Professional Documents
Culture Documents
773 - PDFsam - Morgan Anesthesia 6ed New
773 - PDFsam - Morgan Anesthesia 6ed New
Anesthesia for
Ophthalmic Surgery
KEY CONCEPTS
1 Any factor that increases intraocular 5 Medications applied topically to mucosa are
pressure in the setting of an open globe absorbed systemically at a rate intermediate
may cause drainage of aqueous or extrusion between absorption following intravenous
of vitreous through the wound, serious and subcutaneous injection.
complications that can permanently worsen 6 Echothiophate is an irreversible
vision. cholinesterase inhibitor used in the
2 Succinylcholine increases intraocular treatment of glaucoma. Topical application
pressure by 5 to 10 mm Hg for 5 to 10 min leads to systemic absorption and an
after administration, principally through inhibition of plasma cholinesterase activity.
prolonged contracture of the extraocular Because succinylcholine is metabolized by
muscles. However, in studies of hundreds of this enzyme, echothiophate will prolong its
patients with open eye injuries, no patient duration of action.
experienced extrusion of ocular contents 7 The key to inducing anesthesia in a patient
after administration of succinylcholine. Thus, with an open eye injury is controlling
succinylcholine is not contraindicated in intraocular pressure with a smooth
cases of open eye injuries. induction. Coughing and gagging during
3 Traction on extraocular muscles, pressure on intubation is avoided by first achieving
the eyeball, administration of a retrobulbar a deep level of anesthesia and profound
block, and trauma to the eye can elicit a wide paralysis.
variety of cardiac arrhythmias ranging from 8 The postretrobulbar block apnea syndrome
bradycardia and ventricular ectopy to sinus is probably due to injection of local
arrest or ventricular fibrillation. anesthetic into the optic nerve sheath, with
4 Complications involving the intraocular spread into the cerebrospinal fluid.
expansion of gas bubbles injected by 9 Regardless of the anesthetic technique,
the ophthalmologist can be avoided American Society of Anesthesiologists
by discontinuing nitrous oxide at least standards for basic monitoring must be
15 min prior to the injection of air or sulfur employed, and equipment and drugs
hexafluoride, or by avoiding the use of necessary for airway management and
nitrous oxide entirely. resuscitation must be immediately available.
773
Ophthalmic surgery poses unique problems, includ- TABLE 36–1 The effect of cardiac and
ing regulation of intraocular pressure, control of respiratory variables on intraocular pressure
intraocular gas expansion, prevention of the oculo- (IOP).1
cardiac reflex and management of its consequences, Variable Effect on IOP
and management of systemic effects of ophthalmic
Central venous pressure
drugs. Mastery of general and sedation anesthesia
Increase ↑↑↑
techniques for ophthalmic surgery and a thorough Decrease ↓↓↓
understanding of potentially complicating issues— Arterial blood pressure
including the comorbidities of an increasing geri- Increase ↑
atric patient population—are necessary for optimal Decrease ↓
perioperative outcomes. In addition, the majority of PaCO2
Increase (hypoventilation) ↑↑
ophthalmic procedures are performed under topical Decrease (hyperventilation) ↓↓
or regional anesthesia. The anesthesiologist must be PaO2
familiar with their potential complications, includ- Increase 0
ing those of the accompanying sedation, even if not Decrease ↑
personally administering the topical anesthetic or ↓, decrease (mild, moderate, marked); ↑, increase (mild, moderate,
1
INTRAOCULAR PRESSURE
For example, blinking raises intraocular pressure by
DYNAMICS 5 mm Hg, and squinting (forced contraction of the
Physiology of Intraocular Pressure orbicularis oculi muscles) may transiently increase
The eye can be considered a hollow sphere with a intraocular pressure greater than 50 mm Hg. How-
rigid wall. If the contents of the sphere increase, the ever, even brief episodes of increased intraocular
normal intraocular pressure of 12 to 20 mm Hg will pressure in patients with underlying low ophthal-
rise. For example, glaucoma is caused by an obstruc- mic artery pressure (eg, from systemic hypotension,
tion to aqueous humor outflow. Similarly, intraocu- arteriosclerotic involvement of the retinal artery)
lar pressure will rise if the volume of blood within may cause retinal ischemia.
the globe is increased. A rise in venous pressure will When the globe is opened by surgical incision
increase intraocular pressure by decreasing aque- (Table 36–2) or traumatic perforation, intraocular
ous drainage and increasing choroidal blood vol- pressure approaches atmospheric pressure. Any fac-
ume. Any event that alters arterial blood pressure 1 tor that increases intraocular pressure in the
or ventilation (eg, laryngoscopy, intubation, airway setting of an open globe may cause drainage of
obstruction, coughing, Trendelenburg position) can aqueous or extrusion of vitreous through the wound,
also affect intraocular pressure (Table 36–1). serious complications that can permanently worsen
Alternatively, compressing the globe without a vision.
proportional change in the volume of its contents
will increase intraocular pressure. Pressure on the Effect of Anesthetic Drugs
eye from a malpositioned mask, improper prone on Intraocular Pressure
positioning, or retrobulbar hemorrhage can lead Most anesthetic drugs either reduce intraocular
to a marked increase in intraocular pressure, pos- pressure or have no effect (Table 36–3). Intraocular
sible eye pain, and temporary or permanent visual pressure decreases with inhalational anesthetics in
changes. proportion to anesthetic depth. There are multiple
Intraocular pressure helps to maintain the shape causes for this: A drop in blood pressure reduces
and the optical properties of the eye. Temporary choroidal volume, relaxation of the extraocular mus-
variations in pressure are normally well tolerated. cles lowers wall tension, and pupillary constriction
TABLE 36–2 Open-eye surgical procedures. TABLE 36–3 The effect of anesthetic agents
Cataract extraction
on intraocular pressure (IOP).1
Corneal laceration repair Drug Effect on IOP
Corneal transplant (penetrating keratoplasty) Inhaled anesthetics
Peripheral iridectomy Volatile agents ↓↓
Removal of foreign body Nitrous oxide ↓
Ruptured globe repair Intravenous anesthetics
Secondary intraocular lens implantation Propofol ↓↓
Benzodiazepines ↓↓
Trabeculectomy (and other filtering procedures) Ketamine ?
Vitrectomy (anterior and posterior) Opioids ↓
Wound leak repair Muscle relaxants
Succinylcholine ↑↑
Nondepolarizers 0/↓
1
↓, decrease (mild, moderate); ↑, increase (mild, moderate); 0/↓, no
facilitates aqueous outflow. Intravenous anesthetics change or mild decrease; ?, conflicting reports.
also decrease intraocular pressure, with the excep-
tion of ketamine, which usually raises arterial blood
pressure and does not relax extraocular muscles. imbalance and to determine the type of surgical cor-
Topically administered anticholinergic drugs rection. Nondepolarizing neuromuscular blockers
result in pupillary dilation (mydriasis), which may (NMBs) do not increase intraocular pressure, and we
precipitate or worsen angle-closure glaucoma. Sys- advocate that succinylcholine be reserved for rapid-
temically administered atropine or glycopyrrolate sequence induction.
for premedication are not associated with intraocu-
lar hypertension, even in patients with glaucoma.
THE OCULOCARDIAC REFLEX
2 Succinylcholine increases intraocular pressure
by 5 to 10 mm Hg for 5 to 10 min after admin-
istration, principally through prolonged contracture
3 Traction on extraocular muscles, pressure on
the eyeball, administration of a retrobulbar
of the extraocular muscles. However, in studies of block, and trauma to the eye can elicit a wide vari-
hundreds of patients with open eye injuries, no ety of cardiac arrhythmias ranging from bradycardia
patient experienced extrusion of ocular contents and ventricular ectopy to sinus arrest or ventricular
after administration of succinylcholine. Thus, succi- fibrillation. This reflex consists of a trigeminal (V1)
nylcholine is not contraindicated in cases of open eye afferent and a vagal efferent pathway. The oculocar-
injuries. Nevertheless, dogma often trumps data and diac reflex is most commonly encountered in chil-
ophthalmic surgeons may request that it not be dren undergoing strabismus surgery, although it can
administered in certain circumstances. Unlike other be evoked in all age groups and during a variety of
skeletal muscle, extraocular muscles contain myo- ocular procedures. In awake patients, the oculocar-
cytes with multiple neuromuscular junctions, and diac reflex may be accompanied by nausea.
depolarization of these cells by succinylcholine Routine prophylaxis for the oculocardiac reflex
causes prolonged contracture. The resulting increase is controversial, especially in adults. Anticholinergic
in intraocular pressure may have several effects: it medication is often helpful in preventing the oculo-
will cause spurious measurements of intraocular cardiac reflex, and intravenous atropine or glycopyr-
pressure during examinations under anesthesia in rolate immediately prior to surgery is more effective
glaucoma patients, potentially leading to unneces- than intramuscular premedication. However, anti-
sary surgery, and prolonged contracture of the extra- cholinergic medication should be administered with
ocular muscles may result in an abnormal forced caution to any patient who has, or may have, coronary
duction test, a maneuver utilized in strabismus sur- artery disease, because of the potential for increase in
gery to evaluate the cause of extraocular muscle heart rate sufficient to induce myocardial ischemia.
Ventricular tachycardia and ventricular fibrillation oxide concentration will almost triple the size of
following administration of anticholinergic medica- a 1-mL bubble and may double the pressure in a
tion has also been reported. Retrobulbar blockade or closed eye within 30 min. Subsequent discontinu-
deep inhalational anesthesia may also be of value in ation of nitrous oxide will lead to reabsorption of
preempting the oculocardiac reflex, although admin- the bubble, which has become a mixture of nitrous
istration of a retrobulbar block may itself initiate the oxide and sulfur hexafluoride. The consequent fall in
oculocardiac reflex. intraocular pressure may precipitate another retinal
Management of the oculocardiac reflex includes detachment.
(1) immediate notification of the surgeon and cessa- Complications involving the intraocular expan-
tion of surgical stimulation until heart rate increases;
4 sion of gas bubbles can be avoided by discon-
(2) confirmation of adequate ventilation, oxygen- tinuing nitrous oxide at least 15 min prior to
ation, and depth of anesthesia; (3) administration the injection of air or sulfur hexafluoride, or by
of intravenous atropine (10 mcg/kg) if bradycardia avoiding the use of nitrous oxide entirely. Nitrous
persists; and (4) in recalcitrant episodes, infiltration oxide should be avoided until the bubble is absorbed
of the rectus muscles with local anesthetic. (5 days after air and 10 days after sulfur hexafluoride
injection). Avoiding nitrous oxide seems the sim-
plest approach in these patients.
INTRAOCULAR GAS
EXPANSION
A gas bubble may be injected by the ophthalmolo-
SYSTEMIC EFFECTS OF
gist into the posterior chamber during vitreous sur- OPHTHALMIC DRUGS
gery. Intravitreal air injection will tend to flatten a Topically applied eye drops are systemically absorbed
detached retina and facilitate anatomically correct by vessels in the conjunctival sac and the nasolacri-
healing. Nitrous oxide administration is contraindi- mal duct mucosa (see Case Discussion, Chapter 13).
cated in this circumstance: The bubble will increase One drop (typically, approximately 1/20 mL) of 10%
in size if nitrous oxide is administered because phenylephrine contains approximately 5 mg of drug.
nitrous oxide is 35 times more soluble than nitro- Compare this dose with the intravenous dose of
gen in blood (see Chapter 8). Thus, it tends to dif- phenylephrine (0.05–0.1 mg) used to treat an adult
fuse into an air bubble more rapidly than nitrogen patient with acute hypotension. Medications applied
(the major component of air) is absorbed by the 5 topically to mucosa are absorbed systemically
bloodstream. If the bubble expands after the globe is at a rate intermediate between absorption fol-
closed, intraocular pressure will rise. lowing intravenous and subcutaneous injection. The
Sulfur hexafluoride is an inert gas that is less two patient populations most likely to require eye
soluble in blood than is nitrogen—and much less surgery, pediatric and geriatric, are at particular risk
soluble than nitrous oxide. Its longer duration of of the toxic effects of topically applied medications
action (up to 10 days) compared with an air bubble and should receive at most a 2.5% phenylephrine
can provide a therapeutic advantage. The bubble size solution (Table 36–4).
doubles within 24 h after injection, because nitro- Echothiophate (phospholine iodide) is an irre-
gen from inhaled air enters the bubble more rapidly 6 versible cholinesterase inhibitor used in the
than the sulfur hexafluoride diffuses into the blood- treatment of glaucoma. Topical application leads
stream. Even so, unless high volumes of pure sulfur to systemic absorption and an inhibition of plasma
hexafluoride are injected, the slow bubble expan- cholinesterase activity. Because succinylcholine is
sion does not typically raise intraocular pressure. If metabolized by this enzyme, echothiophate will
the patient is breathing nitrous oxide, however, the prolong its duration of action. Paralysis usually will
bubble will rapidly increase in size and may lead to not exceed 20 to 30 min and postoperative apnea is
intraocular hypertension. A 70% inspired nitrous unlikely. The inhibition of cholinesterase activity
lasts for 3 to 7 weeks after discontinuation of echo- the operation, fear of the eye block procedure, or
thiophate drops. Muscarinic side effects of echothio- unpleasant recall of a previous eye block or local
phate, such as bradycardia during induction, can be eye procedure. General anesthesia is indicated in
prevented with intravenous anticholinergic drugs children and uncooperative patients, as even small
(eg, atropine, glycopyrrolate). head movements can prove disastrous during
Epinephrine eye drops can cause hyperten- microsurgery.
sion, tachycardia, and ventricular arrhythmias; the
arrhythmogenic effects are potentiated by halo-
thane. Direct instillation of epinephrine into the PREMEDICATION
anterior chamber of the eye has not been associated Patients undergoing eye surgery may be apprehen-
with cardiovascular toxicity. sive; however, premedication must be administered
Timolol, a nonselective β-adrenergic antago- with caution and only after careful consideration of
nist, reduces intraocular pressure by decreasing pro- the patient’s medical status. Adult patients are often
duction of aqueous humor. Topically applied timolol elderly, with systemic illnesses such as hypertension,
eye drops, commonly used to treat glaucoma, will diabetes mellitus, and coronary artery disease, and
often result in reduced heart rate. In rare cases, pediatric patients may have associated congenital
timolol has been associated with atropine-resistant disorders.
bradycardia, hypotension, and bronchospasm dur-
ing general anesthesia.
INDUCTION
The choice of induction technique for eye surgery
General Anesthesia for usually depends more on the patient’s other medical
Ophthalmic Surgery problems than on the patient’s eye disease or the
specific operation contemplated. One exception is
The choice between general and local anesthesia the patient with a ruptured globe. The key to induc-
should be made jointly by the patient, anesthesiolo-
7 ing anesthesia in a patient with an open eye
gist, and surgeon. Patients may refuse to consider injury is controlling intraocular pressure with
local anesthesia due to fear of being awake during a smooth induction. Specifically, coughing during
intubation must be avoided by first achieving a deep by the oculocardiac reflex increases the importance
level of anesthesia and profound paralysis. The intra- of closely monitoring the electrocardiogram. In con-
ocular pressure response to laryngoscopy and endo- trast to most other types of pediatric surgery, infant
tracheal intubation can be moderated by prior body temperature may rise during ophthalmic
administration of intravenous lidocaine (1.5 mg/kg), surgery because of head-to-toe draping and mini-
an opioid (eg, remifentanil 0.5–1 mcg/kg or alfent- mal body surface exposure. End-tidal CO2 analysis
anil 20 mcg/kg), or esmolol (0.5–1.5 mg/kg). A non- helps to differentiate this situation from malignant
depolarizing muscle relaxant or succinylcholine may hyperthermia.
be used. Many patients with open globe injuries The pain and stress evoked by eye surgery are
have full stomachs and require a rapid-sequence considerably less than during a major surgical pro-
induction technique to avoid aspiration (see the cedure. “Lighter” anesthesia might be attractive if
later Case Discussion); despite theoretical concerns, the consequences of patient movement were not so
succinylcholine does not increase the likelihood of potentially catastrophic. The lack of cardiovascular
vitreous loss with open eye injuries. stimulation inherent in most eye procedures com-
bined with the need for adequate anesthetic depth
can result in hypotension in elderly individuals. This
MONITORING & problem is usually avoided by ensuring adequate
MAINTENANCE intravenous hydration and by administering small
doses of intravenous vasoconstrictors. Administra-
Eye surgery often necessitates positioning the anes-
tion of nondepolarizing muscle relaxants to avoid
thesia provider away from the patient’s airway, mak-
patient movement is often used in such circum-
ing close monitoring of pulse oximetry and the
stances in order to allow reduced depth of general
capnograph particularly important. Endotracheal
anesthesia.
tube kinking, breathing circuit disconnection, and
Emesis caused by vagal stimulation is a com-
unintentional extubation may be more likely because
mon postoperative problem following eye surgery,
of the surgeon working near the airway. Kinking and
particularly with strabismus repair. The Valsalva
obstruction can be minimized by using a preformed
effect and the increase in central venous pressure
oral RAE (Ring-Adair-Elwyn) endotracheal tube
that accompany vomiting can be detrimental to the
(Figure 36–1). The possibility of arrhythmias caused
surgical result. Intraoperative intravenous adminis-
tration of drugs that prevent postoperative nausea
and vomiting is strongly recommended.
Severe discomfort is unusual following eye sur- anesthesia is preferred to general anesthesia for eye
gery. Scleral buckling procedures, enucleation, and surgery because local anesthesia involves less physi-
ruptured globe repair are the most painful opera- ological trespass and is less likely to be associated
tions. Modest incremental doses of intravenous opi- with postoperative nausea and vomiting. However,
oid usually provide sufficient analgesia. The surgeon eye block procedures have potential complications
should be alerted if severe pain is noted following and may not provide adequate ophthalmic akinesia
emergence from general anesthesia, as it may signal or analgesia. Some patients may be unable to lie per-
intraocular hypertension, corneal abrasion, or other fectly still for the duration of the surgery. For these
surgical complications. reasons, appropriate equipment and qualified per-
sonnel required to treat the complications of local
anesthesia and to induce general anesthesia must be
Regional Anesthesia for readily available.
Ophthalmic Surgery
Options for local anesthesia for eye surgery include RETROBULBAR BLOCKADE
topical application of local anesthetic or place- In this technique, local anesthetic is injected behind
ment of a retrobulbar, peribulbar, or sub-Tenon the eye into the cone formed by the extraocular mus-
(episcleral) block. All of these techniques are com- cles (Figure 36–2), and a facial nerve block is utilized
monly combined with intravenous sedation. Local to prevent blinking (Figure 36–3). A blunt-tipped
A B
FIGURE 36–2 A: During administration of a retrobulbar block, the patient looks supranasally as a needle is advanced
1.5 cm along the inferotemporal wall of the orbit. B: The needle is then redirected upward and nasally toward the apex of
the orbit and advanced until its tip penetrates the muscle cone.
TABLE 36–6 Strategies to prevent aspiration Which induction agents are recommended
pneumonia. in patients with penetrating eye injuries?
Regional anesthesia with minimal sedation1 The ideal induction agent for patients with full
Premedication stomachs would provide a rapid onset of action in
Metoclopramide
Histamine H2-receptor antagonists order to minimize the risk of regurgitation. Propo-
Nonparticulate antacids fol and etomidate have essentially equally rapid
Evacuation of gastric contents onsets of action and lower intraocular pressure.
Nasogastric tube1
Although investigations of the effects of ketamine
Rapid-sequence induction
Cricoid pressure on intraocular pressure have provided conflicting
Rapid induction with rapid onset of paralysis results, ketamine is not recommended in pene-
Avoidance of positive-pressure ventilation via mask trating eye injuries, owing to the increased risk of
Intubation as soon as possible
blepharospasm and nystagmus.
Extubation awake
Although etomidate may prove valuable in
1
These strategies are not recommended for patients with penetrating
eye injuries.
some patients with cardiac disease, it is associ-
ated with an incidence of myoclonus ranging from
10% to 60%. An episode of severe myoclonus may
have contributed to complete retinal detachment
and acidity (see Case Discussion, Chapter 17). The and vitreous prolapse in one patient with an open
risk of aspiration in patients with eye injuries is globe injury and limited cardiovascular reserve.
reduced by proper selection of drugs and anes- Propofol has a rapid onset of action and
thetic techniques. Evacuation of gastric contents decreases intraocular pressure; however, it does
with a nasogastric tube may lead to coughing, not entirely prevent the hypertensive response to
retching, and other responses that can dramatically laryngoscopy and intubation or entirely prevent
increase intraocular pressure. the increase in intraocular pressure that accom-
Metoclopramide increases lower esophageal panies laryngoscopy and intubation. Prior admin-
sphincter tone, speeds gastric emptying, low- istration of fentanyl (1–3 mcg/kg), remifentanil
ers gastric fluid volume, and exerts an antiemetic (0.5–1 mcg/kg), alfentanil (20 mcg/kg), esmolol
effect. It should be given intravenously (10 mg) as (0.5–1.5 mg/kg), or lidocaine (1.5 mg/kg) attenu-
soon as possible and repeated every 2 to 4 h until ates this response with varying degrees of success.
surgery.
Ranitidine (50 mg intravenously), cimetidine How does the choice of muscle relaxant differ
(300 mg intravenously), and famotidine (20 mg between these patients and other patients at risk
intravenously) are H2-receptor antagonists that of aspiration?
inhibit gastric acid secretion. Because they have no Succinylcholine moderately increases intra-
effect on the pH of gastric secretions present in the ocular pressure, but that is a small price to pay
stomach prior to their administration, they have for a rapid onset of action that decreases the risk
limited value in patients presenting for emergency of aspiration and profound muscle relaxation that
surgery. decreases the chance of a Valsalva response dur-
Unlike H2-receptor antagonists, antacids have ing intubation. Advocates of succinylcholine point
an immediate effect. Unfortunately, they increase to the lack of evidence documenting further eye
intragastric volume. Nonparticulate antacids injury when succinylcholine has been used with
(preparations of sodium citrate, potassium citrate, open eye injuries.
and citric acid) lose effectiveness within 30 to Nondepolarizing muscle relaxants do not
60 min and should be given immediately prior to increase intraocular pressure, but the onset of
induction (15–30 mL orally). deep muscle relaxation is much slower than with