FRCA Notes


Intra-ocular pressure


  • The globe is a fixed sphere ensconced in tough connective tissue, within the rigid orbit
  • This makes intra-ocular pressure (IOP) analogous to intra-cranial pressure with regards to its physiological happenings
  • This may be reassuring to those with limited time to learn the ins and outs of intra-ocular pressure and the impacts of anaesthesia

  • Normal IOP is 10 - 20mmHg, though undergoes small physiological fluctuations and a diurnal variation
  • For those fond of equations, IOP = (aqueous production/aqueous outflow) + episcleral venous pressure
  • Unless the patient has a hole in their globe (surgical or otherwise), this means IOP is never lower than episcleral venous pressure (~8-10mmHg)

Vitreous humour volume

  • The volume of the vitreous is relatively fixed and therefore changes to aqueous humour volume are more impactful on IOP
  • Vitreous volume can be affected by mannitol administration

Aqueous humour volume

  • Aqueous humour occupies the anterior chamber of the eye, contributing to IOP
  • It is produced by the ciliary bodies in the posterior chamber through a combination of:
    • Active secretion (80%) via a Na+/K+ ATPase, the rate of which is independent of IOP
    • Ultrafiltration (20%) of plasma, the rate of which is influenced by IOP, venous and oncotic pressure

  • It flows between the iris and anterior lens, through the pupil and into the anterior chamber

  • Aqueous humour outflow occurs via two main routes:
    1. The 'conventional' route (80%)
      • Aqueous is reabsorbed into episcleral veins (at the angle between the cornea and iris i.e. iridocorneal angle) down a pressure gradient via:
        • The trabecular mesh network
        • The canal of Schlemm

    2. The uveoscleral route (20%)
      • There is non-specific outflow through e.g. the suprachoroidal space and choroid itself

  • Increased IOP will increase aqueous drainage (in the otherwise normal eye; this isn't the case e.g. in glaucoma)
  • Increased drainage of aqueous humour is therefore the main compensatory mechanism for alterations to other components of the globe
    • This compensation occurs over approximately 20mins

Autonomic action Physiological effect Effect on aqueous humour
Alpha agonism Vasoconstriction reduces ciliary body blood flow Reduced production
Beta agonism Increased production
Sympathetic activation Mydriasis - pupillary dilation Reduces drainage
Parasympathetic Miosis - pupillary constriction Increases drainage

Choroidal blood volume

  • The retinal artery displays autoregulation down to a SBP of 90mmHg
  • Choroidal blood vessels themselves do not display myogenic autoregulation
  • Otherwise, the factors influencing choroidal blood flow are analogous to that of cerebral blood flow

Choroidal (episcleral) venous pressure

  • The episcleral venous plexus pressure is normally 8-10mmg, only 1-2mmHg below IOP
  • A raised CVP will therefore reduce aqueous humour drainage via this route and thus increase IOP

External pressure

  • Such pressure may be:
    • Pathological e.g. due to retrobulbar haemorrhage (which itself may be secondary to sharp needle regional anaesthesia)
    • Iatrogenic e.g. due to prone positioning or the presence of LA following regional techniques

Increased internal pressure

  • Increased aqueous humour volume e.g. glaucoma
    • There may be a normal iridocorneal angle but a trabecular meshwork which is clogged with extracellular matrix and other detritus (open angle glaucoma)
    • Conversely the iridocorneal angle itself may become narrowed, leading to a physical closure of the trabecular meshwork

  • Increased choroidal blood volume e.g. hypoxia, hypercarbia, hypertension, head down (Trendelenburg), laryngoscopy
  • Increased CVP causing reduced choroidal venous drainage e.g. coughing, straining, vomiting

  • Use of gases to tamponade a detached retina:
    • Sulphur hexafluoride (SF6), especially if it interacts with nitrous oxide thus increasing the gas volume; it typically remains in the eye 3 - 4 weeks post-administration
    • Perfluoropropane (C3F8); it typically remains in the eye 6 - 8 weeks post-administration

Increased external pressure

  • Prone positioning
  • Presence of other fluid in the orbit e.g. blood (retrobulbar haemorrhage), local anaesthetic
  • Surgeons using the patient's face as a hand-rest intraoperatively

Anaesthetic drugs

  • Propofol, soidum thiopentone and etomidate all reduce IOP
  • Ketamine causes a transient rise in IOP over 1min, before it returns to baseline

  • Opioids themselves do directly affect, but can be used to attenuate the pressor response to laryngoscopy
    • Unattenuated, laryngoscopy can cause a 10 - 20mmHg increase in IOP
    • Avoiding intubation e.g. use of supraglottic devices or other pharmacotherapy such as IV lidocaine can also help

  • Neuromuscular blocking drugs
    • Suxamethonium increases IOP for approximately 8 - 10mmHg for 5 - 10mins
    • Non-depolarising agents conversely reduce IOP by reducing extra-ocular muscle tone

  • Volatile agents all decrease IOP
  • Nitrous oxide has no effect in and of itself, but can raise IOP if SF6 used

  • Benzodiazepines cause a slight reduction in IOP

Other drugs which reduce IOP

Drug Effect
Acetazolamide 500mg IV Reduced aqueous humour production
Mannitol 0.5g/kg IV Transient reduction in vitreous humour volume due to osmotic effect
Alpha agonists e.g. bromonidine, apraclonidine Vasoconstrict ciliary body blood supply and reduced aqueous production
Beta-blockers e.g. timolol,levobunolol Reduce aqueous production
Parasympathomimetics e.g. pilocarpine Miosis (pupillary constriction) and increased aqueous drainage
Prostaglandin analogues e.g. latanoprost Increased aqueous drainage via uveoscleral pathway