Radial Nerve


Larger terminal branch of the posterior cord of the brachial plexus, receiving fibres from C5-T1.


Exits the axillary fossa posterior to axillary artery; passes posterior to humerus in the radial groove with the deep brachial artery between the lateral and medial heads of the triceps; perforated the lateral intermuscular septum and enters the cubital fossa, dividing into the superficial (cutaneous) and deep (motor) radial nerves.

Because of its close relation to the humerus, any fracture of the humerus, partial or complete (especially at the humeral neck) has the potential to damage the radial nerve.  The resulting syndrome is weakness in extending the elbow, wrist and fingers, with an associated sensory deficit (see below).


All the muscles of the posterior compartment of the arm (triceps and anconius) and forearm (brachioradialis and extensor carpi radialis longus).  NB the rest of muscles in the posterior compartment of the forearm are supplied by the posterior interosseus nerve, a continuation of the radial nerve.

Skin of posterior and inferolateral arm, posterior forearm and dorsum of the hand lateral to the axial line of digit 4.

It is important to note that the radial nerve does not have an autonomous skin zone. However, complete nerve lesion commonly results in loss of sensation on the radiodorsal aspect of the forearm and the dorsum of thumb (the anatomical snuff box). There is loss of finger extension at the metacarpophalangeal joints, loss of thumb extension, and wrist drop (loss of wrist extension).

The Brachial Plexus

The Brachial plexus is a group of somatic nerves that innervate and receive sensory input from the majority of the upper limb.

Gross anatomy


There are 5 roots involved in the brachial plexus:C5, C6, C7, C8 and T1.  There are several points of interest relating to the nerve roots.

  • Firstly, C5-C7 all leave the spinal cord above the level of corresponding vertebrae.  Spinal nerve C8 exits below vertebra C7 (there is no C8 vertebra), and from then on (including T1 for the purpose of the brachial plexus) spinal nerves exit at below the corresponding vertebral level.
  • Secondly, T1 commonly splits into two.  The larger branch enters the brachial plexus (C5-8 do not encounter ribs) while the small becomes the first intercostal nerve (to innervate the muscles of inspiration)
    • C5-8 pass between the gap between the anterior and middle scalene muscles, with the subclavian artery inferiorly.  The subclavian commonly lies in front of (and covers) T1 before it joins the plexus.


The brachial trunks are formed shortly after the roots exit the intervertebral foramina in the inferior part of the neck.

  • Superior (upper)trunk- the union of C5 and C6
  • Middle trunk– a continuation of C7
  • Inferior (lower) trunk– the union of C8 and T1

NB Injury to these can occur.

    • Erb’s Palsy is a paralysis of the arm- specifically due to damage to the superior trunk, most commonly seen in babies who have had a difficult delivery (usually very large babies) for which forceps or other assistive measures have been required.  The baby doesn’t move the affected arm, reflexes (including the Moro response) are absent or abnormal and the baby may have an associated Horner’s syndrome or respiratory problems.  This is usually self-limiting and will resolve in several weeks.
    • Klumpke’s palsyis caused in similar circumstances but the damage is to the lower trunk.  This causes a claw hand, loss of grip reflex and weakness of the hand muscles.  There also can be associated Horner’s/respiratory problems.


Each trunk then divides into an anterior and posterior division as the plexus passes through the cervicoaxillary canal posterior to the clavicle.

  • Anterior divisions will go on to supply the anterior compartments of the arm (flexor group)
  • Posterior divisions will go on to supply the posterior compartments of the arm (extensor groups)


The cords pass over the 1st rib close to the dome of the lung and continue under the clavicle, and surround the axillary artery (they are named in relation to this artery.

  • Lateral cord– made up of the anterior divisions of the superior and middle trunks
  • Medial cord– continuation of the anterio division of the inferior trunk
  • Posterior cord- made up of the posterior divisions of all three trunks.

Named nerves

NB NOT ALL nerves arise from the cords of the brachial plexus- some originate at the root, trunk and division level.

Broadly speaking, the nerves arising from the brachial plexus can be split into supraclavicular branches and infraclavicular branches depending on whether they arise above or below the clavicle (respectively).

  • Supraclavicular branches
    • Dorsal Scapular
    • Long Thoracic
    • Suprascapular
    • Subclavian nerve (nerve to subclavius)
  • Infrascapular branches
    • Lateral pectoral
    • Musculocutaneous
    • Median
    • Middle Pectoral
    • Medial cutaneous nerve of arm
    • Median cutaneous nerve of forearm
    • Ulnar
    • Upper and lower subscapulars
    • Thoracodorsal
    • Axillary
    • Radial


An astigmatism is essential an uneven curvature of the cornea.


It is usually a congenital condition although rarely can be caused by mechanical damage to the cornea e.g from a large meibomian cyst or from cataract surgery.


The patient will have reduced visual acuity.  As a result, patients may get headaches in trying to accommodate for the astigmatism.

On examination, the corneal reflection may not be smooth or symmetrical.


Corneal topography will show the degree of astigmatism.


Special lenses can be used to correct the refractive error caused by an astigmatism.  It may also be possible to correct the eye’s shape by using a hard contact lens, although this will not always be the case.

Hypermetropia (long-sightedness)

Patients with hypermetropia can see distant things clearly, but have trouble focusing on close things.

The problem can be either:

  • the eye is too small
    • OR
  • the refractive power of the lens is too weak

This results in the image focusing behind the retina.

To tackle this problem, convex lenses (i.e. positive prescription e.g. +1 Diopters) are used for things like reading to bend light inwards and project the image as if it were a distance.  HOWEVER, hypermetropic patients often can accommodate for their long-sightedness by relaxing (and thus thickening) the lens.  Common, hypermetropic patients will present much later (than myopic patients who typically present in childhood) with the need for reading glasses.  In later life, they may require glasses for both reading and distance vision as the power of the lens weakens with age even more.

Patients with severe hypermetropia are at risk of closed angle glaucoma due to their short eyes.

Myopia (short-sightedness)

Patients with myopia can see close things clearly, but have trouble focusing on things in the distance.

The problem can be either:

  • the eye is too long
    • OR
  • the refractive power of the lens is too great

This results in the image focusing in front of the retina.

To tackle this problem, concave lenses (i.e. negative prescription e.g. -1 Diopters for mild to -10 diopters for severe) are used for looking into the distance to bend light outwards and project the image as if it were near.

Patients with severe myopia are at risk of retinal detachment, macular degeneration and primary open angle glaucoma, but usually don’t require reading glasses later in life.

Vitreous Haemorrhage


  • Vitreous haemorrhage is blood in the vitreous chamber of the eye.
  • It is commonly associated with retinal tears and proliferative diabetic retinopathy/ARMD (with the formation of new vessels) (including CRVO)


  • Floaters are the most common symptom.
  • The patient may also have loss of vision (haze) if the haemorrhage is large.
  • There is normally no pain or any other significant problems.  If there are, then a more serious cause should be considered.
  • Examination
    • Haemorrhage may be seen in the vitreous chamber on ophthalmoscopy.
      • It may be difficult to focus on it as it can extend a depth of the vitreous.
    • It may also be difficult to focus on the fundus, depending on the cause of the haemorrhage.
    • The cause should be sought at examination (see ARMD/retinal detachment/diabetic retinopathy).


  • Patients may be advised to keep their head elevated and eyes patched for a while to let the blood settle.
  • The underlying cause, where known, should be treated appropriately e.g. retinal detachment repair; laser treatment for proliferative disease
    • In severe (non-clearing)/recurrent cases, vitrectomy may be required


Retinal vein occlusion

Risk factors/Causes

  • Systemic vascular disease is the most common cause- e.g. hypertension, diabetes mellitus, CVD.  Other causes include inflammatory conditions, blood disorders/clotting disorders, the OCP etc.
  • The exact pathophysiology is not 100% certain but it is hypothesised that the retinal artery/vein can be predisposed to thrombus formation at the point where they enter/exit the optic disc (in the lamina cribrosa).  It is also possible that arteriosclerotic change in the retinal artery causes disturbed blood flow in the retinal vein as it hardens (the two vessels share the same covering- the common adventitial sheath.


  • The patient may be asymptomatic or may only complain of mild visual disturbances in their peripheral field (usually a blurring/loss of field).  If the temporal arcades are blocked and, subsequently, the macula is affected, then patients may complain of a marked visual loss.  This can come on gradually or suddenly.
    • NB if there is a central retinal vein occlusion, there is usually marked loss of vision and there may be pain on movement or the eye or photophobia due to subsequent swelling of the optic disc.
  • Examination
    • There may be reduced visual acuity if the macula is affected.  There may be mild peripheral field defects depending on branch occlusion location and severity.  On fundoscopy:
    • There are classical flame haemorrhages in the affected area.
    • There may be a swollen optic disc in CRVO.
    • There may be cotton wool spots as a result of ischaemic damage to the eye (bad prognostic sign).
    • A RAPD (also poor sign)
  • Patients with ischaemic changes are also at risk of glaucoma and permanent visual loss due to subsequent oedema.  Signs of the former (e.g. raised IOP) should be investigated and managed appropriately.


  • Refer urgently to ophthalmology
  • No immediate treatment available unless IOP is high (in which case beta blockers may be used)
  • Monitor closely for neovascularisation and treat with laser before this progresses
  • Anti-VEGF treatments (as for wet-ARMD) are also now commonly recommended to prevent this.

Retinal Detachment

This is when the retina detaches from the underlying retinal pigement epithelium (RPE).

Risk factors and epidemiology

Patients with a high myopia (short-sightedness- larger than average eye) are at risk of retinal detachment due to the thinly spread retina.  Retinal detachment is also a post-operative risk of cataract surgery (1-2%).  Proliferative diabetic retinopathy can cause a tractional RD.

Although RD is not that common, it is an emergency, since once the macula is involved, the outcome for sight is much poorer.

Types of detachment

  • Rhegmatogenous (most common type)- occurs due to a retinal break/tear/hole that allows fluid from the vitreous cavity between the retina and RPE.
  • Tractional- occurs when fibrous/fibrovascular tissue (usually formed secondary to injury/inflammation/neovascularisation) attaches to the vitreous and pulls the retina from the RPE.  Most commonly due to diabetic retinopathy.
  • Exudative (serous) – detachment due to a build up of fluid underneathe the retina without tear/hole/break.  Usually due to an inflammatory condition, but can also be secondary to hypertension, central retinal vein occlusion (haemorrhage), papilloedema or a retinal tumour.


The 4 F’s:

  • Flashes- due to mechanical traction/trauma to the sensory retina.  This is the differentiating symptom between PVD and a retinal tear.  If they are present, the patient has a retinal tear until proven otherwise.
  • Floaters- usually occur when the vitreous, too, has detached and is casting a shadow onto the retina.
  • Field defects- patients usually report a shadow in their peripheral fields.  This spreads as the retina detaches further.  NB a superior field defect indicates pathology in the inferior retina and vice versa (likewise for left and right).  Commonly this presents in a ‘theatre curtain-like’ fashion, descending from above


  • The patient may have an RAPD
  • check visual fields to try and isolate the location of the tear
  • there may be a characteristic appearance on fundoscopy showing a pale streak across the fundus, superior to which is choroidal tissue- although this may be difficult to focus on
  • there may also be some vitreous haemorrhage on fundoscopy
  • Fall in acuity- this is a bad sign as it is likely that the macula +/- foveal region is detaching.  If the patient loses all acuity, it is likely that this has already happened and the chances of a successful surgical repair are significantly reduced.


USS may be helpful but commonly this is a clinical diagnosis.  It is more useful in exudative forms of retinal detachment, where it can detect the presence of tumours and oedema.  Fundus photography can also help but should not be able to add much more than ophthalmoscopy.


There are a number of ways to fix the tear in the retina- e.g. cryotherapy, retinopexy (gas), laser treatment, scleral buckle surgery etc, depending on the size of the tear/hole and the location.

Posterior vitreous detachment


  • A PVD is largely due to the aging process of the eye.
    • With age, the vitreous loses its strength and elasticity and becomes a little more soft/watery.  As a result, the vitreous can lose its shape and come away from the retina.
    • More common in severely myopic patients


  • Floaters are the predominant feature- as the vitreous comes away, it casts a shadow on the retina
  • Flashes may occur- this is caused by mechanical traction on the retina causing a photopsia (flash)
    • This is a warning sign that the retina is at risk and could tear/detach.  NB retinal detachment is still a rare complication of PVD despite this.
  • A halo of floaters/hairs on the temporal side of vision may be seen.  This occurs as the vitreous detaches from the optic disc area.  This is technically a blind spot, resulting in the shadow causing a halo around it.
  • There is no pain
  • It may be difficult to visualise the retina on fundoscopy


  • Refer urgently to ophthalmology in case of retinal detachment.
  • In most cases, watchful waiting for any signs of retinal tearing is the main management.
  • Most patients’ vitreous gels will continue to degenerate, but symptoms will either become less noticeable or will resolve.
  • If any of the signs (4 F’s) of retinal detachment appear (or worsen after seeing the doctor), refer urgently for repair.
    • Floaters
    • Flashes
    • Fall in acuity
    • peripheral Field loss.



  • A cataract is the result of a gradual thickening of the lens and loss of transparency.
  • The exact mechanism behind cataracts is not known but nuclear sclerosis– which occurs when new cortical layers are added causing compression and hardening of the central nucleus of the lens.
    • A change in the fibrous content of the lens, changes in epithelial growth and death, and a decreased transfer of water and nutrients into the lens is also thought to play a role.
    • Associated with diabetes, smoking, statins, steroid use; eye surgery
  • Cataracts are common (up to 20% of the population will get a cataract; and accounts for almost half of worldwide blindness)
  • Can be classified by type (area of lens affected)
    • Nuclear cataracts- cause reduced contrast and colour intensity; the person has difficulty recognizing faces or car number plates. The person often retains good reading vision for many years.
    • Cortical cataracts- cause problems with glare when driving and difficulty reading; the person finds that sunlight is uncomfortable in winter (due to low sun on the horizon).
    • Subcapsular cataracts- cause difficulty in daytime driving and difficulty reading, and are visually disabling in good lighting


  • A gradual, painless, decrease in visual acuity.
  • Glare is a comon complaint (disproportionate reaction to brightness( which may also manifest as a decrease in contrast sensitivity and/or colour vision.
  • A risk factor for cataracts is myopic vision, and often, at the onset of cataracts, patients will require an increase of their prescription.  This is in contrast to presbyopic patients who can get temporary restoration of their near-sight.
  • On examination
    • The classic sign is an absent/unclear red reflex.
    • Examination of the lens may show general opacification within the lens (nuclear type), opacification in the Posterior subcapsular space, or spoke-like opacification (cortical type).
    • Visual acuity and colour saturation may be reduced.
    • A RAPD may be present if the cataract is preventing a significant amount of light from entering the eye.


  • If the cataract is not causing major problems, the cataract may be left and monitored for any progression.  If the patient is having symptoms, surgical removal and ocular lens implant is the mainstay of management for patients.
    • Most patients will have Phacoemulsification + IOL implant