Head and Neck



  • Scalp and base of skull
  • Brain
  • Pituitary gland
  • Eye and optic tract
  • Nose
  • Sagittal section of head and neck
  • Cross section at C6
  • Larynx with grades at laryngoscopy
  • Triangles of neck


  • Arterial supply of head and neck
  • Great veins of head and neck

Nervous System

  • Cranial nerves – II, V, VII and X
  • Scalp blocks
  • Eye blocks

    • Sub-Tenon’s block
    • Retrobulbar block
    • Peribulbar block

  • Laryngeal nerve blocks
  • Cervical plexus block


  • Scalp and base of skull
  • Brain
  • Pituitary gland
  • Eye and optic tract
  • Nose
  • Sagittal section of head and neck
  • Cross section at C6
  • Larynx with grades at laryngoscopy
  • Triangles of neck

Scalp and Base of Skull

What are the layers of the scalp covering the skull (Figure 1.1)?

Use the SCALP mnemonic

  • Skin with hair follicles and sebaceous glands
  • Connective tissue with neurovasculature of the scalp
  • Aponeurosis (galea aponeurotica)
  • Loose areolar connective tissue which serves as a plane of access in neurosurgery. It is also called the ‘danger zone of the scalp’ as infection from scalp can reach the meninges through emissary veins.
  • Periosteum
Figure 1.1 Layers of scalp.

Which bones make up the skull?

The skull is made up of eight bones which are interconnected by sutures which are immovable fibrous joints.

  • One each of the frontal, sphenoid, occipital and ethmoid bones
  • Two of the parietal and temporal bones

Briefly describe the structures that pass through the various foramina in the base of the skull.

Out of the different foramina, there are a few which are easy to remember: foramen caecum in front of the crista galli, cribriform plate, superior orbital fissure, foramen magnum, stylomastoid foramen, hypoglossal canal on either side of the foramen magnum.

The other foramina can be remembered as

OROS LAJ – in order of their appearance as shown in the figures (Figures 1.2 and 1.3).

Figure 1.2 Base of skull – inferior surface.
Figure 1.3 Base of skull – inner surface.

The base of the skull with its foramina and contents is shown in Table 1.1.

Table 1.1 Major Cranial Foramina and the Structures Passing Through



Foramen caecum

Emissary vein from nose to superior sagittal sinus

Cribriform plate

Olfactory nerve

Anterior ethmoidal nerve

Superior orbital fissure

(Live Frankly To See Absolutely No InSult)

Lacrimal nerve (branch of ophthalmic nerve)

Frontal nerve (branch of ophthalmic nerve)

Trochlear nerve

Superior branch of oculomotor nerve

Abducens nerve

Nasociliary nerve (branch of ophthalmic nerve)

Inferior branch of oculomotor nerve

Superior and inferior ophthalmic vein

Optic canal

Optic nerve

Ophthalmic artery

Foramen rotundum

Maxillary nerve (V2)

Foramen ovale


Mandibular nerve (V3)

Accessory meningeal nerve

Lesser petrosal nerve

Emissary vein

Foramen spinosum


Middle meningeal artery and vein

Emissary vein

Nervus spinosus

Foramen lacerum


Meningeal branch of ascending pharyngeal artery

Emissary vein

Traversed partially by Internal carotid artery

Greater petrosal nerve

Auditory meatus

Facial nerve

Vestibulocochlear nerve

Labyrinthine vessels

Jugular foramen

Inferior petrosal sinus/sigmoid sinus

Glossopharyngeal nerve

Vagus nerve

Accesory nerve

Occipital artery

Carotid canal

Internal carotid artery with venous and sympathetic plexus

Hypoglossal canal

Hypoglossal nerve

Meningeal branch of hypoglossal nerve

Emissary vein

Stylomastoid foramen

Facial nerve

Posterior auricular artery

Foramen magnum

Medulla oblongata


Spinal accessory nerves

Spinal arteries

Dural veins

For completeness, the foramina through which the cranial nerves exit the skull are summarised in Table 1.2.

Table 1.2 Foramina Through which the Cranial Nerves Exit the Brain

Cranial nerve


I – olfactory

Cribriform plate of ethmoid

II – optic

Optic canal of sphenoid

III – oculomotor

Superior orbital fissure

IV – trochlear

Superior orbital fissure

V – trigeminal

V1 – ophthalmic – superior orbital fissure

V2 – maxillary – foramen rotundum

V3 – mandibular – foramen ovale

VI – abducens

Superior orbital fissure

VII – facial

Internal auditory meatus ⟶ facial canal ⟶ stylomastoid foramen

VIII – vestibulocochlear

Internal auditory meatus

IX – glossopharyngeal

Jugular foramen

X – vagus

Jugular foramen

XI – accessory

Enters by the foramen magnum, exits by the jugular foramen

XII – hypoglossal

Hypoglossal canal


What is the normal cerebral blood flow to the grey and white matter? What is the overall cerebral blood flow to the brain? What percentage is this of cardiac output?

The normal cerebral blood flow to grey matter is 70 ml/100 g/min and to white matter is 20 ml/100 g/min. The overall cerebral blood flow to the brain is 50 ml/100 g/min.

The percentage of cardiac output is approximately 14% (700 ml/min).

Describe the meningeal layers that surround the brain and the spinal cord.

The brain and spinal cord are surrounded by three layers of membranes called the meninges. A tough outer layer (dura mater), a delicate middle layer (arachnoid mater) and an inner layer firmly attached to the surface of the brain (pia mater).

Describe the arterial supply to the dura mater.

The arterial supply to the dura mater consists of

  • Anterior meningeal arteries which are branches of the ethmoidal artery
  • Middle and accessory meningeal arteries arising from the maxillary artery
  • Posterior meningeal artery which is a branch of the ascending pharyngeal artery
  • Meningeal branches from the occipital artery and vertebral artery

What is the innervation of the dura mater?

The dura mater is supplied by the meningeal branches of all three divisions of the trigeminal nerve (V1, V2 and V3) and the first, second and third cervical nerves.

Pituitary Gland

The pituitary gland is located in the sella turcica of the sphenoid bone at the base of the skull. The roof is formed by an incomplete fold of dura, the diaphragma sella, which is traversed by the pituitary stalk and optic chiasm. The fossa is limited posteriorly by the clivus of the sphenoid and inferiorly and anteriorly by the sphenoidal air sinuses. The lateral walls are in close relation to the cavernous sinus, internal carotid artery, CN III, IV, V1, V2 and VI (Figures 1.4 and 1.5).

The pituitary gland weighs 500–900 mg and is divided into the anterior and posterior glands. The two parts of the pituitary gland function as separate endocrine organs with different cell populations and functionality.

The anterior pituitary gland (adenohypophysis) is an evagination of the ectodermal Rathke’s pouch. The anterior lobe is further divided into the par distalis, pars tuberalis and par intermedia.

The posterior pituitary (neurohypophysis) is divided into the pars nervosa and the infundibulum. Developmentally the posterior pituitary arises from the forebrain and is an extension of the hypothalamus.

Arterial supply

  • Superior and inferior hypophyseal arteries, which are branches of the internal carotid artery. They form a capillary network with the hypothalamo-hypophyseal portal system. The primary capillary network lies at the pituitary stalk, where the hypothalamic hormones are released. This capillary bed is drained by a set of long portal veins that give rise to the second capillary bed in the anterior pituitary. The veins originating in the neurohypophyseal capillary plexus give rise to the short portal veins that will also contribute to the adenohypophyseal capillary plexus and connect the two circulatory systems.
  • This hypothalamo-hypophyseal portal system creates a communication between the endocrine and neural cells providing an easy short loop feedback between the two sets of cells.

Venous drainage

  • Venous drainage from the gland is into the cavernous sinus and then onto the petrosal sinus and finally into the jugular vein.

What is a portal circulation and what are the other examples in the body?

A portal circulation begins and ends in capillaries. Arterial capillaries normally end up forming a vein that enters the right side of the heart. In a portal circulation, the primary capillary network drains into a vein known as a portal vein. This then branches to form a second set of capillaries before draining into the venous system. Other examples of a portal circulation are the hepatic portal, placental, renal, ovarian and testicular circulations.

Figure 1.4 Pituitary gland – structure.
Figure 1.5 Pituitary gland – anatomical position and relations.

Which hormones are released by the pituitary?

  • Anterior pituitary – growth hormone (GH), adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinising hormone (LH) and prolactin
  • Posterior pituitary – antidiuretic hormone (ADH) and oxytocin

What are the types of pituitary tumours? What are their clinical manifestations?

Pituitary tumours are classified by size into


  • <10 mm in diameter, most commonly occurring pituitary adenomas
  • Clinical effects are mainly due to hormonal hyper-secretion
  • The commonest pituitary hormone secreted by these tumours is prolactin (35%), followed by GH (20%) and ACTH (7%)


  • >10 mm in size
  • Non-secretory tumours
  • Clinical effects are usually due to mass and pressure effects leading to visual disturbances, increased intracranial pressure and hypopituitarism due to destruction of pituitary tissue.

Hyperprolactinaemia – due to increased prolactin secretion

  • Male – impotence, reduced facial hair and galactorrhoea
  • Female – weight gain, menstrual disturbance, infertility and galactorrhoea

Acromegaly – due to increased GH, after epiphyseal closures

  • Musculoskeletal features – prognathism, prominent supraorbital ridges, increased skull size, large hands and feet
  • Soft tissues – macroglossia, enlarged nose, thickening of the laryngeal and pharyngeal soft tissues, laryngeal stenosis, hoarse voice due to recurrent laryngeal nerve palsy
  • Heart – myocardial hypertrophy, interstitial fibrosis and cardiomegaly leads to ischaemic heart disease and left ventricular dysfunction
  • Miscellaneous – sleep apnoea, hypertension and diabetes mellitus secondary to the anti-insulin effect of growth hormone

Cushing’s disease – due to increased ACTH

  • Central weight gain and obesity, moon face, extra fat around neck (‘buffalo hump’), hirsutism, thin skin, abdominal striae, easy bruising, poor wound healing
  • Proximal myopathy, fatigue, depression
  • Hypertension and hyperglycaemia

What are the anaesthetic concerns for a patient undergoing surgery for acromegaly?

Anaesthetic concerns can be classified into

Neurosurgical anaesthesia and its complications

  • Haemodynamic instability
  • Maintenance of cerebral oxygenation
  • Prevention of perioperative complications such as venous air embolism in the sitting position
  • Rapid emergence to facilitate neurological assessment
  • Adequate postoperative analgesia and antiemesis

Acromegaly and its implications

  • Airway – the clinical features of acromegaly lead to an increased risk of a difficult ventilation and intubation. An awake fibreoptic intubation may be necessary.
  • Respiratory – coarsening of features leading to upper airway obstruction leads to an obstructive picture on spirometry. Also, obstructive sleep apnoea can increase the risk of difficulties with ventilation and intubation and sensitivity to opioids.
  • Cardiovascular – myocardial hypertrophy, interstitial fibrosis, hypertension and cardiomegaly lead to ischaemic heart disease and left ventricular dysfunction.
  • Neurological – compression of surrounding structures leading to visual disturbances, increased ICP and cavernous sinus thrombosis.
  • Endocrine – impaired glucose tolerance and diabetes mellitus complicates more than 25% of acromegalic patients hence the need for careful glucose monitoring and management.

Which electrolyte is most commonly affected after pituitary surgery?

After pituitary surgery the most commonly affected electrolyte is sodium. This can be due to diabetes insipidus (DI) due to decreased secretion of ADH. Inappropriate water loss leads to hypernatraemia and increased serum osmolality in the context of large volumes of dilute urine. Treatment aims at replacement of water and ADH. Intranasal or intravenous desmopressin (Deamino D Arginine Vasopressin, DDAVP) has been the mainstay of treatment.

The criteria for diagnosis of DI include

  • Increased urine volume >3 L/day
  • Increased serum sodium >145 mmol/L
  • Increased serum osmolality >300 mOsm/kg
  • Decreased urine osmolality <300 mOsm/kg
  • Decreased urine specific gravity <1.005


  1. Griffiths, S., & Perks, A. (2010). The hypothalamic pituitary axis Part 2: Anaesthesia for pituitary surgery. Anaesthesia Tutorial of the Week, 189.
  2. Krishnachetty, B., & Sethi, D. S. (2015). The Final FRCA Structured Oral Examination: A Complete Guide. CRC Press: Boca Raton, FL.


What makes up the bony structure of the orbit?

The bony structure of the orbit can be described as follows

  • General shape

    • Pyramidal
    • Apex points towards the optic canal

  • Boundaries

    • Roof – frontal bone
    • Floor – zygoma, maxilla
    • Medial wall – sphenoid, maxilla, ethmoid, lacrimal bone
    • Lateral wall – zygoma, sphenoid

Can you name the important foramina contained within the orbit, and the structures passing through each?

There are a total of nine foramina or fissures within the orbit. The most important are shown in Figure 1.6.

  • Optic foramen

    • Optic nerve, ophthalmic artery

  • Superior orbital fissure (see also Scalp and Base of Skull)

    • Oculomotor, trochlear, abducens nerves, ophthalmic division (V1) of trigeminal nerve
    • Superior and inferior ophthalmic veins

  • Inferior orbital fissure

    • Infra-orbital nerve (branch from maxillary division (V2) of trigeminal nerve) and vessels
Figure 1.6 Superior and inferior orbital fissures and structures passing through.

What is the general structure of the eyeball?

  • Axial length approximately 25 mm in diameter
  • Three layers

    • Outer layer – sclera (posterior and opaque) and cornea (anterior and transparent) form the fibrous outer layer. Sclera receives attachments to the extraocular muscles, and is perforated posteriorly by the optic nerve.
    • Middle layer – choroid, ciliary body and iris form the vascular middle layer. Choroid lines the inside of the sclera, and is continuous with the iris anteriorly and is perforated by the optic nerve posteriorly.
    • Inner layer – retina forms the innermost layer within the posterior chamber and comprises of neural tissue.

  • Two segments

    • Anterior segment

      • (further divided into anterior and posterior chambers; anterior chamber extends from cornea to iris and posterior chamber from iris to lens)
      • One sixth of the eyeball
      • Contains transparent watery fluid called aqueous humour

  • Posterior segment

    • Five-sixths of the eyeball
    • Contains transparent, gelatinous mass called vitreous body

What are the constituents of aqueous humour?

Aqueous humour is a clear gelatinous fluid contained within the anterior and posterior chambers of the eye supplying nutrients to the avascular cornea and lens and maintaining the intraocular pressure.

The fluid has similar composition to plasma but with less protein and glucose and more lactic acid and ascorbic acid.

It is produced predominantly by active secretion mechanisms (80%) with the Na+/K+ ATPase enzyme creating an osmotic passage of water into the posterior chamber. The other method of production of aqueous humour is through ultrafiltration of the plasma (20%).

The rate of production is approximately 2.5 μL/min, its total volume being 250 μL.

Can you describe the anatomy of the production and drainage of the aqueous humour?

It is produced by the ciliary processes of the ciliary body and is secreted into the posterior chamber. It then flows between the iris and lens and into the anterior chamber through the pupil. Most exits the anterior chamber via the trabecular meshwork at the iridocorneal angle into the canal of Schlemm. The canal of Schlemm is a scleral venous sinus which drains into the anterior ciliary veins (then into the superior ophthalmic vein and the cavernous sinus), with some exitting via the uveoscleral route being absorbed through the ciliary muscle into the sclera (Figure 1.7).

Figure 1.7 Drainage of aqueous humour.

How does pupil size affect drainage of the aqueous humour?

Pupillary dilatation narrows the iridocorneal angle and reduces the rate of drainage.

What are the determinants of intraocular pressure (IOP)?

The normal IOP is 10–25 mmHg.

Internal factors (due to the volume of the globe contents)

  • Arterial blood pressure – blood flow to the eye is autoregulated, therefore a fall in blood pressure will decrease IOP. Significant increases in arterial blood pressure outside of the range of autoregulation will therefore increase IOP.
  • Venous blood pressure – coughing, straining, vomiting and the Valsalva manoeuvre will increase venous congestion therefore increasing IOP. Head-up positioning of the patient will decrease venous congestion and IOP.
  • Partial pressures – partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) affect blood vessel tone and therefore IOP. The effect is the same as the factors which affect cerebral blood flow.
  • Aqueous humour production and drainage – can affect IOP, such as in glaucoma
  • Vitreous humour volume – haemorrhage in the vitreous can increase IOP
  • Presence of a foreign body – sulphur hexafluoride bubble or tumour

External factors (extraocular compression)

  • Extraocular muscle tone – can increase IOP (such as is caused by a depolarising muscle relaxant) and therefore cause a decrease in IOP when paralysed
  • Extrinsic compression – due to an improperly applied facemask, prone positioning or expanding orbital haematoma due to regional block complication can increase IOP
  • Drugs – can both increase and decrease IOP depending on their mechanism of action (listed below)

How can drugs affect intraocular pressure?

  • Induction agents: all anaesthetic induction agents and inhalational agents apart from ketamine reduce IOP. Etomidate can cause myoclonus and should probably be avoided. The fall in IOP is independent of their effect on blood pressure, central venous pressure and extraocular muscle tone. It is more likely to be as a result of direct action on central control mechanisms.
  • Opioids: have no direct action on IOP but will attenuate elevated pressure caused by intubation and can increase IOP due to respiratory depression and increased PaCO2.
  • Muscle relaxants: suxamethonium causes a small transient rise in IOP (5–10 mmHg for 5–10 minutes due to prolonged contraction of the extraocular muscles), whilst non-depolarising muscle relaxants produce no change or even a fall in IOP.
  • Mannitol can be given (0.5 mg/kg IV) as an osmotic diuretic which works by removing fluid from the vitreous chamber. Acetazolamide is a carbonic anhydrase inhibitor (500 mg IV) which acts by decreasing aqueous humour production by the ciliary body.

What pharmacological agents are used to reduce IOP?

Reducing aqueous humour production

  • Beta blockers such as timolol reduce aqueous humour production through adenylate cyclase inhibition.

Increasing the drainage of aqueous humour

  • Prostaglandin analogues such as latanoprost work by increasing the outflow of aqueous humour via the uveoscleral route.
  • Cholinergic medications such as pilocarpine, and anticholinesterase inhibitors such as neostigmine contract the ciliary body and increase drainage through the trabecular network.

Both mechanisms

  • Sympathomimetics such as ephedrine reduce aqueous humour production and increase drainage through ciliary body vasoconstriction and adenylate cyclase inhibition.
  • Alpha 2 agonists such as brimonidine work by decreasing aqueous humour production and increasing uveoscleral outflow.

What is SF6? What are the implications of its use for anaesthetists?

Sulphur hexafluoride is an inert, highly insoluble gas used by ophthalmic surgeons to provide tamponade for retinal surgery.

Nitrous oxide should not be used in patients where SF6 has been used in their surgery (visual loss up to 6 weeks after the procedure due to nitrous oxide use has been reported). Exposure to nitrous oxide when SF6 is present can lead to diffusion of nitrous oxide into the bubble faster than inert insoluble gases leave thereby increasing IOP.

How would you anaesthetise an unstarved patient requiring urgent surgery for a penetrating eye injury?


  • Unstarved patient – risk of aspiration and hence the need for rapid sequence induction
  • Urgent surgery – no time to wait for a starved status
  • Penetrating eye injury – avoid increased IOP for the fear of expulsion of eye contents
  • Depolarising muscle relaxants aiding rapid sequence (to avoid aspiration) risks the rise of IOP

This was a problem in the pre-rocuronium (and sugammadex) era, where adjuncts were given to reduce the IOP rise with the use of suxamethonium.

Current practice: in an unstarved patient, a modified RSI induction would be indicated to minimise aspiration risk. Rocuronium at a dose of 1– 1.2 mg/kg would be preferred to suxamethonium due to non-depolarising muscle relaxants having minimal effect on IOP. A smooth induction using an appropriate induction agent (propofol) and volatile agent for maintenance (sevoflurane), with a short acting opioid should be used to attenuate the elevation in pressure due to intubation (remifentanil or alfentanil). Ventilation to control PaO2 and PaCO2 to reduce the risk of an increase in IOP due to derangements in these parameters. A head-up position should be maintained if possible during intubation and surgery to help with venous drainage. A plan for smooth extubation should be in place such as using remifentanil to minimise the risk of coughing. Prevention of nausea and vomiting by giving appropriate antiemetics during the surgery is vital to smooth emergence and recovery post eye surgery.

Explain the pathways involved in the pupillary light reflexes. See also Chapter 7.

  • Afferent pathway: light is sensed by the optic nerve which is transmitted via the optic tract to the pretectal nucleus of the high midbrain. This signal is then transmitted to the Edinger-Westphal nucleus (of CN III).
  • Efferent pathway starts via parasympathetic fibres which run from the Edinger-Westphal nucleus in the oculomotor nerve (CN III), synapsing in the ciliary ganglion. From here post ganglionic short ciliary nerves leave the ciliary ganglion and innervate the iris sphincter which causes pupil constriction.

Contraction of the pupillary muscles to dilate the pupil is triggered via sympathetic impulses along the short and long ciliary nerves originating in the superior cervical ganglion. These axons run along the internal carotid artery.

Sagittal Section of Neck

The candidates are shown an image of the sagittal section of the head and neck pertaining to the airway and asked to point out the structures of importance.

Figure 1.8 Sagittal section of the head and neck.

Make yourself familiar with Figure 1.8 and the structures.

  1. 1. Tongue
  2. 2. Hard palate
  3. 3. Soft palate
  4. 4. Hyoid bone (C3)
  5. 5. Thyroid cartilage (C4–C5)
  6. 6. Cricoid cartilage (C6)
  7. 7. Thyroid gland
  8. 8. Epiglottis
  9. 9. Vocal cords
  10. 10. C6 vertebral body


The nose is made of bones and cartilage and features the external cartilaginous nose, nares and nasal cavity. The nasal cavity is divided into right and left by the septum which comprises the ethmoid bone, vomer and septal cartilage.

The lateral wall of the nose has three nasal conchae (superior, middle and inferior) forming turbinates (horizontal bones with fibrovascular tissue) and four openings

  • Sphenoethmoid recess – opening for the sphenoidal sinus
  • Superior nasal meatus – opening for the posterior ethmoidal sinuses
  • Middle nasal meatus – opening for the frontal sinus, maxillary, middle and anterior ethmoidal sinuses
  • Inferior nasal meatus – opening for the naso-lacrimal duct

Arterial supply

The overall arterial supply of the nose is by branches of internal and external carotid arteries.

  • External nose – branches of facial, ophthalmic and maxillary arteries
  • Lateral nasal wall – sphenopalatine, anterior and posterior ethmoid arteries
  • Nasal septum – sphenopalatine, anterior and posterior ethmoid arteries and superior labial and the greater palatine arteries. Little’s area or Kiesselbach’s plexus is situated in the antero-inferior part of nasal septum just above the vestibule and marks the confluence of different supplies (Figure 1.9).

Venous drainage

Submucous venous plexus draining into the cavernous sinus.

Nerve supply

In short, the nose is supplied by the first two branches of the trigeminal nerve (Figures 1.10 and 1.11)

  • Sensory

    • External nose – infratrochlear, infraorbital and nasociliary nerve
    • Nasal cavity – palatine nerves from pterygopalatine (or sphenopalatine) ganglion and anterior ethmoidal nerve

  • Special sensory (smell) carried via olfactory nerves
  • Motor innervation to the nasal muscles is via the facial nerve
Figure 1.9 Nasal septum – arterial supply.
Figure 1.10 Nasal septum – nerve supply.
Figure 1.11 Lateral wall of nose – nerve supply.

When would you cannulate the nose?

  • Provide oxygen via nasal specula
  • Insertion of nasopharyngeal airway
  • Nasotracheal intubation
  • Insertion of nasogastric tubes or temperature probes

What are the indications and contraindications for the nasal route for intubation?


  • Surgical access
  • Angioedema of the tongue
  • Mechanical obstructions to mouth opening from mandibular fixation
  • Trismus
  • Intraoral mass lesions
  • Fixed neck contracture or severe degenerative cervical spine disease

Absolute contraindications

  • Suspected epiglottitis
  • Midface instability
  • Severe coagulopathy
  • Base of skull fracture
  • Impending respiratory arrest

What is the ‘danger area’ of the face?

The lower part of external nose and the upper lip is called the dangerous area of the face as an infection in this region may spread to cavernous sinus through the inferior ophthalmic vein via the valveless anterior facial vein.

How would you topicalise the nose for awake fibreoptic intubation?

The nasal cavity is innervated by the greater and lesser palatine nerves and the anterior ethmoidal nerve.

Local anaesthetic can be given by spray or the use of atomiser, placement of swabs soaked with local anaesthetic, by inhalation via nebuliser or by performing nerve blocks of the palatine and anterior ethmoidal nerve.

These nerves can be blocked by taking a cotton-tipped applicator soaked in local anaesthetic and passing it along the upper border of the middle turbinate to the posterior wall of the nasopharynx, where it is left for 5–10 minutes.


The tongue is a boneless, muscular organ which facilitates swallowing, speech and sensation of taste.

Muscles of the tongue

  • Intrinsic – change the shape and size of the tongue
  • Extrinsic – attached to the adjacent structures, e.g. hyoglossus, styloglossus, palataglossus

Blood supply

  • Lingual artery (a branch of the external carotid artery) and tonsillar artery (a branch of the facial artery)

Venous drainage

  • Lingual vein

Nerve supply

  • Anterior 2/3

    • Sensory – lingual nerve (Trigeminal V3)
    • Special sensory – facial nerve

  • Posterior 1/3

    • Sensory – glossopharyngeal nerve
    • Special sensory – glossopharyngeal nerve

  • Motor

    • All muscles except palatoglossus – hypoglossal nerve
    • Palatoglossus – vagus nerve


The pharynx is a tubular structure that lies posterior to the nasal cavity, oral cavity and larynx with muscles that help with swallowing and speaking. Arterial supply is via branches of external carotid artery and drainage into internal jugular vein. The sensory and motor supply of the pharynx is from the trigeminal (maxillary branch), glossopharyngeal and the vagus nerves.


In the Primary FRCA OSCE, an image may be provided either of the sagittal section of the neck or the laryngeal complex with cartilages and muscles and the candidate is required to name specific structures followed by issues with nerve injury. This question is generally answered badly, and the overall opinion is that the image provided is quite difficult to decipher. The candidate might also be asked to perform surgical cricothyroidotomy in a manikin.

In the Final FRCA SOE, a more detailed knowledge of the anatomy with its clinical application is required for a satisfactory pass.

Clinical application topics

  • Cricothyroid puncture or surgical airway
  • Anaesthesia of the larynx for awake fibreoptic intubation
  • Nerve palsies
  • Laryngeal injuries
  • Post thyroidectomy airway emergency

The larynx is the organ of phonation and an important structure for anaesthetists in many clinical contexts.

The larynx extends from C3 (hyoid bone) to C6 (cricoid cartilage), at which level the trachea originates. It consists of three paired and three unpaired (single) cartilages and hyoid is the only bone in the pharyngo-laryngeal complex.

Unpaired/single cartilages

  • Epiglottis (leaf-shaped)
  • Thyroid (shield-like)
  • Cricoid (signet ring-like)

Paired cartilages

  • Arytenoid (pyramidal)
  • Cuneiform (cylindrical)
  • Corniculate (triangular)

A knowledge of the names of the cartilages and their relative positions will help name the structure attached to them. For example, the structure that connects the thyroid and the cricoid cartilages could only be the cricothyroid ligament (membrane) or cricothyroid muscle. The ligament is more central connecting the inferior border of the thyroid and the superior surface of the cricoid. Whereas the muscle is more lateral attaching to the inferior horn of the thyroid cartilage to the cricoid cartilage.

  • Epiglottis: the epiglottis is leaf-shaped and connected to the hyoid bone by the hyo-epiglottic ligament. The vallecula is the pouch between the epiglottis and the base of the tongue where the tip of the laryngoscope is placed during direct laryngoscopy in adults.
  • Thyroid cartilage: the thyroid cartilage is in the shape of a shield and gives the anterior laryngeal prominence. It is quadrangular with superior and inferior cornu which articulate with the hyoid and cricoid respectively through specific ligaments.
  • Cricoid cartilage: the cricoid cartilage is positioned below the thyroid cartilage with the thinner portion attaching to the thyroid cartilage via the avascular cricothyroid membrane. The broader part is posterior and houses the arytenoid cartilage on the top.
  • Arytenoid, cuneiform and corniculate cartilages: these cartilages are present at the back of the larynx between the thyroid and the cricoid cartilages. They connect to the epiglottis by the aryepiglottic folds which are further strengthened by the cuneiform and corniculate cartilages which are found embedded in these folds (Figure 1.12).
Figure 1.12 Cartilages of the larynx.

Vocal cords

The vocal cords are formed by the thickening of the upper edge of cricothyroid membrane connecting to the arytenoid cartilage posteriorly. The white colour of the cords is because of the absence of the submucosal covering.


Extrinsic muscles – move the larynx as a whole

  • Elevators – suprahyoid muscles (stylohyoid, geniohyoid, mylohyoid, thyrohyoid and stylopharyngeus)
  • Depressors – infrahyoid muscles (omohyoid, sternothyroid, sternohyoid and thyrohyoid)

Intrinsic muscles – control the vocal cords and the glottic opening (Figure 1.13)

The intrinsic muscles connect between cartilages as listed below (T, thyroid; C, cricoid; A, arytenoid) (Table 1.3).

Table 1.3 Muscles of the Larynx

T – C


T – A


T – A


C – A

Cricoarytenoid – lateral

C – A

Cricoarytenoid – medial

A – A

Transverse arytenoid

Cricothyroid muscle – the only TENSOR of the cord.

Posterior cricoarytenoid muscle – the only ABDUCTOR of the cord.

All other intrinsic muscles are responsible for relaxation and adduction of the cords.

Figure 1.13 Muscles of the larynx.

Arterial supply

Superior and inferior laryngeal arteries which arise from the superior and inferior thyroid arteries which in turn are branches of the external carotid artery.

Venous drainage

Superior and inferior laryngeal veins drain into the superior and inferior thyroid veins which in turn empty into the internal jugular veins and left brachiocephalic veins, respectively.

Lymphatic drainage

Deep cervical and upper tracheal lymph nodes drain the upper and lower half, respectively.

Nerve supply

The sensory and motor supply of the larynx is by the vagus via the superior and recurrent laryngeal nerves.

Superior laryngeal nerve (SLN)

The SLN originates from the inferior ganglion (C1 level) of the vagus nerve and descends posterior to the carotid artery towards the larynx. At the level of greater horn of hyoid bone, it divides into external and internal branches. The internal branch (iSLN) provides sensory innervation of mucous membrane of the larynx above the level of vocal cords including base of the tongue and epiglottis. The external branch (eSLN) provides motor supply to cricothyroid muscle.

The iSLN can be injured during surgical interventions of the anterior neck such as carotid endarterectomy and after cervical spine injury.

The eSLN is in close proximity to the superior thyroid vascular pedicle at the superior pole of the thyroid and there is a risk of injury during thyroid surgery.

Recurrent laryngeal nerve (RLN)

The right RLN is a branch of right vagus nerve and it loops the right subclavian artery and runs parallel to the tracheoesophageal groove.

The left RLN originates from the left vagus nerve as it crosses the aortic arch and it loops the arch and descends parallel to the tracheoesophageal groove. The longer course of the left RLN makes it more prone to injury than the right RLN.

In the neck, both nerves accompany the inferior thyroid pedicle and it is at high risk of injury during thyroid surgery (Figure 1.14 and Table 1.4).

Figure 1.14 Nerves of the larynx.

Table 1.4 Innervation of the Larynx




Base of tongue, epiglottis, larynx above the level of vocal cords (iSLN)

Larynx below the level of vocal cords


Cricothyroid muscle only (eSLN)

All other intrinsic muscles

What are the causes of laryngeal nerve palsy?

Damage to vagus, SLN or RLN can be due to

  • Trauma
  • Iatrogenic causes, secondary to

    • Surgical – thyroid, lung, heart or cervical spine surgery
    • Anaesthetic – prolonged intubation, nerve blocks

  • Neoplastic – lung malignancy and metastatic lesions
  • Infective – viral
  • Miscellaneous

    • Cardiovocal syndrome (Ortner’s syndrome) – hoarseness due to a left recurrent laryngeal nerve palsy caused by cardiovascular pathology
    • Neurological syndromes – various neurological syndromes are named secondary to the level of lesion of vagus nerve; Wallenberg – lateral medulla, Vernet’s – jugular foramen

What happens when the vagus nerve is damaged at the base of skull (with respect to laryngeal innervation)?

High vagal lesions cause complete unilateral vagal paralysis affecting both SLN and RLN.


  • Unilateral loss of the sensation of larynx


  • Loss of abductors and adductors – ipsilateral cords in the paramedian (cadaveric) position
  • Dysphagia from unilateral palatal weakness
  • Palatal droop on the ipsilateral side and deviation of the uvula to the contralateral side

When the injury is unilateral, the loss of function can be temporary and less pronounced as opposed to bilateral damage (Tables 1.5 and 1.6).

Table 1.5 Summary of SLN (Superior Laryngeal Nerve) Damage

Unilateral SLN

Bilateral SLN



Unilateral sensory loss above the cord

Bilateral sensory loss above the cords


Unilateral cricothyroid palsy

Bilateral cricothyroid palsy



Temporary hoarse voice

Hoarse voice

Risk of aspiration



Airway obstruction



Table 1.6 Summary of Bilateral RLN (Recurrent Laryngeal Nerve) Damage

Partial RLN damage*

Complete RLN damage*



Sensory loss below the cords

Sensory loss below the cords


Paralysis of abductors (posterior cricoarytenoid)

– cords in closed position

Paralysis of all intrinsic muscles (except cricothyroid)

– cords in open position



Hoarseness, dysphonia


Risk of aspiration



Airway obstruction



The RLN carries the abductor and adductor fibres and hence its injury results in damage to both. Varying degrees of damage result in involvement of abductors more than the adductors according to Semon and Rosenbach. Semon’s law is based on the assumption that the nerve fibres supplying the abductors lie in the periphery of the recurrent laryngeal nerve and any progressive lesion involves these fibres first as they are more susceptible to pressure before involving the deeper adductor fibres.

In summary, bilateral partial RLN damage (0.2% after thyroidectomy) causes complete acute airway obstruction whilst in bilateral complete damage (1–2%) the cords are open and increases the aspiration risk.

So if RLN palsy is unavoidable choose a complete injury!

How can you prevent laryngeal nerve damage during surgical procedures?

  • Preoperative laryngoscopy to rule out preoperative nerve involvement
  • Good surgical conduct – complete dissection and exploration of RLN during surgery
  • Awareness of anatomical variations
  • Continuous RLN monitoring may be useful in certain cases

What are the causes of airway complications post thyroidectomy?

Airway complications are more prevalent in the recovery period compared to during induction and intubation.

General causes

  • Laryngospasm
  • Foreign body
  • Obesity/obstructive sleep apnoea syndrome
  • Inadequate reversal of neuromuscular blocking drug

Specific to thyroidectomy

  • Haematoma (1–2%)
  • The commonest cause for acute airway obstruction in the first 24 hours. Definitive therapy is surgical evacuation of haematoma. If re-intubation is necessary consideration should be given to awake fibreoptic intubation due to airway distortion.
  • Laryngeal oedema (0.1%)
  • Bilateral RLN palsy or paresis (<2%)
  • Hypoparathyroidism/hypocalcaemia (3–5%)
  • The commonest cause of airway compromise after 24 hours, hypocalcaemia usually manifests 24–48 hours post surgery as tingling in lips followed by laryngeal stridor and airway obstruction, carpopedal spasm, tetany, laryngospasm, seizures, QT prolongation and cardiac arrest. It is usually managed with intravenous calcium gluconate and CPAP for associated airway compromise.
  • Tracheomalacia
  • Rare and considered historical as it is nearly obsolete in modern day thyroidectomies. Confounding factors could be long standing goitre with retrosternal extension and presence of tracheal compression.

How can the cricothyroid membrane be used for oxygenation in an emergency?

  • Cricothyroid cannula and jet ventilation
  • Surgical cricothyroidotomy and ventilation
  • Seldinger mini-tracheostomy

NAP4 suggests that cricothyroid cannulation has a higher failure rate than surgical cricothyroidotomy in an emergency. The scalpel-bougie-cricothyroidotomy technique or the ‘three-step’ technique is considered as the most efficient and reliable method of obtaining emergency front of neck access (FONA) in ‘can’t intubate can’t oxygenate’ situations.

Other possible questions

  1. 1. Describe the technique of front of neck access (FONA) or demonstrate in a manikin in OSCE.
  2. 2. How would you anaesthetise the airway for an awake fibreoptic intubation?


  1. Batuwitage, B., & Charters, P. (2017). Postoperative management of the difficult airway. BJA Education, 7(17), 235–241.
  2. Burdett, E., & Mitchell, V. (2011). Anatomy of the larynx, trachea and bronchi. Anaesthesia & Intensive Care Medicine, 12(8), 335–339.
  3. Erman, A. B., Kejner, A. E., Hogikyan, N. D., & Feldman, E. L. (2009, February). Disorders of cranial nerves IX and X. Seminars in Neurology 29(01), 85–92.

Grades at Laryngoscopy

Cormack-Lehane classification describes laryngeal view at direct laryngoscopy (Figure 1.15).

  • Grade 1: full view of glottis
  • Grade 2a: partial view of glottis
  • Grade 2b: only posterior extremity of glottis seen or only arytenoid cartilages
  • Grade 3: only epiglottis seen, none of glottis seen
  • Grade 4: neither glottis nor epiglottis seen

Intubation is likely to be difficult with a Grade 2b view or worse.

Figure 1.15 Grades at laryngoscopy.


  1. Krage, R., Van Rijn, C., Van Groeningen, D., Loer, S. A., Schwarte, L. A., et al. (2010). Cormack–Lehane classification revisited. British Journal of Anaesthesia, 105(2), 220–227.

Cross Section of Neck at C6 Level

Figure 1.16 shows the structures at the level of cross section at C6 or C7 vertebra.

Figure 1.16 Cross section of neck at C6 level.

Easily identifiable structures

  • Skin and subcutaneous tissue
  • Platysma, sternohyoid and sternothyroid muscles
  • Thyroid gland, trachea, oesophagus
  • Carotid sheath with contents (common carotid artery medially, IJV laterally and the vagus nerve)
  • C6 or C7 vertebra

The structures laid out in Table 1.7 might not be easy now, but you will certainly be able to identify them after reading this topic!

Table 1.7 Important Structures in the Neck at the Level of C6



Scalene muscles

Longus colli


Recurrent laryngeal nerve

Phrenic nerve

Brachial plexus (or C6 nerve root)

Sympathetic trunk

Superficial cervical plexus


Vertebral artery and vein

Fascial planes of deep cervical fascia

Investing layer

Pretracheal layer

Prevertebral layer


Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Nov 27, 2021 | Posted by in ANESTHESIA | Comments Off on 1 HEAD AND NECK

Full access? Get Clinical Tree

Get Clinical Tree app for offline access