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*Department of Anesthesia and University of Toronto Hand Program, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada
Address correspondence to R. J. Sawyer, MB BCh, FRCA, Department of Anesthesia, Derriford Hospital, Derriford Road, Plymouth, Devon, PL6 8DH, England. Address e-mail to rjsawyer1@ hotmail.com.
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Abstract |
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IMPLICATIONS: This case report describes an uncommon complication (blindness) occurring after an inadvertent overdosage of a frequently used local anesthetic (lidocaine) during a regional anesthetic procedure. The discussion focuses on the suspected pathophysiology of the blindness.
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Introduction |
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Case Report |
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Basic monitoring was initiated (BP, electrocardiogram, and pulse oximetry) and IV access established on the contralateral hand via a 20-gauge cannula connected to an infusion of 0.9% normal saline. Midazolam 2 mg was administered IV as an anxiolytic. A 22-gauge cannula was inserted on the dorsum of the operative hand and after placing a double-cuffed tourniquet on the upper arm, the arm was exsanguinated by elevation and wrapping with an Esmarch bandage. The tourniquet cuff was then inflated to a pressure of 250 mm Hg.
A dose of 30 mL of 2% lidocaine (600 mg) was injected IV via the 22-gauge cannula. This was an inadvertent drug error resulting from a misreading of the vial label and was immediately recognized. The decision was made to continue with the procedure. The dose administered was the equivalent of 12 mg/kg. The procedure proceeded uneventfully and total tourniquet time was 45 min.
Toward the end of the procedure, the patient started to complain of severe tourniquet pain in her left arm. Before the distal cuff could be inflated or the tourniquet could be deflated slowly, a member of the operating room staff inadvertently deflated the cuff without the anesthesiologist’s knowledge. This was an unfortunate result of a communication error between staff members.
Within seconds of cuff deflation, the patient developed a tachycardia of 140 bpm, complained of visual changes (she could only see red), lost consciousness, and then became unarousable. She had seizure-like activity affecting her upper limbs lasting for approximately 30 s. Vital signs (SaO2 = 98%, BP 90/60, pulse rate 140 bpm) and airway were maintained. Initial management included administration of 100% oxygen, monitoring vital signs, and midazolam 2 mg IV bolus. The patient maintained her own airway and her tachycardia resolved to 100 bpm without any treatment. There was no associated hypotension. The seizure-like activity settled after the administration of midazolam. The IVRA cuff was not reinflated during this time. After approximately 5 min in the operating room the patient became responsive to pain but did not respond to verbal commands appropriately. Her Glasgow Coma Scale score was 11/15 (eyes 3/4, verbal 3/5, motor 5/6). It was decided that she was stable enough to be transferred to the postanesthesia care unit (PACU). This was uneventful.
In the PACU, the patient became more lucid and was able to communicate appropriately with the staff. She immediately complained of seeing only "white before her eyes." Immediate visual examination demonstrated reduced vision: she could not differentiate fingers, faces, or even color. Eye movements were intact, pupils reacted equally, and further neurological examination was normal. Although we were able to communicate with the patient appropriately and reassure her, she became distressed at her blindness, and a further bolus dose of midazolam 2 mg IV was administered.
A neurology opinion was sought with the view of investigating the patient further, possibly with a magnetic resonance imaging (MRI) scan. The differential diagnosis of the cause of blindness included an acute cerebrovascular accident. The results of the neurology examination were normal (cranial nerves, motor, sensation, and reflexes), except for her reduced vision. These symptoms resolved such that after 5 min in the PACU she was able to differentiate colors and outlines. Within 10 min, the patient’s visual acuity, visual fields, and extraocular eye movements were entirely normal. It was therefore decided that no further investigations (MRI) should be undertaken, and the patient was transferred back to the ward.
The patient was discharged completely well from the hospital the next morning and at 1-month follow-up she had no residual visual symptoms. A literature search revealed that a case such as this has not been previously reported in humans.
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Discussion |
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Large doses of local anesthetics can lead to acute cardiovascular and central nervous system (CNS) toxicity. Lidocaine toxicity usually results in symptoms of perioral/tongue numbness, restlessness, visual hallucinations (objects appear to oscillate), slurring of speech, seizures, and ultimately respiratory failure, coma, and death. Cardiovascular toxicity may result in profound bradycardia, arrhythmias, and asystole (3). Unusual symptoms and signs have been previously reported after acute lidocaine toxicity and include acute reversible aphasia (4) and complete reversible loss of brainstem reflexes (5).
After tourniquet release, this patient received a large, rapid IV bolus dose of lidocaine. It is unfortunate that a serum lidocaine concentration was not obtained. However, the pharmacokinetics of IV lidocaine have been well studied (6,7), and most studies indicate that symptoms and signs of toxicity appear at venous levels of 5 µg/mL or more (8).
Calculated serum concentration (Cpmax= drug dose/VD) would be 6.59 µg/mL, after the initial bolus injection. However, this does not account for a significant percentage (20%–80%) of the drug bound to the arm tissues as a result of forearm isolation (7). An inverse relationship exists between cuff occlusion time and plasma concentrations of lidocaine (7) and the effect of varying tourniquet deflation cycling technics would have resulted in a slower time (Tmax) to peak arterial concentration (Cpmax), but would not have significantly influenced Cpmax (9).
Elucidating the exact mechanism of this patient’s bilateral blindness is difficult. Blindness may also be caused by emboli to the retinal arterioles or visual cortex, or it may result from venous thrombosis resulting in venous congestion of the retina. In this patient, we excluded this diagnosis because of the swift and progressive resolution of the visual symptoms while in the PACU. If the symptoms had persisted, a MRI scan would have been an appropriate investigation to check for cerebrovascular blood flow changes.
Lidocaine has a number of pharmacodynamic effects in the CNS and inhibits conduction across sodium channels within neural tissue. The site of action of lidocaine causing blindness could have been at the level of the retina, optic nerve, optic radiation, or cortex. Lidocaine has quantitatively different effects on different parts of the brain (10,11).
The cortical effects of progressive lidocaine toxicity have been investigated in cats and demonstrate a tetraphasic action. This action extends from diffuse electroencephalogram slowing to a stage of convulsion (12).
Local anesthetics, including lidocaine, inhibit the release of GABA, an inhibitory neurotransmitter (13). A reduction in 
-aminobutyric acid (GABA)-ergic activity on subcortical nerve terminals results in stimulation of central nuclei, particularly the amygdaloid nuclear complex and thalamus. Any resultant stimulatory effect arises from an imbalance of these GABA inhibitory pathways.
The visual symptoms could thus be explained as a manifestation of either occipital lobe seizure activity or subcortical stimulation being precipitated by the acute large cerebral lidocaine drug concentration. Visual manifestations, including visual auras, hallucinations, ictal blindness, and abnormal ocular movements, are well-known symptoms of occipital lobe cortical seizure activity (14). Ictal blindness in the form of a whiteout or blackout has been reported, including a prolonged form described as status epilepticus amauroticus. These symptoms can occur with or without subsequent loss of consciousness.
We surmise that this patient’s transient bilateral symptoms were as a result of lidocaine-induced ictal blindness, possibly a result of cerebral stimulation within the occipital lobe or at subcortical centers. The speed of spontaneous resolution of the patient’s symptoms and signs is consistent with the pharmacokinetics (redistribution and elimination) of lidocaine as the plasma concentration returned to within the therapeutic range.
Had the cuff not been inadvertently deflated, our recommendations in managing this patient would have been as follows: a second cuff can be positioned and inflated over the forearm, thus effectively halving the isolated toxic dose of lidocaine. This technique has proven efficacy in the studies by Chan et al. (15) and Plourde et al. (16). The proximal arm cuff could then be deflated cyclically three times with fixed 10-second periods of deflation as recommended by Sukhani (9). Once the proximal arm cuff has been deflated, the forearm cuff can then be deflated in a similar fashion. This would result in a reduction of Cpmax and a significantly prolonged Tmax.
We would like to reiterate the importance of ensuring that the correct dosage of local anesthetic is used in IVRA procedures and that all operating room staff are suitably aware of the safe management of tourniquet cuffs during IVRA procedures.
In summary, we have presented a case of transient, reversible, bilateral blindness occurring as a result of an acute toxic overdose of lidocaine in a young fit woman. There were no long-term neurological or visual sequelae. A literature search revealed that a case such as this has not been previously reported in humans.
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  D. L. ORR II and W. J. CURTIS Obtaining written informed consent for the administration of local anesthetic in dentistry J Am Dent Assoc, November 1, 2005; 136(11): 1568 - 1571. [Abstract] [Full Text] [PDF]
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