Principles of Ophthalmic Anaesthesia

McGoldrick, KE. - J.Clin. Anaesthesia(1989):1,4: 297
Fry and Henderson - Anaesthesia (1989); 45: 14017
Thornton, SP - Current Opinioon in Anaesthesia (1993)
Calobrisi, BL and Lebowitz, P - Int Anaesthesiology Clinics (1990); 28,2: 83
Cousins - Neural Blockade (1980)

Most paediatric patients require GAs.
In adults the prime determinant is often duration and nature of surgery.
Anterior segment work < 2 hours -> retrobulbar block.
Retinal surgery usually GA.
Preference of the surgeon is important.
Ability of patient to cooperate, speak English, lie still and avoid coughing with an open eye are important.
LA is not always safer than GA - complications of retrobulbar block include:
- retrobulbar haemorrhage - higher incience with retrobulbar blocks ~1.4%,
- stimulation of OC reflex,
- puncture of posterior globe,
- IV injection of LA,
- intraocular injection,
- central retinal artery occlusion,
- subdural injection,
- brainstem anaesthesia - (delayed onset LOC and resp. depression),
- blindness,
- penetration of the optic nerve.
Globe perforations more common with - axial length > 26 mm (myopic patients),
- long, sharp and "Atkinson" type needles,
- staphyloma.
LA can track via the optic chiasm to the midbrain resulting in contralateral EOM paralysis.
IV propofol/Methohexitone/thiopentone prior to insertion of block -> comfort and amnesia.
AVOID excessive sedation -> loss of reflex airway protection & patient cooperation.
2 ml lignocaine 2%, bupivacaine 0.5% 3 ml, and hyaluronidase 75 units often used.
Volume injected depends on the degree of proptosis and the size of the orbit.
Facial nerve anaesthesia by blocking extraorbital branches.
Cardiac patients - adrenaline or not? - 1/200,000 dilution is safe in most cases.
No significant difference between retro- and peribulbar techniques in terms of effectiveness and safety.
Peribulbar provides same degree of anaesthesia and akinesia, but marginally less visual extnction.

2. TECHNIQUE OF RETROBULBAR BLOCK (Cousins pages 457-458)
Patient supine with nose pointing towards the ceiling, looking towards the opposite side to the eye being injected, looking slightly up, never down
Palpation of inferior orbital margin at its most lateral and inferior aspect.
This is the site of injection.
25g, 35mm needle inserted through a skin wheal directed toward the top of the orbital pyramid, just skirting below the globe.
Because the eye is rotated, inferior oblique has been turned out of the path of the needle, which should penetrate only orbital fat.
Needle is slowly introduced to the hub.
Penetration of the orbital septum may produce a brief resistance, but any greater or sustained resistance may indicate contact with the globe, a muscle of the optic nerve.
Needle is withdrawn and redirected more vertically under these circumstances.
Aspiration prior to injection of ~ 2ml LA solution, applying gentle pressure 2-4 minutes.
Increasing proptosis suggests retrobulbar haemorrhage.
Akinesis of the orbicularis:
(i) van Lint Method
Nerve block close to outer canthus injecting 30-35 mm subcutan. towards eyebrow then again towards IO foramen.
(ii) O'Brien
Paralysis of VII anterior to the condyloid process of the mandible. Needle directly to the bone then injection as it is withdrawn.
Retrobulbar block - nerves blocked are those within the cone (annulus of Zinn):
1. Optic,
2. Oculomotor - superior and inferior branches,
3. Nasociliary, and
4. Abducens.
Peribulbar block - those within SOF, annulus and IOF:
1. Lacrimal,
2. Frontal,
3. Trochlear,
4. Oculomotor - S/I branches,
5. Nasociliary,
6. Abducens,
7. Infraorbital, and
8. Zygomatic.
Reduced risk of retrobulbar haemorrhage, central retinal artery occlusion, optic nerve injury, globe perforation, intradural injection.
Simple to perform with low incidence of even minor complications.
Supine position, head on small pillow.
Solution - 500 units hyaluronidase (when available);
- 10 ml - 2% lig., 0.5% bupiv. equal proportions;
Skin wheal lower lid just above inferior orbital rim, 1.5 cm from lateral canthus;
Repeat for upper lid 1-2 mm medial and inferior to supra-orbital notch;
1.25" "Atkinson needle" advanced through skin wheal bevel towards orbit feeling pop as lower orbital septum penetrated, advanced toward equator of eye angled in superomedial direction;
4 ml LA injected after aspiration at depth of 2.5 cm;
Proptosis and conj. oedema common and benign;
Repeat above the globe advancing to depth of 2 cm then a further 0.5-1 cm medially, injecting 2-3 ml solution;
Needle withdrawn injecting 1 ml in orbicularis on the way out;
Honan pressure cuff for 10 minutes;
Complete akinesia is excellent end point - further injection below for inferolat. movement and above for superomedial movement.
Spread subcutaneously to other eye;
Periorbital ecchymoses;
Transient brightness on initial exposure to operating microscope;
Less visual extinction.
10 - 22 mmHg normal.
3 main determinants - (i) extrinsic pressure on the eye,
(ii) scleral rigidity,
(iii) alterations in intraocular contents, either semisolid or liquid.
Rate of formation and drainage of AH is most important factor.
IOP= K[(OPaq - OPpl) + CP]
K = coefficient of outflow;
OPaq = osm. pressure of aqueous,
OPpl = osmotic pressure of plasma,
CP = capillary pressure.
Small changes in solute conc. result in rapid changes in IO hence value of mannitol.
Diameter of Fontana's space determines outflow of aqueous.
Pupillary dilatation closes Fontana's space and causes an increase in IOP 2deg. to reduced aqueous drainage.
V. sensitive to fluctuations in venous pressure - vomiting, straining, coughing, laryngoscopy increases IOP 2deg. to increased capillary pressure.
Increases in already elevated IOP can result in glaucoma and permanent visual loss.
Penetrating injuries - IOP = atmospheric \ increases in IOP can extrude contents.
Glaucoma patients require - miotic drops preop, avoidance of overhydration and venous congestion.
Hypotension exposes these patients to retinal vein thrombosis.

(i) CNS depressants.
Inhalational agents - dose-dependent decrease in IOP - relaxation of IOMs;
- [[arrowdown]] aqueous production;
- [[arrowup]] " reabsorption.
Virtually all CNS depressants lower IOP.
Ketamine probably has little or no effect.
(ii) Ventilation
Low PaCO2 decreases IOP 2deg. to vasoconstriction.
(iii) Neuromuscular blockers
Sux - [[arrowup]]IOP 2deg. to tonic contracture of EOMs, choroidal vessel dilatation, relaxation of orbital smooth muscles, (NDNMBs lower IOP).
- lasts ~ 7 minutes,
- up to 8 mmHg increase in IOP,
Non-depolariser pretreatment only partly effective preventing the rise.
Acetazolamde, propranolol also used with some effect - all methods imperfect.
(iv) Adjuvant drugs
Ganglion blockers, hypertonic solutions, acetazolamide (via carbonic anhydrase inhibition) lower IOP.

Topical drugs drain via nasolacrimal duct to the nose and are systemically absorbed. particularly important are -
- atropine,
- cocaine (rarely used),
- timolol,
- echothiophate (organophosphate) - benefit from preop atropine to block muscarinic effects and obtund vagal reflexes. Sux, ester LAs require reduced doses.
- adrenaline - 2% topical to decrease AH secretion and enhance outflow in open angle glaucoma - systemic symptoms in some cases.
-phenylephrine - mydriatic and cycloplegic - severe myocardial ischaemia in CAD, cerebral aneurysm rupture reported.
- scopolamine - myd/cyclo - systemic toxicity reported.
- intraocular ACh - bradycardia, hypotension, salivation, bronchospasm etc.
- SF6 - Sulfur hexafluoride - gas bubble in retinal detachment - N2O will increase the size and increase IOP.
- mannitol and other hypertonic solutions.

Bradycardia due to - traction on the EOMs, conjunctiva, orbital structures,
pressure on the globe,
retrobulbar block,
ocular trauma,
pressure on tissue remaining after enucleation.
Trigeminal afferent, vagal efferent.
Also causes - any arrhythmia including VT, and rarely asystole.
Incidence highest in children - 90% if no atropine pretreatment.
IM atropine not useful - delayed onset acutely, brief duration as premed.
In adults prophylaxis not usually indicated.
In children 0.02, or glyco. 0.01 prior to commencing surgery is indicated.
Treatment - removal of stimulus, anticholinergics IVI, check depth of anaesthesia, lig. if VEBs a problem.

Intercurrent illness is common in eye patients.
If GA planned intubation is necessary - head is draped, anaesthetist is away from the head.
Gentle brief laryngoscopy.
Adequate anaesthetic depth, lignocaine 1.5 prior to intubation.
Monitoring - ECG, FiO2, BP (NI), SpO2, capnography, PNS.
Intraocular procedures require great attention to detail.
Deep NMB mandatory.
Antiemetic intraoperatively is useful to limit postop N&V.

Most common eye operation. Paediatric mainly.
High incidence of OC reflex, increased incidence of MH - (strabismus assoc. with MH sensitivity).
Masseter muscle spasm 3x higher in children undergoing strabismus repair.
When present, postpone surgery and obtain muscle biopsy.
Avoid sux routinely - intubate under deep halothane anaesthesia or with NDNMB only.
Sux interferes with forced duction manoeuvres.
IV atropine or glycopyrrolate limits OC reflex in children.
Capnography particularly important to detect MH.
Vomiting common - IV antiemetic given at start of case useful.

Maintenance of intraoperative MIOSIS.
Interactions between anti-glaucoma medication and anaesthetics.
Avoid venous congestion (retinal vein thrombosis).
Avoid hypotension (retinal artery thrombosis).
Low normal IOP essential to prevent extrusion of contents when the eye is opened.
Premed with antiemesis in mind.
Atropine in normal doses is not harmful in glaucoma.
Any volatile is OK; deep NMB is mandatory; extubate under lignocaine to minimise coughing.

SF6 tamponades the retina; dramatic rise in IOP as N2O enters the gas space in the globe.
\ avoid N2O for 10 days.
Basically an extraocular procedure but drainage of subretinal fluid opens the eye.

Prevention of additional increase in IOP is the goal.
Exclude other injuries, eg CHI, chest, abdominal etc.
H2 antagonist, metoclopramide and non-particulate antacid is indicated.
NO attempt to insert NG tube should be made when awake.
Barbiturate and non-depolariser only for intubation risks aspiration while waiting for muscular relaxation.
Premature attempts may cause coughing with increased IOP +++.
Priming dose (10% of relaxant dose ) of NDNMB 4 minutes prior to definitive dose minimises the IOP effect.
Thiopentone 4-6 PLUS sux often advocated because of the excellent intubating conditions and minimisation of aspiration risk.
Alternative is to use supra-normal dose of atracurium eg 0.6-0.7, or vecuronium 0.25 and intubate after one minute with cricoid pressure still applied, after maximal preoxygenation.

1. safer,
2. lower incidence of PE,
3. less PONV,
4. less postop restlesness,
5. less postop lung complications,
6. less postop cardiac and cerebrovascular complications,
7. less bleeding,
8. no clear benefit in reducing memory loss in the elderly.

Libonati et al (1985) - 74/100 patients with open eye injuries received SCh either by infusion or after ND pre-treatment -> no evidence for any clinically significant change in condition of the globe following administration.
Also stated over 10 years 0/2,200 patients requiring GA for open eye injuries (most of whom received SCh) was associated with vitreous extrusion.
Potential theoretically always exists.

Strategies to reduce risk
(i) Non-depolariser pre-treatment
Some reduction in IOP but not absolute.
Meyers et al (1980) assessed IOP using this technique and applanation tonometry and found a significant proportion of patients increased their IOP.
(ii) Small "self-taming" pre-dose SCh
Followed by "intubating" dose SCh. Refuted by Meyers.
(iii) Lignocaine pre-treatment
1-2 pre-SCh -> also ineffective.
But lig 1.5, thiopentone and then SCh in some reports showed to reduce the increase in IOP.
(iv) Nifedipine pre-treatment
10 mg S/L 20 minutes prior to induction -> reduced rise in IOP without major effect on systemic BP.
Correlated with attenuation of BP rise with intubation -> proposed as the mechanism of action of this technique.

Atracurium and vecuronium given after induction of anaesthesia controlling for as many variables as possible (opioid pre-med, topical LA to cords and trachea, IV droperidol) cause no rise in IOP above baseline.
Other studies looking at supra-maximal intubating doses of atra and vec confirm an absence of IO hypertension.
Shortening interval from dose to intubation
(a) Supra-maximal dosing - Atra and vec at 5-6 times ED95 doses investigated (vec - 0.25, atra - 1.5
Mean onset time ~ 1 minute.
Atracurium at this dose -> moderate hypotension; vecuronium -> minimal CVS effect.
Vec 0.2-0.4 -> mean onset time = 95 and 87 seconds respectively (80% twitch height depression).
Onset time probably realistically ~ 100 seconds.
Attempted intubation before adequate relaxation -> rise in IOP.
(b) Priming principle
Based on the theory that small dose of ND relaxant can block large numbers of ACh receptors at the NMJ before appreciable clinical reduction in NM transmission.
Second larger dose blocks remaining receptors and effects more rapid onset of intubation conditions.
Optimal priming dose - atracurium - 0.08-0.09;
- vecuronium - 0.01-0.012
Some patients will experience muscle weakness at these doses -> potential loss of airway protection, regurgitation etc \ caution.