A Disunion of the Literature – NSAIDs and Fracture

The Gist:  Currently, practice and literature are divisive with regard to issues of non-steroidal anti-inflammatory medications (NSAIDS) and bone healing in fractures; however, analgesic dosed NSAIDs are probably ok in the acute fracture process in most patients.  Check out this open access article by Yates et al.

The Case:  A 11 y/o male presented to Janus General with left forearm edema and deformity after falling during a basketball game.  Imaging demonstrated a non-displaced, transverse radius fracture with less than ten degrees of volar angulation. The patient received ibuprofen, was placed in a splint, and follow up with orthopedics was arranged.  Later, the orthopedist instructed me not to give NSAIDs to patients with fractures "because they delay healing."  I was marginally acquainted with the controversy from reading these bits of FOAM (Free Open Access Medical education) previously: The Trauma Professional and Jacobi EM's take, but I was startled enough by the physician's rigid statement of fact to review the literature myself.

Why the worry?
  • Non-union is a feared, delayed complication of fracture and is estimated to occur in ~1% of long bone fractures although this rate is higher in other fractures and influenced by individual factors (1).
  • Studies of NSAIDs in fracture healing conducted in rats tend to show delayed fracture healing, delayed callus formation, and increased prevalence of non-union -see Table 1 in this article (2,3).  
  • The biologic plausibility - The initially inflammation generated by a fracture plays a role in creating the environment for bone healing (5).  NSAIDs inhibit cyclo-oxygenase (COX), decreasing the presence of some prostaglandins (2). Prostaglandins such as PGF2A and PGE2 aid in bone healing by stimulating osteoblasts.  These prostaglandins are also thought to play a role in angiogenesis necessary for bone repair/regeneration as well as bone metabolism (3).  Thus, COX inhibition and interference with these cytokines may interrupt the body's natural way of repairing itself.
The Human Literature:  Oftentimes, animal studies and in vitro experiments don't translate into how things work in the human body and it appears this is the case with NSAIDs and fracture, as the data is a wash.  Why might this be?
  • No prospective RCTs with sufficient power have been conducted that reflect NSAIDs dosed for analgesia in patients with acute fracture.  
  • Clinical practice contains far more variables than a well designed laboratory study, thus confounding the data.  For example, mechanism of injury, smoking and glycemic control can affect fracture healing rates but these vary individually (1).  
  • Studies look at various kinds of fractures that have disparate expected rates of non-union (ex: post-op spinal surgery has 10-15% rates of non-union vs 1-5% of long bone fractures) (4).
  • Retrospective studies examining NSAIDs and delayed healing often involved routine, protracted dosing of NSAIDs or may have been more common in patients with more complicated fractures or signs of complications, as they consumed more NSAIDs.  
This free, full text article by Wheeler et al summarizes the human studies with NSAIDs in fracture healing in Table 2 on the second page.  Below are some of the highlights from the literature: 

Burd et al Retrospective, increased incidence of non-union in NSAID group (26% vs 7%, p = 0.004) and those with worse fractures.
  • Note: The patients in this study received indomethacin 25 mg TID x 6 weeks, which is not consistent with our acute pain dosing (they were looking at inhibiting heterotopic bone formation).
Bhattacharyya et al  Retrospective database review, looking at patients who filled prescriptions for an NSAID in the 90 days after humeral shaft fracture.  The study only showed a significant difference in non-union in patients exposed to NSAIDS between 61-90 days (RR 3.9, 95%CI 2.0–6.2)
  • Limitation: NSAID use was neither quantified nor specified by type.  Of note, this cohort of 9995 patients predominantly included older adults (mean age = 77)
Adolphson et al.  n=42, RCT with piroxicam in post-menopausal women with distal radius fractures with dorsal displacement (Colles), no delay in fracture healing.

Dodwell et al - meta-analysis, inconclusive.  The pooled odds ratio for nonunion was significantly higher in patients exposed to NSAIDs when the heterogeneous studies of variable quality were analyzed together (OR 3.0, 95% CI 1.6-5.6). The higher quality studies alone did not demonstrate an increased odds of non-union (OR 2.2, 95% CI 0.8-6.3).
  • Limitations: Case control and cohort studies only, long bone and spine surgeries pooled together, variable NSAID and dosing.
What I've taken away for my practice:
  • Ensure adequate immobilization of fractures to mitigate pain (5).
  • Provide analgesia to patients using my pain algorithm, which will continue include NSAIDs (such as ibuprofen 400 mg) or acetaminophen as needed for pain in patients with fracture. 
  • Consider the individual patient and factors that may put them at risk for impaired healing (high risk fracture, osteoporosis, smoking status, diabetes, etc).
  • Encourage patients to use the lowest effective dose of NSAIDs for the shortest period of time as the data suggests that higher doses of NSAIDs may be associated with delayed healing (4*,6).
  • Avoid aggravating colleagues and continuing dialogue on this evolving topic, when possible, by factoring in which orthopedist is on-call when prescribing NSAIDs. 
2.  Pountos I, et al.  Do Nonsteroidal Anti-Inflammatory Drugs Affect Bone Healing? A Critical Analysis. ScientificWorldJournal. 2012; 2012: 606404
3.  Kurmis et al. The effect of nonsteroidal anti-inflammatory drug administration on acute phase fracture-healing: a review. J Bone Joint Surg Am. 2012 May 2;94(9):815-23. doi: 10.2106/JBJS.J.01743. 
4.  Reuben SS.  High dose nonsteroidal anti-inflammatory drugs compromise spinal fusion. Can J Anaesth. 2005 May;52(5):506-12.  *note: this study is authored by an individual who had 21 other publications retracted due to falsified studies, so findings should be taken with a grain of salt.
5.  Menkes J.  Tintinalli's Emergency Medicine.  7th ed. New York: McGraw Hill Medical. 2011.  p.1789
6. Dodwell ER, et al.  NSAID exposure and risk of nonunion: a meta-analysis of case-control and cohort studies.
Calcif Tissue Int. 2010 Sep;87(3):193-202. 

Tackling The Most Commonly Abnormal ED "Vital Sign"

The Gist:  Pain is subjective and ubiquitous in the emergency department (ED).  Treatment of pain in the ED varies widely between practitioners and is often not formally taught as part of the curriculum, lending this aspect of EM to often be characterized as "art."  I came up with a rough pain control algorithm for acute pain or recurrent pain as I get started in Emergency Medicine, roughly based on an evidence based template from Lipp et al (note: I'm not an expert and this is far less useful for complex pain complaints such as migraine and does not address procedural sedation).
Check out this article by Dr. Leon Gussow of The Poison Review on the darker side of the emphasis of pain as a Joint Commission mandated vital sign in the ED.  

Regional Analgesia - It appears that, with the aid of ultrasound, nerve blocks are increasingly common in the ED. These are great for orthopedic and soft tissue injuries, and there seems to be a movement to increase utilization for hip fractures (Haslam et alHaines et al)
Upsides:   Patient may not need sedation or sedating analgesics, thereby preserving mentation, respiratory drive, and hemodynamics.  Great, targeted analgesia 
Downsides: Potentially time consuming, invasive, disrupts neuro exam, potential for systemic toxicity (use ultrasound!).  
    • Practice these on an anesthesia rotation. 
    • Use ultrasound:  Ultrasound Guided Nerve Block EducationPart IPart IIFemoral Nerve BlocksSonoguide.com.  Sonospot.com has many useful posts on publications and tipstricks for ultrasound guided nerve blocks (searchable).
    • Perform a solid neurovascular exam before performing the block.  Monitor patients afterward. 
    • Work with consultants (ex: ortho for blocks for femur and hip fractures).
Non-opioid Analgesics - Acetaminophen (APAP) and Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for mild to moderate pain (2).
Upsides:  NSAIDs are especially useful in prostaglandin-potentiated conditions, such as dysmenorrhea, gout, rheumatoid arthritis, and ureteral colic (1, 2).  APAP is safe in pregnancy (1,3).
    • Dose-limiting adverse effects on the gastrointestinal tract (NSAIDS). Must be cognisant of total APAP load across all medications so 4g/day is not exceeded  (1,2).
    • NSAIDS may have untoward effects in patients on other medications including: warfarin (bleeding), diuretics/lithium/ACE-I/methotrexate (renal insufficiency and subsequent therapeutic index issues) (1).
    • NSAIDS may induce or worsen renal insufficiency in elderly patients, those with pre-existing renal disease, or in the setting of dehydration (3).
    • Ceiling dose for analgesia from ibuprofen lies in a 400mg dose (higher ceiling dose for anti-inflammatory effect), discussed in this blog post by Dr. Chris Bond. 
    • Parenteral keterolac offers no better analgesia compared with ibuprofen or naproxen, and costs much more (Dr. Bond's postArora et al, 2, 4).
    • IV APAP, used internationally with success, has made an appearance in the US over the past couple of years, but comes at a cost of more than $10 USD per 1g dose without drastically better analgesia.  The focus on IV APAP is the potential opioid sparing effect (Kwiatkowski et al)
Opioid Analgesia - These get the most attention in the ED, partially due to the focus on abuse.  There are many drugs in this category but they tend to fall into groups:  
  • Opiates (derived from the opium plant) - morphine, codeine
  • Semi-synthetics - hydrocodone, oxycodone, hydromorphone, oxymorphone, buprenorphine, heroin 
  • Synthetics - fentanyl, alfentanil, sufentanil, remifentanil, methadone, tramadol, propoxyphene, meperidine
    • Good analgesia for visceral and somatic pain
    • Many opioids are titratable
    • Respiratory depression
    • Histamine release - pruritus, flushing, hives, and/or hypotension.
    • Released from mast cells, may be mistaken for allergic reaction (which has an immunologic component). 
      • Opiates tend to cause more histamine release than the semi-synthetics and synthetics (6).
    • Potential for abuse/dependence
    • IV morphine starting dose for moderate-to-severe pain = 0.1 - 0.15 mg/kg. 
      • Patients in severe pain or opioid-tolerant, will not obtain adequate analgesia with a single 0.1-mg/kg dose and may require additional doses.
    • Oral opioids (hydrocodone) may take 30-60 min to achieve analgesia (3). 
      • This may be off-set by time to establish an IV, etc (Miner et al)
    • Oxycodone starting dose 0.125 mg/kg (Miner et al) in most patient populations.
    • IV hydromorphone starting dose 1mg, with an additional 1mg dose if analgesia not achieved (5).
      • less renal clearance so may be better in patients with renal insufficiency (2,4)
      • less histamine release (6).
    • When discharging a patient home with opioids, consider checking the state monitoring program online (ACEP clinical policy, Level C).  This can be time consuming and is generally limited to a single state.  Listen to Dr. Scott Weingart's Practical Evidence podcast on this.
    • When prescribing, prescribe a short course (ex: 3 days).
    • It's widely accepted that analgesia doesn't "mask" surgical pathology, which was a historic concern in patients with suspected intra-abdominal pathology (1-4).
Poppies in Turkey
1.  Miner J, Paris P, Yealy D.  "Pain Management."  Rosen's Emergency Medicine.  7th ed. p 2410-2428.  
2.  Lipp C, Dhaliwal R, Lang E.  Analgesia in the emergency department: a GRADE-based evaluation of research evidence and recommendations for practice.  Critical Care 2013, 17:212 
3.  Ducharme, J.  "Acute Pain Management in Adults."  Tintinalli's Emergency Medicine.  7th ed.  p 259-265.
4.  Heins, Alan. Focus On: Effective Acute Pain Management.  October 2005.  ACEP. 

#InternLife – Setting Up an RSS Feed Aggregator

The Gist:  RSS feed aggregators act as a one-stop shop and bring information from blogs, websites, etc to you.  Setting one up is easy and most have free applications that allow seamless interfacing between web browsers, tablets, and smart phones...check out the video below for how I do it.

  • Yes, I realize the irony of posting this on a blog and is not useful for most folks, but I wanted a single link to refer people to when there's a paucity of time to help people set things up.

Getting Started:

1.  Pick an RSS Aggregator (Feedly, Flipboard, etc)
2.  Add content.  The steps will be essentially the same as above.  Here are some of my favorite blogs to follow. You can also get articles from journals as they are published (or before, by following the articles in press feeds).  Here's how I approach that (note: uses GoogleReader but steps are the same in Feedly).
3.  Read.


  • Start slowly and steadily, as it's easy to get overwhelmed by information overload (see Dr. Chris Nickson's talk on FOAM overload).  For example, I often start people out with 3-4 blogs.
  • You can add journals (anything from Annals of EM to Journal of Medical Toxicology) and videos, too!  Examples include Amal Mattu's EKG videos, EM in 5 (core EM distilled into digestible 5 minute chunks), and HQMEDED (an assortment of excellent EM cases and talks, most of which are brief)

LOC – How Much Does It Matter in Neuroimaging Decision-making?

The Gist:  Loss of consciousness (LOC) in mild traumatic brain injury (mTBI) in adults isn't easily established as we think but often marks a decision point for imaging.  Use the patient's clinical status and risk factors to determine the need for neuroimaging and follow up in cases of mTBI.  Dr. Chad Kessler has a great free open access (FOAMtalk on the subject.

The Cases:  Initially, as a medical student confronted with a patient with mild head injuries in the emergency department, I spent a good portion of the history attempting to establish the presence and exact duration of loss of consciousness and post-traumatic amnesia.  A few attendings harped on this point early on in my training, thus I felt it was crucial to establish with accuracy.  Take, for example, the following cases of GCS 15, neurologically intact patients with normal vital signs and otherwise asymptomatic. Which one needs a head CT?
  • 16 year old volleyball player fell at practice, certain she was out for "minutes."  Pain free, doing homework in exam room.
  • 20 year old restrained driver in an MVC with a tree, unable recall the accident or the few minutes following the accident. Abrasions on legs, no vomiting.
  • 68 year old restrained driver on ASA 81 mg daily with facial trauma requiring sutures on the forehead, denies LOC, recalls entire accident, conversant.
  • 3 year old fell from the sofa unwitnessed, hit her head with epistaxis that stopped spontaneously at home, and was "possibly" out for a moment before the baby sitter ran into the room
Major decisions in these mild head injury patients:
  • Who needs a CT scan to identify clinically important injuries?
    • Or, in Europe or the future in the US, we may need to ask who needs an increasingly popular sensitive but poorly specific S100-B biomarker (Study: Zongo et al, Responses: Graham et al, Taira et al)
  • Who is at risk for deterioration? 
  • Who can be sent home after a normal CT scan?  Who needs intervention?  What follow up/precautions are advised?
Why do we care about LOC/retrograde amnesia when we work up these patients?
  • It's scary to the patient and family/bystanders.  It can be important for building rapport and shared decision making to recognize that the experience of LOC/post-traumatic amnesia can be frightening.
  • Witnessed LOC or retrograde amnesia over 30 minutes before the trauma marks an entry point into clinical decision aids such as the Canadian CT Head Rule and New Orleans Criteria.  Here is my post on a comparison between the two decision aids.  
  • LOC also serves as a high risk criterion in PECARN (for pediatric patients).
  • Questionable indicator of severity of injury.  
    • Longer durations of LOC (> 5 minutes) associated with higher likelihood of significant injuries.  These are, perhaps, more likely to be witnessed or documented.
    • Some cite a study by Owings et al to demonstrate the preponderance of badness associated with patients with only a transient LOC; however, this study selected for really sick patient   (Inclusion criteria in one phase was admission to OR or ICU).
How do we determine LOC after mTBI?
  • Self-reporting is unreliable.  
    • Mayou et al conducted a study in which patients with blunt head trauma in a motor vehicle accident were asked whether they definitely had LOC, definitely did not have LOC, or were uncertain.  
      • n=124 patients reported definite LOC.  15% of those definitely had LOC and 23% (n=29) probably had LOC.  
      • Essentially, 2/3 of patient's reporting LOC did not actually have LOC.  
    • Confounders:  alcohol, drugs, PTSD, pain, perception of time, pediatric patients.
      • Pediatric patients may not be able to communicate or identify LOC.
    • For neuroimaging purposes, the data suggest that we probably don't need to split hairs over whether someone had LOC for a few seconds or a minute.  Estimates of time are likely inaccurate - was it many minutes or just 1-2?
  • Talk to paramedics, bystanders, parents, etc to better establish whether LOC occurred. 
How much does LOC matter for the things we care about?
  • 15% of mild TBI patients have intracranial pathology (Jagoda et al).
  • 0.5-1% have clinically significant injuries requiring neurosurgical intervention (Jagoda et al).
  • Do not have to have LOC to have mild TBI or significant cognitive dysfunction.
    • Normal neuroimaging may be falsely reassuring to a patient with mTBI.
    • Good follow up, precautions, and discharge instructions should still be given to these patients (CDC recommendations)
  • LOC alone is not predictive of need for neurosurgical intervention.  Smits et al noted that LOC/PTA plus other risk factors were associated with more significant injuries (note: this cohort was a little higher risk than some other mTBI studies, including patients with GCS 13-14 or high risk criteria + GCS 15).
What do we do in practice?
  • Wide variation between emergency physicians with regard to ordering head CTs in the context of head trauma (Stiell et alPrevodello et al).  
    • The figure below demonstrates variations between providers in one academic ED in ordering a head CT in patients with head trauma (Limitation: may be confounded by variable injury severity level.
Prevedello LM, Raja AS, Zane RD, et al.Variation in use of head computed tomography by emergency physicians.  Am J Med. 2012 Apr;125(4):356-64. 
    • Lowest ordering rates not necessarily associated with greater pathology or "misses" requiring further neurosurgical intervention (Stiell et al).
  • Probably don't use clinical decision aids like the CCHR properly.  Reductions in CT scanning in these populations have not panned out as expected, likely secondary to gaps in knowledge translation (Morton et al, Curran et al)
What can we do?  
  • Educate ourselves with excellent free, open access resources (FOAM): Life in the Fast Lane has a great review of Mild TBI workup and disposition and EBMedicine - evidence based review.  
  • Know how to use decision aids properly and use one that suits one's community and risk tolerance as providers: PECARN, CCHR, NOC
  • Engage in shared decision making with patients.  In patients who don't need neuroimaging, discuss the limitations of scans with regard to concussions and emphasize measures they can take (follow up, precautions, rest, etc).
  • ACEP's clinical policy can also serve as a guide: Order a non-contrast head CT if the patient looks like they have badness or at high risk (following clinical features - Level A if they also have LOC, Level B without LOC):
    • Focal neurologic deficit
    • GCS <15
    • Coagulopathy/on anticoagulants
    • Vomiting
    • Headache (Severe Headache without LOC)
    • >60-65 years old 
Or, if the patient has LOC/PTA AND: 
    • Drug or alcohol intoxication
    • Deficits in short-term memory
    • Physical evidence of trauma above the clavicle
    • Post-traumatic seizure
    • Physical signs of a basilar skull fracture
    • Dangerous mechanism of injury: ejection from a motor vehicle, a pedestrian struck, or fall from a height of greater than 3 feet or five stairs
Case Resolution:  The 68 year old and 20 year old received CT scans although family members in the other cases wanted scans.  The 20 year old didn't meet NOC or CCHR criteria and the scan was negative.  The 68 year old patient without LOC had a subdural hemorrhage on CT which was expansile and required neurosurgical drainage within a few hours.

The FOAM Forecast – Better Than The Weather Guy/Gal

The Gist:  Old news in the Free Open Access Medical Education (FOAM) world often predates alterations in guidelines and bedside practice.  Thus, while we may regurgitate things solely for test taking purposes or to sate the local practice patterns, it may behoove us to acquaint ourselves with changing schools of thoughts prior to these changes trickling down in standard ways.  FOAM can serve as a means of preconditioning one's way of thinking and actions to mitigate the knowledge translation window.

The example: I recently completed my second iteration of ACLS testing with the 2010 guidelines and I encountered the following:
LBBB is a STEMI equivalent?  I was told this by an attending as a third year medical student but, through Twitter, I recalled recently noting that the 2013 AHA Guidelines state that new or presumed new LBBB, in isolation, is not an indication for a patient to proceed directly to PCI or thrombolysis (I.e. no other concerning features on ECG or sick patient status).   As I marked up my algorithm, wandering whether this distinction had clinically relevance, I recalled the following case from nearly a year prior...

The Case:  A 48 year old obese male presented to the Janus General ED with some new chest pain and mild dyspnea at 0300.  His vital signs were within normal limits and he appeared uncomfortable and anxious but in no distress.  A 12-lead ECG demonstrated a LBBB that failed to meet any of the Sgarbossa criteria.  My supervising physician instructed me to page the cardiology fellow to see the patient and push for PCI after my database search failed to produce an old ECG to look for a prior LBBB.  The cardiology fellow came in and, after seeing the ECG and the patient, stated he would take him to PCI later, perhaps the following day.  The patient had no bump in troponin and ultimately left the hospital without a diagnosis of an MI.
  • Interestingly just one week prior, I watched this brief tutorial from Dr. Amal Mattu on LBBB and MI, one of several times I'd heard this same trope on podcasts.  I followed the directives and waited until after shift to check into LBBB and MI a little further, knowing I shouldn't blindly accept something I watched on the internet.
How FOAM forecasted the guidelines and provided updated education: 
  • 2011an EMCrit episode featured a discussion with Dr. Stephen Smith regarding reading STEMI on  ECGs with an LBBB, introducing the ST/S ratio 
    • A ratio of the amplitude of the ST segment to the S wave >-0.25 is suggestive of ischemia/STEMI and increases the sensitivity of the Sgarbossa criteria (full text article), awaiting further validation 
  • July 2012: Dr. Mattu foretold the changing guidelines in 20 minute video on LBBB and MI.
  • December 2012:  EMS 12-lead Blog educates EMS providers on the removal of LBBB as a STEMI equivalent in the 2013 AHA guidelines
  • June 2013: Dr. Mattu's ECG tutorial of the week re-emphasized the ability to read MI on an ECG with a LBBB.   
These created a reading list on LBBB and MI - reinforcing life-long learning skills of reading:
  • Kontos et al
    • n=401 patients with LBBB undergoing AMI rule out
    • No difference in incidence of MIs between chronic and new LBBB
    • Concordant ST changes (n=14) were the most important predictor of AMI (OR 17, 95% CI 3.4-81, P < .001
    Chang et al
    • Observational cohort of ED patients with ACS symptoms
    • No difference in the rate of AMI between the 3 groups: 
      • new or presumed new LBBB - 7.3% (RR 1.1; 95% CI, 0.47-2.84)
      • old LBBB - 5.2% (RR, 0.84; 95% CI, 0.41-1.69)
      • no LBBB -6.1% 
    Jain et al
    • Retrospective single-center analysis. N =36 patients with new/presumed new LBBB and ACS symptoms (~1-2% of AMI population in this system), 12 diagnosed with AMI
    • 30/36 underwent emergent cath
    • Sgarbossa criteria performed poorly in terms of sensitivity (Score of at least 5, sensitivity ~14%)
    Neeland et al - Excellent review of LBBBs.
How may this translate into clinical impact?  
  • Cath lab activation.  Garvey et al demonstrated that among 14 cath centers, 72% of cancellations were due to ECG reinterpretations.
    • Prehospital setting: As noted in the EMS 12-lead Blog, prehospital ECGs and providers can directly activate the cath lab.  Thus, the use of the modified Sgarbossa criteria and knowledge that a new LBBB alone does not necessarily qualify a patient for cath lab activation. 
    • ED: Improve the ways in which one can read an MI on a LBBB on an ECG (modified Sgarbossa with ST/S ratio)
  • Potentially spare patient unnecessary emergent revascularization. 
  • Ease communication with consultants.  Many cardiologists (such as the one in the above case) have stopped taking patients to PCI based solely on a new LBBB.  
  • So, it's not really about the LBBB, rather the diffusion of knowledge.  Training courses such as ACLS are updated every five years. Thus, if a provider takes a course towards the end of that five years, it may be a few years before they provider is updated.  It often takes even longer to unlearn practices, especially in non-teaching centers. Sites such as TheSGEM and RuralDoctors.net specifically target knowledge translation that may allow for more broad information sharing/collaboration and, perhaps, ultimately improved patient care.
Limitations - There's a fine balance in being an early adopter, a cautious practitioner, a diplomat, a pot stirrer, and a skilled test taker.  Preparing for shifts in thought/practice, "dogmalysis" (word credit to Dr. Cliff Reid) through digestible bits of FOAM, may at least induce greater discussion and consideration in order to achieve this balance.

House of God’s Law #3 (Revised)

At a cardiac arrest, the first procedure is to take your own pulse...and nobody else's once CPR is begun. 
(adapted from The House of God by Samuel Shem)

The Gist:  Worldwide resuscitation guidelines de-emphasize pulse checks using palpation due to poor sensitivity and increased no-flow time (1).  Yet, many in-hospital resuscitations still pause compressions for pulse checks, which is associated with poorer survival outcomes (2,3).  New* opportunities exist, taken within the context of the patient, to gauge return of spontaneous circulation (ROSC) including end-tidal CO2 (etCO2) and ultrasound that may lessen interruption in chest compressions.

The Case:  During one of my first official shifts in an ED as a medical student, I participated in a well executed code at Janus General.  Each individual had a clear role and my task was to feel for a pulse.  I kept my hand glued to the patient throughout the code, frightened that I might erroneously call something that was or wasn't actually present.  Eventually, after buckets of fluid, some epinephrine, and sodium bicarbonate (suspected DKA with profound hyperkalemia, which turned out to be the case),  I felt a bounding pulse in our patient and spoke up, still worried that it was the reverberation of my own heartbeat.

This case brought forth three questions, one of which was easily answered:
1.  What about the significance of the time off the chest?
  • I've seen a great deal of interruption in chest compressions throughout codes, mostly for transfers or provider switches, pulse checks, and defibrillation.  I began noticing these interruptions more frequently after I discovered that there's a 50% decrease in chance of ROSC for every 10 seconds of hands-off time (4).  I addressed defibrillation here, but pulse checks seem like a non-controversial, more intuitive, and easier means for intervention.
2.  Why aren't we following the guidelines?
3.  Was I crazy to be so worried that I would mis-judge the pulse? We're physicians, surely we can feel a pulse, right?

The FOAM (Free Open Access Medical Education):  On a recent Broome Docs podcast, Dr. Matt Dawson provided reassurance that my fear was not unprovoked.  He recounts a pediatric case in which the discrepancy between cardiac echo and palpation for pulse were not aligned and how that changed the resuscitation.

Do people really still stop for pulse checks?  Yes, and more than we think.
  • National guidelines and popular emphasis on uninterrupted CPR may be executed well in the FOAM world, simulation, and many centers; however, chest compressions are still interrupted more than we think. 
    •  A recent article by Souchtchenko et al in the Journal of Emergency Medicine articulates this point and provides some points for intervention.  
  • We often underestimate interruptions in chest compressions.  This is likely multifactorial, due to recall bias, overconfidence, and cognitive load.  It's easier to gauge CPR quality on the periphery of a code, where our minds have a lessened cognitive load.  Furthermore, it's difficult to accurately gauge elapsed time in such situations, particularly when even a 5 second pause has deleterious consequences on cerebral perfusion pressure (3).  Also, we're more likely to look kindly upon our own skills and actions when we are closer in proximity to the action.   
    • A study (n=40 resuscitations) by McInnis et al showed a 30% non-compliance with AHA guidelines regarding compressions and also demonstrated that providers often failed to recognize interruptions in chest compressions.  In a survey, the code leaders explained interruptions in compressions mostly as a result of pulse checks (37%) and defibrillation (24%).  
  • Knowledge translation likely plays a role in the discrepancy between what the guidelines recommend and what we practice.  Some community institutions may be more susceptible to slow uptake and implementation of new/changing practices.  Also, CPR is often one of those times in which rescuers run off of their ingrained algorithms, which can be difficult to change in the heat of practice.  
  • Equipment/Training.  We may very well know what we're supposed to do, but this may not translate into execution.  Capnography and ultrasound are not available in all resuscitation areas, despite what the FOAM world may have one believe.  
Pulse Palpation Literature: During cardiopulmonary resuscitation (CPR), pulse palpation lacks sensitivity and specificity and typically interrupt chest compressions thus, the guidelines advise against it (1).  According to some studies, only 55% of rescuers can identify a pulse within 60 seconds (6).  Furthermore, most equipment in the hospital allows for rhythm checks during compressions thereby obviating the need for that pause (during which some providers historically integrated a pulse check).  So, even if we're not pausing compressions solely for a pulse check, checking for a pulse may not be that helpful (except to occupy an eager medical student).

Tibballs et al 2010 (full text) was similar to a studies in adults by Dick et al and Eberle et al.
  • 209 health care professional "rescuers" were asked whether a pulse was palpable or not in a cohort of pediatric patients receiving forms of extracorporeal life support where some forms generated a palpable pulse while others did not.  Information regarding pressures and pulse forms was obscured
  • Pulse palpation: Correct determination 78% of the time.  Rescuer sensitivity 86%, specificity 64%.  Often took up to 30 seconds.
  • Limitations: pediatric population, gold standard, site of pulse check, on ECLS (supposedly blinded)
What now?: Ultrasound and capnography (ETCO2) offer ways to predict ROSC with limited to no interruption of chest compressions.  Dr. Reuben Strayer has a detailed cardiac arrest vector demonstrating resuscitation flow with no pulse checks and an Academic Life in Emergency Medicine post offers insight into achieving successful cardiac arrest outcomes.

Ultrasound: This is well-covered by FOAM sources, especially after an article by Blyth et al.  Highlights include the following posts: BestBets (see for landmark articles), EM Lit of Note, ScanCrit.
If you're an EMRAP subscriber, check out the Jan 2013 discussion.
  • Lack of cardiac activity on point of care limited echo is associated with poor likelihood of ROSC with a pooled negative LR of 0.18 (95% CI = 0.10 to 0.31), and a positive likelihood ratio of 4.26 (95% CI = 2.63 to 6.92).
  • Use the echo in the context of the individual patient/resuscitation. Experts such as Dr. Matthew Dawson suggest that echo be used in two situations: 
    • (1) Rule out reversible causes such as tamponade or massive PE.  
    • (2) After rounds of CPR as an excuse to cease CPR when resuscitation seems futile (3).
  • Limitations:  typically involves interruption in chest compressions, very rare occasions exist when a patient may not have cardiac activity on ultrasound and go on to walk out of the hospital.
  • On the horizon? Transesophageal echo during CPR, which limits interruptions but takes far more skill (Blaivas et al).  
Capnography.  There are excellent posts by St. Emyln's, ScanCrit, and a short PK talk by Jon Schonert of EMChatter on this topic so I won't rehash these.
  • Given consistent ventilation, the partial pressure etCO2 (PetCO2) correlates well with cardiac output during CPR.  During CPR, the carbon dioxide in the lungs is primary delivered by cardiac output.  
    • A rise in PetCO2 to ~35-40 mmHg or a sudden rise of 10mmHg over baseline during CPR has found to predict ROSC (Pokorna et al).  
    • Similarly, PetCO2 levels <10mmHg have been associated with unlikely ROSC or need to improve CPR quality. 
  • There are limitations to PetCO2 in the context of CPR.  
    • Cause of cardiac arrest may alter the PetCO2.  A respiratory cause may increase PetCO2 whereas large pulmonary embolism may cause very low PetCO2 although this is not currently an acceptable diagnostic modality by itself (see this meta-analysis).
    • Administration of sodium bicarbonate may increase PetCO2.
*Use of "new" is relative, as literature such as Salen et al is over a decade old.
1.  Berg RA, Hemphill  R, Abella  B, et al.  2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. Circulation. 2010; 122: S685-S705.
2. Cunningham LM, Mattu A, O'Connor RE, Brady WJ.  Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions in cardiac arrest resuscitation.  Am J Emerg Med. 2012 Oct;30(8):1630-8. 
3.  Mattu A, Bond M, Tewelde S, Brady W.  The Cardiac Literature 2010.  Am J Emerg Med.  2012 May;30(4):615-25.  (full text)
4.  Eftestøl T, Sunde K, Steen PA.  Effects of Interrupting Precordial Compressions on the Calculated Probability of Defibrillation Success During Out-of-Hospital Cardiac ArrestCirculation.2002; 105: 2270-2273
5.  Dawson, M.  Comments on Notes from the Community: Cardiac Ultrasound. .Jan 24, 2013.  Available at http://www.emrap.org/episode/2013/january/notesfromthe Accessed June 13, 2013. 
6.Dick WF, Eberle B, Wisser G, Schneider T. The carotid pulse check revisited: what if there is no pulse?Crit Care Med. 2000 Nov;28(11 Suppl):N183-5