Author: Ryan Radecki

EMS Blood Pressures Aren’t Unreliable

Ever since a trauma patient billed as normotensive with stable vital signs rolled off the elevator with CPR in progress having “just lost pulses”, I’ve been somewhat skeptical of my prehospital report, including vital signs.  This study, at least, supports a position that, barring untruthfulness, EMS providers vital signs are usually not clinically significantly different than vital signs obtained on arrival to the Emergency Department – even if observed techniques for EMS providers weren’t perfect.

The first phase study looked at 100 patients arriving in the Emergency Department.  BP measurements were obtained within 5 minutes of arrival, and compared to the reported measurement from EMS.  There was approximately a 17mmHg +/- spread to the systolic pressures measured by EMS compared to the first BP in the Emergency Department.

The second phase of the study had observers riding with EMS and documenting the technique at which they used to find vital signs – and then having the research assistants performing the same measurement in the field as well.    In this phase, EMS providers systolic pressure was only a 10.1mmgHg +/- spread away from the research assistant – despite having ideal technique deficiencies and a terminal digit preference for numbers ending in zero.

The article concludes that EMS providers measurements had poor agreement with subsequent measurements, and that the differences were clinically significant.  However, based on the distribution of error in their Bland-Altman plots, I disagree that assessment, as most of the variability occurred throughout a range of inconsequential systolic pressures between 120 and 170.  They unfortunately had very few patients with clinically important hypo- or hypertension, so the question really remains unanswered whether EMS measurements at the clinically important extremes are reliable.

I do find it rather entertaining that their methods included a “specially trained research assistant” to measure blood pressure, referred to in the title as an “expert”.  You can be an “expert” in anything nowadays, apparently.

“Agreement between emergency medical services and expert blood pressure measurements.”
www.ncbi.nlm.nih.gov/pubmed/21982624

A Third of TPA Patients Do Not Have Stroke

…but they almost all do well!  Only 5.1% of patients without stroke who receive TPA end up with intracerebral hemorrhage – so it’s OK that we give TPA to a ton of patients without a confirmed diagnosis of stroke, right?

This is a retrospective Finnish registry study of 1,104 consecutive TPA patients enrolled in a prospective cohort.  Of these, 119 had basilar artery occlusion, which is angiographically proven prior to treatment, and are excluded from their analysis, and a couple others were excluded for other reasons.  This left 985 patients who were initially diagnosed with ischemic stroke, and, eventually, 14 of those patients were diagnosed as a stroke mimic such as migrane, epilepsy, or a demyelinating disorder.  The authors then go on to say that stroke mimics such as these accounted for a mere 1.4% of all TPA patients, and none of them had ICH.

But, this isn’t exactly a true reading of their data.  The authors also state that 275 of their patients had “neuroimaging negative ischemic stroke”, which is to say, their follow-up MRI detected no sign of infarct.  Now, there is a false-negative rate on DWI MRI for stroke, but it’s in the range of 5% for acute infarcts, and generally involves small lacunar, small cortical, and some posterior circulation strokes.  Not only that, it’s reasonable to suggest that around 40% of TIAs actually have DWI or FLAIR sequence abnormalities as well.

So, some of their “neuroimaging negative ischemic stroke” group probably does have ischemic stroke with false negative MRI – but not 30% of the study population.  And, some of their neuroimaging positive group is likely false positive from TIA as well.  These numbers for stroke mimics are also far below other reported case series, which have estimated 10-30% incidence, depending on whether TIAs are included.

I absolutely cannot fathom this line of reasoning and distortion Neurology is developing in justify recklessly pushing TPA onto a larger population.

“Stroke Mimics and Intravenous Thrombolysis”
http://www.ncbi.nlm.nih.gov/pubmed/22000770

Preventing Mechanical Ventilation in Newborns

This is lovely article regarding the treatment of respiratory distress in newborns.  It is not a new concept to use surfactant in clinically indicated situations to improve ventilation in the newborn in distress – however, the typical treatment involves endotracheal intubation and mechanical ventilation prior to application.  This is a randomized, controlled trial of surfactant administration prior to mechanical ventilation.

This involves 220 preterm infants in Germany who were selected for the trial, essentially, if they were on CPAP requiring more than 30% inspired O2.  In the intervention group, patients received intratracheal surfactant if stable on CPAP and 30% O2.  Outcome measures were the portion of patients mechanically ventilated at any time or at day 2 or 3 after birth.  Minimal differences between groups, although the control group was a few grams lighter at birth.

Overall, 33% of all intervention infants required mechanical intervention vs. 73% of the control group.

Simple takeaway – surfactant isn’t just useful after intubation, but may also prevent mechanical ventilation.

“Avoidance of mechanical ventilation by surfactant treatment of spontaneously breathing preterm infants (AMV): an open-label, randomised, controlled trial”
www.ncbi.nlm.nih.gov/pubmed/21963186

Ultrasound In Undifferentiated Infant Vomiting

Is there anything ultrasound can’t do?  Trauma, vascular access, undifferentiated abdominal pain – and another nice case report for vomiting in children.

These authors are using ultrasound in the projectile-vomiting infant looking at the pylorus, and, after finding a normal pylorus, they scan the rest of the abdomen.  Lo and behold, they identify intussusception.  I am not entirely certain I would be able to well-identify the pylorus, but I can definitely see potentially noting the intussusception.  The authors include several nice images as teaching points.

As the barriers to routine ultrasound use in the ER decrease, hopefully we will all become more facile with using it in many more clinical situations.

“Use of Emergency Ultrasound in the Diagnostic Evaluation of an Infant With Vomiting”
www.ncbi.nlm.nih.gov/pubmed/21975504

Hypertonic Saline In Cardiac Arrest

There is a physiologic phenomenon observed in animal studies that a small increase in plasma osmolarity using hypertonic saline increases microperfusion, including myocardial and cerebral blood flow.  Therefore, in theory, hypertonic saline administration during resuscitation from cardiac arrest should be efficacious in improving survival and neurologic outcome.

These authors conduct a randomized prospective trial in which they prove that 100 patients in each arm is not enough to make valid claims about a secondary endpoint for which the study was not designed to evaluate.  There is no difference between groups in mortality – and not even non-significant trends – but a small, significant, absolute difference in neurologic impairment, 4.9% without neurologic impairment in the control group and 13% in the intervention group.

So, another study suggesting further study is needed.  If anything, it demonstrates how impossibly hard it is to evaluate treatments in the heterogenous population of out-of-hospital cardiac arrest, and to ensure internal and external validity.

“Randomised study of hypertonic saline infusion during resuscitation from

out-of-hospital cardiac arrest.”

Stroke After-Care Is Far More Important

Somewhere in the rush to but up billboards and focus the medical establishment on experimental revascularization interventions for acute stroke (e.g., time is brain), we’ve overlooked what truly matters – follow-up care after the ischemic event.  This is a lovely study that reminds us of what we probably knew once, but have forgotten – that even in the absence of acute therapy, simple protocols to prevent fever, prevent hyperglycemia, and prevent aspiration pneumonia lead to profound differences in the number of patients with zero or minimal disability after stroke.

This is a prospective interventional study in which acute stroke units in New South Wales Australia were randomized to either no protocolized intervention, or an intervention with nursing protocols named above.  At the end of the three-year intervention period, 42% of the control group had mRS 0 or 1 at 90 days, and 58% of the intervention group had mRS 0 or 1 at 90 days.  There were small differences in the type of stroke, education level, and prior ability to work that probably favored the intervention group, but the differences at baseline were far smaller than the magnitude of the treatment effect.  In short, a basic nursing protocol intervention improved outcomes more than any other intervention for acute stroke.

“Implementation of evidence-based treatment protocols to manage fever, hyperglycemia, and swallowing dysfunction in acute stroke (QASC): a cluster randomised controlled trial.”
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)61485-2/fulltext

Yes, Let MONA Fade Away

These authors make a brief argument regarding the inappropriateness of the commonly taught acronym of “MONA” for the initial treatment of acute coronary syndrome.  It is probably the case that well-read Emergency Physicians have since moved on, but it bears repeating.

 – Morphine, which has been associated with worsened outcomes in CRUSADE, but the results are confounded by other factors.  Narcotics are still probably reasonable for nitrate-resistant pain.
 – Oxygen, in which hyperoxia is associated with coronary vasoconstriction, exacerbates reperfusion injury and infarct size.  It is currently recommended that oxygen only be used for patients who are hypoxic.
 – Nitrates, suitable for the relief of anginal symptoms in selected patients.
 – Aspirin, the only element of MONA proven to be strongly beneficial.

And, presumably, future trials will involve the use of newer anti-platelet and other agents in the inital treatment of ACS.

The market is ripe for a replacement acronym!

“Initial treatment of acute coronary syndromes.  Is there a future for MONA acronym after the 2010 guidelines?”
http://www.ncbi.nlm.nih.gov/pubmed/21982924

High-Sensitivity Troponin For Better Or Worse

The premise of this article seems fine – as we all learned in medical school, the LDH CK-MB Troponin is now our most sensitive and specific assay for myocardial injury, but, we were also taught that it takes a certain amount of time for the assay to turn positive.  Thus, the inpatient rule-out with multiple sets of cardiac enzymes.  These investigators looked a new assay, with a lower detection limit, and hope to prove that it has 100% sensitivity with a single measurement, obviating the need for additional enzymatic testing.
There were two phases – a cohort observational portion and a clinical deployment portion.  The observational phase was intended to verify prior data suggesting 99% sensitivity for the assay and, of their 703 patients, 195 had initial hs-cTnT levels of <3ng/L – and none had acute MI in their 6 month follow-up period (97.8 to 100% sensitivity).  In their clinical deployment phase, they collected 915 patients who received two sets of the hs-cTnT assay, and found that only one patient had a subsequent hs-cTnT rise after an initially undetectable hs-cTnT, giving a sensitivity of 99.8% (99.1-100).
So, they say, there is no longer any realistic need to get multiple sets of cardiac enzymes in a patient if the first level is undetectable.  This is probably true, but whether it reduces inpatient stays and follow-up invasive cardiac testing is another matter.  My guess is that widespread availability of this assay would lead to clinicians ordering troponins on patients they wouldn’t have previously ordered them on, and – perhaps you know how this story will probably play out – a story in which use of the d-Dimer assay would decrease chest imaging for pulmonary embolism, but didn’t.  Too many clinicians are applying it incorrectly and using its weak positive likelihood ratio to light up patients unnecessarily, and I expect this to lead to more patients being kept for testing, not fewer, as the authors propose.

“Rapid Exclusion of Acute Myocardial Infarction in Patients With Undetectable Troponin Using a High-Sensitivity Assay”
www.ncbi.nlm.nih.gov/pubmed/21920261

Popular Dehydration Scales Fare Poorly In 3rd-World Use

I like the author’s use of the word “popular” to describe pediatric clinical dehydration scales.  In case you’re not part of the “in crowd”, today’s “popular” dehydration scales include the World Health Organization scale, the Gorelick scale, and the Clinical Dehydration Scale.
This article is a prospective application of each of the three scales by a healthcare provider upon admission to one of three hospitals in Rwanda.  Children were weighed on admission and then on discharge, and the gain in weight was used as the gold standard for comparison to each standardized dehydration scale.
So, bad news:  each of these dehydration scoring scales is too complicated to hold in working memory, and you’d have to have it posted on a wall.
But, good news:  in the words of the authors, “The WHO scale, Gorelick scale, and CDS did not have an area on the ROC curve statistically different from the reference line.”
Which means, you get to save your wall space because the dehydration scales gave false negatives or false positives as frequently as they gave true negatives and true positives.  More research is necessary to derive more accurate clinical assessment of children presenting with possible dehydration.
“Comparing the accuracy of the 3 popular clinical dehydration scales in children with diarrhea.”

600mg Is Probably Your Best Clopidogrel Loading Dose

Most STEMI is the result of an acute thrombotic event, so, more thrombotic inhibition is better, right?  Italy, Hungary, Serbia and Belgium band together for ARMYDA-6 to test a randomized, prospective 600mg vs. 300mg clopidogrel loading dose prior to PCI in STEMI.
They didn’t look at mortality and only followed 30-day outcomes – probably because they didn’t have statistical power from only 201 patients to detect a difference – but their surrogate markers of infarct size, successful PCI, LVEF and 30-day “major cardiovascular events” all favored clopidogrel.  Unfortunately, almost every nonsignificant difference between the two clinical groups favored the 600mg group – younger, less diabetes, fewer prior MIs, higher LVEF at baseline, faster loading and cath lab times, less multivessel disease, more TIMI flow >1 pre-PCI.
That being said, it’s consistent with the prior ARMYDA-1 and CURRENT-OASIS studies, and even if this isn’t a fabulous study, it’s another but of evidence to consider.
“Outcome Comparison of 600- and 300-mg Loading Doses of Clopidogrel in Patients Undergoing Primary Percutaneous Coronary Intervention for ST-Segement Elevation Myocardial Infarction”