Ophthalmic complications of dental anesthesia are rare and almost always transient. They include ocular motor cranial nerve paresis, Horner syndrome, and visual loss. Symptoms generally develop immediately after injection of the anesthetic solution, persist no more than several hours, and are attributed to the anesthetic reaching the orbit or cavernous sinus. There are, however, a few reports of complications that cannot be attributed simply to the anesthetic effect, either because of delayed onset or persistent deficits (1-3). We present three new cases, two involving optic neuropathy, and one involving abduction paresis and mydriasis.
The patients in this study were accrued by a detailed retrospective card review conducted on all patients evaluated on the neuro-ophthalmology service at the Carmel Medical Center, Haifa (JH) and the Sapir Medical Center, Kefar-Saba, Israel (YA) from January 2000 through December 2004. We tabulated details of the dental anesthesia and clinical manifestations. A Medline search was conducted for articles published in English from 1960 to the present using the following keywords: dental anesthesia and ocular, dental anesthesia and visual complications, and dental anesthesia and ophthalmoplegia.
A 30-year-old woman underwent tooth extraction from her right upper jaw because of a dento-alveolar abscess. After the procedure, she reported blurred vision in her OD. Ophthalmic examination a few hours later revealed visual acuity was 20/25 OD and 20/20 OS. A partial abduction deficit was present OD. Pupils measured 7 mm OD and 5 mm OS in dim light. The pupil OD reacted incompletely to direct light and a near target. There was no relative afferent pupillary defect, and the anterior segment, fundus, and visual fields were normal. Follow-up examination 1 day later showed no ophthalmic abnormalities.
A 45-year-old healthy man noticed sudden visual loss in his OS 3 hours after root canal treatment in tooth 25 (left upper jaw). On examination 6 hours after the dental treatment, visual acuity was 20/20 OD and 20/100 OS. There was a relative afferent pupil defect OS and color vision was impaired OS. Ophthalmoscopy revealed a small crowded disc OD and a pale swollen disc with flame shaped hemorrhages OS. Visual field OD was normal and demonstrated a lower altitudinal defect OS. A computed tomography scan of the brain and orbits was normal. A month later, visual acuity was unchanged and the optic disc OS was pale. One year later, the patient noticed sudden visual loss in his OD without provoking factors. Visual acuity was 20/80 OD and 20/100 OS. Ophthalmoscopy revealed a swollen disc with flame-shaped hemorrhages OD and a pale optic disc OS. Visual fields demonstrated lower altitudinal defects OU.
A 26-year-old woman underwent root canal treatment in tooth 27 (left upper jaw). She reported loss of vision OS immediately after the procedure. Examination 6 days later revealed a visual acuity of 20/20 OD and 20/200 OS, a relative afferent pupillary defect, and markedly impaired color vision OS. Fundus examination was normal in both eyes. Visual fields revealed an inferior altitudinal defect OS. A computed tomography scan of the orbits and brain demonstrated swelling over tooth 27 with no signs of sinus infection; the orbits and optic nerves appeared normal. She was treated with intravenous methylprednisolone 1 g/d for 3 days followed by oral prednisone 1 mg/kg for 11 days that was tapered down over a few days. Ten days later, visual acuity had recovered to 20/20 OS, the relative afferent pupil defect and color vision deficit had disappeared, and the visual field had returned to normal.
We have described two patients with ipsilateral optic neuropathy and one patient with an ipsilateral abduction deficit and a dilated pupil occurring immediately after dental procedures involving the upper jaw. In one patient, the optic neuropathy did not recover; in the other, it recovered completely within 10 days. The single patient with an ocular motor disturbance recovered completely within 1 day.
Thirty-nine cases of ophthalmic complications resulting from dental anesthesia have been published in the English literature since 1960, most of them in dental journals. Thirty-six reports have described transient manifestations that disappeared within 5 hours of administration of the anesthetic. Because of the usually benign and transient nature of the manifestations, most patients were never examined by an ophthalmologist. Therefore, the nature of the deficits is not well documented.
Of the 36 reported cases, 23 have occurred after upper jaw anesthesia (posterior superior or a middle superior alveolar block) (Table 1); 13 have occurred after lower jaw anesthesia (mandibular block) (Table 2). The commonest symptom has been diplopia, mostly secondary to lateral rectus palsy. Other manifestations have been visual loss, ptosis, mydriasis, and Horner syndrome. The exact mechanism by which the anesthetic causes the deficits remains unsettled.
In upper jaw anesthesia, the anesthetic is believed to cause neuro-ophthalmic manifestations by any of the following mechanisms:
- Simple diffusion from the pterygomaxillary fossa to the orbit through defects in the bone or via the vascular, lymphatic, and venous networks that link these spaces (4,5).
- Inadvertent injection into the orbit through the inferior orbital fissure (6).
- Inadvertent intra-arterial injection into the superior alveolar artery with retrograde flow to the internal maxillary artery and then to the middle meningeal artery. A middle meningeal branch occasionally penetrates the superior orbital fissure and anastomoses with the lacrimal branch of the ophthalmic artery (7,8). In support of this theory is the observation that blanching and anesthesia of the skin of the lateral upper and lower eyelids, supplied by the lacrimal nerve and artery, are sometimes described in conjunction with transient ophthalmic manifestations. The risk of penetrating an arterial lumen increases when using a non-aspirating syringe and injecting rapidly under pressure.
- Inadvertent venous injection into the pterygoid venous plexus (4,9). From there the solution can reach the orbit through the cavernous sinus which receives drainage from the pterygoid venous plexus via emissary veins through the foramen ovale and drainage from the orbit via the inferior and superior ophthalmic veins. The pterygoid venous plexus also communicates with the inferior ophthalmic vein through the inferior orbital fissure (4,9,10).
- Inadvertent scraping of the wall of an artery. The trauma sets up a sympathetic impulse that travels from the anterior, middle, or posterior superior alveolar arteries back to the internal carotid plexus and from there through the ophthalmic artery to the orbit. Decreased sympathetic activity would then produce vasoconstriction caused by the unopposed parasympathetic tone that in turn would cause ischemic deficits (11).
The mechanism of transient injury after lower jaw anesthesia can hardly be explained by simple diffusion of the anesthetic solution, because the injection site is too far from the orbit. Instead, the proposed mechanism is inadvertent intra-arterial injection (6,12,13). Because the inferior alveolar artery, a branch of the internal maxillary artery, lies adjacent to the alveolar nerve, an accidental intravascular injection is possible. In fact, the chances of penetrating the inferior alveolar artery during mandibular block are much higher than penetrating the posterior or middle superior alveolar arteries during upper teeth anesthesia, not only because of its proximity to the alveolar nerve, but because its lumen is relatively large.
The mechanism of Horner syndrome after inferior alveolar nerve anesthesia remains difficult to explain. It is proposed that inadvertent cervical sympathetic block results from a misdirected injection into the pterygomandibular space. From there the anesthetic would reach the pre-vertebral space and cause transient sympathetic chemical denervation (14).
Three cases have been reported in which ophthalmic complications were delayed, prolonged, or permanent and thus cannot be easily explained by a direct effect of the anesthetic drug (1-3). Hyams (1) reported a young woman who fainted immediately after the injection. The next day she noticed diplopia. Paresis of third and fourth cranial nerves was diagnosed. Tomazzoli-Gerosa et al. (2) described a young woman who experienced complete hemifacial sensory and motor paralysis immediately after an inferior alveolar nerve block. Several hours later, she lost vision in the ipsilateral eye. Two months later, optic disc pallor was observed, phenomena that resemble our case 2. Another unusual report (3) was that of a 14-year-old girl who “complained of blurred/double vision and occasional light flashes” in her OS 4 hours after the dental treatment was completed. The symptoms persisted the next morning and finally disappeared approximately 24 hours after the injection. No explanation is given.
Permanent loss of vision has been reported after anesthetic injections in other parts of the face, particularly during rhinosurgical procedures (15-17). In these cases, visual loss has been attributed to the vasospastic effect of adrenaline. This supposition is supported by the finding that ophthalmic artery pulse pressure is reduced by 50% after retrobulbar injections of Xylocaine and adrenaline (18).
In our case 1, diffusion of the anesthetic to the orbit or cavernous sinus alone could have explained the ophthalmic manifestations because they disappeared as the anesthetic effect wore off. Our case 2 experienced a permanent loss of vision with a course that resembled anterior ischemic optic neuropathy. We believe that the vasospastic effect of the adrenaline may have triggered this process. We cannot entirely rule out a coincidence, inasmuch as the same condition occurred in the fellow eye 1 year later without an identifiable trigger.
Our case 3 is difficult to explain because the period of optic neuropathy lasted longer than the anesthetic effect. It is possible that the neuropathy was secondary to the effect of lidocaine. Animal studies have demonstrated a possible toxic effect of lidocaine on rat retinal ganglion cells (19).
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