ESA 4 Clinical Conditions Flashcards
Spread of infection within fascial planes
Superficial - None (simple cellulitis)
Retropharyngeal space (anterior to alar fascia) - Down to mediastinum (results from URTIs)
Danger space (posterior to alar fascia) - Down to diaphragm (results from URTIs)
Parapharyngeal space - Down to T2/3 (affecting carotid sheath structures,
Prevertebral fascia - Down to T2/3 results from bad dentition/quinsy)
Branchial cysts/fistulae
Arise as a failure of the pharyngeal clefts to recede (1 st one remains and becomes the ear canal). Cysts are fluid filled pockets, whereas fistulae are openings between two epithelia. Both types are visible along the anterior border of SCM within the neck.
Carotid atheroma formation
Carotid sinus is a bulge that leads to turbulent blood flow, which damages epithelia and kick-starts atheroma formation.
If an atheroma or thrombosis breaks off and travels to the brain it can result in a stroke or TIA.
Carotid sinus hypersensitivity
Carotid sinus is extremely sensitive, so a small touch can be perceived as a huge rise in pressure, sending signals down CN IX (afferent) and CN X (efferent), activating the baroreceptor reflex and causing a drop in blood pressure.
More common in men, manifests as being unable to wear a tie or shave without feeling faint.
Scalp laceration
Blood supply is rich so bleeds profusely. Blood vessels are embedded in dense connective tissue layer so vessels have restricted ability to constrict.
Also, lacerations to the epicranial aponeurosis cause contraction in both directions (occipital and frontal bellies) leading to a wound being held open.
Cavernous sinus thrombosis
Facial veins are valveless so blood can drain both ways i.e. facial veins can drain into the cavernous sinus. An infection that tracks back causes thrombosis within the cavernous sinus which can compress CN III, CN IV, CN VI, CN V 1 or the ICA (this method of infection tracking back can also cause meningitis)
Danger triangle of face
Area bound by the canthuses of the mouth and the bridge of the nose. Infection increasingly likely to track back here vs other areas of the face (see cavernous sinus thrombosis)
Enlarged lymph node(s)
Generally speaking, lymph nodes are enlarged due to either or infection.
Obviously, infection is almost always the cause for enlargement. Malignant lymph nodes are hard, matted and non tender, and importantly immobile.
Lymphadenopathy secondary to infection leads to tender, firm and importantly mobile lymph nodes
Tonsillitis
Refers to inflammation of the palatine tonsils usually (back of mouth). Leads to odynophagia and fever. Prone to reinfection in some people, tonsillectomy is performed in these cases
Whiplash
An acute and large force applied across the C spine leads to overstretching of the tendons and ligaments of the spine, causing intense and sharp pain.
Common cause is a car crash, the seatbelt immobilises the thoracic spine but the head keeps moving, and the collision of the forces stretches the spine
Burst/Jefferson fracture
Huge force applied to atlas i.e. falling on face from height. Bilateral fractures occur in the posterior portion, accompanied with avulsion of the anterior arch, so atlas bursts into pieces. As fragments travel outwards spinal cord injury may not occur
Hangman’s fracture
Hyperextension of the neck (landing on chin) leads to bilateral fractures of pars interarticularis, damaging the spinal cord and leading to death
Fractured pterion
Middle meningeal artery lies deep to the pterion (point on lateral side of skull where sphenoid, temporal, parietal and frontal bones fuse), thinnest portion of skull. A fracture here (the ‘temple’) leads to rupture of this artery and subsequent extradural haematoma
Coning
Increased ICP forces the cerebellar tonsils through the foramen magnum of the occiput, putting pressure on the brainstem and leading to immediate death (due to cease of respiratory function)
Consequences of Premature birth to the calvaria
Suture lines not completely formed at birth leading to bones having manoeuvrability to allow for manipulation (and interlocking) within the birth canal.
Bones are too far apart in premature babies so cannot fuse together, leading to brain damage. Premature babies usually delivered by C section
Fractures of the skull
Depressed fracture – fracture caves inwards, pressing on the brain, common in squamous parts of the skull, especially the pterion (where temporal, sphenoid, parietal and frontal bones meet) - Pterion fractures damage the anterior branch of the middle meningeal artery and cause an
Linear fracture – lines spread out from the impact bone in several directions but bone doesn’t cave inwards - Can be seen in the frontal bone
Comminuted fracture – skull is split into several distinct pieces of bone, also usually involves a break in the skin
Countercoup fracture – force travels round skull and occurs on the opposite side to the point of impact
Basilar fracture – occurs on the back of the head (basilar part of occipital bone) extradural haematoma
Fractures of the mandible
Coronoid process fracture – unusual and usually unilateral
Condylar process fracture – usually result in avulsion and/or dislocation of the TMJ
Angle of mandible fracture – can damage the 3 rd molar socket
Body of mandible fracture – tend to occur at the area of a canine tooth
Lateral cleft lip
Failure of MNP and maxillary prominence to fuse leading to split in mucosa up to the nostril
Cleft palate
Failure of palatal shelves to fuse in midline leading to a difficulty suckling and with speech
Foetal alcohol syndrome
Results on the foetus of alcohol intake during pregnancy.
Alongside alcohol related neurodevelopmental delay (combined as foetal alcohol spectrum disorder) incidence is 1/100 births
Physical features
Short palpebral fissures (small eyes) No philtrum Small head Underdeveloped jaw Thin upper lip
Mental features
Behavioural disorders e.g. ADHD
Learning disorders e.g. thinking, speech, social skills
Hearing and sight problems
CN I lesion
Usually a result of cribriform plate fracture (accompanied by CSF rhinorrhoea) or meningitis. Leads to anosmia
CN II lesion
Can be due a number of things, including central retinal artery occlusion, compression by a pituitary adenoma etc. Loss of vision depends on where the lesion is along the nerve but leads to reduced visual acuity, visual fields and defective direct and consensual pupillary reflexes. Can also show a relative afferent pupillary defect (both eyes show a consensual pupillary reflex by side with damaged CN II causes both pupils to constrict less)
Differentiating CN II lesions
Proximal to the optic chiasm – CN II is carrying all sensory input from one eye, so this leads to a total loss of vision in this one eye. This manifests as reduced vision on the lateral field of vision on the same side (specifically, the loss of the medial fibres of that eye – the lens flips the image before it hits the retina)
At the optic chiasm (bitemporal hemianopia) – here, the medial fibres supplying sensory information from the lateral fields of vision cross, and are both damaged. This leads to reduced vision at the peripheries, known as tunnel vision. This is most commonly caused by an enlarging pituitary adenoma
At the optic tract (homonymous hemianopia) – here, the fibres that receive information from the other side’s field of vision (e.g. left optic tract carries information from right FOV) are damaged, and so leads to loss of vision in the contralateral field of vision (not the contralateral eye, it’s slightly different). Commonly caused by a parietal lobe tumour
CN III lesion
Can be a result of a number of things but a common one is cavernous sinus thrombosis. Increased ICP is also a common cause.
Displays ptosis (loss of levator palpebrae superiorus) and down and out pupil (unopposed actions of superior oblique and lateral rectus). If parasympathetic fibres are involved (they usually are) then also shows loss of accommodation reflex and a blown (dilated) pupil due to loss of constrictor pupillae
Horner’s syndrome
Damage to the sympathetic trunk e.g. due to a Pancoast tumour leads to ptosis (loss of superior tarsus), a constricted pupil (myadrisis due to loss of dilator pupillae) and anhydrosis (loss of sympathetically mediated sweating)
CN IV lesion
Can be caused by cavernous sinus thrombosis. Leads to diplopia when looking down and in (action of superior oblique lost). Can also see patient has a head tilt as they try to compensate for the loss of intortion
CN V lesion
Damage to fibres leads to loss of sensation. V 1 and V 2 purely cause sensory loss in their distributions, but V 3 damage leads to loss of mastication muscle bulk (e.g. masseter) as well. Sympathetic fibres that hitch hike the nerve to the relative distributions also damaged leading to vasodilation and anhydrosis
Harlequin syndrome
Damage to the sympathetic fibres that hitch hike CN V at the level of the sympathetic trunk/thoracic cord leading to vasodilation and anhydrosis across the entire half of the face
Trigeminal neuralgia
Severe sharp pain within the distribution of the trigeminal nerve that lasts for a few seconds to a few minutes. Triggered by sudden movements, wind or just idiopathic
CN VI lesion
Usually seen as one of the first signs of increased ICP. As such, CN VI palsy can be misdiagnosed as falsely localising whereas in fact it is due to a whole brain pathology. Paralysis of lateral rectus leads to diplopia on attempted lateral gaze in the affected eye
CN VII lesion (Facial nerve palsy)
A lesion to the ‘clinical’ facial nerve i.e. containing the parasympathetic fibres is much more common than one of the anatomical ‘proper’ facial nerve i.e. just the motor and sensory roots. It is at risk in a number of locations:
Parotid gland (parotitis or malignancy) – affects only motor functions
Facial canal (inflammation) – doesn’t affect the pterygopalatine ganglion but can affect stapedius (leading to hyperacusis) and submandibular ganglion (taste sensation, sublingual and submandibular glands). Also affects motor function
Forceps delivery – affects the extracranial portion only motor functions affected
As shown the damage depends on the level/structure at which CN VII is damaged. Tends to be permanent
Bell’s palsy
Idiopathic damage to CN VII. Tends to be motor functions only i.e. affects the nerve extracranially (but can have intracranial Bell’s palsy leading to parasympathetic and sensory damage). Many cases thought to be caused by inflammation due to Herpes zoster but this is difficult to prove. Tends to resolve spontaneously
Stroke (in the context of CN VII)
Lesion to one hemisphere of the brain can cause infarction of the facial motor nucleus. However, the branch of CN VII that supplies frontalis (temporal) receives fibres from both the right and the left facial motor nuclei. This is true for CN VII on both sides. This means that someone with a stroke will be unable to perform most facial actions but they will be able to wrinkle their forehead/raise their eyebrows
CN VIII lesion
As the vestibulocochlear nerve is comprised of the vestibular (balance) and cochlear (hearing) nerves you would expect some dysfunction in either of these. Damage to the vestibular portion leads to inability to balance and subsequent vertigo. Damage to the cochlear portion leads to sensorineural hearing loss (air conduction still > bone conduction but hearing reduced vs the contralateral side)
Vestibular schwannoma
Benign tumour of the Schwann cells of CN VIII. Leads to symptoms seen with a CN VIII lesion/palsy. If it grows large enough it can begin to impinge on CN VII within the facial canal, which shows both changes in hearing (hyperacusis due to paralysis of stapedius) and taste (loss of chorda tympani), alongside facial paralysis
CN IX lesion
Damage to CN IX leads to a loss of function in stylopharyngeus, which is a key muscle involved in elevating the larynx during swallowing, to position the epiglottis correctly. It also supplies taste to the posterior 1/3 rd of the tongue, so this could be tested with a specific kit. However, CN IX cannot be examined alone, and is instead examined alongside CN X with things such as the gag reflex or getting the patient to cough/swallow
CN X lesion(s)
There are two key types of CN X lesion (in the context of the head and neck i.e. not considering its distribution throughout the thorax and abdomen), but there are some features that may be common to both. Any deviation in the uvula away from the lesion may be evident, as musculus uvulae will contract to pull the uvula towards the unaffected side.
Also, any damage to the vagus nerve may damage the pharyngeal constrictors, leading to disorders of swallowing.
There are two key branches that may provide differing symptoms when considering phonation:
External/superior laryngeal nerve – solely provides innervation to cricothyroid, which tenses and elongates the vocal cords, allowing for a higher pitch and is known as the ‘singers muscle’. Damage to this nerve leads to a monotone voice and loss of strength (loudness) of phonation
Recurrent laryngeal nerve – provides innervation for the other intrinsic muscles of the larynx, the most important of which is the posterior cricoarytenoids, which abduct the vocal cords. They also innervate the lateral cricoarytenoids, which adduct the vocal cords. Total damage to the nerve less to loss of both of these muscles leading to the vocal cord being stuck between abducted and adducted. This may produce a hoarse voice
Partial paralysis adversely affects the posterior cricoarytenoids, leading to a vocal cord that is locked in the adducted position. If this occurs bilaterally, the larynx cannot open and it is a surgical emergency that requires a needle cricothyroidotomy to resolve
Can easily undergo iatrogenic damage during any thyroid surgery – care must be taken to identify and avoid these nerves
CN XI lesion
Lesions to CN XI lead to denervation atrophy of trapezius and SCM, along with weakness of shrugging the shoulders and rotation of the head
CN XII lesion
Damage leads to fasciculations of the tongue and a deviation in movement towards the affected side. This is because when sticking the tongue out, the transverse intrinsic muscle on both sides contracts to elongate/narrow the tongue. If this is paralysed on the right side, it stays short on the right side, so it will deviate towards this side.
Orbital (blowout) fractures
Certain walls of the orbit are much thinner than others and as such are prone to fractures when a large force is applied across the orbit. All fractures usually give some degree of diplopia, enopthalmos, lid swelling, pain, reduced vision and reduced visual fields. Common types are:
Floor (aka maxillary) – results from relatively minor trauma directly to the orbit
Leads to inferior displacement of the eye and relevant apparatus, this means the inferior rectus can get trapped and this results in inability to raise the eye (leading to diplopia on vertical gaze)
Also may lead to enopthalmos, as the eye is pushed posterior and inferior within the socket
Can be accompanied by infraorbital anaesthesia (lower eyelid and upper lip), due to damage of the infraorbital nerve (branch of CN V 2 )
Medial (aka ethmoidal) – results from relatively minor trauma directly to the orbit
Rarely isolated and usually seen in combination with other fractures
Can trap the medial rectus, leading to horizontal diplopia on medial gaze
Damage to the ethmoidal air cells within the ethmoid sinus can lead to surgical emphysema
Lateral (aka zygomatic arch) – results from major trauma due to the relative thickness of the frontozygomatic suture
Usually found alongside other facial injuries
Can trap the lateral rectus, leading to horizontal diplopia on lateral gaze
Retinal detachment
The retina and the choroid have different embryological origins, and as such can easily become detached from each other if force is applied to them e.g. trauma. Outer layers of the retina are supplied by the choroid, and inner ones by the central retinal artery. As such, loss of the choroid leads to avascular necrosis of the retina and subsequent loss of vision
Open angle glaucoma
Increased fluid formation within the anterior chamber of the eye leads to the iris being displaced anteriorly and the angle of the trabecular network getting wider i.e. more open.
This progresses gradually and increases intraocular pressure until the optic nerve is compressed, leading to a loss of vision
Closed angle glaucoma
Different pathology to open angle glaucoma, in this the iris is forced against the trabecular network (i.e. posteriorly), leading to acute vision loss
Central retinal artery occlusion
Interruption of this artery (running within CN II) leads to painless and instantaneous vision loss, very difficult to fix as the nerve begins to die shortly after. Shows on fundoscopy as a pale retina (blood supply delivered by this artery), aside from the macula/fovea which is entirely perfused by the choroid
Central retinal vein occlusion
Interruption of this venous drainage (running within CN II), usually due to dehydration or thrombophlebitis, leads to acute but not instantaneous vision loss due to a backup of pressure. Shows on fundoscopy as a ‘stormy sunset’ picture
Papilloedema
Swelling of the optic disc as a result of (usually) increased ICP, but can in rare cases be due to bad, untreated hypertension as well. On fundoscopy appears as a red, angry picture with a bulging optic disc and raised retinal arteries
Meibomian cyst
Blocked tarsal gland found on the eyelid. Not infected per se but may become so (so can be treated just with a hot compress)
Styes
Infected ciliary gland found within the margin of the eyelid. By definition are infected so require antibiotics to treat
Thyroid eye disease
Usually a result of poorly controlled hyperthyroidism (Grave’s disease is the usual cause). Swelling of the tissues within the orbit causes exophthalmos as they have no where else to go.
Symptoms
Ocular irritation
Red eyes
Diplopia
Symptoms
Proptosis/exophthalmos
Lid retraction
Restrictive myopathy
Lid lag
The severity can be graded by using the NOSPECS mnemonic:
No signs OR symptoms
Only signs, no symptoms
Soft tissue involvement e.g. lid oedema
Proptosis (exophthalmos)
Extraocular muscle involvement (e.g. restrictive myopathy)
Corneal abrasion (eyelids not closing properly due to lid oedema)
Sight loss
Starting with no signs or symptoms at 0, you gain a point as you head down the scale. Anything >3 needs referring for imaging and steroids to prevent permanent vision loss
Conjunctivitis
Inflammation of the bulbar conjunctiva giving a red appearance to the sclera of the eyeball. Usually self limiting and does not require any treatment
Periorbital cellulitis
Inflammation of the soft tissue structures within the orbit itself. Differentiated from simple conjunctivitis by the presence of swollen eyelids. Accompanied by visual dysfunction, relative afferent pupillary defect, fever and exophthalmos. Infection is at a high risk of tracking back into either the ocular structures themselves e.g. CN II or the brain itself e.g. leading to meningitis so needs IV antibiotics and admission
Orbital mass lesions
Several different types, but essentially some sort of accumulation of cells/fluid that leads to swelling in or around the orbit, pain, inflammation, diplopia, proptosis and restricted eye movements. These are just some of the types:
Mucocoele – a blocking of the sinus openings in the nose leading to back up of secretions into the area of the orbit
Dermoid cysts – congenital cysts that can be superficial or deep and are often well circumscribed, they tend not to cause pain
Wegener’s granulomatosis – these lesions are a result of necrotising vasculitis and as such are prone to infection if the necrotic tissue is not removed properly (corticosteroids may reduce the necrosis formation)
Dacryoadenitis – inflammation of the lacrimal glands, can commonly be caused by mumps or gonhorrea
Pseudotumour – idiopathic diagnosis of exclusion after the lesion has been biopsied
Capillary haemangioma – aka strawberry nevus, tend to be congenital, superficial ones are easily identified on the eyelid
Cavernous haemangioma – a benign tumour of dilated and well vascularised blood vessels (through which blood moves slowly), they tend to be found deep within the orbit (in the intraconal space, posterior to the eyeball but bound either side by the rectus muscles) and as such may caus proptosis/exophthalmos
Corneal abrasion
Any foreign body can scratch the cornea, the fibrous layer that overlies the pupil/iris (technically overlies the anterior chamber). This is usually mitigated by the blink reflex; cornea is supplied by CN V 1 , which when stimulated leads to contraction of orbicularis oculi, blinking out the foreign body. If this is lost e.g. the nerve is damaged, then the eye can be damaged. Abrasions usually heal on their own but antibiotic eye drops may be needed
Antihelix deformity
Lack of the antihelix fold of the pinna, leading to a ‘dumbo ear’ appearance
Pinna malform
Congenital hypoplasia or aplasia of the pinna
Pre-auricular pit
Small hole immediately anterior to the EAM within the pinna
Pre-auricular skin tag
Small swelling immediately anterior to the EAM within the pinna
Traumatic rupture of pinna
Pinna is ‘ripped apart’ due to trauma. Tends to look worse than it is due to the tendency of elastic cartilage to rip apart when it is damaged due to elastic fibres providing recoil, pulling the edges of the wound further apart
Pinna haematoma
Accumulation of blood between cartilage and perichondrium (usually secondary to trauma), which if not treated may lead to avascular necrosis of the pinna as the cartilage’s ‘blood supply’ has been stripped leading to cauliflower ear
Cauliflower ear
‘Collapsed down’ pinna due to avascular necrosis (usually secondary to a pinna haematoma)
Otitis externa
Infection of the external ear, commonly caused by Staphylococcus spp., leads to an inflamed, sore external ear, which can be accompanied by discharge and some degree of hearing loss
Foreign body insertion (external ear)
Small objects lodged in the ear canal lead to pain and a degree of conductive hearing loss. Can also lead to tympanic rupture if left in situ without prompt removal
Tympanic membrane rupture
Occurs either due to trauma (cotton buds!) or pressure difference on either side of the membrane (otitis media leading to a bulging and then ruptured membrane due to the build up of pus is common). As the membrane is now not in tact its ability to vibrate is reduced, leading to a degree of hearing loss. Tears can be minor, or central holes or subtotal perforations
Acute otitis media
Infection of the middle ear, almost always a result of tracking of an upper respiratory tract infection via the Eustachian tube (especially common in children due to the fact it is shorter, narrower and at a less oblique angle). Leads to pain, conductive hearing loss and retraction of tympanic membrane, however in some cases the build-up of pus can lead to bulging and subsequent rupture of the eardrum
Otitis media with effusion
Thick effusions develop behind the eardrum as a result of consistent negative pressure (such as a chronically collapsed Eustachian tube in children) leading to reduced ability to hear (conductive hearing loss) and a predisposition to an infection, creating a vicious cycle. Can be treated with grommet insertion into the tympanic membrane to provide an alternate route for pressure to equalise
Mastoiditis
Infectious spread to the air cells of the mastoid process of the temporal bone (via the epitympanic recess), leading to swelling of this bone. Can be seen externally as post-auricular inflammation, and pushes the ipsilateral pinna anteriorly, which can be spotted on examination. Spreads very easily and so can cause intracranial infection (e.g. meningitis) and death. Requires antibiotics and surgical clear-out of the mastoid air cells
Cholesteatoma
Retraction pockets appear (as a result of –ve pressure) and accumulate dead skin cells, forming a necrotic mass of dead cells that multiplies and spreads through adjacent structures. Acts cancerous but isn’t cancerous. The most lateral portion of a cholesteatoma can be spotted in the attic/pars flaccida of the tympanic membrane
Benign positional paroxysmal vertigo
Displacement of otolith (stone within the canal) that keeps moving when the fluid stops (like sediment within water), so you perceive movement when you are actually still (mismatch between vision and vestibular system is unpleasant). Only lasts a few seconds
Meniere’s disease
Overaccumulation of endolymph leads to vertigo, tinnitus, hearing loss and aural fullness
Motion sickness
Very common complaint of many people. Occurs when there is a mismatch between vestibular and visual systems, which the brain perceives as poisoning and activates the vomiting centres as a defence mechanism. Common example is seasickness; vestibular system perceives rocking of boat whereas your eyes see you’re steady (if you look within the boat/close your eyes), so can be remedied by focussing on the horizon so your eyes know you’re not steady
Nasal fractures
Most common fracture of the facial skeleton. Occurs when a force is applied across the nose e.g. a punch. If it heals misaligned, then the entire nose (including the cartilage) is misaligned permanently
Septal haematoma
Trauma to the nose can also cause a septal haematoma, which like a pinna haematoma strips the perichondrium from the cartilage, leaving the nasal septum at risk of avascular necrosis. If this happens the patient can end up with a deviated septum, leading to snoring or even sleep apnoea (temporary cessation of breathing in sleep)
Rhinitis
Umbrella term for any inflammation and irritation of the nasal mucosa, which manifests as the feeling of a blocked, stuffy nose, with some alteration to speech, inability to breath through the nose and discharge from the nose. Many causes/types:
Viral/bacterial infection Allergic rhinitis (hayfever) Nasal polyps (benign collections of eosinophilic cells that grow close to the middle meatus)
