Download The Anesthetic Management of Ocular Trauma

The Anesthetic Management
of Ocular Trauma
Rajpal Kohli, MD
Harvinder Ramsingh, MD
Benu Makkad, MD
University of Cincinnati College of Medicine
Cincinnati, Ohio
’
Introduction
Ocular trauma is a worldwide problem that affects people of all
ages.1 Approximately 2 million eye injuries occur each year in the
United States. According to one study looking at ocular trauma from
1992 to 2001, the most frequent type of eye injury was superficial injury
to the eye and adnexa (41.6%), followed by a foreign body on the
external eye (25.4%), contusions (16%), and open wounds (10.1%).
The most common etiology of these ocular injuries was foreign body
(41.7%), followed by, strike by an object (19.4%), fight or assault (6.8%),
fall (5.9%), vehicle-related (4.0%), and cutting/piercing objects (3.1%).
The morbidity and economic impact of ocular injuries is significant,
accounting for approximately 1 to 3 billion dollars annually. The
purpose of this review is to focus on the relevant ocular anatomy/
physiology and anesthetic management of the most common injuries
associated with ocular trauma.
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Anatomy
The eye is the extension of the central nervous system (CNS) that
rests in the orbit. Seven cranial bones form the orbit: frontal, zygomatic,
sphenoid, maxilla, palatine, lacrimal, and ethmoid2 (Fig. 1). The optic
foramen contains ophthalmic vessels, the optic nerve, and sympathetic
innervations from carotid plexus. Within the superior orbital fissure lies
the oculomotor, trigeminal, trochlear, and abducens nerves. The
REPRINTS: DR RAJPAL KOHLI, MD, UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE, 234 GOODMAN STREET,
PO BOX 670764, CINCINNATI, OH 45267-0764, E-MAIL: [email protected]
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Figure 1. Skeletal anatomy of the orbit. (Kiser AC, O’Brien SM, Detterbeck FC. Blunt
tracheobronchial injuries: treatment and outcomes. Ann Thorac Surg. 2001;71:2059–2065. Figure
22-1. Reprinted by permission).
infraorbital fissure contains infraorbital and zygomatic nerves. Within
the infraorbital foramen lies the infraorbital nerve, artery, and vein.
The eye is made up of 3 layers consisting of the sclera, uveal tract,
and retina2 (Fig. 2). The sclera is the dense fibrous structure that
maintains the shape of the eye. The cornea is the transparent anterior
portion of the sclera that allows passage of light to the retina. The iris,
ciliary body, and the choroid make up the uveal tract. The iris divides
the anterior segment of the eye into anterior and posterior chambers.
The ciliary body is the site for aqueous humor production and contains
ciliary muscles for accommodation of the lens. The choroid is highly
vascular and supplies blood to the 10 layers of retina that convert light to
neural impulses. These nerve impulses travel to the retinal ganglion, the
axons of which penetrate the sclera to form the optic nerve.
The aqueous humor occupies the anterior and posterior chambers
of the eye. Its volume is primarily responsible for intraocular pressure
(IOP) regulation. The volume of vitreous humor is more constant than
that of aqueous humor. Blood is supplied to the eye and the orbit
through branches of internal and external carotid arteries. The first
branch of internal carotid artery, the ophthalmic artery divides into
central retinal artery and long/short ciliary posterior arteries supplying
the retina. The anterior part of optic nerve is perfused by posterior
ciliary arteries with significant individual variation predisposing some
patients to anterior ischemic optic neuropathy after period of hypotension. The posterior optic nerve is perfused by pial vessels from the
ophthalmic artery. The ophthalmic veins drain the orbit while the
Anesthetic Management of Ocular Trauma
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Figure 2. Anatomy of the anterior eye. (Perchinsky M, Long W, Rosoff J, et al. Traumatic.
Rupture of the tracheobronchial tree in a 2 year old. J Pediat Surg. 1998;33:1707–1711. Figure
22-2. Reprinted by permission).
central retinal vein provides ocular drainage. All venous drainage is
transmitted to the cavernous sinus.
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Physiology
IOP is defined as the pressure exerted by the contents of the eye
against its wall.3 Normal IOP is 10 to 22 mm Hg and may differ by 5 mm
Hg between the 2 eyes.4,5 A pressure above 25 mm Hg at any age is
considered abnormal. The normal IOP is significantly higher than tissue
pressure6–8 (2 to 3 mm Hg) and intracranial pressure (7 to 8 mm Hg).
Additionally, there is a diurnal variation with an increase in IOP in the
morning (2 to 3 mm Hg) due to dilation of pupils during sleep,
recumbent position, and pressure of the eyelid.
Two thirds of the aqueous humor is formed by the ciliary bodies in the
posterior chamber and one third in the anterior chamber facilitated by
carbonic anhydrase/cytochrome oxidase enzymes.5,9 The production of
aqueous humor is augmented by sympathetic stimulation and suppressed
by parasympathetic control. The aqueous humor produced in the
posterior chamber flows through the pupil into the anterior chamber
and then exits from the eye through Fontana’s spaces into Schlemm’s
canal, episcleral veins, and finally emptying into the cavernous sinus.9
The aqueous humor outflow is primarily determined by the diameter of
Fontana’s spaces is illustrated in the following equation:
r4 ðPiop Pv Þ
A¼
8Zl
where A = volume of aqueous humor/time, r = radius of Fontana’s
spaces, Piop = intraocular pressure, Pv = venous pressure, Z = viscosity,
l = length of Fontana’s spaces.
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With mydriasis caused by a-1 stimulation, Fontana’s space narrows,
and resistance to outflow is increased along with IOP. Thus, it needs to
be avoided in patients with glaucoma. Although b-stimulation has no
effect on pupillary diameter, both b-agonists and antagonists are known
to paradoxically decrease IOP. Parasympathetic stimulation produces
miosis and decreases IOP.2
Changes in solute concentration of plasma affect aqueous humor
formation and thus IOP as well. The variations in osmotic pressure of
aqueous humor/plasma affect aqueous humor formation as shown by
the following equation2:
IOP ¼ k½ðOPaq OPplÞ þ Pc
where k = coefficient of outflow, OPaq = osmotic pressure of aqueous
humor, OPpl = osmotic pressure of plasma, Pc = capillary perfusion
pressure.
Thus, hypertonic solutions, like mannitol, aid in lowering IOP by
increasing the osmotic pressure of plasma. Lastly, carbonic anhydrase
inhibitors like acetazolamide can directly inhibit aqueous humor
formation by interfering with sodium channel function.
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Physiologic Determinants of IOP
Three primary determinants of IOP are:
Changes in intraocular volume of blood and aqueous humor
(most important)
Intrinsic compliance of scleral and corneal walls
External compressive forces by extraocular muscle tone and
periorbital structures
Factors Affecting Intraocular Blood Volume
They include changes in blood pressure, central venous pressure,
and intraocular vascular tone.
Effect of Changes in Systemic Blood Pressure The arterial supply
of the eye is autoregulated.7 Overall, minor increases in systemic
pressure have minimal effects on IOP. However, sustained hypertension/
hypotension seems to be directly correlated with increased IOP.
Chronically elevated hypertension will cause adaptation of choroidal
vessels resulting in normalization of IOP.
Effect of Changes in Venous Pressure Increased venous pressures
on the other hand can dramatically increase IOP by increasing choroidal
blood volume and tension of the orbit by inhibiting the blood efflux. As
a result putting the patient in the head-up tilt position helps to reduce
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IOP. Any increase in venous pressure (coughing, vomiting, Trendelenberg position, or Valsalva maneuver) will cause an increased resistance to
ocular outflow and will increase IOP.3
Effect of Changes in Basal Intraocular Blood Volume The basal
intraocular blood volume in the eye is primarily a result of intraocular
vascular tone, mainly dictated by arterial PCO2 and by central
controlling areas in the diencephalon.4,7 There is a direct straight-line
correlation between IOP and end-tidal concentration of CO2 due to
resultant vasodilatation within the eye. The central control of IOP is
complex as it involves control of vascular and extravascular muscle tone
apart from a possible direct effect on IOP.
Factors Affecting Intraocular Aqueous Volume
They include changes in the rate of formation and drainage of
aqueous humor.
Effect of Change of Aqueous Humor Formation on IOP Both
stimulation and depression of aqueous formation seen after the
administration of drugs with sympathetic and parasympathetic effects.
Acetazolamide by inhibition of carbonic anhydrase decreases the
aqueous humor formation.
Effect of Change of Aqueous Humor Drainage on IOP The
primary controller of outflow seems to be the trabecular meshwork
between the anterior chamber and Schlemm’s canal. Ciliary muscle
contraction decreases the resistance to outflow by opening the trabecular
network. Resistance to outflow drainage is also influenced by adrenergic
stimulation. a-Stimulation induced mydriasis increases outflow resistance
and IOP, whereas b-stimulation decreases IOP without affecting
pupillary size or outflow resistance by altering the blood flow.
External Compressive Forces Affect on IOP
Sudden external compression by digital eyelid pressure, forceful
masking during preoxygenation, surgical retraction to the eyelids, or
spasm of extraocular muscles after succinylcholine administration can
occur which increases IOP. However, at the same time compensatory
effects are induced that offset this increase in pressure by increasing
aqueous outflow.
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Preoperative Evaluation
Fully understanding ocular anatomy and physiology, especially how
IOP is regulated will allow the anesthesiologist to tailor the anesthetic
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plan to provide the least risk to the trauma patient while preserving
ocular function. Many of the drugs used in normal trauma anesthesia
can have detrimental effects on IOP of the eye and decisions must be
made according to the risks and benefits of different approaches of
airway and anesthetic management of the patient.
For every ocular trauma case, the anesthesiologist should achieve
the following main objectives10:
1.
2.
3.
4.
5.
6.
7.
8.
Overall patient safety
Avoidance of elevated IOP
Avoid external ocular pressure
Provide a stable operative field
Analgesia
Avoidance or obtundation of the oculocardiac reflex (OCR)
Minimize bleeding
Smooth induction and emergence
Generally, a trauma patient poses a unique challenge because the
immediate goal in a trauma is to secure the airway as quickly as possible,
prevent aspiration of gastric contents, and also prevent sudden increases
in IOP that may cause further eye damage. Thus rapid sequence
intubation with succinylcholine would be appropriate as it provides the
advantages of swift onset, superb intubating conditions, and brief
duration of action. In open-globe injury, the use of succinylcholine
increases IOP, and loss of intraocular contents could cause irreversible
damage. However, no published reports have shown increased eye
damage in open-globes despite increase in IOP associated with
succinylcholine.7
Patient safety is a primary concern and each case must be assessed
for risk of aspiration. There are alternative management options
available that will be discussed below which may not increase the risk
of ocular injury and still provide patient safety.
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Type of Injury—Open-globe Versus Closed-globe
Traumatic eye injuries can be accompanied by more severe bodily
injuries. An eye injury will usually not be the cause of mortality, but
inappropriate management can be the cause of significant and
devastating morbidity. The type of eye injury will also determine the
urgency of surgery.
The numerous eye injuries that can occur can easily be categorized
as being either open-globe or closed-globe injuries to help in our
management. In open-globe injuries, the IOP is already atmospheric so
the pharmacologic changes that occur with anesthetic drugs are not
significant to patient outcome. Here, a smooth induction to prevent
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coughing/straining, patient immobilization during surgery, and a
smooth emergence are keys to prevent loss of intraocular contents.
Closed-globe injuries require significant planning and preparation
in order to prevent further damage to the eye by an increase in IOP.
They also require smooth induction and emergence, as patient
coughing/bucking will cause a detrimental increase in IOP. In a
closed-globe injury, the pharmacologic and physiologic management
of IOP is the center point of anesthetic management and this will be the
focus of this chapter.
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History and Physical
A standard history and physical are always the best way to prevent
unnecessary complications and to prioritize the obstacles in anesthetic
management for the trauma patient. Documentation in the chart of
preoperative visual acuity or loss is important to determine the urgency
of the surgery. A full visual examination should be carried out
postoperatively also to ascertain any ongoing pathology and/or damage
that might have occurred from surgical or anesthetic complications.
The full extent of the trauma must be taken into consideration.
Because many ocular injuries are associated with head and neck trauma,
such as skull fractures or intracranial hemorrhage, a thorough survey of
the patient should be undertaken. A study examining the National
Pediatric Trauma Registry showed that 25% of children with ocular
trauma had other major injuries and were more likely to have a basilar
skull fracture or orbital wall fracture. In a majority of these major
trauma cases, the child was the nonrestrained passenger in a motor
vehicle accident.11 Thus, one must take into consideration possible
thoracic or abdominal bleeding, rib fractures, splenic or liver lacerations,
and pelvic fractures when considering management for major ocular
trauma. A full preoperative evaluation for major trauma should include
a head computed tomography to visualize periorbital structures and
possibly a chest, abdominal, or pelvic computed tomography depending
on the mechanism of injury.
Through a detailed history and physical in conjunction with detailed
discussion with the surgeon before, during, and at the end of surgery will
help optimize patient outcome without anesthesia-induced complications.
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General Versus Regional Anesthesia
Once the extent of bodily injury and ocular damage is ascertained,
the choice of general anesthesia versus regional anesthesia can be
discussed with the input of the surgeon. General anesthesia is a must
for most trauma patients for repair of penetrating eye injuries, retinal
surgery, un-cooperation, intoxication, and most pediatric patients.
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General anesthesia provides the surgical benefit of immobilizing the eye
and eliminating the need for patient cooperation while also allowing
control of factors affecting IOP.
Regional anesthesia can be safely used with a cooperative patient in
the setting of a limited corneal/eyelid laceration repair or foreign body
removal where the potential for extrusion of intraocular contents is
minimal.
There are 3 major blocks used for ocular surgery: retrobulbar,
peribulbar, and sub-Tenon’s block. The retrobulbar or intraconal block
involves injecting local anesthetic into the posterior cone of the extraocular
muscles. Complications include OCR, retrobulbar hemorrhage, penetration of the posterior globe or optic nerve, intravascular, subdural or intraocular injection, central retinal artery occlusion, and brainstem anesthesia.
OCR
This is mostly elicited by preoperatively performing intraorbital or
retroorbital injections and intraoperatively by the traction on the
extraocular muscles or pressure on the eye.
The OCR is mediated by afferent pathways via long and short ciliary
nerves to the ciliary ganglion and then to the gasserian ganglion along
the ophthalmic division of the trigeminal nerve terminating in the main
trigeminal sensory nucleus in the floor of the fourth ventricle. The
efferent pathway is through the vagus nerve. The most common
manifestation of the reflex is sinus bradycardia, but more ominous
manifestations including atrioventricular block, ventricular bigeminy,
ventricular tachycardia, and asystole. Most studies define significant
OCR-related bradycardia as a 10% to 20% decrease in the resting heart
rate that is sustained for 5 seconds or longer.
Recent evidence has shown that the neither pretreatment with
atropine nor retrobulbar block prevent or attenuate the OCR reflex.
The reflex ceases when stimulation ends. The first step in treating OCR
is to stop stimulation. Fortunately, sustained and repeated stimulation
usually causes the OCR to fatigue. If bradycardia persists, treatment
with atropine or glycopyrrolate intravenous (IV), or local injection of
lidocaine near the eye muscle may be necessary2 (Fig. 3).
The peribulbar block involves injecting local anesthetic outside of
the muscle cone. The advantages of this block are a low complication
rate and that it can be performed easily with minimal pain. The
disadvantages include the need to inject a larger volume (possibly
increasing IOP) and a slower onset time and potential to perforate the
globe. If the inferior rectus is injected, the patient will have vertical
diplopia from myotoxicity.
A sub-Tenon block involves the injection of local anesthetic into the
posterior sub-Tenon space with use of blunt dissection. A blunt probe is
Anesthetic Management of Ocular Trauma
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Figure 3. Anatomy and physiology of the OCR. (Kiser AC, O’Brien SM, Detterbeck FC. Blunt
tracheobronchial injuries: treatment and outcomes. Ann Thorac Surg. 2001;71:2059–2065. Figure
22-3. Reprinted by permission).
used to spread the extraocular muscles so that local anesthetic can
diffuse into the retrobulbar space. It is painless and provides reliable
anesthesia with minimal risk of serious complications.
’
Premedication
The main goal of preoperative medication is to avoid any significant
increases in IOP due to bucking, coughing, or straining by using
judicious sedation and to provide aspiration prophylaxis to trauma
patients who are regarded as full stomach.
Preventing Aspiration
In general, the most commonly used anesthetic premedications do
not affect ocular physiology. Gastric emptying and reducing gastric
acidity to prevent the risk of aspiration pneumonitis are a priority in
trauma patients. Metoclopramide, sodium citrate solution, and histamine-2-receptor blockers can be used in almost all cases without causing
increased IOP.
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Sedation/Amnesia
As a class, narcotics and benzodiazepines lower IOP by decreasing
anxiety and providing sedation. Diazepam, given IV, a few minutes
before induction of anesthesia has been shown to lower IOP, probably by
centrally mediated muscle relaxant properties.7 Midazolam was shown
to have similar effects on IOP as diazepam and thiopental.3,5,7 Oral or
nasal midazolam can be used in children.
Oral clonidine can also be used in adults or children to provide
anxiolysis and to decrease the incidence of postoperative nausea and
vomiting.
Morphine given intramuscularly (IM) has been shown to decrease
IOP.12 In patients with glaucoma, appropriate use of narcotics has
minimal effect or even help to lower IOP.
Anticholinergics/Antisialogogics
Anticholinergics, when used topically, have significant effects on
the eye. They will cause mydriasis and increase IOP. When used as
antisialagouges and given IM or IV (atropine, scopolamine, and
glycopyrrolate), there is no significant effect on IOP.7
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Intraoperative Management
Induction
Rapid control of the airway with minimal hemodynamic changes
is a key goal in the trauma patient. When ocular trauma is involved,
the methods used to induce anesthesia can play a significant role in
the morbidity of the patient. For this reason, the anesthesiologist
must formulate a plan that will consider the specific ocular injury.
Preoxygenation with gentle placement of the facemask is important with
care taken not to apply undue pressure on the injured eye.
Most commonly used induction agents, with the exception of
ketamine, actually provide a protective effect on IOP. Induction with
thiopental can cause a significant decrease in IOP.13 Propofol’s effect on
IOP is similar to that of thiopental.14
Etomidate has also been shown to significantly decrease IOP within
1 minute of injection.15 There is no current evidence that etomidate has
caused an increase of IOP from myoclonus, although in theory it could
have detrimental effects. The benefit of the use of etomidate to maintain
hemodynamic stability during induction needs to be weighed on a caseby-case basis against the possibility of increasing IOP if the patient does
experience myoclonus.
Ketamine has been used regularly by ophthalmologists to facilitate
examination of the eye in uncooperative children. One study showed
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that premedication with diazepam and meperidine before giving
ketamine does not affect IOP, and that it may even lower IOP in
children when given IM.16 Older studies have shown that IOP is
significantly increased with ketamine.16–18 Additionally, ketamine has
the side effects of blepharospasm and nystagmus and increased rate of
postoperative nausea/vomiting that further contradict its use in ocular
surgery. Thus, a majority of studies show that ketamine will increase IOP
and until further studies are published, ketamine should not be a
recommended induction agent for ocular trauma surgery.
These IV induction agents work by centrally depressing the CNS
areas that control IOP by either effecting vascular tone or extraocular
muscle tone as shown by animal studies.
IV agents have also shown to facilitate aqueous drainage.
The use of standard narcotics and volatile inhaled anesthetics also
depress these centers and thus keep IOP low.3 Narcotics and volatile
anesthetics reduce IOP through relaxation of extraocular muscles,
depression of CNS controlling centers in the diencephalon, enhancement of aqueous outflow, decrease in aqueous humor production, and
lowering central venous pressure.
Muscle Relaxants
Depolarizing muscle relaxants like succinylcholine are the mainstay
for muscle relaxation during trauma cases because of its rapid onset and
quick recovery if airway management becomes difficult. In ocular trauma,
the use of succinylcholine can be a preventable cause of major morbidity.
Succinylcholine has been shown to significantly increase IOP by 10
to 20 mm Hg for up to 6 minutes.6 Tracheal intubation during this time
frame increased IOP even further, but did not prolong the duration of
effect.19 Pretreatment of patients with benzodiazepines,20,21 b-blockers,
lidocaine, small doses of nondepolarizing muscle relaxant, and even
subparalytic doses of succinylcholine to blunt the increase in IOP have
produced inconsistent results, and in most cases do not prevent IOP
from rising.7 The full mechanism of how succinylcholine increases IOP
is not clear. Postulated theories include increasing extraocular muscle
tension, choroidal vascular dilatation, contraction of extraocular smooth
muscles, and cycloplegic action resulting in deepening of the anterior
chamber and increased outflow resistance.
Unlike succinylcholine, nondepolarizing muscle relaxants reduce
IOP by relaxing the extraocular muscles. A rapid sequence technique
with a supramaximal intubating dose of nondepolarizing muscle
relaxant such as vecuronium (0.2 mg/kg), rocuronium (1.2 mg/kg), or
cisatracurium (0.4 mg/kg, 8xED95) can be used to achieve fairly rapid
onset of muscle relaxation (60 to 90 s) for favorable endotracheal
intubation.3,22,23
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Even though succinylcholine is documented to increase IOP, there
are no clinical case reports of further eye damage, loss of vitreous
humor, or other complications in open eye surgery with administration
of succinylcholine.24 The judgment of the anesthesiologist must come
into play and the risk of further ocular injury with the use of
succinylcholine must be weighed against the risk of aspiration and
long-term paralysis with nondepolarizing muscle relaxants and a
possible unknown difficult airway.
Endotracheal Intubation
IOP also increases with direct laryngoscopy and endotracheal
intubation by 10 to 20 mm Hg6,25 with subsequent extrusion of
intraocular contents probably related to sympathetic cardiovascular
responses. Several pretreatment regimens to blunt this response to
tracheal intubation have also been shown to inhibit the increase in IOP.
IV lidocaine (1.5 mg/kg), sufentanil (0.05 to 0.15 mg/kg), or remifentanil
(0.5 to 1 mg/kg) 3 to 5 minutes before induction have kept IOP from
rising.7,26 Thiopental (6 mg/kg IV) or propofol (3 mg/kg IV) will help
prevent coughing and bucking during endotracheal intubation.
Oral administration of clonidine (5 mg/kg) 2 hours before induction
of anesthesia will also blunt the IOP response to tracheal intubation.27
Placing the patient in reverse Trendelenberg will help to decrease
venous return and thus keep IOP low during intubation.7
Laryngeal Mask Airway
Airway management with a laryngeal mask airway and induction
with propofol has shown to keep IOP within normal ranges.28
Unfortunately, because most patients are considered trauma patients,
only endotracheal intubation is appropriate to protect the airway from
aspiration. Also in ocular cases, the airway is not readily accessible by the
anesthesiologist, thus endotracheal intubation is the preferred method
of airway management.
’
Monitoring and Maintenance
Standard anesthetic monitoring including observation of arterial
blood pressure, electrocardiography, pulse oximetry, FiO2, capnography, and peripheral nerve stimulation monitoring should be carried out
for all cases.
The goal will be to either decrease IOP or keep it very near normal
levels. It is important to maintain an adequate level of anesthesia with
volatile inhaled anesthetics along with the use of a nondepolarizing
muscle relaxant to provide a motionless field of operation. Volatile
anesthetics are known to reduce IOP proportionally with the depth of
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anesthesia and reduce coughing or bucking that can increase central
venous pressure thereby increasing choroidal blood volume/IOP.3,7 Full
muscle relaxation is extremely important for cases with open-globe
injuries, where coughing or patient movement can have catastrophic
effects.
By maintaining normocapnia with controlled ventilation, volatile
inhaled anesthetics have been shown to reduce IOP from 18% to
40%.29–31 Respiratory acidosis and hypercapnia can increase IOP. There
is a linear effect between IOP and increasing partial pressure of CO2. At
low levels of PaCO2, the choroidal blood vessels are constricted, thus
lowering IOP and the formation of aqueous humor is decreased owing
to reduced carbonic anhydrase activity.3 During episodes of hypoxia, the
choroidal circulation dilates which will in turn increase IOP.
Additionally, those patients more prone to a reactive airway like
smokers would benefit from the use of IV lidocaine/fentanyl to help aid
in cough suppression during extubation.
Retinal Detachment
Severe trauma to the face or eye can result in retinal detachment. In
these cases, the surgeon may inject a bubble of gas [generally sulfur
hexafluoride(SF6)] into the vitreal cavity. Because nitrous oxide is 117
times more diffusible than SF6, it rapidly enters the gas bubble causing
the bubble to increase from 2 to 3 its original size. This can cause IOP
to increase from 14 to 30 mm Hg from baseline. SF6 gas bubbles can
remain for 3 to 4 weeks.32,33 For this reason, it is advisable to avoid N2O
when intravitreal gas injection is used or has been used in the past
month, owing to possible reexpansion of the bubble and increase IOP
on subsequent exposure to N2O.
’
Emergence
Awakening a patient while keeping the IOP low can be a challenge.
Several techniques can be employed to ensure smooth emergence with
no coughing or bucking. Standard medication for muscle relaxant
reversal can be used. The patient must be deeply anesthetized before
reversal to prevent any movement. Neostigmine and atropine or
glycopyrrolate to reverse the effects of nondepolarizing muscle relaxants
does not increase IOP.3
One method used in simple ocular surgery is to extubate the trachea
while the patient is still deeply anesthetized and maintains the airway by
mask ventilation until the patient is conscious. Unfortunately, the
trauma patient is assumed to have a full stomach and general anesthesia
with an unprotected airway, even for a short period of time, allows the
possibility of aspiration. If there is an orbital fracture that has not been
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repaired, mask ventilation of the patient can cause more damage.
Another factor making deep extubation unacceptable for emergence is
that the pressure of the mask can be communicated to the globe, thus
increasing IOP.7
Another option is to use intratracheal administration of lidocaine to
inhibit the gag reflex upon emergence. This can have unpredictable
results in longer cases. In short cases, instilling lidocaine just below the
vocal cords seems to work consistently. In longer cases, the airway needs
to be sprayed closer to emergence and spraying through the
endotracheal tube does not allow anesthetic to reach the upper airway.
Also anesthetizing the upper airway can put a trauma patient with a full
stomach at risk of aspiration owing to loss of their gag reflex.
Another option is to give IV lidocaine at a dose of (1.5 mg/kg IV)
approximately 5 to 10 minutes before awakening. This can cause
delayed awakening due to the sedating effects of lidocaine and does not
always prevent coughing and bucking.
Yet another method that has had consistent results with rapid
emergence and little chance of reacting to tracheal extubation is using a
short acting opioid and little or no volatile agent at the end of the case.
Remifentanil 0.5 to 0.7 mcg/kg IV may be administered and any volatile
agent discontinued approximately 5 minutes before the end of surgery.
Many anesthesiologists allow the CO2 to rise to help initiate patient
breathing at the end of the case. In ocular trauma cases where a rise in
CO2 can cause an increase in IOP, continuing controlled mechanical
ventilation or using pressure support ventilation will ensure normocarbia and thus stable IOP.
A high-dose opioid and naloxone method may require a longer time
for emergence, but the chances of reaction to the airway are minimal.
The patient is purposefully overnarcotized by the end of the case. Once
the volatile anesthetic is off and the case is over, 10 to 20 mcg of naloxone
at a time is administered until the patient wakes up and follows
commands.
The anesthesiologist must use the method with which he or she is
most comfortable. Use of these techniques during a regular case will
allow smooth implementation during a case when it is needed.
’
Postoperative Period
Most of the strategies to prevent increases in IOP pertain to the
postoperative period as well. Nausea and vomiting after ophthalmic
surgery is very common. Vomiting increases IOP, which can be detrimental after surgical or traumatic trespass of the globe. Thus, prophylaxis should be provided by administering clonidine as a premedication,
avoiding nitrous oxide (controversial), limiting opioid analgesics,
and administering prophylactic medications (such as ondansetron,
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dexamethasone, or transdermal scopolamine) for postoperative nausea
and vomiting. Treatment of postoperative pain should be reviewed with
the patient and the surgeon. Most common ophthalmic procedures have
minimal postoperative analgesic requirements that can be met by small
doses of ketorolac and opioids titrated to effect.
’
Conclusions
Management of ocular trauma can be challenging. Customary
anesthetic methods may not be the best management choices for ocular
trauma because of the unique pharmacologic and physiologic requirements of these cases. By understanding the ocular effects of our
commonly used medications, the anesthesiologist can ensure optimal
operating conditions and protect the eye from further trauma.
’
References
1. McGwin G Jr, Hall TA, Xie A, et al. Trends in eye injury in the united states, 19922001. Invest Ophthalmol Vis Sci. 2006;47:521–527.
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