Anatomy Of The Nose

Foundations and mechanisms

Structural organisation and functional compartments

The nose comprises the external nose, nasal vestibule and paired nasal cavities separated by the septum. For anaesthetic practice, the key conceptual division is between the structural airway (nares, vestibule, septum, turbinates and choanae), the neurovascular mucosa governing reflexes and bleeding, and the paranasal sinus drainage system, which influences infection, obstruction and surgical access. The nasal cavities extend from the nares to the choanae, opening into the nasopharynx at approximately the level of the hard palate posteriorly.

The roof is narrow and formed by nasal bones, frontal bone, cribriform plate of ethmoid and sphenoid. The floor is formed by the hard palate. The medial wall is the septum: quadrangular cartilage anteriorly, perpendicular plate of ethmoid superiorly and vomer posteroinferiorly. The lateral wall carries the inferior, middle and superior conchae, which create the corresponding meatuses. The inferior meatus receives the nasolacrimal duct; the middle meatus receives the frontal, maxillary and anterior ethmoidal sinuses; the superior meatus receives posterior ethmoidal cells; the sphenoethmoidal recess receives the sphenoid sinus.

Region	Key anatomical feature	Anaesthetic relevance
Nasal vestibule	Keratinised squamous epithelium, vibrissae, relatively narrow	Trauma during nasopharyngeal airway or nasal intubation; topicalisation less effective than respiratory mucosa
Respiratory mucosa	Pseudostratified ciliated columnar epithelium with venous sinusoids	Drug absorption, humidification, warming, bleeding and mucosal oedema
Olfactory cleft	Superior septum, superior concha and roof; olfactory epithelium	Cribriform plate vulnerability; anosmia risk; avoid instrumentation directed superiorly
Posterior nasal cavity	Choanae adjacent to nasopharynx	Correct path for nasal tubes: along floor, not upwards

Airflow, resistance and conditioning

The nose contributes approximately 50% of total upper airway resistance during quiet nasal breathing, although this varies with the nasal cycle, posture, mucosal congestion and disease. Resistance is greatest at the nasal valve, the narrow segment bounded by the septum, upper lateral cartilage and inferior turbinate; its cross-sectional area is commonly cited as approximately 55–100 mm². Because flow is partly turbulent, small reductions in radius markedly increase resistance; Poiseuille’s relationship remains a useful conceptual model, with resistance proportional to 1/r⁴ under laminar conditions.

The nose conditions inspired gas: warming towards core temperature, humidifying towards near-saturation, and filtering particles. At the trachea, inspired gas is normally approximately 37°C and 100% relative humidity, corresponding to an absolute humidity of about 44 mg H₂O/L. Bypassing the nose with tracheal intubation removes this conditioning and contributes to mucociliary dysfunction, secretion thickening and heat loss.

Vascular anatomy and mechanisms of epistaxis

The nasal mucosa is highly vascular, supplied by branches of both internal and external carotid systems. The clinically dominant anterior plexus is Kiesselbach’s plexus on the anteroinferior septum, where septal branches of the superior labial, sphenopalatine, greater palatine and anterior ethmoidal arteries anastomose. Posterior epistaxis more often arises from the sphenopalatine artery and is more difficult to control.

Arterial source	Parent system	Principal contribution
Anterior and posterior ethmoidal arteries	Ophthalmic artery; internal carotid system	Superior septum and lateral wall; important in skull base and ethmoid surgery
Sphenopalatine artery	Maxillary artery; external carotid system	Posterior septum and lateral nasal wall; major vessel in posterior epistaxis
Greater palatine artery	Maxillary artery	Inferior septum via incisive canal
Superior labial artery	Facial artery	Anterior septum and vestibule

Venous drainage parallels arterial supply to facial, ophthalmic and pterygoid plexus pathways. The valveless communications with the cavernous sinus explain the classical, though uncommon, risk of intracranial septic spread from the midface. Mucosal venous capacitance is under autonomic control; sympathetic stimulation causes vasoconstriction and reduced airway resistance, whereas parasympathetic activity increases glandular secretion and congestion.

Innervation and reflex physiology

General sensation is via trigeminal branches. The anterior superior nasal cavity is supplied by the anterior ethmoidal nerve from the nasociliary branch of V1; posterior and inferior regions are supplied by V2 via nasopalatine and posterior superior lateral nasal branches from the pterygopalatine ganglion. Olfaction is mediated by CN I through the cribriform plate. Parasympathetic secretomotor fibres arise from the facial nerve via the greater petrosal nerve and pterygopalatine ganglion; sympathetic fibres arise from the superior cervical ganglion via the deep petrosal nerve.

Nasal stimulation may provoke sneezing, coughing, lacrimation, laryngospasm or haemodynamic responses. In anaesthesia, instrumentation of the nasal cavity can activate trigeminal afferents with reflex vagal effects, particularly in lightly anaesthetised patients. Topical local anaesthesia and vasoconstriction reduce both nociceptive input and mucosal trauma.

Classification and high-yield anatomical hazards

• Nasal septal deviation: may be cartilaginous, bony or combined; clinically relevant when selecting the nostril for nasotracheal intubation or nasopharyngeal airway insertion.
• Turbinate hypertrophy: commonly inferior turbinate enlargement; increases resistance and bleeding risk with blind instrumentation.
• Basal skull fracture risk: suspected with CSF rhinorrhoea, periorbital ecchymosis, Battle’s sign, haemotympanum or severe midface trauma; nasal instrumentation is classically avoided because of cribriform plate disruption.
• Choanal obstruction: unilateral disease may be occult; bilateral choanal atresia presents neonatally because neonates are preferential nasal breathers for the first weeks of life.

Topical pharmacology relevant to nasal instrumentation

Drug	Typical adult nasal use	Key limits and cautions
Lidocaine	2–4% topical spray, pledgets or atomisation	Maximum usually 3 mg/kg without adrenaline and 7 mg/kg with adrenaline; reduce in frailty, hepatic impairment and combined routes
Co-phenylcaine	Lidocaine 5% with phenylephrine 0.5%, commonly 1–2 sprays per nostril depending on preparation	Beware hypertension, ischaemic heart disease, thyrotoxicosis and monoamine oxidase inhibitor use
Phenylephrine	0.25–1% topical solution or spray	Alpha-1 vasoconstriction; systemic absorption may cause hypertension, reflex bradycardia and arrhythmia
Oxymetazoline	0.05% spray, typically 1–2 sprays per nostril	Alpha-adrenergic vasoconstrictor; rebound congestion with prolonged use beyond approximately 3–5 days
Cocaine	4% topical solution in ENT practice	Local anaesthetic plus vasoconstrictor; maximum commonly 1.5 mg/kg or 100–200 mg depending on local policy; avoid in significant cardiovascular disease

The practical mechanism of safe nasal passage is therefore anatomical rather than force-based: vasoconstrict, anaesthetise, choose the more patent side, advance parallel to the hard palate along the floor of the nose, and avoid superior angulation towards the cribriform plate.

Clinical assessment and investigations

Clinical presentation and targeted anatomical assessment

Assessment of the nose in anaesthetic practice is directed at identifying obstruction, bleeding risk, infection, deformity and anatomical hazards to instrumentation. Symptoms should be anatomically localised: anterior obstruction suggests septal deviation, inferior turbinate hypertrophy, vestibular stenosis or valve collapse; posterior obstruction suggests choanal pathology, adenoidal tissue, polyposis or nasopharyngeal mass. Unilateral persistent obstruction, epistaxis, crusting, facial pain, paraesthesia or anosmia are red flags for neoplasia, invasive fungal disease or granulomatous disease. Clear unilateral rhinorrhoea exacerbated by leaning forward suggests cerebrospinal fluid leak, particularly after craniofacial trauma or trans-sphenoidal surgery.

For Primary FRCA purposes, clinical assessment is particularly relevant before nasotracheal intubation, fibreoptic nasendoscopy, nasogastric tube placement and high-flow nasal oxygen. Enquire specifically about previous septal surgery, nasal fractures, recurrent epistaxis, anticoagulants, cocaine use, granulomatosis with polyangiitis, hereditary haemorrhagic telangiectasia, and symptoms of obstructive sleep apnoea. Examination should compare nostril patency by occluding each side during quiet inspiration; forced inspiration may exaggerate dynamic nasal valve collapse. The Cottle manoeuvre—lateral traction on the cheek improving airflow—suggests internal nasal valve compromise, although diagnostic specificity is poor. Anterior rhinoscopy assesses Little’s area, septal spurs, perforation, crusting, turbinate hypertrophy and discharge. Flexible nasendoscopy defines posterior septal deviation, polyps, choanae, nasopharynx and laryngeal inlet, and is more informative than anterior inspection when planning awake nasal fibreoptic intubation.

Presentation	Important differential diagnoses	Assessment implication
Unilateral nasal obstruction	Septal deviation/spur, foreign body, antrochoanal polyp, inverted papilloma, malignancy	Prefer contralateral nostril for instrumentation; consider nasendoscopy/CT if persistent or bleeding
Bilateral obstruction	Allergic/non-allergic rhinitis, turbinate hypertrophy, chronic rhinosinusitis with polyps, pregnancy rhinitis	May respond to vasoconstrictor; increased resistance to nasal oxygen and tubes
Epistaxis	Kiesselbach plexus trauma, hypertension association, anticoagulation, posterior sphenopalatine bleed, tumour	Correct coagulopathy where possible; avoid traumatic nasal instrumentation
Clear rhinorrhoea after trauma/surgery	CSF leak, allergic rhinitis, lacrimal drainage	Avoid nasal tubes; investigate beta-2 transferrin and skull base imaging
Midface trauma/periorbital bruising	Le Fort fracture, cribriform plate fracture, septal haematoma	Nasal intubation is contraindicated if skull base disruption suspected

Bedside scoring and functional tests

The Nasal Obstruction Symptom Evaluation score is a validated patient-reported instrument comprising 5 items scored 0–4 and multiplied by 5, giving a 0–100 score; values above 50 generally represent at least moderate obstruction and are used in septoplasty outcome studies rather than acute airway decision-making. Peak nasal inspiratory flow is simple and reproducible: adult values are commonly approximately 100–150 L min^-1, but interpretation requires comparison with baseline, age and sex. A low value is non-specific but supports clinically significant obstruction. For OSA risk, relevant because nasal obstruction worsens CPAP tolerance and perioperative airway risk, STOP-Bang ≥3 has high sensitivity for moderate-to-severe OSA but low specificity; ≥5 denotes high risk and should prompt enhanced postoperative monitoring rather than delaying urgent surgery.

Investigations and interpretation

Most nasal pathology is diagnosed clinically. Investigations are reserved for trauma, suspected mass, complicated infection, CSF leak, severe/recurrent epistaxis, or when nasal instrumentation is planned in a high-risk patient.

Investigation	Indication	Interpretation/thresholds
Flexible nasendoscopy	Posterior obstruction, recurrent epistaxis, suspected mass, pre-awake nasal intubation assessment	Identifies septal spur, polyps, posterior bleeding, choanal stenosis and nasopharyngeal lesions; also permits dynamic assessment of airway collapse
CT facial bones/sinuses	Midface trauma, suspected skull base fracture, chronic rhinosinusitis failing treatment, tumour mapping	Thin-slice CT, typically 0.5–1.25 mm, is preferred; far superior to plain radiographs for nasal and midface fractures. Look for cribriform plate disruption, pneumocephalus, orbital wall injury and Le Fort patterns
MRI	Sinonasal malignancy, perineural spread, intracranial/orbital extension, encephalocele	Better soft tissue discrimination than CT; complementary rather than first-line in acute bony trauma
Beta-2 transferrin or beta-trace protein	Suspected CSF rhinorrhoea	Beta-2 transferrin is highly specific for CSF, with reported sensitivity and specificity commonly >90–95%; glucose dipstick testing is unreliable and should not guide airway decisions
FBC, PT/INR, APTT, fibrinogen, group and save	Major/recurrent epistaxis, anticoagulant use, liver disease, massive transfusion risk	For invasive haemostasis aim platelets >50 × 109 L-1; consider reversal if INR significantly elevated, particularly >1.5 with active bleeding

Preparation for nasal instrumentation

Choice of nostril is based on history, patency testing and, when available, endoscopic findings. Resistance during passage is clinically meaningful: force risks mucosal avulsion, turbinate trauma, septal perforation and epistaxis. Nasotracheal tube bleeding is reduced by vasoconstriction, lubrication, warming/softening the tube and using the smaller effective internal diameter, commonly 6.0–6.5 mm in adult females and 6.5–7.0 mm in adult males, adjusted to patient size and surgical requirements.

Drug	Typical topical dose	Key cautions
Co-phenylcaine spray	Common UK preparation: lidocaine 5% with phenylephrine 0.5%; 1 spray is approximately 0.1 mL, delivering about 5 mg lidocaine and 0.5 mg phenylephrine	Account for total lidocaine dose; avoid excessive phenylephrine in severe hypertension, ischaemic heart disease or thyrotoxicosis
Lidocaine	Maximum commonly cited dose without adrenaline 3 mg kg-1; with adrenaline 7 mg kg-1	Include nebulised, sprayed and transtracheal doses; toxicity risk rises with mucosal absorption
Oxymetazoline/xylometazoline	Usually 0.05–0.1% spray, 1–2 sprays per nostril	Alpha-adrenergic vasoconstriction; rebound congestion with prolonged use, but useful acutely

Absolute or near-absolute contraindications to blind nasal instrumentation include suspected basal skull fracture, severe midface trauma, known cribriform plate defect, recent trans-sphenoidal surgery, obstructing nasal mass and severe coagulopathy. In these circumstances, oral, fibreoptic-guided, surgical or image-informed alternatives should be selected.

Management, pharmacology and procedures

Peri-operative relevance: nasal airway optimisation and nasotracheal intubation

The nose is a high-resistance, highly vascular conduit; anaesthetic manipulation must respect the septum, turbinates and Kiesselbach’s plexus. Nasal instrumentation is indicated for maxillofacial, dental and oropharyngeal surgery, but is relatively contraindicated in suspected basal skull fracture, midface instability, coagulopathy, severe septal deviation, nasal polyposis, recent trans-sphenoidal surgery and significant epistaxis. The right nostril is often favoured because bevel orientation of a standard tracheal tube tends to reduce septal trauma, although the more patent side should be selected clinically.

1. Assessment: ask about obstruction, previous epistaxis/surgery, anticoagulants and cocaine use; inspect septum and turbinates where possible. A simple patency test or fibreoptic assessment is useful in anticipated difficulty.
2. Preparation: topical vasoconstrictor plus local anaesthetic, warmed well-lubricated tube, progressive dilation with nasopharyngeal airways if needed.
3. Technique: advance along the floor of the nose, parallel to the hard palate, not cephalad. Resistance at the inferior turbinate or septal spur should prompt withdrawal and use of the contralateral nostril, smaller tube or fibreoptic guidance.
4. Complications: epistaxis, turbinate avulsion, retropharyngeal dissection, bacteraemia, sinusitis, pressure necrosis of ala nasi, cuff damage, intracranial placement in cribriform plate disruption, and aspiration of blood.

Drug/intervention	Typical adult dose/use	Key pharmacology and cautions
Co-phenylcaine spray	Usually lidocaine 5% with phenylephrine 0.5%; 1–2 sprays per nostril according to preparation	Provides mucosal anaesthesia and α1-mediated vasoconstriction. Avoid excess in hypertension, severe coronary disease, arrhythmias and hyperthyroidism.
Lidocaine	Maximum commonly 3 mg/kg plain, 7 mg/kg with adrenaline; reduce in frailty, pregnancy, liver disease	Amide local anaesthetic; onset 2–5 min. Systemic toxicity: circumoral paraesthesia, seizures, myocardial depression. Account for all topical, nebulised and infiltrated doses.
Phenylephrine	Topical 0.25–0.5%; IV bolus 50–100 micrograms if treating anaesthetic hypotension	Direct α1 agonist; reflex bradycardia. Topical systemic absorption may cause severe hypertension, especially in children and small adults.
Oxymetazoline/xylometazoline	0.05% adult spray, 1–2 sprays per nostril	Imidazoline α-agonists; duration 6–12 h. Limit to ≤3–5 days to avoid rhinitis medicamentosa.
Tranexamic acid	Topical: 500 mg in 5 mL applied on pledget; IV: 1 g over 10 min when indicated	Antifibrinolytic inhibiting plasminogen activation. Useful adjunct in epistaxis, especially antiplatelet-associated bleeding; caution in active thromboembolic disease.

Acute epistaxis: structured management

Epistaxis is usually anterior from Little’s area but posterior bleeding from sphenopalatine branches is more likely in older, hypertensive or anticoagulated patients and may threaten the airway. Management follows an ABCDE approach: sit forward, suction, quantify haemorrhage, obtain IV access, FBC, coagulation studies, group and save/crossmatch, and reverse anticoagulation only when clinically appropriate. Direct pressure should be applied to the cartilaginous nose for 10–15 minutes continuously. Hypertension is usually reactive; treat severe persistent hypertension but do not delay haemostasis.

Stepwise haemostasis

• Topical vasoconstrictor and anaesthesia: pledgets soaked in lidocaine with phenylephrine or oxymetazoline improve visualisation and patient tolerance.
• Cautery: if a discrete anterior bleeding point is seen, silver nitrate cautery for 5–10 seconds around then onto the point. Avoid bilateral septal cautery at the same sitting due to septal perforation risk.
• Anterior packing: expandable sponge, ribbon gauze with antiseptic lubricant, or balloon tamponade. Pack parallel to the nasal floor. Observe for hypoxia, vagal episodes and aspiration.
• Posterior epistaxis: dual-balloon catheter or Foley catheter temporisation with ENT involvement. Definitive treatment is endoscopic sphenopalatine artery ligation or selective arterial embolisation.

Admission is indicated for posterior packs, haemodynamic compromise, significant comorbidity, ongoing anticoagulation concerns, hypoxaemia, frailty or lack of supervision. Packed patients require analgesia, antiemesis, head elevation and monitoring; toxic shock syndrome is rare, and routine systemic antibiotics for all anterior packs are not universally supported, but many ENT protocols use co-amoxiclav or doxycycline for prolonged packing, prosthetic valves or immunocompromise. Packs are commonly removed at 24–48 h; posterior packs often require monitored care because they may precipitate airway obstruction, bradyarrhythmias or obstructive sleep apnoea.

Trauma and septal complications

Nasal fracture management is primarily functional rather than cosmetic in the acute phase: exclude septal haematoma, CSF rhinorrhoea, ocular injury and midface fracture. Septal haematoma appears as a soft, bilateral septal swelling and requires urgent incision and drainage plus packing/splinting and antibiotics; delay risks cartilage necrosis from perichondrial separation, causing saddle-nose deformity and septal abscess. Closed reduction of displaced nasal fractures is usually performed after swelling subsides, ideally within 7–10 days in adults and 3–7 days in children, before bony union.

Long-term nasal disease relevant to anaesthesia

Chronic obstruction from allergic rhinitis, turbinate hypertrophy, septal deviation, polyps or chronic rhinosinusitis affects mask ventilation tolerance, nasotracheal access and peri-operative sleep-disordered breathing. Intranasal corticosteroids such as fluticasone propionate 50 micrograms/spray, 1–2 sprays per nostril daily reduce mucosal inflammation with minimal systemic bioavailability; maximal effect may require several days to weeks. Saline irrigation improves crusting and postoperative sinus care. Antihistamines help allergic symptoms; first-generation agents increase sedation and anticholinergic burden. Long-term topical decongestant use causes rebound congestion through receptor downregulation and mucosal ischaemia.

Follow-up and safety-netting

After epistaxis or nasal instrumentation, patients should avoid nose blowing, heavy exertion, hot drinks and digital trauma for 24–48 h, use topical emollients if crusting, and seek urgent review for recurrent bleeding, fever, increasing pain, obstruction or black discharge. After nasal surgery or packing, follow-up assesses septal integrity, synechiae, infection, olfaction and airway patency. For anaesthetic records, document nostril used, tube size, degree of trauma, topical drug doses and any contraindication to future nasal instrumentation.

Exam controversies and advanced synthesis

Nasal instrumentation: anatomy determines safety

In Primary FRCA vivas, the nose is rarely examined as isolated descriptive anatomy; it is tested through complications of nasotracheal intubation, nasopharyngeal airway insertion, epistaxis, skull-base trauma and topical pharmacology. The central principle is that instruments should pass posteriorly along the floor of the nose, not superiorly. The inferior meatus lies beneath the inferior turbinate and overlies the hard palate; the cribriform plate is superior, thin, and vulnerable in facial trauma. Misquoting this direction is a common viva pitfall.

Clinical manoeuvre	Anatomical target	Key hazard	Exam point
Nasopharyngeal airway	Floor of nose, bevel towards septum initially	Epistaxis; intracranial placement in basal skull fracture	Contraindicated in suspected anterior cranial fossa/base of skull fracture
Nasotracheal intubation	Most patent nostril; tube advanced parallel to hard palate	Turbinate avulsion, septal trauma, bacteraemia, retropharyngeal perforation	Warm/soften tube, vasoconstrict, lubricate, consider fibreoptic guidance
Nasogastric tube	Inferior meatus to nasopharynx	Intracranial passage in skull-base fracture	Orogastric route preferred if craniofacial trauma suspected

Controversies: base-of-skull fracture and “relative” contraindications

The traditional teaching is absolute avoidance of nasal instrumentation in suspected basal skull fracture. In practice, the risk is highest with cribriform plate disruption, severe midface trauma, CSF rhinorrhoea, periorbital ecchymosis, Battle sign, haemotympanum, or radiological anterior skull-base injury. The controversy is that many trauma patients have uncertain findings and require urgent airway control. For FRCA purposes, the safe answer is: avoid blind nasal insertion; if a nasal route is essential, use imaging, expert ENT/maxillofacial input and fibreoptic visualisation. Blind force is indefensible.

Epistaxis anatomy and haemorrhage control

Most epistaxis is anterior, arising from Kiesselbach’s plexus/Little’s area, where septal branches of the sphenopalatine, greater palatine, superior labial and anterior ethmoidal arteries anastomose. Posterior epistaxis is commonly from the sphenopalatine artery or Woodruff’s plexus and is more likely to cause airway contamination, aspiration and haemodynamic compromise. In anaesthetic practice, even “minor” nasal bleeding may be clinically important because it obscures fibreoptic views and increases aspiration risk.

Bleeding site	Likely vessel	Clinical implication
Anterior septum	Kiesselbach’s plexus	Common, visible, usually controlled with pressure/cautery
Posterior nasal cavity	Sphenopalatine artery branches	Greater blood loss; may need posterior pack or endoscopic ligation
Superior septum/lateral wall	Anterior/posterior ethmoidal arteries	Orbital and anterior cranial fossa proximity; avoid blind superior trauma

Topical preparation: useful but not benign

Vasoconstriction reduces mucosal bleeding but introduces systemic toxicity risks because nasal mucosa is highly vascular. Cocaine remains pharmacologically attractive because it provides local anaesthesia and vasoconstriction by inhibiting noradrenaline reuptake, but it is arrhythmogenic, hypertensive and interacts with volatile agents, tricyclics, MAO inhibitors and sympathomimetics. Many units therefore prefer lidocaine plus phenylephrine or oxymetazoline.

Agent	Typical nasal use	Important limits/pitfalls
Cocaine	4% solution; pledgets or spray	Maximum commonly quoted 1.5 mg/kg, often capped at 200 mg; avoid in significant IHD, arrhythmia, severe hypertension
Lidocaine	2–4% topical; atomised or pledgets	Total dose matters: usual maximum 3 mg/kg plain, 7 mg/kg with adrenaline; topical absorption is unpredictable
Phenylephrine	0.25–0.5% topical	Alpha-1 agonist; hypertension, reflex bradycardia, myocardial ischaemia if excessive
Oxymetazoline	0.05% spray	Alpha agonist; less anaesthesia, useful vasoconstrictor; rebound congestion with repeated use

Airflow physiology and high-flow nasal oxygen

The nose contributes approximately 50% of total upper-airway resistance in quiet breathing, with resistance varying across the nasal cycle due to autonomic venous engorgement of turbinate erectile tissue. High-flow nasal oxygen exploits nasal anatomy by delivering warmed, humidified oxygen at flows commonly up to 60–70 L/min, producing pharyngeal dead-space washout, high inspired oxygen concentration and modest positive airway pressure. In adult studies of apnoeic oxygenation, including the THRIVE observational work, prolonged apnoea with preserved oxygenation was reported, but carbon dioxide still rises, typically around 0.15 kPa/min initially and faster after prolonged apnoea. Thus, HFNO does not equal ventilation; this distinction is a frequent examination trap.

Viva-level integration and common pitfalls

• Do not say “insert upwards”. Nasal airways, tubes and NG tubes pass backwards along the hard palate.
• Do not confuse innervation. General sensation is trigeminal: anterior ethmoidal nerve anteriorly, nasopalatine and greater palatine branches septally, and maxillary nerve branches posteriorly. Olfaction is confined to superior olfactory mucosa.
• Do not omit venous drainage. Nasal veins communicate with facial, ophthalmic and pterygoid venous systems; this explains cavernous sinus relevance.
• Remember paediatrics. Infants are preferential nasal breathers; nasal obstruction can cause disproportionate respiratory distress. Neonatal choanal atresia classically presents with cyclical cyanosis relieved by crying.
• Recognise surgical relevance. Septal deviation, turbinate hypertrophy, polyps, previous surgery and coagulopathy increase failure and bleeding during nasal intubation.
• Be precise about contraindications. Suspected base-of-skull fracture, severe midface trauma, obstructing nasal pathology and uncontrolled coagulopathy are major red flags for nasal instrumentation.