Month: August 2012

Mistakes Were Made

This is a fascinating series in Pediatric Emergency Care in which interesting cases from published medical malpractice verdicts are featured.  Each case – typically ending poorly – is followed by a short editorial on the underlying disease processes, with pearls regarding treatment, diagnosis, and the case outcome.  Reading these cases, hopefully, will not contribute to recency bias, and ideally serve simply as brief reminders of clinical features of the rare sick children lurking in the haystack of walking well.


Medicine – as much as or greater than any other profession – is a delicate mix of confidence, humility, and the recognition of the underlying biases in our cognition and practice.  Most of this blog focuses on practicing based on evidence, applying the rules and probabilities of populations as guides towards the diagnosis and treatment of individual patients.  Therefore, when reading these Legal Briefs, I simply want to reinforce the dangers of anecdote-based medicine.

“Pediatric Emergency Medicine:  Legal Briefs”

Here Comes Gonorrhea (Again)


Good news for the monogamous – bad news for the rest – Neiserria gonorrhoeae is rapidly becoming resistant to cefixime, an oral third-generation cephalosporin.  The resistance rates are low – a maximum of 17% in Honolulu – but the fear is that continued cefixime use will carry-over into an increased resistance for ceftriaxone.


This follows the 2007 declaration that fluoroquinolone resistance had obviated their use.


For now, the CDC recommendations have narrowed to 250mg IM/IV ceftriaxone plus 1g oral azithromycin once or 100mg oral doxycycline BID for seven days.

“Update to CDC’s Sexually Transmitted Diseases Treatment Guidelines, 2010: Oral Cephalosporins No Longer a Recommended Treatment for Gonococcal Infections”
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6131a3.htm?s_cid=mm6131a3_e

Ketamine – Cure For Everything

There aren’t many medications I love using more than ketamine.  I use it for adjunctive pain control, to control agitation, and for induction prior to intubation.  Now, chances are, it’s probably useful in seizures.


This is a case report and review of the literature for the use of ketamine in the control of refractory status epilepticus.  The literature is profoundly weak – the “review” is essentially a review of case reports.  And, the patient outcomes describe in the case reports are replete with “All died” or “Survived but severely disabled.”  However, this is primarily due to the serious cause of the underlying disorders – encephalitis, neurosyphilis, meningitis, anoxic brain injury – and less likely the ketamine, although this does not provide the evidence to that effect.  The proposed mechanism is via NMDA receptor antagonism, which the author proposes works better by synergy with GABA antagonism, rather than either as monotherapy.


Seems like a fair physiologic mechanism, and it’s nice to have something additional to consider in refractory disease.  Ketamine also was noted in this case report to counteract the hypotensive effects of midazolam and propofol, consistent with prior literature describing its beneficial effect on cerebral perfusion pressure.  It’s pretty much a “I tried this and I like it” article, but I think it’s probably likable and not the last we’ve heard about ketamine for status.


“Early Ketamine to Treat Refractory Status Epilepticus”

When Do Patients Need Blood Cultures?

Another lovely JAMA Rational Clinical Examination article relevant to the Emergency Department – this time regarding the utility of blood cultures.  Blood cultures are frequently requested for febrile inpatients, however, the incidence of false positive ranges between 2.5% and 8%.  This leads, unfortunately, to additional patient harms from additional treatment or observation.


This article is a systematic review of several studies gathering clinical features of patients for whom blood cultures were requested, as well as the clinical outcomes of the cultures, in an attempt to identify features predictive of positive or negative cultures.  They also examine a couple validated clinical decision instruments to determine their potential utility in stratifying the appropriateness of cultures.


Essentially, based on a few pieces of decent evidence and a few pieces of poor evidence, the authors determine a few general categories of infectious etiology with varying pretest probability for bacteremia.  These are:
 • Cellulitis, community-acquired pneumonia, community-acquired fever: low (<14%) probability
 • Pyelonephritis: mid (19-25%)
 • Severe sepsis, septic shock, bacterial meningitis: high (38-69%)


In general, however, no individual clinical feature had a positive or negative likelihood ratio of sufficient magnitude to guide testing.  Combinations of clinical features – such as patients with SIRS – were capable of excellent sensitivity & negative likelihood ratios, but only had specificities of 0.27 to 0.47.


However, the more important clinical aspect of blood cultures and bacteremia is not addressed in this article, which is how frequently the true positives even change clinical management.


“Does This Adult Patient With Suspected Bacteremia Require Blood Cultures?“

www.ncbi.nlm.nih.gov/pubmed/22851117

Vancouver Chest Pain Rule in Tehran

Iran and Canada would be considered by most to be very different places.  However, from a cardiovascular standpoint, it seems they’re not so disparate.


This is a prospective, validation study of the Vancouver Chest Pain Rule.  The Vancouver rule is one of many 2-hour accelerated rule-outs operating under the presumption that all disease can never be detected – sensitivity will never be 100%, but this assumes a context in which a discussion may be had with the patient about outpatient disposition.  Essentially, any patient under 40 years without a history of coronary artery disease and a normal EKG simply gets discharged.  Older than 40 and atypical chest pain is discharged either immediately after a CK-MB < 3.0 µg/L, or receives a 2-hour delta + repeat EKG if > 3.0 µg/L.  Essentially, the rule is designed only to ensure all unusual NSTEMIs are picked up.


In the initial study, the 30-day ACS rate for the discharged group was 1.2%.  In this Iranian study, the 30-day ACS rate of 292 very-low-risk patients is 1.3%.  Two of the four patients meeting criteria for discharge by CK-MB had positive troponins.  Considering CK-MB is nearly considered anachronistic now, most modern EDs would have not have discharged these patients based on troponin testing.  A third patient had EKG changes on the second EKG – which should fail the Vancouver rule, so I’m uncertain why it was included in their very-low-risk group.  Finally, the last patient had an entirely normal evaluation and a subsequent 70% lesion discovered on angiography a week later.  No mention of the hemodynamic significance/relation to ischemia of this lesion is noted.


A few hundred patients is hardly a definitive validation, but it’s a nice demonstration that 50% of their cohort could have been discharged in two hours – and with the same 30-day event rate as the poor people being made to glow in the CCTA studies.


“Validation of the Vancouver Chest Pain Rule: A Prospective Cohort Study”

Tramadol: A Myth of Safety

For me, tramadol lands squarely in the gap between oral analgesics I might use for “no pain” – ibuprofen, acetaminophen – and analgesics I might use for “real pain” – hydrocodone derivatives.  The literature describing the analgesic properties of tramadol is bizarre, with multiple comparisons with placebo, nerve blocks, adjunctive epidural anesthesia, etc., and very few head-to-head comparisons to the sorts of medications we routinely use.  When there are comparative efficacy reports, they typically conclude that tramadol is effective…just as effective as the NSAIDs its being compared with.

The theory I’ve heard people use when considering use of tramadol is that it has a better safety profile than hydrocodone and is less dependence-forming.  These claims may be true, but I do not believe they are true to the extent that it is clinically relevant.  Tramadol still generates an opioid withdrawal syndrome and, as this article describes, overdose/abuse still results in apnea with need for ventilatory support.

Additionally, tramadol is a GABA antagonist, lowering seizure threshold.  Of the 525 patients overdosing primarily on tramadol retrospectively identified at this Iranian hospital, 19 experienced apnea and 242 (46.1%) experienced seizures.  This is retrospective and co-ingestants cannot be fully ruled out, but the propensity for seizure is far more surprising than the incidence of apnea.

Tramadol has a role in pain control prescribing, but, in my practice, that role is tiny.

“Tramadol-induced apnea”
http://www.ncbi.nlm.nih.gov/pubmed/22809771