RETROBULBAR HEMORRHAGE

Retrobulbar hemorrhage occurs in approximately 0.44 to 3% of retrobulbar anesthetic cases.47,48 Given the extensive vascular plexus within the orbit, any vessel may be nicked and caused to bleed. This potential may be aggravated in patients taking anticoagulants, antiplatelet aggregation medications (e.g., aspirin), steroids, or nonsteroidal antiinflammatory medications.18 Systemic conditions such as hematologic abnormalities, thrombocytopenia, or even the presence of poorly controlled hypertension may be additional contributing factors. Excessive manipulation of the needle during insertion and injection increases the risk of hemorrhage.

Retrobulbar hemorrhages vary in severity. Although some are venous in origin and may spread slowly, arterial hemorrhages tend to accumulate blood rapidly. They produce aggressive orbital swelling, with rapid onset of marked proptosis, immobility of the globe, and massive subconjunctival and eyelid blood staining. The sudden elevation of intraocular pressure may rapidly cause serious vascular compromise to the intraocular structures of the globe.49,50

TREATMENT AND PREVENTION

Treatment of this condition is dependent on its severity. If a tense orbit and globe are observed, prompt treatment is essential to avoid permanent visual loss. The central retinal artery should be immediately assessed. If it is seen to be pulsatile or closed, immediate decompression of the anterior orbit must be accomplished. This is achieved by performing a lateral canthotomy, and if necessary, a complete disinsertion of the lateral canthal tendon and incision of the lower fornix may be necessary to provide further decompression. The patient should be observed until the vision and circulation are stabilized, and periodic frequent measurement of visual acuity should be made for several hours until it is determined that the eye is stable and there is no further accumulation of hemorrhage. In this setting it is wise to postpone surgery until the eye has recovered.

In more mild cases, immediate compression of the globe with digital pressure, intravenous mannitol, and observation may be sufficient to limit the spread of blood. It is not unreasonable to proceed with surgery if the hemorrhage is sufficiently innocuous that, on ballottement of the globe, it is soft, and there is no intraocular circulatory compromise. Visualization of the anterior segment must unimpeded and intraoperative maintenance of the anterior chamber during the procedure must be assured. If, after a seemingly small retrobulbar hemorrhage, surgery is initiated, and there is difficulty maintaining the anterior chamber after the

initial incision, the surgery should be abandoned prior to capsulorrhexis. If the intregrity of the anterior capsule has already been violated with the beginning of the rhexus, and, due to persistent shallowing of the anterior chamber, it is difficult to continue, the surgery should be abandoned. If it is initially difficult to maintain the anterior chamber due to positive posterior pressure, every step throughout the entire surgery will be more difficult. Multiple chamber collapse and potential posterior capsular rupture with vitreous loss is a likelihood. The procedure can be completed 3 to 7 days later, without risk to the patient, and with a significantly increased likelihood for success.

Retrobulbar hemorrhage may be avoided in most cases by taking several precautions. First, gentle yet decisive insertion of the needle without tilting, jiggling, or continually stabbing will minimize the risk of piercing a vessel. Second, a small-diameter, short-bevel, disposable needle that does not exceed the desired orbital depth of penetration is preferable. A needle length of less than 31 mm will limit needle penetration depth, thus avoiding needle access to the posterior vessels of the orbital apex,51 where the largest vessels in the orbit reside. A small-bore needle (27 gauge or less) will limit the amount of bleeding that may occur in the event that a vessel is pierced, because a smaller rent in the vessel will be created. Aggressive aspiration through the syringe to rule out an intravascular injection may cause traction on and subsequent rupture of a blood vessel. Aspiration should be performed gently, if at all, prior to injection, withdrawing the needle slightly if intravascular position is suspected.

The anterior orbit is relatively avascular in three sites: (1) the inferotemporal quadrant (junction of the lateral one-third and medial two-thirds), (2) the superotemporal quadrant in the sagittal plane of the lateral limbus, and (3) directly nasally in the compartment nasal to the medial rectus. This lack of vessels makes them ideal sites for orbital injection.52 The superotemporal quadrant is particularly suitable for periconal injection. The superonasal area is to be avoided because the end vessels of the ophthalmic artery and the trochlea of the superior oblique are located there (see Fig. 1–3).

SUBCONJUNCTIVAL HEMORRHAGE

Less severe than retrobulbar hemorrhage, subconjunctival hemorrhages occur with regularity. Unfortunately, the presence of this minor problem is often one of the criteria by which patients evaluate their immediate postoperative success. Aside from the cosmetic appearance, these hemorrhages are of no medical significance. If a postoperative patch is applied, patients will initially be unaware of the problem. They should be warned of the presence of such

a hemorrhage on patch removal and reassured as to the benign nature of the condition.

EXTRAOCULAR MUSCLE PARESIS

Transient and reversible akinesia is the hallmark of most injectible anesthesia. Many surgeons use this as the end point to determine the adequacy of the block. Recently, the introduction of ropivacaine 1% as an agent for injection has been shown to have less motor neuron effect. With this agent, a similar anesthetic effect53 with a decrease in intraand postoperative akinesia is expected. In cases where peribulbar anesthesia is given, neither amaurosis nor akinesia will occur, obviating to some extent the need to patch the eye at the conclusion of the procedure.

Rarely the injection of local anesthetic has been shown to cause persistent or even permanent extraocular muscle paresis. This may be due to preexisting strabismus masked by the cataract, commonly from prolonged occlusion or preexisting ocular palsy.54 Further, some postoperative diplopia is based on optical problems, for example anisometropia.55 However, in many cases the diplopia is likely due to injury related directly to the anesthetic injection. Hamed54 postulates that there may be a mechanical injury due to injection directly into the belly of the extraocular muscle. Another mechanism of muscle damage may be laceration of the anterior ciliary arteries, causing an intrasheath hematoma, with subsequent elevation of pressure within the sheath. The resultant “compartment syndrome” consists of hypoperfusion, ischemia, and inflammation. Permanent muscle fiber damage may then ensue. The inferior rectus muscle is most likely to be damaged.56,57

The role of direct chemical myotoxicity from the anesthetic agents has been studied but remains unclear. Animal studies using bupivacaine, lidocaine, and mepivacaine58,59 have established that when injected in the region of, but not directly into, the extraocular muscles, there was a negligible toxic effect that was fully reversible in time. However, when these drugs were injected directly into the extraocular muscles, there were histologic changes deemed severe enough to cause strabismus. These findings are in contrast to the high degree of myotoxicity of anesthetic agents demonstrated in other skeletal muscles.

Of interest is that an increase in persistent postoperative diplopia was noted in patients undergoing cataract surgery with retrobulbar and peribulbar anesthesia at a time when Wydase (hyaluronidase, Wyeth) was unavailable.55 One theory to explain this finding is that the absence of the hyaluronidase may have caused a pooling of anesthetic near the muscle for a prolonged period of time. This may have caused more toxicity than is usual.

BRAINSTEM ANESTHESIA AND

INJECTION INTO THE OPTIC NERVE

The optic nerve sheath is anatomically continuous with the dura of the brain. Injection beneath the sheath can result in injectate tracking back into the subarachnoid or subdural space. Symptoms of such “brainstem” anesthesia are erratic and may include respiratory arrest, cardiopulmonary arrest,60,61 hypertension, tachycardia, dysarthria,62 confusion, marked shivering, convulsions, loss of consciousness, hemiplegia, paraplegia or quadriplegia, and contralateral blockade of the optic nerve or the third, sixth, and twelfth cranial nerves.63,64 Hamilton65 has explained the occurrence of hypertension and tachycardia on the basis of a parasympathetic blockade after the anesthetic enters the cerebrospinal fluid. An alternate explanation suggests vagal blockade at the brainstem.66 The onset of manifestations of brainstem injection is not immediate, but occurs 2 to 10 minutes after injection and then resolves over the ensuing several hours. It is therefore advisable that patients should be monitored carefully for 15 minutes following retrobulbar injection so that, in the event this crisis occurs, immediate recognition is possible.61 Although the consequences of undetected brainstem anesthesia can be dreadful, with immediate diagnosis and appropriate supportive treatment the result is usually uneventful. Treatment consists of vigilant monitoring, ventilatory support, intravenous fluids, and, as indicated, the use of systemic pharmacologic agents such as vasopressors, vasodilators, or adrenergic blocking agents. Rarely, injection directly into the optic nerve may cause severe vision loss.67

Intravenous injection during retro/peribulbar block will cause a constellation of findings similar to optic nerve sheath injection. Intraarterial injection will cause the rapid onset of grand mal seizure. This problem may be prevented in the same way that other needle-related complications are prevented, that is, proper placement of the needle with respect to orbital position and depth, avoidance of the classic Atknison positioning of the eye, and awareness of the axial length of the eye.

LIMITATION OF OCULAR BLOOD FLOW

Restriction of blood flow from a retrobulbar hemorrhage has been discussed above. Studies by Findl et al68 have shown that peribulbar and retrobulbar anesthetics have a harmful effect on the choroidal and retinal blood flow. Commonly, this phenomenon may not be clinically significant. However, in patients with compromised circulation such as diabetics, hypertensives, and those in whom normal autoregulation of ocular blood flow is impaired, such as those with diabetic retinopathy or glaucoma, this

phenomenon may take on increased significance. In this circumstance even a small reduction in ocular perfusion may result in ischemia.

Ocular compression devices, commonly used to enhance the spread of anesthetic and reduce intraocular pressure prior to surgery, have also been implicated in the production of ischemia. Blood flow to the retina is influenced by a balance between intraocular and extraocular arterial blood pressure. The application of external pressure from devices such as the Honan’s balloon or the “superpinky” may cause an initial increase in intraocular pressure.69–72 The additional intraocular pressure is another cause of reduced ocular blood flow. In those patients noted above, the damage may be significant.73–75

Finally, the use of epinephrine in the injectate may similarly be implicated in production of ischemia.76 Epinepherine was considered important in the past, as the vasoconstriction it created was used to prolong the action of the retrobulbar block. Now, however, surgery is usually brief. Long-lasting blocks are unnecessary. If a long-acting block is desirable for any reason, a long-acting anesthetic such as Marcaine can be employed. Therefore, epinephrine is unnecessary and should be avoided.

OCULOCARDIAC REFLEX

The oculocardiac reflex is frequently seen in conjunction with ocular surgery. Most commonly it is noticed under general anesthesia when the extraocular muscles are stretched. Additionally, it can be seen in conjunction with retrobulbar block which, according to Hamilton,52 is attributable to the use of large-bore, dull needles. The dull needle is thought to push on the intraorbital structures, and the rapid filling of the orbit with anesthetic through the large-bore needle allows nerve transmission of pressure before adequate anesthesia to block neuronal transport. Hamilton postulates that because the afferent limb of this reflex is trigeminal, arising from within the orbit, and the efferent limb is vagal, ablation of this reflex may be accomplished by administration of retrobulbar lidocaine with a sharp, small-bore needle.77 Additionally, administration of atropine78 (2 to 3 mg in an adult) will prevent this problem.

FACIAL NERVE BLOCK

Rarely used as a separate injection during routine cataract surgery, seventh nerve blockade using the Van Lint, O’Brien, or Nadbath technique is, at times, required. Complications from this technique are reported, most commonly with the Nadbath technique. In this procedure injection in or near the stylo-

mastoid foramen is accomplished. The problems encountered include swallowing difficulty (spread to the glossopharyngeal nerve), and respiratory difficulty (vagus and spinal accessory blockade). Permanent facial palsy is most commonly reported with the Nadbath approach as well. Thus, separate injection of the seventh nerve is best avoided. With an orbital injection of hyaluronidase, a sufficient volume of anesthetic, and an ocular decompression device, eyelid akinesia is accomplished by spread to the lids through the orbital septum. Therefore, the need for separate, percutaneous nerve block is unnecessary.52 In situations where the separate injection is required as a supplement, avoidance of hyaluronidase and limitation to superficial injection (no deeper than 12 mm) is recommended.79,80

CORNEAL EXPOSURE

The cornea may remain anesthetic for a variable period of time following surgery. It is prudent to take appropriate measures to protect it against inadvertent injury, particularly when lid akinesia exists concomitantly. An occlusive eye patch is most commonly employed for this purpose. However, the patch may not be necessary. By employing shortduration anesthetics and giving appropriate patient counseling for frequent application of lubricating drops, forced blinking, and avoidance of touching or rubbing the eye, the cornea should be protected until sensation returns. Advantages of using an occlusive dressing must be weighed against the potential hazards such as contribution to the development of postoperative ptosis,81 increased moisture and temperature enhancing the growth of pathogenic organisms,82 and the patient’s loss of peripheral vision and stereopsis.

ATONIC PUPIL

Postoperative atonic pupil is a rare but reported complication of cataract surgery. Suggestions that this may be related to damage to the ciliary ganglion or adjacent parasympathetic branches83 by injection anesthesia have been countered by the observation that pilocarpine instilled in these eyes did not induce pupillary constriction. This would suggest a direct iris sphincter malfunction as the etiology.84

CONCLUSION

Complications related to regional orbital anesthesia occur with low frequency, but their consequences can be substantial. Awareness of the potential for these problems, with meticulous attention to detail,

and the ability to institute prompt corrective measures optimize the outcomes in these cases.

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