Give me all the answers to the question on septum, nasal septum, and all of its disorders for 10 marks each, each consisting of definition, etiology, pathogenesis, clinical features, stages, complications, treatment, investigations, and management separately for each of the diseases coming under the chapter nasal septum and its disorders. It should mainly consist of deviated nasal septum, nasal perforation, nasal septal hematoma, septal perforation, septal abscess, etc.

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Nasal Septum and Its Disorders - 10-Mark Answers


1. DEVIATED NASAL SEPTUM (DNS)

Definition

Deviated nasal septum (DNS) is a displacement of the nasal septum from the midline, resulting in asymmetry of the two nasal cavities. It is one of the most common causes of unilateral (or bilateral) nasal airway obstruction. The septum may deviate in the vertical plane (C-shaped or S-shaped), or there may be a horizontal spur.

Etiology

1. Congenital/Developmental:
  • Intrauterine moulding forces on the fetal nose
  • Trauma during birth (forceps delivery, passage through a narrow pelvic canal) - this can cause early septal deviation or deviation that is not evident until puberty
  • Asymmetric chondrocyte growth leading to bending away from the side of injury
2. Traumatic:
  • The most common cause in adults
  • Any nasal or midfacial trauma can cause fracture and displacement of the septal cartilage
  • Minor trauma early in life causes microfractures; healing causes bending of cartilage away from the injury site
3. Growth-related:
  • During active growth at puberty, asymmetric cartilage growth may cause deviation
  • Differential growth of the septum versus the surrounding bony structures
4. Racial/Hereditary factors:
  • Hereditary tendencies in facial bone and cartilage growth patterns

Pathogenesis

The nasal septum is formed by the quadrilateral (quadrangular) cartilage anteriorly and the perpendicular plate of the ethmoid and vomer posteriorly. Any deforming force - traumatic, growth-related, or pressure - displaces cartilage or bone from the midline. When this occurs early in life, asymmetric nasal growth can result due to interruption of chondrocyte growth, leading to asymmetry of the entire nasal structure. The mucosa on the concave (narrow) side undergoes compensatory hypertrophy, while the mucosa on the convex (wider) side undergoes atrophy. The turbinate on the side opposite the deviation often hypertrophies compensatorily (compensatory turbinate hypertrophy).
Airflow through the nose is disturbed - instead of the normal laminar flow, turbulent airflow develops, leading to:
  • Reduced olfaction
  • Impaired warming, humidification, and filtering of inspired air
  • Reduced oxygen inflow
  • Paradoxical nasal obstruction on the contralateral side (patients feel obstruction on the side opposite the deviation because of turbinate hypertrophy)

Classification (Types/Stages)

Mladina Classification (most commonly used):
TypeDescription
Type IVertical ridge on one side, not reaching the nasal valve
Type IIVertical ridge reaching the nasal valve on one side
Type IIIVertical ridge involving the nasal valve area, extending to the floor
Type IVS-shaped deviation (two ridges, one on each side)
Type VLarge horizontal spur on one side, floor of nose
Type VIGroove/trench combined with spur
Type VIIMore than two of above combined
Simple Classification:
  • C-shaped deviation - deviation to one side
  • S-shaped deviation - deviation in two planes
  • Spur - localized bony/cartilaginous projection
  • Dislocation - inferior border of the septal cartilage displaced off the vomerine groove into one nasal passage

Clinical Features

Symptoms:
  1. Nasal obstruction - unilateral or bilateral; may be intermittent due to the nasal cycle
  2. Epistaxis - from drying and irritation of mucosa over the convexity of the deviation; septal varices may develop from the deviation causing turbulent airflow
  3. Headache - from contact point between the deviated septum and lateral nasal wall (contact headache, Sluder's neuralgia)
  4. Rhinitis - from impaired mucociliary clearance
  5. Snoring and mouth breathing
  6. Anosmia or hyposmia - from impaired airflow to the olfactory cleft
  7. Sinusitis - chronic, recurrent; from impaired drainage
Signs:
  1. External nasal deformity (deviation of nasal dorsum in severe cases)
  2. Anterior rhinoscopy: deviated septum, spurs, compensatory turbinate hypertrophy on the contralateral side
  3. Cottle maneuver - positive in nasal valve compromise
  4. After decongestion: assessment of the full extent of septal deviation, high septal deviations that impinge on the internal nasal valve
Paradoxical Nasal Obstruction: The side with the wider nasal passage (away from the deviation) is perceived as obstructed by the patient due to turbinate hypertrophy. This must be explained carefully.

Investigations

  1. Anterior rhinoscopy with nasal speculum - identifies the deviation, spurs, turbinate hypertrophy
  2. Nasal endoscopy - rigid 0° or 30° endoscope for complete evaluation including posterior spur, high deviations, polyps, and sinus ostia
  3. CT scan of paranasal sinuses - axial and coronal cuts; identifies the extent of septal deviation, associated sinusitis, and anatomical relationships before surgery
  4. Acoustic rhinometry - objective assessment of nasal airway cross-sectional area
  5. Rhinomanometry - objective measurement of nasal airway resistance
  6. X-ray PNS (Waters' view) - limited value; may show associated sinus disease

Complications

  1. Chronic sinusitis (frontal, ethmoidal, maxillary)
  2. Recurrent epistaxis
  3. Middle ear disease (secondary Eustachian tube dysfunction)
  4. Hypertrophy of the contralateral inferior turbinate
  5. Atrophic rhinitis on the wide side (from turbulent airflow)
  6. External nasal deformity
  7. Obstructive sleep apnea

Treatment and Management

Conservative:
  • Nasal decongestants (short term) for symptomatic relief
  • Nasal saline irrigation
  • Treatment of associated sinusitis
  • Nasal steroid sprays for associated mucosal inflammation
Surgical Indications:
  • Persistent nasal obstruction causing significant morbidity
  • Recurrent epistaxis from septal varices
  • Recurrent sinusitis secondary to DNS
  • Sleep-disordered breathing
  • Before access surgery for sinus/pituitary/lacrimal operations
  • Associated external nasal deformity
Surgical Options:
1. Septoplasty (preferred)
  • Conservative operation preserving as much septal cartilage as possible
  • Hemitransfixion or Killian's incision
  • Mucoperichondrial flaps elevated
  • Deviated cartilage and bone removed, scored, or repositioned
  • L-strut of at least 1 cm dorsal and 1 cm caudal preserved to maintain tip and dorsal support
  • Bilateral mattress sutures (5-0 plain) to approximate mucoperichondrial flaps
  • Endoscopic septoplasty allows improved visualization
2. Submucous Resection (SMR) / Killian's operation (older technique)
  • More cartilage removed; can cause saddle nose deformity
  • Largely replaced by septoplasty
  • Indicated only when cartilage is needed for grafting in rhinoplasty
  • Preserves dorsal and caudal strut (L-strut)
Postoperative:
  • Nasal packing (not routine - causes pain and does not provide benefit per evidence)
  • Thin pliable Silastic sheets may be used for septal perforations or synechia prevention
  • Antibiotics if packing is left >36 hours (risk of toxic shock syndrome from S. aureus)
  • ENT follow-up at 24-36 hours if packing placed
Complications of Surgery:
  • Perforation (if bilateral mucosal tears not repaired; interposition graft required)
  • Saddle nose deformity (excessive cartilage removal)
  • Loss of tip support (full transfixion incision or open approach)
  • Septal haematoma, abscess
  • Persistent deviation (~20-30% patients; <10% with optimal technique)
  • Epistaxis, cerebrospinal fluid leak (rare)

2. NASAL SEPTAL HEMATOMA

Definition

Nasal septal hematoma is a collection of blood in the potential space between the septal cartilage and its overlying mucoperichondrium (submucoperichondrial space), resulting in stripping of the perichondrium from the cartilage and disruption of the cartilage's blood supply.

Etiology

  1. Nasal trauma - the most common cause; occurs in 0.8-1.6% of nasal trauma cases
  2. Nasal fracture - mechanical force ruptures perichondrial blood vessels
  3. Postsurgical - following septoplasty or SMR (bilateral mucosal tears not recognized)
  4. Nasogastric tube injury
  5. Spontaneous (rare) - in patients on anticoagulants, hemophilia, other coagulopathies
More common in: males and children (mucoperichondrium is less adherent in children, increasing risk)

Pathogenesis

The vascular supply to the septal cartilage is entirely derived through the perichondrium (it is avascular cartilage). When trauma ruptures perichondrial blood vessels, blood accumulates in the submucoperichondrial space. This:
  1. Lifts the perichondrium off the cartilage
  2. Disrupts the blood supply to the cartilage
  3. If untreated, leads to ischemic necrosis of the septal cartilage (within 3-4 days)
  4. The pooled clotted blood acts as a nidus for infection, leading to septal abscess
  5. Loss of enough septal cartilage results in loss of the nasal dorsum and tip support, causing saddle nose deformity

Clinical Features

Symptoms:
  1. History of nasal trauma (usually recent)
  2. Nasal obstruction (bilateral, severe, worsening - distinguishes from post-traumatic mucosal edema alone)
  3. Nasal pain, tenderness
  4. Fever (if infection has set in)
Signs:
  1. Widened nasal septum on anterior rhinoscopy
  2. Bilateral, smooth, boggy, bluish/purple swellings on the septum
  3. Swellings are fluctuant and non-reducible (unlike mucosal edema which reduces with decongestion)
  4. Nasal airway severely compromised
  5. Tenderness over the septum
Key Clinical Distinction: Septal hematoma does NOT shrink with vasoconstrictors, whereas mucosal edema does.

Stages

  1. Acute (0-72 hours): Fresh blood clot; fluctuant, compressible swelling; no infection
  2. Organizing (3-7 days): Clot organizes, becomes firmer; cartilage necrosis begins; risk of secondary infection
  3. Infected/Abscess (>72 hours if untreated): Systemic signs of infection; purulent material; septal abscess
  4. Chronic/Calcified (weeks-months): Fibrocartilage formation or calcification; firm swelling

Investigations

  1. Clinical diagnosis - primarily clinical; anterior rhinoscopy is diagnostic
  2. Aspiration - needle aspiration confirms hematoma (blood, not air)
  3. CT scan - if intracranial extension or facial fractures suspected; shows homogeneous septum widening
  4. Blood cultures - if abscess suspected
  5. CBC, coagulation studies - if spontaneous hematoma or recurrent

Complications

  1. Saddle nose deformity - the most feared complication; from cartilage necrosis
  2. Nasal obstruction - permanent, from cartilage loss and fibrosis
  3. Septal abscess - from superinfection of hematoma
  4. Septal perforation - from necrosis and abscess
  5. Cavernous sinus thrombosis - from spread of septal abscess
  6. Meningitis - from intracranial extension
  7. Epidural abscess, intracranial abscess - serious life-threatening complications
  8. Osteomyelitis - of adjacent bony structures

Treatment and Management

Immediate treatment is mandatory to preserve cartilage viability.
Incision and Drainage (I&D) - Step-by-Step:
  1. Position patient in "sniffing position" with adequate anterior rhinoscopy setup (nasal speculum, light source, suction)
  2. Anesthesia: three cotton pledgets soaked in 1:1 mixture of 4% topical lidocaine + epinephrine 1:1000 for 5 minutes; followed by infiltrative anesthesia if required
  3. Sterile technique as much as possible
  4. Small horizontal incision through the mucosa over the most dependent part of the hematoma - do NOT incise the cartilage
  5. Evacuate the clot with Frazier suction or forceps
  6. Bilateral anterior nasal packing with antibiotic-coated nasal tampons to prevent reaccumulation and keep septum midline
  7. 24-hour ENT follow-up; if packing <36 hours, prophylactic antibiotics may not be required
Postoperative:
  • Daily or 48-hourly review to ensure no reaccumulation
  • Mattress (quilting) sutures through both sides of the septum may be placed to obliterate the dead space and prevent reaccumulation
  • Systemic antibiotics: consider amoxicillin-clavulanate or first-generation cephalosporin to prevent abscess formation
  • If abscess already present: IV antibiotics, culture-directed therapy (see Septal Abscess section)

3. SEPTAL ABSCESS

Definition

Septal abscess is a collection of pus between the septal cartilage and its overlying mucoperichondrium (or in the subperiosteal space over the perpendicular plate of ethmoid/vomer). It is an infected septal hematoma and constitutes a surgical emergency.

Etiology

  1. Infected septal hematoma - the most common cause; septal hematoma that is untreated or inadequately drained becomes infected
  2. Nasal trauma - direct injury introducing organisms
  3. Nasogastric tube injury (iatrogenic)
  4. Furunculosis - of the nasal vestibule spreading inward
  5. Sinusitis - direct extension from adjacent sphenoiditis or ethmoiditis
  6. Dental infection - spread from maxillary teeth
  7. Iatrogenic - following septoplasty with inadequate hemostasis or septal mucosal tear

Pathogenesis

The hematoma provides a culture medium for bacteria. Avascular necrosis of the cartilage begins within 3-4 days if blood supply via the perichondrium is not restored. Bacteria reach the hematoma either hematogenously or by direct spread. Once infected, the purulent collection rapidly destroys cartilage through enzymatic and ischemic mechanisms, causing septal perforation and saddle nose deformity. The rich venous connections of the nose (valveless facial vein, angular vein communicating with superior ophthalmic vein, pterygoid plexus) allow rapid spread of infection intracranially and to the cavernous sinus.

Causative Organisms

  • Staphylococcus aureus - 70% (most common; including MRSA)
  • Haemophilus influenzae
  • Group A beta-hemolytic Streptococcus (Streptococcus pyogenes)
  • Streptococcus pneumoniae
  • Klebsiella pneumoniae
  • Enterobacteriaceae (less common)

Clinical Features

Symptoms:
  1. History of recent nasal trauma or septal hematoma
  2. Severe nasal pain (disproportionate to trauma)
  3. Marked nasal obstruction (bilateral)
  4. Fever, malaise, rigors - systemic signs of infection
  5. Headache
  6. Swelling of the nasal tip and columella (external soft tissue involvement)
Signs:
  1. Tender, red/erythematous nasal tip and vestibule
  2. Bilateral, fluctuant, purple/dusky septal swellings obstructing the airway
  3. Widened, boggy septum on anterior rhinoscopy
  4. Cervical lymphadenopathy
  5. High-grade fever, tachycardia (sepsis features in advanced cases)
  6. Periorbital swelling (if orbital extension)
  7. Signs of meningism (if intracranial extension)

Investigations

  1. Anterior rhinoscopy - diagnostic; bilateral purple/fluctuant septal swellings
  2. Aspiration - pus confirms abscess; send for Gram stain, culture and sensitivity
  3. Full blood count - leukocytosis (neutrophilia)
  4. Blood cultures - if septicemia suspected
  5. CT scan of paranasal sinuses and brain - assesses extent, orbital or intracranial spread; essential before surgery if complication suspected
  6. MRI - better soft tissue delineation for intracranial complications
  7. ESR, CRP - elevated, non-specific markers of infection

Complications

  1. Saddle nose deformity - from destruction of quadrilateral cartilage (most common sequela)
  2. Nasal valve collapse - from loss of structural support
  3. Septal perforation - from full-thickness necrosis
  4. Facial cellulitis - external spread
  5. Orbital cellulitis and abscess - via periorbital spread
  6. Cavernous sinus thrombosis - via superior ophthalmic vein; life-threatening
  7. Meningitis - intracranial spread; potentially fatal
  8. Epidural abscess, intracranial abscess - neurosurgical emergency
  9. Septicemia / Sepsis - systemic spread

Treatment and Management

A surgical emergency - prompt action is mandatory.
Surgical:
  1. Operative incision and drainage (I&D) - under general or local anesthesia
    • Incise most dependent part of the septum
    • Evacuate all pus
    • Irrigate with saline
    • Place a corrugated drain or pack to maintain drainage
    • Ensure bilateral drainage if bilateral abscess
  2. Send pus for Gram stain, culture and sensitivity
  3. Quilting/mattress sutures to obliterate dead space after drainage
Antibiotic Therapy:
  • Empirical (pre-culture): IV broad-spectrum antibiotics covering S. aureus and Gram-positives; e.g., co-amoxiclav (amoxicillin-clavulanate) IV + metronidazole; or IV flucloxacillin + amoxicillin
  • Adjust to culture-directed therapy once sensitivities available
  • MRSA coverage (vancomycin, teicoplanin, or daptomycin) if risk factors present or no response to initial therapy
  • Continue antibiotics for 7-14 days
  • IV antibiotics continued until systemic improvement, then step down to oral
Complications Management:
  • Cavernous sinus thrombosis: IV antibiotics (including antistaphylococcal), anticoagulation (controversial), ophthalmological and neurosurgical review
  • Intracranial abscess: Neurosurgical drainage + IV antibiotics
  • Saddle nose deformity (late complication): Reconstructive rhinoplasty with cartilage or bone graft once infection fully resolved (minimum 6 months)

4. SEPTAL PERFORATION

Definition

Septal perforation is a full-thickness defect (hole) in the nasal septum, involving both the mucosa and the underlying cartilage or bone. It creates a communication between the two nasal chambers.

Etiology

Traumatic:
  • Nose picking (digital trauma - most common cause of anterior small perforations)
  • Following nasal/septal surgery (septoplasty, SMR) - if bilateral mucosal tears are not repaired
  • Following septal hematoma or abscess with cartilage necrosis
  • Nasogastric tube injury, nasotracheal intubation
  • Cauterization of the septum (bilateral simultaneous cautery)
Inflammatory/Infective:
  • Syphilis (tertiary - typically posterior, large, bony)
  • Tuberculosis - granulomatous destruction
  • Wegener's Granulomatosis (Granulomatosis with Polyangiitis, GPA) - midline destructive lesion; mucosal granulations destroy cartilage; associated with sinusitis, lung, and kidney involvement
  • Leishmaniasis
  • Leprosy
Toxic/Occupational:
  • Cocaine (intranasal use) - vasoconstriction causes ischemic necrosis; typically anterior cartilaginous perforation
  • Chrome salts (occupational exposure in plating/tanning industry)
  • Industrial chemicals: arsenic, phosphorus
Neoplastic:
  • Primary nasal or sinus tumors eroding through the septum
Iatrogenic:
  • Overuse of topical nasal medications (prolonged vasoconstrictor use)
  • Nasal steroid spray directed at the septum
Idiopathic:
  • No identifiable cause in some cases

Pathogenesis

A perforation results from full-thickness destruction of the septal mucosa on both sides simultaneously, allowing the two raw areas to coalesce and the cartilage (if not already destroyed) to become exposed and necrotic. Once the cartilage loses its mucosal blood supply bilaterally, it undergoes avascular necrosis, completing the perforation. The hole disrupts normal laminar airflow, creating turbulence, with the following consequences:
  • Excessive evaporation from nasal mucosa at the perforation edges
  • Crust formation
  • Mucosal drying and inflammation
  • Epistaxis from granulation tissue at edges
  • Whistling (from air moving through a small-to-medium perforation)
Perforations rarely heal spontaneously once established.

Clinical Features

Symptoms:
  1. Nasal obstruction - from turbulent airflow; paradoxical (may feel worse on the unaffected side)
  2. Nasal crusting - extensive; from turbulent airflow and drying
  3. Epistaxis - from granulation tissue and crusted mucosa at perforation edges
  4. Whistling - characteristic high-pitched whistle on breathing, especially with small-to-medium anterior perforations
  5. Cacosmia - foul smell from crusted, infected debris within the perforation
  6. Saddle nose deformity - if large perforation (loss of cartilaginous dorsal support)
Signs:
  1. Anterior rhinoscopy/nasal endoscopy: visible hole in the septum, surrounded by crusting, granulations, or dried blood
  2. Location:
    • Anterior cartilaginous perforations: traumatic, cocaine, nose-picking, iatrogenic
    • Posterior perforations (bony): syphilis, TB; often asymptomatic
  3. Saddle nose deformity in severe cases
  4. Associated stigmata: skin/ocular/renal involvement (GPA); chancre (syphilis); drug use history

Investigations

  1. Anterior rhinoscopy and nasal endoscopy - visualize the perforation; assess size, location, edge characteristics
  2. CT scan - assess the extent of the perforation, bony involvement, associated sinus disease
  3. Nasal biopsy - if GPA, TB, tumor, or syphilis suspected
  4. Serology:
    • c-ANCA / PR3-ANCA - for Granulomatosis with Polyangiitis (Wegener's)
    • VDRL, TPHA, FTA-ABS - for syphilis
    • Ziehl-Neelsen stain, TB culture - for tuberculosis
    • ESR, CRP, urinalysis - for GPA (impaired creatinine clearance, haematuria)
  5. Urine toxicology - for cocaine use
  6. CXR - for TB, sarcoidosis, GPA (lung involvement)

Complications

  1. Progressive enlargement of the perforation
  2. Saddle nose deformity (large perforations)
  3. Chronic crusting, infection, and epistaxis
  4. Aspiration pneumonia (from posterior drainage)
  5. Whistling - socially distressing
  6. Anosmia (if large/posterior)

Treatment and Management

Conservative (symptomatic):
  1. Regular nasal saline irrigation (Ringers or saline douching) to remove crusts
  2. Topical antiseptic/antibiotic ointments (Bacitracin, Polysporin) to moisturize and prevent crust adherence
  3. Humidification of environment
  4. Treat underlying cause - antibiotics for TB; immunosuppressives (cyclophosphamide + prednisolone) for GPA; cessation of cocaine/nasal decongestants
Prosthetic:
  • Septal button (Silastic biflanged prosthesis) - inserted to occlude the perforation; effective for perforations up to ~2 cm; reduces whistling, crusting, and epistaxis; does not require surgery; well tolerated
  • Custom-made buttons available for larger perforations
Surgical (for small-to-medium perforations amenable to repair):
  1. Bilateral mucoperichondrial flaps - most common technique; advancement flaps from both sides of the septum cover the defect
  2. Interposition graft - temporalis fascia, costal perichondrium, or crushed cartilage placed between bilateral mucoperichondrial flaps as a framework
  3. Composite grafts (for very small perforations)
  4. Turbinate flap - inferior turbinate mucosa rotated to cover the defect
  5. Enlargement of the perforation - if posterior edge causes significant bleeding/whistling; mucosa is folded around the posterior edge to stabilize it (palliative)
Note: No single surgical technique has met with universal success. Success rates are inversely proportional to perforation size. Very large or posterior perforations are best managed conservatively or with a septal button.

5. NASAL SEPTAL ABSCESS vs. SEPTAL HEMATOMA - DIFFERENTIAL DIAGNOSIS

FeatureSeptal HematomaSeptal Abscess
OnsetPost-trauma (hours)Days after untreated hematoma or trauma
FeverAbsentPresent (high-grade)
PainMild-moderateSevere
SwellingBluish, smooth, boggyRed, erythematous, fluctuant, purple/dusky
AspirationBloodPus
TreatmentI&D (urgent)I&D + IV antibiotics (emergency)
Systemic signsAbsentSepsis features possible

6. ANATOMY OF THE NASAL SEPTUM (Background Knowledge)

The nasal septum is a median partition of the nose consisting of:
  • Quadrilateral (quadrangular) cartilage - the main anterior component; supported by the maxillary crest and vomerine groove below, by the nasal bones and perpendicular plate of ethmoid above
  • Perpendicular plate of ethmoid - the superior bony component
  • Vomer - the posteroinferior bony component
  • Maxillary crest and palatine crest - form the floor
Functions:
  • Separates nasal airway into two distinct chambers
  • Supports the nasal dorsum (via the dorsal quadrilateral cartilage)
  • Maintains shape of the columella and tip
  • Contributes to humidification and filtration of air

SUMMARY TABLE

DisorderKey FeatureEmergencyTreatment
DNSNasal obstruction, epistaxisNoSeptoplasty/SMR
Septal HematomaBoggy bilateral septal swelling post-traumaUrgentI&D + packing
Septal AbscessInfected hematoma; fever; pusEmergencyI&D + IV antibiotics
Septal PerforationHole in septum; whistling; crustingNoSeptal button/flap repair

Sources:
  • Cummings Otolaryngology Head and Neck Surgery (Kridel & Sturm), Ch. 29 - The Nasal Septum, pp. 567, 569
  • K.J. Lee's Essential Otolaryngology, Ch. on Septal Abscess, p. 582
  • Bailey and Love's Short Practice of Surgery, 28th Ed., Ch. 51 - Septal Perforation, p. (Summary Box 51.10)
  • Tintinalli's Emergency Medicine, Ch. 244 - Nasal Septal Hematoma, pp. 1617-1619
  • Textbook of Family Medicine, 9e - Nasal Trauma, Septal Hematoma, p. 281All five comprehensive 10-mark answers are compiled above. Here's a quick guide to what's covered:

What's Included

1. Deviated Nasal Septum (DNS)
  • Full Mladina classification (Types I-VII) and C/S-shaped/spur types
  • Pathogenesis of nasal cycle, paradoxical obstruction, compensatory turbinate hypertrophy
  • Investigations: rhinoscopy, endoscopy, CT, rhinomanometry
  • Septoplasty technique in detail (L-strut, Killian's incision, mattress sutures) vs. SMR
2. Nasal Septal Hematoma
  • Pathogenesis of ischemic cartilage necrosis (perichondrium as sole blood supply)
  • 4-stage progression (acute → organizing → abscess → calcified)
  • Step-by-step I&D procedure from Tintinalli's
  • Key clinical sign: does NOT shrink with vasoconstrictors
3. Septal Abscess
  • Causative organisms with percentages (S. aureus 70%)
  • Full complication spectrum up to cavernous sinus thrombosis and intracranial abscess
  • Antibiotic regimens including MRSA coverage
  • Management of late saddle nose (delayed reconstruction ≥6 months)
4. Septal Perforation
  • Complete etiology (trauma, cocaine, chrome salts, syphilis, TB, GPA, iatrogenic)
  • Targeted investigations (c-ANCA for GPA, VDRL for syphilis, urine tox for cocaine)
  • Conservative (saline, ointments), prosthetic (septal button), and surgical options (bilateral mucoperichondrial flaps + interposition graft)
5. Differential Table comparing hematoma vs. abscess side-by-side for quick revision
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