Monthly Archives: September 2017

Pupillary Paralysis

Imagine this scenario — a patient arrives in the ED, GCS 3, and is intubated for airway protection prior to the arrival of neurosurgery, who evaluates the patient and announces that the pupils are fixed and dilated, and laments that the pupillary exam is unreliable because the patient was given neuromuscular blocking agents, or paralytics to accomplish endotracheal intubation. Are they right? Does the use of depolarizing or non-depolarizing agents affect the pupillary light reflex?

I have heard multiple answers to this question, which often contradict each other, so I did some reading. I found one study from my home institution done by anesthesiologists and one done by emergency physicians that evaluated this prospectively. Andrew Gray and colleagues from UCSF did a prospective study of 20 patients receiving endotracheal intubation for elective surgery, and used pupillometry (a fun device invented here) to measure the PLR in patients randomized to saline, pancuronium or vecuronium. One thing I liked in their paper was the mention of the story of Scott Smith, a physician who self-administered curare to investigate its effects as an analgesic. He was found to be paralyzed but to have intact pupillary reflexes. They found that 100% of the patients in this series continued to exhibit intact pupillary light reflexes after administration of paralytics.

The second study by Caro et al. studied 94 emergency department patients undergoing rapid sequence intubation, with 67 receiving succinylcholine and 27 receiving rocuronium. In this series, which while small and single-center is probably more relevant to emergency medicine practice, two blinded physicians assessed patients for pupillary reflexes following administration of paralytics for RSI, approximately one minute after administration of medications. They too found preserved PLR in the vast majority of patients (91% of those getting succinylcholine and 100% of those getting Rocuronium). For a more exhaustive review and critical appraisal of this one, see the Annals of EM August 2011 Journal Club, in which this paper was covered.

So what to take away from all of this? If someone has a fixed/dilated pupil after the administration of paralytics, do not assume it is from the medication. It probably isn’t, at least according to these data. Induction medications and other agents (especially atropine) can obviously affect pupillary size, but any abnormal findings in the setting of the altered ED patient needing intubation should probably be attributed to badness, and not to the medications given for intubation.

References

Caro DA1, Andescavage S, Akhlaghi M, Kalynych C, Wears RL. Pupillary response to light is preserved in the majority of patients undergoing rapid sequence intubation. Ann Emerg Med. 2011 Mar;57(3):234-7. PMID: 21220175. [PubMed] [Read by QxMD]

Photoplethysmographic pulsus paradoxicus!

Say that three times fast.

We had a challenging case in our emergency department recently involving a patient with a self-inflicted stab wound to the anterior chest, which resulted in a pericardial effusion, prompting concern for the development of tamponade. A challenging element of the case involved thinking about the patient’s stability, and the urgent/emergent need for operative intervention v percutaneous intervention v observation — how could we determine whether this patient was, in fact, in cardiac tamponade or on their way towards developing this condition?

A classic teaching is to assess for a pulsus paradoxus, or an exaggerated decrease in the arterial blood pressure with inspiration. Traditionally this is done using a stethoscope and manual blood pressure cuff (I will not try to spell the S-word). If the difference in BP between the first expiratory Korotkoff sound and the first Korotkoff sound that no longer disappears with inspiration (the pulsus) is greater than 10 mmHg, a pulsus paradoxus is present.

Has anyone ever checked for one of these, or has this technique become like with many other physical exam findings, something that people are aware of but don’t really know how to check for? I’m not sure — I personally have never checked for one, and reach for the ultrasound when trying to risk stratify patients with pericardial effusions. Is there an easier way, or one that doesn’t require PoC echo?

These authors evaluate the utility of pulse oximetry, or plethysmography in the assessment of tamponade. They suggest that the difference between the inspiratory decrease in the magnitude of the waveform and the expiratory increase has been shown to correlate with intraarterially measured pulsus paradoxus. Unfortunately it turns out that this finding is not pathognomic for cardiac tamponade — it is linked to a number of other conditions (e.g. elevated intrathoracic pressures from asthma), and may be absent in patients who actually have tamponade physiology.

The most relevant article to this particular case is probably the study from Stone et al., “Respiratory changes in the pulse-oximetry waveform associated with pericardial tamponade.” from 2006, when they measured phasic respiratory variability in the pulse-oximetry waveform of patients undergoing aspiration of pericardial effusions. They found that the degree of respiratory variability in the pulse-oximetry waveform was significantly increased in these patients compared to effusion-less patients, and increased with the hemodynamic consequences of the tamponade. When the effusions were aspirated and drained, the variability disappeared.

So, is this something to hang your hat on? Probably not useful entirely for ruling OUT pericardial tamponade, but in a patient with an effusion if you’re asked by the consultant you wake up in the middle of the night whether you’ve checked for a pulsus yet, this might be an easier way than busting out your manual BP cuff and Googling how to check one the traditional way.

References

Clark JA1, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004 Jan;158(1):48-51. PMID: 14706958. [PubMed] [Read by QxMD]

Sunglasses Sign

I came across this piece from a 2008 issue of Neurology recently, and wanted to keep it here for posterity. The conclusions of the study were clearly communicated by the title: “The “sunglasses sign” predicts nonorganic visual loss in neuro-ophthalmologic practice.”

In this seminal article, Bengtzen and colleagues performed a prospective analysis of all patients wearing sunglasses in clinic, and patients receiving diagnoses of “non-organic vision loss”, which was a technical term new to me. They report on a number of co-variates of this diagnosis, including the wearing of sunglasses inside the exam room, alongside “highly positive review of systems, workers’ compensation claim, disability, and lawsuit”.

Specifically, the reported sensitivity of wearing sunglasses for non-organic vision loss (NOVL) was 0.46 (95% CI 0.33 to 0.59). The prevalence of NOVL in the entire study population was 4.3% but  79% in sunglasses-wearing patients. The specificity of sunglasses for the diagnosis of NOVL was 0.995 (95% CI 0.989 to 0.998).

I found this interesting if only because it supports existing stereotypes about the wearing of sunglasses indoors. The article does not comment on why this relationship exists, nor does it suggest that the performance characteristics of this finding allow you to use it to rule in or rule out true vision threats, but it does shed some light on the patterns that shape our practice and color our perceptions.

References

Bengtzen R1, Woodward M, Lynn MJ, Newman NJ, Biousse V. The “sunglasses sign” predicts nonorganic visual loss in neuro-ophthalmologic practice. Neurology. 2008 Jan 15;70(3):218-21. PMID: 18195266. [PubMed] [Read by QxMD]