: Trauma (shear force) ruptures perichondrial vessels → blood collects in the potential space → cartilage is avascular.

Incidence: Occurs in 0.8–1.6% of nasal traumas. More common in males and children (mucoperichondrium is less adherent in children → greater risk). — K.J. Lee's Essential Otolaryngology

Clinical presentation:

Bilateral nasal obstruction (blood collects on both sides of the cartilage)
Purple/dusky, fluctuant, "grape-like" swellings on the septum
Significant nasal pain (unlike simple deviation)
Saddle-nose deformity if left untreated (avascular necrosis of cartilage)

Complications if untreated:

Avascular necrosis of septal cartilage → saddle-nose deformity
Secondary infection → septal abscess
Septal perforation, nasal valve collapse

Treatment: Prompt incision and drainage (I&D) — make an incision in the mucosa, evacuate the clot. After drainage, prevent reaccumulation by:

Quilting sutures or nasal packing (bilateral)
Incising a piece of mucosa before packing to provide drainage
If it reaccumulates: repeat drainage

7. Septal Abscess

Definition: Suppurative infection within the submucoperichondrial space — most commonly a complication of an untreated or infected septal hematoma.

Causes:

Secondary infection of a septal hematoma (most common)
Nasogastric tube injury to septum
Furunculosis
Direct extension from sphenoiditis
Dental infection
Iatrogenic (post-septoplasty)

Microbiology: Staphylococcus aureus (70%), Haemophilus influenzae, Group A beta-hemolytic streptococcus, Streptococcus pneumoniae, Klebsiella pneumoniae, Enterobacteriaceae. — K.J. Lee's Essential Otolaryngology

Clinical features:

Severe nasal pain and tenderness
Fever, malaise
Widened septum with bilateral dusky/erythematous, fluctuant swellings
Complete nasal obstruction
Erythema of the nasal vestibule

Complications (severe, potentially life-threatening):

Saddle-nose deformity (cartilage necrosis)
Nasal valve collapse
Facial cellulitis / preseptal cellulitis
Cavernous sinus thrombosis (via facial vein/pterygoid plexus)
Orbital extension / orbital cellulitis
Intracranial extension: epidural abscess, meningitis, intracranial abscess
Sepsis

Treatment:

Prompt surgical incision and drainage (operative)
IV antibiotics — empiric coverage for S. aureus (including MRSA consideration) and gram-negative organisms; guided by intraoperative cultures
Bilateral drainage with nasal packing after I&D
Close monitoring for intracranial/orbital complications

Summary Table

Condition	Key Feature	Treatment Priority
Anterior epistaxis	Kiesselbach's plexus, 90% of cases	Compression → cautery → anterior packing
Posterior epistaxis	Sphenopalatine artery, elderly, severe	Posterior tamponade, admit, ± embolization
Nasal fracture	Most common facial fracture	Rule out hematoma, reduce 6–10 days post-injury
Septal hematoma	Fluctuant bilateral septal swelling	Urgent I&D, packing
Septal abscess	Fever, severe pain, purulent, bilateral	Emergency I&D + IV antibiotics

Sources: Roberts and Hedges' Clinical Procedures in Emergency Medicine; Rosen's Emergency Medicine; K.J. Lee's Essential Otolaryngology; Cummings Otolaryngology Head and Neck Surgery; Textbook of Family Medicine 9e; Goldman-Cecil Medicine; Robbins Pathology

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