Written by Zach Adams, OSUEM resident // edited by Michael Barrie, OSUEM Assistant professor
EMS brings in an unconscious man. They are bagging the patient in the hallway of the ED and tell you that they found the patient “down” at home, unresponsive, and with agonal respirations. The patient is obviously altered, unresponsive, and not protecting his airway. You and the team respond rapidly, performing rapid assessment on this undifferentiated patient. Rapid sequence intubation is performed to protect the airway, and you go down your algorithm. The patient was not moving spontaneously, and you’d like to assess pupillary status. But he’s intubated, sedated, and just received etomodate and rocuronium. The pupils appear dilated and unresponsive. But is the pupil exam reliable after a paralytic?
Assessment of neurological status is important in all critically ill patients, and the pupillary response to light can give us some good information. In the scenario above, if we assess the pupillary response to light, does it give us any information after a paralytic?
There are two pathways involved in the reflex: an afferent limb controlled by CN II (optic nerve), and an efferent limb controlled by CN III (oculomotor nerve). When the optic nerve, or more precisely photosensitive retinal ganglion cells, sense light, the message is relayed via the optic nerve to the pretectal nucleus of the midbrain. From here, the message passes to the bilateral Edinger-Westphal nuclei (EWN). Preganglionic parasympathetic neurons from the EWN synapse with the ciliary ganglia. The ciliary ganglia then send postganglionic parasympathetic neurons via the short ciliary nerve to the sphincter papillae, which contract the iris in response to binding of acetylcholine. For a fun video, check out
In our average patient, shining a light into one eye should lead constriction of the iris in the involved eye, as well as consensual constriction in the opposite eye, indicating the pathway is intact. If the involved eye constricts, but the opposite eye does not respond, this suggests a motor deficit of the oculomotor nerve or Edinger-Westphal nucleus in the midbrain. If the response is normal in the ipsilateral eye (both eyes constrict), but on shining light in the opposite eye there is no response, there is an afferent (optic nerve) defect, and vice versa. What does this information tell us? It gives us a general idea of brainstem function, brain stem death, optic nerve and oculomotor nerve function, and the possibility of depressant drugs in the patient’s system (i.e. narcotics, etc.). That’s a lot of information. But what if our patient has undergone RSI? Are we out of luck?
During RSI, drugs of choice for paralysis include depolarizing (i.e. succinylcholine) and non-depolarizing (i.e rocuronium) neuromuscular blockade (NMB). Paralysis by depolarizing NMB agents involves two phases. In phase I, depolarizing neuromuscular blockade by succinylcholine involves direct binding of succinylcholine to motor endplate acetylcholine receptors. This causes opening of Na/K ion channels, leading to depolarization of the cell. Depolarization leads to calcium release, which causes muscle cell contraction (i.e. fasciculations). Acetylcholine release by peripheral motor neurons is rapidly degraded by acetylcholinesterase, allowing repolarization of the muscle for another contraction. On the other hand, succinylcholine is not degraded as quickly, and stimulation continues, blocking repolarization. Moreover, plasma cholinesterase is the enzyme responsible for degradation of succinylcholine, which takes some time. During phase II, prolonged paralysis occurs when a large amount of succinylcholine is given by desensitization of the motor endplate acetylcholine receptors, and they remain refractory to further stimulation. Hence, paralysis.
Paralysis by non-depolarizing NMB involves competitive inhibition of acetylcholine for motor endplate acetylcholine receptors. Binding by non-depolarizing NMBs prevents acetylcholine binding, and, therefore, muscle contraction and paralysis.
Both of these mechanisms involve the inhibition of acetylcholine. In this manner, it would be reasonable to believe that the pupillary light reflex would also be impacted, as acetylcholine release from the postsynaptic parasympathetic fibers of CNIII cause pupillary constriction in response to light. Reasonable, but it would be fortunate if this were not true.
Fortunately for us, the supposition appears to be incorrect. In a study by Caro, et. Al, they looked prospectively at 94 patients assessed by two blinded emergency physicians and the pupillary light response after neuromuscular blockade and intubation. They excluded patients without an intact response prior to intubation, with the primary outcome being clinically observable pupil response. Sixty-seven patients had received succinylcholine, and 31% received rocuonium.
Of those that received succinylcholine, 91% maintained an intact pupillary response after completion of RSI. 100% of patients receiving rocuronium demonstrated a preserved pupillary reflex. 100%! They concluded that pupillary light reflex in patients undergoing RSI is not inhibited by succinylcholine or rocuronium, the medications we most often use in our ED for RSI.
When the pupils are fixed and dilated, they’re fixed and dilated it appears, RSI or not. This doesn’t impact our resuscitation necessarily, but it should be noted and documented.
For more information on succinylcholine versus rocuronium for intubation, check out http://lifeinthefastlane.com/ruling-the-resus-room-004/ – great quick read (unlike the above).
Here’s the link to the paper cited http://www.ncbi.nlm.nih.gov/pubmed/21220175 I think it’s mentionable. Next time you call out pupillary response, pre or post-intubation, you can at least be confident that the response is the response for most patients.