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Respiratory Arrest in the Eye Clinic* FREE TO VIEW

Marc A. Simon, MD; Gregory Cosgrove, MD; Clifford W. Zwillich, MD; Edward D. Chan, MD, FCCP
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*From the Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center and Department of Medicine, National Jewish Medical and Research Center, Denver, CO.

Correspondence to: Edward D. Chan, MD, FCCP, K613e, Goodman Building, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO 80206; e-mail: chane@njc.org

Chest. 2001;119(6):1953-1955. doi:10.1378/chest.119.6.1953
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A 66 -year-old man underwent retrobulbar anesthesia for repair of a detached retina. Anesthesia consisting of 5 mL of a 1:1 mixture of 2% lidocaine and 0.5% bupivacaine was injected with a 1-inch, 23-gauge needle into the retrobulbar space. There was no sanguinous return during pullback of the syringe plunger just before the injection. The patient had received this combination of medications during prior ophthalmologic procedures without any adverse effects. Three minutes after the injection, he became unresponsive with a respiratory rate of 3 to 5 breaths/min. Bag-mask ventilation was administered, and he was transferred to the emergency department.

One month before hospital admission, surgical repair of his recurrent right retinal detachment was unsuccessful. On the day of hospital admission, he underwent a pneumatic retinopexy, also known as a fluid-gas exchange procedure, of the right eye in an attempt to salvage the failed surgery. This procedure consists of injection of an inert expandable gas into the vitreous cavity in an attempt to close retinal breaks.

His medical history was significant for legal blindness of the left eye secondary to chronic uveitis of unknown etiology, glaucoma of the right eye, and previous laser surgery for a right retinal detachment 10 years previously. He had no known drug allergies, and his outpatient medications included several eye drops, including dorzolamide, flurbiprofen, hydroxypropyl, prednisolone, and timolol.

In the emergency department, he was afebrile with a BP of 157/60 mm Hg and a heart rate of 100 beats/min. He remained bradypneic for a total duration of approximately 1 h, with oxygen saturation of 95% on 100% supplemental oxygen via bag-mask ventilation. Head and neck examination was notable for bilateral mydriasis and subcorneal air in the right eye secondary to the fluid-gas exchange procedure. The lungs were clear to auscultation. Cardiac examination findings were normal. There was no clubbing, cyanosis, or edema of the extremities. Neurologic examination findings were remarkable for unresponsiveness and absence of pupillary reflexes in both postsurgical eyes. Deep tendon and Babinski reflexes were normal. The serum electrolytes, CBC count, and troponin I levels were all within normal limits. ECG revealed normal sinus rhythm and no evidence of acute ischemia.

What is the most likely cause of the respiratory arrest?
Diagnosis: Retrobulbar anesthesia-induced central respiratory arrest

Lidocaine and bupivacaine are commonly used local anesthetics for ophthalmologic procedures. Retrobulbar injection in the region between the lateral rectus muscle and optic nerve anesthetizes the nerve supply to all of the extraocular muscles with the exception of the superior oblique. It also anesthetizes the globe and the ciliary ganglion, with resultant mydriasis. Local ophthalmic anesthetics also minimize the risk of wound rupture associated with coughing during extubation after general anesthesia. Lidocaine is the most commonly used anesthetic because of its rapid onset and long duration of action (1 to 2 h). Bupivacaine is frequently mixed with an equal amount of lidocaine to further prolong the duration of anesthesia (up to 6 to 10 h). The maximum safe dose of lidocaine is considered to be 4.5 mg/kg and of bupivacaine is 200 mg. Hyaluronidase is frequently included in the injection to shorten the onset of action and to increase the spread of anesthetic.

Respiratory arrest is a rare complication of retrobulbar anesthesia. One prospective study of 3,123 retrobulbar injections reported a nearly 10-fold higher incidence of respiratory arrest with the use of 4% lidocaine mixed with 0.75% bupivacaine, occurring in 7 of 888 injections (0.79%), compared to 2% lidocaine mixed with 0.75% bupivacaine, noted in 2 of 2,235 injections (0.089%). Most of these patients also received oral or IV sedation as well as retrobulbar hyaluronidase. The risk was found to be independent of underlying medical condition, age, or sex. Respiratory arrest typically occurred 2 to 8 min after injection. Duration of apnea ranged from 5 to 55 min, with three cases lasting > 30 min and requiring intubation. Of the nine patients with respiratory arrest, two patients had hypotension and bradycardia that were responsive to atropine, and one patient had transient hypertension. Serum levels of lidocaine and bupivacaine of patients who had respiratory arrest were not significantly higher than the 20 control subjects, and all levels were below the toxic range. All affected patients recovered without adverse long-term effects.

Although the precise mechanism for respiratory arrest with retrobulbar injection of anesthetic is not known, retrograde movement of the anesthetic along the optic nerve sheath to the respiratory center in the brainstem has been postulated (Fig 1 ). According to this theory, because the average retrobulbar space is only 1.6 mL as measured in cadaveric eyes but the average injected volume is 5 mL, the excess anesthetic travels along the path of least resistance. In most patients, this is through Tenon’s capsule and into the eyeball. However, in a small percentage of patients, Tenon’s capsule is too impermeable and the anesthetic, under pressure, diffuses into the potential space around the optic nerve sheath, traveling to the brainstem. This potential space has been documented using dye studies.

Respiration and level of arousal are functions of the diffusely organized reticular formation located throughout the brainstem. The diffusely organized reticular formation is a group of neurons located outside of the major nuclear groups of the brainstem with far-reaching axons that extend superiorly to the thalamus and inferiorly to the spinal cord. The optic nerve tract passes laterally between the inferior edge of the thalamus and the midbrain, and then terminates in the lateral geniculate body of the posterior thalamus. Therefore, anesthetic traveling along the optic nerve tract to the thalamus may adversely affect the diffusely organized reticular formation, resulting in apnea.

In addition to retrograde movement of anesthesia along the optic nerve sheath, other hypothesized mechanisms of respiratory arrest from retrobulbar anesthesia include direct accidental injection into the optic nerve sheath and inadvertent injection into the ophthalmic artery with retrograde flow into the cerebral circulation. However, intravascular injection of bupivacaine is known to cause immediate cardiovascular collapse as opposed to delayed respiratory arrest seen in our patient.

After his initial assessment in the emergency department, the patient developed bradycardia at a rate of 50 beats/min, believed to be because of increased vagal output from the apnea and transient hypoxemia. Atropine was administered, and the heart rate increased to 80 beats/min. Within 60 min of the respiratory arrest, he spontaneously regained consciousness and his bradypnea resolved. When asked about the incident, he denied losing consciousness and stated he was audibly aware of his surroundings but was unable to talk or move. The etiology of his motor paralysis was unclear. The patient was discharged after an overnight observation in the ICU and recovered completely without any sequelae.

  1. Respiratory arrest is an uncommon but potentially catastrophic complication of retrobulbar anesthesia. The probability of respiratory arrest is related to the amount of anesthetic injected. Cases have been reported with the use of lidocaine, bupivacaine, or mepivacaine alone and with various combinations of anesthetics.

  2. Hypothesized mechanisms for retrobulbar anesthesia-induced respiratory arrest include diffusion and retrograde spread of anesthetic along the potential space of the optic nerve sheath into the respiratory center, or direct injection of anesthetic into the optic nerve sheath or into the ophthalmic artery.

  3. Optimal management of retrobulbar anesthesia-induced respiratory compromise requires prompt recognition, maintenance of airway patency and, not infrequently, mechanical ventilation.

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Figure Jump LinkFigure 1. Proposed mechanism of retrobulbar anesthetic-induced respiratory depression. CN = cranial nerve.Grahic Jump Location


Figure Jump LinkFigure 1. Proposed mechanism of retrobulbar anesthetic-induced respiratory depression. CN = cranial nerve.Grahic Jump Location



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