Postoperative Complication of Periocular Anesthesia

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  • 7/29/2019 Postoperative Complication of Periocular Anesthesia

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    -Postoperative Complications

    of Periocular Anesthesia

    Ignatius C. Cyriac, M.D.

    Roberto Pineda, II, M.D.

    Even as current trends move away from retrobulbar blocks and topical

    anesthesia gains greater widespread acceptance, ocular anesthesia still is most

    commonly administered with a needle. Although rare, numerous complications

    associated with the administration of periocular anesthesia have been described,

    ranging from the innocuous hemorrhage to life threatening systemic situations.Early recognition is paramount, and judi cious management of these

    complications can result in more favorable visual outcomes and significantly less

    morbidity.

    The local anesthetic ocular complications that are reviewed include

    retrobulbar hemorrhage, globe perforation, optic nerve trauma, and mus cl

    injury. As systemic complications can be associated with direct central nervous

    system (eNS) spread of anesthetic, signs and symptoms of this situation also are

    addressed.

    Techniques

    The aim of retrobulbar anesthesia administration is to direct the tip of theretrobulbar needle toward the orbital apex within the muscle cone to allow

    diffusion of anesthetic within this space. When the ocular motor nerves (III and

    VI) and sensory nerves (V) are blocked, akinesia and anesthesia is achieved.

    Ophthalmic surgery has been performed with local anesthesia for more than

    100 years. Herman Knapp was the first to describe retrobulbar anesthesia with

    cocaine in 1848. However this method fell into disrepute because of serious and

    fatal complications. The modern technique of retrobulbar anesthesia using

    lidocaine was described by Atkinson in 1948. This technique of retrobulbar

    anesthesia as described by Atkinson has undergone various modifications in

    general use but essentially is un-

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    86 Cyriac Q,~ Pineda

    changed from his original method. Atkinson originally recommended the

    technique of positioning the globe in an up and inward gaze using a blunted

    needle of no longer than 35 mm. Because of the blind approach of this

    technique, Unsold and associates' performed studies that involved scanning

    orbits of cadavers after introducing a retrobulbar needle. They demonstrated

    the optic nerve, ophthalmic artery, superior orbital vein, and posterior pole of

    the globe to be in close proximity to the needle. The authors recommended

    placing the globe in primary position or in a down and outward gaze,

    suggesting that the optic nerve, vessels, and inferior oblique are placed outside

    the path of the anesthetic needle.

    Peribulbar anesthesia administration seeks to avoid the optic nerve,

    ophthalmic artery and vein, and posterior globe by placing the anesthesia

    outside the retrobulbar space just posterior to the equator. Akinesia and

    anesthesia is achieved through diffusion of anesthesia in this area. The actual

    technique is more varied in its use than is the retrobulbar method of

    administration. The technique described by Davis and Mandel/ serves as

    representative example of this block. With the eye in primary position, a 12-

    mm 27-gauge needle injects a diluted 1 % lidocaine solution into the anteriororbit inferotemporally. In this same area, an 18 to 24-mm 23 to 26-gauge

    needle is used to inject a solution of lidocaine, marcaine, and wydase.

    Supplemental blocks of this same preparation are administered into the

    superonasal or inferonasal orbit as needed.

    Peribulbar anesthesia has been believed to be less painful and to result infewer postoperative complications than is retrobulbar anesthesia. Fewer cases

    of retrobulbar hemorrhage, globe perforation, and brainstem anesthesia have

    been reported.f

    Anatomical Considerations

    To understand the mechanisms of complications from periocular nerve

    blocks first requires knowledge of orbital anatomy. Motor nerves (cranial

    nerves III, IV, and VI) insert into rectus muscles between the pos terior and

    middle thirds of the muscle belly. Thus, the muscular branches of the third

    nerve may be blocked within the muscle cone in the posterior orbit, notably in

    the area of the optic nerve and ophthalmic vein, whereas the inferior oblique'snervous and vascular branches insert more anteri orly on the muscle and,

    therefore, are more susceptible to damage by blocks provided along the orbital

    floor. The origin of the superior oblique in the posterior-superotemporal orbit

    and its relative immobility render superotemporal blocks perilous.

    Needle length with relation to anatomical dimensions also can increase the

    risk of complications for a particular block. It has been shown that the average

    length from the lateral one-third of the inferior orbital rim to the orbital apex is

    48 mm or less. 4 Also, the intracanalicular portion

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    Complications of Periocular , nosia - 87

    of the optic nerve is relatively immobile and extends anteriorly from here. Risk

    from using long needles then becomes apparent. Using blunt needles was

    thought to resolve this risk, but complications have been reported with blunt

    needles as well. 5

    Local Complications

    Hemorrhage

    The most common complication of periocular anesthetic administra tion i

    retrobulbar and periocular hemorrhage. Incidence of hemor rhages with

    retrobulbar blocks is between 1 and 3% and, when combined with peribulbar

    blocks, incidences of 1 : 1,000 to 1 : 60 have been re ported." However, most of

    these cases are mild in nature. Acquired vascu lar disease is thought to be a risk

    factor for this occurrence.

    The vast majority of orbital and periocular hemorrhages are venous in

    origin. Usually, they are not vision-threatening and more often require

    postponement of surgery than any intervention. Alternatively, arterial he

    morrhages can produce proptosis, ecchymosis, and chemosis. In the pres ence o

    rapid orbital swelling causing a tight orbit, marked proptosis, oph thalmoplegia,

    and blood-staining of periorbital tissues, a retrobulbar hemorrhage of arterial

    origin should be suspected. Vision loss occurs as a result of the tamponade

    effect of the periorbital swelling wherein the in traorbital pressure rises higher

    than does the intraarterial pressure. Also, occlusion of the microvasculature of

    the optic nerve can occur, causing a late optic atrophy.

    If the diagnosis of retrobulbar hemorrhage is suspected, pressure

    measurement and ophthalmoscopy are indicated. Treatment is immedi ate latera

    canthotomy-cantholysis and close follow-up of intraocular pres sure (lOP) and

    vision. Emergent orbital decompression surgery may be considered if the optic

    nerve is compromised.

    Permanent impairment of vision in such patients has not been shown to

    occur. Direct arterial trauma is the suspected cause, and no modifica tion in

    technique has demonstrated avoidance of this complication.

    Globe Perforation

    Globe perforation is one of the most dreaded complications of local

    anesthesia. Several retrospective studies reported isolated cases of globe

    perforation. Incidence of globe perforation ranges from 1: 1000 to 1 : 4200 in

    reported cases and, in patients with axial lengths greater than 26 mm, the

    incidence increases to 1 : 140. 7 In addition, axial myopes also have thinner

    sclera, placing them at further risk. Other risk factors for globe perforation

    include enophthalmos or nanophthalmos, multiple injections or injection sites,

    and a history of a scleral buckling procedure.

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    88 Cyr.,.; and Pineda

    Whether advantages accrue to sharp rather than blunt needles is un known. Use

    of blunt needles has been thought to avoid this risk, but cases of blunt-needle

    perforation have occurred. Also, performing strictly peribulbar blocks does not

    obviate the risk of perforation, although the incidence is lower with the

    peribulbar technique.f Because techniques and needle types vary, determining

    the relative risk of globe perforation is difficult. The risk of perforation has not

    been proven in any controlled study.

    Symptoms of ocular penetration include severe pain and sudden loss of

    vision, and signs include hypotony, sudden increase in lOP, and sub -conjunctival hemorrhage. When suspected, indirect ophthalmoscopy should be

    performed to confirm the diagnosis, but scleral exploration is not necessary, as

    the perforation sites often are small and self-sealing. If the media are not clear

    enough to allow visualization of the retina, the sur geon may proceed with

    cataract surgery. Otherwise, treatment entails immediate cryopexy or episcleral

    implant for anterior perforations or laser photocoagulation to posterior

    perforations. Systemic antibiotics should be administered to reduce the risk of

    endophthalmitis.

    Complications of perforation include subretinal, retinal, and vitreous

    hemorrhage; retinal holes; or detachment. The degree of postoperative visual

    recovery depends on the location of the perforation (although the majority are

    below the fovea), presence of a retinal detachment, and development of

    proliferative vitreoretinopathy.

    Muscle Injury

    Although exceedingly rare, another complication oflocal ocular anes thesia

    is direct muscle trauma with subsequent diplopia. The cases reported most

    commonly are of inferior rectus palsies or contracture after blocks .m d of

    superior rectus overaction. Increased use of peribulbar blocks has been

    implicated as a cause, given the multiple injections or injection sites used with

    this method; however that the use of hyalu ronidase is thought to improve the

    efficacy of this technique, thereby re quiring less injection of anesthetic.

    The mechanism of muscle injury is speculative. One theory contends that

    direct injection of anesthetic into the recti and subsequent myotoxic ity cause

    postoperative strabismus. Studies by Rainin and Carlson" sug gested that

    surrounding an isolated rectus muscle with high concentra tions and volume of

    anesthetic can cause muscle fiber destruction. Trauma to nerves and needle

    damage of the rectus muscles also are spec ulated to be causes of postoperative

    strabismus.

    Another accepted theory is that muscle injury occurs in one of two ways:

    Laceration of anterior ciliary vessels causes a hematoma ora large volume of

    anesthetic is injected into this same intramuscular or perimus cular space." The

    compressive effect of blood or anesthetic is thought to

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    Complications of Periocular, sthesla- 89

    result in vascular compromise and subsequent muscle fibrosis and con tracture.Overall, muscle paresis after cataract surgery is noted to be temporary,

    but cases of permanent muscle injury have been described. These cases of

    permanent strabismus are thought to be the result of a myotoxic effect of the local

    anesthetic, but the lack of pathological studies in these cases cannot confirm the

    etiology.'?

    Optic Nerve Injury

    Injury to the optic nerve with the anesthetic needle is a great concern in

    administering periocular anesthesia. Severe visual deficit on the first

    postoperative day may be the clinical presentation.

    Direct needle trauma to the optic nerve is not thought to be the mech anism

    optic neuropathy after surgery. In fact, optic nerve injury and dysfunction

    occurring after local ocular anesthesia is related inherently to retrobulbar

    hemorrhage and to central artery occlusion.

    Retrobulbar hemorrhage can cause a marked rise in lOP or intraor bi

    pressure, thereby causing a central retinal artery occlusion. Intravas cular injectio

    of anesthetic also can cause a central vein or artery occlu sion via vasospasm. A

    third mechanism for vasoocclusion is the injection of anesthetic into the nerve

    sheath, causing a compressive effect first on the venous circulation and later

    compromising arterial inflow. Direct needle trauma to the retinal artery in the

    posterior orbit, prior to its pen etration of the optic nerve, also is thought to occur.

    All these mechanisms cause optic atrophy as a result of vascular compromise.

    Needle penetration of the optic nerve rarely causes vision loss but, if

    associated with a central retinal artery occlusion, visual dysfunction can be

    profound and permanent.

    CNS Complications

    CNS complications oflocal anesthetic injection can have lethal effects.

    In extremely rare instances, after receiving periocular anesthesia, a pa tient m

    experience cardiovascular and pulmonary problems, such as hy potension a

    respiratory arrest. Drug toxicity can be a cause and may manifest initially as

    tremors, agitation, slurred speech, and (eventually) seizure activity. Moreover,

    overall nervous system collapse causing respira tory depression an

    cardiovascular collapse can occur.

    The fisk of nerve trauma or subsequent intrathecal administration of

    anesthesia (or both) are thought to be linked. A study of CNS complica tions a

    retrobulbar block demonstrated an incidence of 1: 375. Reported rates of CNS

    complications range from 0.09% to 1.50%. A life threatening complication ca

    occur in 0.13%.11 Effects included apnea

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    90 Cyriac and Pineda

    and respiratory depression, convulsions, and cardiopulmonary arrest. In -

    terestingly, no reported cases occurred in studies wherein a needle length shorter

    than 1.5 inch was used. In peribulbar anesthesia, many suggest using needles no

    longer than 25 mm.

    The clinical picture of CNS anesthesia can be varied. Affected patients may

    experience confusion and agitation (which may be normal consider ing

    administration of intravenous sedation), dizziness, tremors (ranging from

    shivering to marked convulsions), ophthalmoplegia or amaurosis of the fellow

    eye, tinnitus or deafness, and problems with speech or breath ing. The onset ofsymptoms usually occurs within a few minutes, peaking at approximately 15

    minutes after anesthesia administration. For this rea son, we recommend that the

    patient be observed, without drapes, for 15 minutes after administering

    anesthesia. The average duration of these symptoms is 2 to 3 hours.

    Signs of CNS anesthesia include loss of consciousness, apnea, and limb

    paralysis. CNS blockade can manifest as arterial hypertension and tachycardia or

    hypotension and bradycardia with cardiac arrest and pul monary edema. These

    signs and symptoms can occur in any combination, whereas the earliest findings

    are contralateral eye signs and loss of con sciousness. With proper diagnosis and

    prompt treatment, full recovery is normal. Treatment is specifically directed

    toward seizure control, hemo dynamic support and, in some cases, administration

    of cardiopulmonary resuscitation. The nature of this complication of ocular

    anesthesia emphasizes the need for careful monitoring of the patient by aqualified anesthesia staff.

    The mechanism of this complication is debated. Intravenous or in traarterial

    administration has been postulated, but blood levels in patients were not in the

    toxic range. Also, doubt has been cast on the intraarterial theory, because no

    reports have cited blood in syringes or retrobulbar hemorrhages. Intravascular

    injection should produce immediate seizure activity. Grand mal seizure activity

    usually is the predominant sign but is not necessarily always present. Respiratory

    depression and cardiovascular collapse also should occur injust a few seconds.

    This clinical picture after periocular anesthesia has not been reported.

    The most widely accepted explanation is direct injection into the nerve

    sheath, and it has been shown through orbitography studies using radiocontrast

    dye. 12 Anesthetics can gain access to the cranial nerve roots, pons, midbrain, and

    spinal cord. Also, the cerebrospinal fluid analysis of patients who developed

    respiratory arrest demonstrated lido caine and bupivicaine.P The neurologicalsigns or vision loss from this mechanism are thought to be short-lived, and no

    permanent effects have been noted. Direct injection into the subarachnoid space

    would cause respiratory arrest within a few minutes, and this is the common

    clinical scenario.

    Complications of Periocular Anesthesia - 91

    Conclusion

    No method or technique of local ocular anesthesia is free of compli cation.

    We recommend that surgeons perform their preferred technique properly and with

    the globe in primary position. The use of blunted, shorter needles 33 mm for

    retrobulbar blocks and 20 mm for peribul bar blocks) also is recommended.

    Furthermore, the peribulbar technique, although not proved, appears to have an

    advantage over the retrobulbar technique in reducing the risk of complications.Many advances in technique have enabled surgeons to achieve excel lent

    surgical anesthesia and akinesia. With careful monitoring by qualified individuals

    with experience in local ocular anesthesia, the vast majority of cases result in no

    serious complication. However, because the administra tion of anesthesia is

    essentially a "blind" maneuver, risk of damage to vital neurovascular structures,

    orbital tissues, and even to the globe itself is inherent. Therefore, occasional

    complications should be expected.

    References

    12. Unsold R, Stanley .lA, Deg-root J . The CT-topography of retrobulbar anesthesia: anatomic-cinical correlation of complications and suggestion of a modified technique. Graefes Arch

    Clin Exp Ophthalmol 1981 ;217:125-136

    13. Davis DB, Mandel MR. Posterior peribulbar anesthesia: an alternative to retrobulbar

    anesthesia.J Cataract Refract Surg 1986;12:182-184

    14. Davis DB, Mandel MR. Efficacy and complication rate of 16,224 consecutive peri bulbar

    blocks. J Cataract Refract Surg 1994;20:327-335

    15. Katsev DA, Drews RC, Rose BT. An anatomic study of retrobulbar needle path length.

    Ophthalmology 1989;96:1221-1224

    16. Hay A, Flynn HW, Hoffman .II, Rivera AH. Needle penetration of the globe during

    retrobulbar and peri bulbar injections. Ophthalmology 1991 ;98: 1017-1024

    17. Edge KR, Martin .I, Nicoli V. Retrobulbar hemorrhage after 12,500 retrobulbar blocks.

    Anesth Analg 1994;76:1019-1022

    18. Duker JS, BelmontJB, Benson WE, et al. Inadvertent globe perforation during retrobulbar

    and peribulbar anesthesia. Ophthalmology 1991;98:519-526

    19. Rainin EA, Carlson BM. Postoperative diplopia and ptosis. Arch Ophthalmol 1985; 102:1337

    20. Hamed LM. Strabismus presenting after cataract surgery. Ophthalmology 1991;98: 247-25221. Esswein MB, Von Noorclen CK. Paresis of a vertical rectus muscle after cataract extraction.

    Am J Ophthalmol 1993; 116:424-430

    22. McGoldrick KE. Anesthesia for ophthalmic and otolaryngologic surgery. Philadelphia:

    Saunders, 1992

    23. Drysdale DB. Experimental subdural retrobulbar injection of anesthetic. Ann Ophthal

    1984;16:716-718

    24. Kober, KA. Cerebrospinal fluid recovery of lidocaine and hupivicaine following respiratory

    arrest subsequent to retrobulbar block. Ophthalmic Surg 19H7;lH:II-13