Interesting descriptive study of a decade’s worth of children transferred/admitted to Texas Children’s in Houston with intra-orbital or intra-cranial extension of their sinusitis. It’s really just a summary of the clinical and hospital courses of 118 patients identified through retrospective chart review.
– Of these patients, 40% had been prescribed outpatient courses of antibiotics prior to the time of diagnosis of intra-cranial or intra-orbital extension.
– All patients with intra-orbital involvement presented with eye swelling.
– Intra-cranial extension had substantially (and significantly) more headache and vomiting, and only 67% received antibiotics prior to transfer.
– Identical numbers in each group – 16% – of patients were afebrile upon presentation.
– 33% of patients with intracranial extension of sinusitis did not complain of a URI-like syndrome at presentation.
– Frontal sinus involvement was associated with 84% of their intra-cranial extension.
– All organisms recovered were sensitive to clindamycin or vancomycin plus cefotaxime except for a single pseudomonal infection.
– There were no deaths, and four patients had persistent neurologic or visual sequelae.
Short summary – orbital cellulitis was a little more straightforward in diagnosis than intracranial extension of sinusitis, and a significant minority of both groups would definitely diagnostic challenges. CT imaging, anathema as it may be, is the diagnostic modality of choice.
Not as helpful an article as I hoped when I pulled it to peruse. Part of the issue is the surveys are administered to psychiatry and emergency department residents regarding their evaluation of the patient, so you’re almost certain to have a lot more variability – not just in assessment, but in level of understanding of language and the process of acute psychiatric assessment.
Where I’m not surprised we have a low kappa with our psych colleagues are areas like mood disorders – as emergency physicians are looking more at threat to themselves, threat to others, acute psychosis, and other factors affecting their global level of function to determine whether they are safe for discharge. What’s interesting are the 2×2 tables regarding things like suicidality, where psychiatry is eliciting suicidality in a significant number of individuals where that was not reported by the emergency physician. Out in community practice where psychiatry is not always readily available, the discharge of psychiatry patients is a high-risk endeavor – and I would have expected the emergency physician to be more attuned to suicide risk and document a lot more concern for suicidality that was deemed not an issue for the consulting team.
Mostly just an article to read out of passing curiosity that won’t impact your practice.
I don’t know if I’m the only one who gets depressed by these sorts of articles. You have the progression through medical school and residency, you finally start feeling up-to-date on current treatment, your Grand Rounds invited speakers present results from some trials, and you think you’re fully armed to provide the best care modern medicine can provide.
And, then you discover that it’s all a stack of cards predicated on results influenced by pharmaceutical funding.
This article is from JAMA, again, very important topic given studies performed with pharmaceutical funding have a fourfold greater chance of reporting positive results. They looked at meta-analysis, one of the techniques we try to use to increase statistical power in our reading of the literature. They discovered that nearly no meta-analyses included comment on whether the included studies were funded by pharmaceutical literature – even though 60% of the studies reported funding sources, and 70% of those studies reported receiving funding from the pharmaceutical industry – and the same sort of dismal reporting for author conflicts of interest. What it means – it’s another cautionary tale regarding how pervasive the masking of conflicts of interest really is, and how easily it creeps into the medical literature without our knowledge.
This falls into the “don’t use etomidate” pile of literature. Well-demonstrated, primarily in the pediatric literature, that etomidate and its association with adrenal insufficiency results in poorer outcomes in shock. This article doesn’t look at etomidate, but rather it describes relative or absolute adrenal insufficiency in pediatric shock, and finds it relatively pervasive. It then finds an association between their two definitions of adrenal insufficiency and length of stay, length of ventilator days, and required doses of vasopressors. They only 5% mortality in their study, so they can’t comment on any mortality association.
So, this is another study that helps describe why etomidate may be contributing to poorer outcomes. The days of ketamine + rocuronium RSI are coming (we’ll save the succinylcholine vs rocuronium debate for another day).
There are nice studies in the U.S. defining and validating a rule that determines which patients are unlikely to have ROSC or survival to hospital discharge, e.g. BLS-TOR. This is a study from France that looks at people who do have ROSC to see, not just if they’ll survive, but survival where the patient is not severely disabled or vegetative. One of the nice things about Europe is that their cultural perception of “life” really has to do more with living, and not just simply “being alive”. So, whether we can actually implement something like this in the U.S. may be difficult.
It’s a chart review, which limits its quality to some extent. The other real issue I have with this OHCA score is its complexity – it incorporates initial rhythm, no-flow and low-flow intervals, and admission levels of creatinine and lactate. The U.S. validation cohort had 34% therapeutic hypothermia, which is pretty good – the derivation cohort was only at 11%. Predictors of good neurologic outcome, consistent with other articles: ventricular fibrillation, bystander CPR, lower creatinine and lactate.
Unfortunately, for this rule to get up to 100% specificity, the sensitivity drops to 19%. Alternatively, you could say that’s 20% of out-of-hospital arrest ROSC that shouldn’t have further intervention, which would be an important cost and medical resource utilization savings.
So, this is something that your colleagues in critical care are going to use to discuss prognosis, although I’d like to see something along these lines that helps attenuate the number of people we resuscitate until our post-resuscitation care demonstrates much, much improved outcomes.
From the critical care literature, looking at whether the ICU admission represents a “teachable moment” for counseling against health-endangering behaviors. It’s a review article asking the question whether interventions at the time of admission to an ICU – i.e., a close brush with death – are effective.
This is relevant to the Emergency Department for those situations where you want to shake your patients and tell them “you did this to yourself, you fool!”
They look at the literature for nicotine cessation and for alcohol cessation. The nicotine cessation literature is rather bleak. They break down the interventions to <15 minutes vs. >15 minutes, and then whether contact after hospital discharge is helpful. Pretty much, unless you have a mechanism for prolonged after-discharge contact and counseling, you won’t get any meaningful results.
As far as alcohol goes – there are good studies that support questionnaires, lab work, or scoring systems to identify individuals at risk for alcohol-related injuries or illness. However, all the studies in their review show regardless of behavioral intervention, no decrease in alcohol consumption at discharge is seen.
So, sadly, almost assuredly, the ED, with the minimal time and follow-up available to us, is unlikely to be a place where impactful counseling is feasible.
Ultrasound guidance and visualization of anatomy and/or the needle tip during jugular venous cannulation is, essentially, the standard of care given the frequency of complications using anatomic landmarks alone – not to mention the “growing” U.S. population that has outgrown their landmarks. It’s also the standard of care because residents finishing their training right now have never done an IJ without the ultrasound.
So, what do we do when we don’t have ultrasound? Then you’re left with the decision to do subclavian or femoral.
Well, ultrasound-guided subclavians are well-described in the literature, and this is an article from our critical care colleagues with 400 subclavian access attempts – half with landmarks and half with ultrasound. Fewer complications, fewer attempts, less time to access. Hard to argue with that. If you aren’t getting familiar with ultrasound, I would start thinking about ways to become more comfortable.
Doom and gloom from the Netherlands regarding antibiotic resistance in E. coli. Although they focus on the resistance rates to fluoroquinolones, the more interesting take-home point from this article is the risk factors described for polypharmacy resistance.
Depending on your local resistance patterns, 88% susceptibility to E. coli for fluoroquinolones either sounds great or it sounds terrible. What’s interesting is that the strains of E. coli in this study that had fluoroquinolone resistance also had 33% resistance to amoxicillin-clavulanate, 65% resistance to TMP-SMX, and 14% had an ESBL gene. So, you can really extend their findings to more a listing of predictive factors for resistance to multiple antibiotics. In there study, the main univariate risk factors were indwelling catheter (OR 6.0) and prior fluoroquinolone use within six months (OR 18.6). Less prominent, but still statistically significant were underlying urinary tract disorder (OR 2.3), recurrent UTI (OR 2.2), or recent hospitalization (OR 2.3).
Their conclusion that the presence of any of these risk factors should result in a urine culture being sent, which is reasonable – although even in the absence of risk factors, there was still an 8.2% chance of fluoroquinolone resistance.
Last day of Journal Club for April.
It is very interesting how generational medical practice is – currently training physicians are accustomed to using norepinephrine for virtually everything as the vasopressor of choice (except, well, when there’s a medication shortage like this past month), while previous generations have a comfort zone with dopamine.
This is a very nice study in a lot of ways and it does a good job if illustrating that dopamine and norepinephrine have very small but relevant clinical effects. Some of their inclusion criteria are a little odd – hypoperfusion/decreased CVP after only 1000mL of crystalloid or 500mL of colloid? And 246 of their patients suffered from hypovolemia due to acute hemorrhage – so you can really question why anyone was reaching for a pressor instead of a Cordis or the OR – and, there are a few other instances with small numbers where neither dopamine or norepinephrine is your vasopressor of choice (e.g., anaphylactoid shock, spinal shock).
But, they had good randomization and their treatment groups are very similar. And what did they find? No difference.
Well, not completely true – no difference in ICU mortality with a p = 0.07 in favor of norepinephrine and no difference in in-hospital mortality with a p = 0.24 favoring norepinephrine. So, norepinephrine is favored, but statistically the results are not bulletproof. I think the trends are reasonable, but it’s certainly worth keeping an open mind. Alternatively, if you wanted to never use dopamine again, you can definitely argue that norepinephrine is no worse.
Secondary outcomes generally trend in favor for norepinephrine with a few reaching significance – although, when you look at 20 secondary outcomes, you’re bound to find some significant differences. The most important difference is the incidence or arrhythmias, primarily atrial fibrillation, which occurred in 24% of the dopamine group and 12.4% of the norepinephrine group at a p = <0.001.
It’s an important paper to have around to be on the same page as the critical care colleagues.
Dredged up for Journal Club from The Year 2000 (that was the future, once).
You might scoff at this article because it enrolls a grand total of 25 participants with acute urticaria, ten of which receive diphenhydramine and fifteen receive famotidine. You might be more impressed to know that this is pretty reflective of the evidence we have regarding H2-blockers in the treatment of urticaria. Another study from 1993 compares diphenhydramine, famotidine, and cromolyn sodium – and only enrolls 20!
It is mildly amusing to see them report there is no significant difference between the groups when they don’t have the power to detect any. Regardless, our H2 blockers provide some relief, it’s likely additive, and they’re inexpensive and safe.
The “definitive” study at present supporting our H1 + H2 blocker for acute urticaria or allergic reaction in the emergency department enrolls 91, and it shows diphenhydramine + cimetidine is superior to diphenhydramine alone.