Monday, October 17, 2011

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."

Sunday, October 16, 2011

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

Friday, October 14, 2011

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

Thursday, October 13, 2011

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

Tuesday, October 11, 2011

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."

Monday, October 10, 2011

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"

Saturday, October 8, 2011

Not Long, But Short QT

Another rare channelopathy that I was not previously aware of, but that carries the same risks of sudden death as long-QT syndromes.

This is a longitudinal observational study of the European Short QT Registry - which has a grand total of 53 patients - who were followed for, on average, 5 years.  The diagnosis of short QT does not have a generally accepted definition, but typically means a QTc less than 340 or 360, and the other literature shows a high association with sudden death and QTc less than 340.  In their registry 23% had a HERG gain-of-function mutation identified, and there is also an autosomal dominant inheritance pattern identified.

Based on their follow-up for events, or for cardiac events recorded by implantable defibrillators, there was a 4.9% incidence of syncope, defibrillator shocks, or nonsustained polymorphic ventricular tachycardia.  Prophylactic treatment involves either the implantable defibrillator or daily hydroquinidine therapy to prolong QT.

Something new to look for on EKGs that you'll probably never see, but will seem really smart if you do.

"Long-term follow-up of patients with short QT syndrome"
www.ncbi.nlm.nih.gov/pubmed/21798421

Friday, October 7, 2011

Lack of IV Access, Harbinger of Death

Interesting observational study of 56,332 patients picked up in an EMS system in King County, looking at IV access and outcomes.

For reasons they don't look into in this study, they find that IV access is an independent predictor of decreased in-hospital mortality.  Not for the less-acute patients, but for patients of high-acuity, lack of IV access shows a pretty significant trend towards poor outcomes.  They don't look at fluid therapy, medication therapy, etc. as confounding variables - so we don't know what it is specifically about IV access that confers a survival advantage.

They do a brief breakdown of the systolic blood pressure and the percentage of patients receiving IV access, and, as expected, more IVs are attempted at the extremes.  This leads me to believe there are patients who were high acuity, required IV access, but had failed IV access attempts - but there's no data on that either.

This is a study that could end up telling us something, or nothing.  Interesting, nonetheless.

"Intravenous Access During Out-of-Hospital Emergency Care of Noninjured Patients: A Population-Based Outcome Study"
http://www.ncbi.nlm.nih.gov/pubmed/21872970

Wednesday, October 5, 2011

C-Collars Cannot Stabilize Unstable Injuries

This is another cautionary anatomic study that demonstrates cervical collars are not adequate immobilization devices - except in patients who already do not need them.

This is a cadaveric spinal immobilization study in which C5/C6 instability was induced, and the Ambu extrication collar, the Aspen collar, and no collar were evaluated for range of bending and rotation during a bed transfer simulation.

The results are pretty straightforward.  Before the instability was induced, patients had minimal neck movement, whether immobilized or not.  After instability was induced, the patients all had significant bending and rotation - nearly the same for the patients in the collars as in no collar at all.

This is consistent with the small amount of prior work done in actual unstable spines; most of the cervical collar data is in healthy volunteers.  The limitations of a cervical collar should be recognized, and patients should have their cervical spine evaluated and cleared or intervened on immediately.

"Cervical collars are insufficient for immobilizing an unstable cervical spine injury."
www.ncbi.nlm.nih.gov/pubmed/21397431

Tuesday, October 4, 2011

Linezolid Is Superior To Vancomycin For Pneumonia

This is consistent with prior studies and not particularly earthshaking, but if you needed more literature to support switching antibiotics in the case of treatment failure, this would be another one.

This is in pigs, and it's an animal model of MRSA ventilator-associated pneumonia.  Four groups - controls, twice-daily vancomycin, continuous vancomycin infusion, and linezolid.  Treatment was initiated after 12 hours of bacterial inoculation in ventilated pigs.  At the end of their 96 hour treatment period, 75% of controls, 11% of each vancomycin group, and 0% of linezolid pigs were BAL positive for MRSA by culture.  Likewise, pathologic sections also showed decrease inflammation and damage in the linezolid group.

Short story, linezolid is better - but not quite better enough that we can't still start with vancomycin and keep it in reserve.

Sponsored by Pfizer and Eli Lilly.

"Efficacy of linezolid compared to vancomycin in an experimental model of pneumonia induced by methicillin-resistant Staphylococcus aureus in ventilated pigs"
www.ncbi.nlm.nih.gov/pubmed/21926613

Sunday, October 2, 2011

N-acetylcysteine Overdose With Anaphylactoid Reaction and Myocardial Infarction

This is another toxicology case that illustrates a point I make (probably too often) to my residents - that every action we take has a risk of harm, whether known or unanticipated.  I'm probably the only attending who cancels their IM ketorolac orders and changes them to PO ibuprofen.  Why?  Because of cases like this.

This is an entirely appropriate therapy - N-acetylcysteine given for hydrocodone-acetaminophen overdose - gone wrong because of a mixing error resulting in 10-fold overdose (126,000mg loading dose!).  Anaphylactoid reactions are known side effects in N-acetylcysteine, and, unfortunately, this patient's reaction was more severe than most, suffering an inferior MI with a peak troponin of 658ng/mL.  He expired 17 hour after the N-acetylcysteine overdose.

I've seen epinephrine given IV instead of SQ more than once (one time resulting in an MI), many medications are tissue toxic if they extravasate, you can get sterile abscess formation from intramuscular injections, etc.  The fewer interventions and the less invasive the interventions, the less risk at which we place our patients.

"Fatal myocardial infarction associated with intravenous N-acetylcysteine error"

Saturday, October 1, 2011

Ethanol Hand Sanitizer Abuse

I imagine every department has a frequent-flier patient like this - they keep getting referred to rehab, but they don't stop bouncing back.  And the hand cleanser keeps mysteriously running out.

This is case report and literature review of the National Poison Data System that documents the accidental and intentional exposures to ethanol-containing hand sanitizer.  And, really, their numbers probably underestimate the issue - considering the cases reported to poison control are primarily in children under age 6.  There are plenty of teenagers and other adults abusing these substances as well, but they are far less likely to be reported to a poison control center.

The case report is rather amusing - a teenager with a g-tube "looking for a buzz" who put 500mL of 61% ethanol hand sanitizer into the tube and subsequently required intubation and then dialysis when his first ethanol level was 720mg/dL.

"The rising incidence of intentional ingestion of ethanol-containing hand sanitizers"
www.ncbi.nlm.nih.gov/pubmed/21926580

Friday, September 30, 2011

Featured on ERCast

Was fortunate enough to be invited to appear on one of the premier Emergency Medicine podcasts - ERCast, by Dr. Rob Orman (@emergencypdx).

We had a lovely chat about two posts from August, clearance of C-spine by CT vs. MRI (link) and CT within 6 hours for the diagnosis of SAH (link).  The esteemed Dr. Scott Weingart of EMCrit also weighs in on the CT article.

He's been podcasting far longer than I've been writing, and he has a lot of fantastic content and has been featured on EM:RAP as well.  If you haven't discovered it yet, you're missing out.

Thursday, September 29, 2011

Back Pain, Harbinger of Death

In Perth, Western Australia, clearly back pain is a different sort of entity than back pain here in the United States.  This is a retrospective review of 22,000 back pain representing 1.9% of all visits over a five year period simply as an epidemiologic overview with descriptive statistics.

And, fascinating statistics they are.  Highlights:
 - 43.8% of patients were diagnosed with simple muscular back pain.
 - 17.1% of muscular back pain patients required admission to the hospital with a mean length-of-stay of 6.4 days, and one that was hospitalized for 163 days!
 - Patients at the extremes of age (< 15 years, > 75 years) were simple muscular back pain less than 40% of the time.
 - Of the medical diseases found in the non-muscular group, the top were renal colic, sciatica, UTI/pyelonephritis.
 - 24 myocardial infarctions, 53 pulmonary emboli, 17 aortic dissections, and 18 ruptured AAA were diagnosed in patients with a primary complaint of back pain.

How do 17.1% of simple muscular back pain patients get admitted to the hospital?  For six days?  It boggles the mind.

Finally - back pain at the harbinger of death - there was a 1.2% 30-day mortality rate in all patients presenting for any complaint of back pain, and 0.8% with non-specific or muscular back pain.  That's almost as lethal as our low-risk chest pain cohort here in the U.S.

Fascinating.

"Analysis of 22,655 presentations with back pain to Perth emergency departments over five years"
www.ncbi.nlm.nih.gov/pubmed/21923920

Wednesday, September 28, 2011

No Reversing The Harm of Etomidate

A small, but growing body of evidence is starting to correlate the physiologic adrenal suppression of etomidate with worsening clinical outcomes.  This study is a French prospective cohort that really likes etomidate for RSI, so, they decided to ask the question whether a continuous hydrocortisone infusion has any substantial effect on cardiovascular parameters in the setting of etomidate use.

Short answer, no.

Their randomized groups are awfully small - 45 patients in each group - so their power to detect a difference is not great.  But, at the minimum, there's no profoundly obvious difference or any seemingly clinically significant trend between the two groups.

I trained using etomidate for everyone, but I've almost completely moved to alternative agents, ketamine being the most prominent of those agents.  Most significantly, ketamine differs from the other agents in terms of having analgesic properties as well, and I think it is reasonable to provide some treatment for the pain associated with laryngoscopy.  There is evidence that ketamine is a myocardial depressant and may be deleterious in patients with limited cardiac reserve, but so far in limited literature it holds up clinically well against etomidate and midazolam.

"Corticosteroid after etomidate in critically ill patients: A randomized controlled trial"
http://www.ncbi.nlm.nih.gov/pubmed/21926601

"Intubating ICU patients with ketamine: adverse effects that can occur."
http://www.ncbi.nlm.nih.gov/pubmed/18079246

Monday, September 26, 2011

Blocking Frizzled Proteins Reduces Infarct Size

This is another window-to-the-future article that caught my eye because, really, I just wanted to see what a Frizzled signal was.

And, it turns out, it's mildly interesting.

My area of expertise is not cell signaling and infarct-related myocardial fibroblast migration/inhibition, so the first few pages of cell plating and luciferase expression measurement are not my cup of tea.  However, eventually, the authors get around to injecting UM206 into a mouse MI model and find significant reductions in infarct size, increased myofibroblasts, and, more importantly, increased ejection fraction/decreased mortality from heart failure.

Give it another five years, and maybe we'll be giving our ACS patients aspirin, clopidogrel, and a Frizzled-antagonist.

"Blocking of Frizzled Signaling With a Homologous Peptide Fragment of Wnt3a/Wnt5a Reduces Infarct Expansion and Prevents the Development of Heart Failure After Myocardial Infarction."
circ.ahajournals.org/content/.../CIRCULATIONAHA.110.976969.abstract

Sunday, September 25, 2011

MRI After Negative CT in Obtunded Trauma

In contrast to the recently reviewed study showing 5 surgical injuries in 174 patients complaining of neck pain after a negative CT c-spine, this study of MRI in obtunded trauma patients with a negative CT c-spine showed no surgical injuries.

Specifically, this is a retrospective review from U.C. Davis in which they looked at 512 patients who underwent both CT c-spine and MRI c-spine.  They found 150 patients who were confused/obtunded, had otherwise normal neurologic examination, and had a negative initial CT c-spine.  Half of these patients had an injury identified on their MRI, but none of them were unstable ligamentous injuries or structural abnormalities requiring surgical intervention.

This is more relevant to our trauma colleagues who need to mobilize people in the ICU to prevent other complications, and external validity is limited in a single-center study, but it's a mark on the side of keeping the standard of care at CT and not proceeding to MRI in an irrational manner.

"The Value of Cervical Magnetic Resonance Imaging in the Evaluation of the Obtunded or Comatose Patient With Cervical Trauma, No Other Abnormal Neurologic Findings, and a Normal Cervical Computed Tomography."
www.ncbi.nlm.nih.gov/pubmed/21857257

Friday, September 23, 2011

Hyperbaric Oxygen Therapy for Carbon Monoxide

Another mini-review where I agree with the Cochrane Review that essentially concludes: too much cost/risk, not enough proven benefit.


Hyperbaric oxygen therapy is of proven value in rapidly clearing carboxyhemoglobin from the serum - half-life approaches 20 minutes at 3 atmospheres vs. 1 hour on 100% face mask and several hours at lower concentrations of oxygen.  In addition, HBO has all sorts of beneficial effects in terms of preventing the damaging intracellular effects of carbon monoxide, including impairment of cytochrome oxidase a3 and of lipid peroxidation.  Lipid peroxidation, as you might imagine, in a brain full of lipids, is where you really end up in trouble with permanent neurologic sequelae.


Unfortunately, the first animal models that prove how well HBO works go directly from CO poisoning into multiple atmospheres of therapy.  As few HBO centers there are in the U.S., this is absolutely not a clinically relevant model because of the delays to therapy - and that's why the human literature is less conclusive.


There are essentially three large studies that contribute most of the weight to the 2011 Cochrane Review - one from 1989 that demonstrates no benefit, a second from 2002 in the New England Journal of Medicine that has a broad following, and, finally, a 2011 publication in Intensive Care Medicine.  Most toxicologists who are pro-HBO base their opinions on the 2002 Weaver article.


The good news about the Weaver article - it's a great study.  It enrolls a lot of patients, it enrolls all kinds of patients, it dives them to three atmospheres, it does three dives in a 24 hour period, and it has excellent objective testing and subjective evaluation follow-up.  This study was well-designed to give us the answers.  And, in the end, it finds a significant difference in objective neurologic function in the HBO group and a subjective difference in memory ability in the HBO group.  What is odd, however, is that there were many objective tests of cognitive function.  Most trended towards favoring the HBO group, but only one of them reached statistical significance - a trail marking test in which a line was drawn between similar numbers.  The absolute change in cognitive function between treatment and follow-up wasn't that much different between the two groups.  And, unfortunately, the larger issue for me is the baseline difference between the two groups in amount of time exposed to CO which trended towards much higher in the NBO group - 22 +/- 64 hours in the NBO group and 13 +/- 41 hours in the HBO group.


This difference is much more important because animal studies have demonstrated it's not the carboxyhemoglobin concentration that matters as much as the dissolved CO that diffuses intracellularly.  There's a fabulous study in dogs demonstrating this difference.  In one group, they exposed dogs to CO to get their carboxyhemoglobin concentration to 68% - and they all died.  In a second group, they bled dogs until they had lost 68% of their hemoglobin - in theory, the same level of deoxygenation as the CO group - and they all lived.  Third, they bled dogs down until they had lost 68% of their hemoglobin, then exposed that hemoglobin to CO in vitro and re-transfused it back into the dogs - in theory, the same 68% carboxyhemoglobin level as group 1 - and those dogs lived.  The difference between group 1 and 3 was the amount of dissolved CO in the blood and intracelluarly, and it was demonstrated that their cytochrome oxidase a3 activity was normal in group 3 despite the carboxyhemoglobin levels.


So, that's where I can't take the Weaver evidence as strong enough as the sole large study favoring HBO, even though it was well-designed.  The 2011 evidence, as mentioned before, is a study by Annane in Intensive Care Medicine.  This is the more recent study showing no benefit.  However, if you thought the Weaver study had flaws, this one is even worse.  They enrolled patients between 1989 and 2000 - but didn't publish until 2011, which is a massive red flag.  Their endpoint is fuzzier, as they simply have a questionnaire and a physical examination as their follow-up without a lot of details.  But, for what it's worth, they found HBO was futile in non-comatose patients and harmful in comatose patients.  They also do not dive as low or as long as the patients in the Weaver study.


Each of these studies makes it in the Cochrane Review which finds a cumulative nonsignificant trend towards minimal improvement in the HBO group.   The problem is, HBO therapy is expensive, causes hyperoxic seizures, barotrauma, anxiety, oxidative stress and both hyperthermia and hypothermia.  Weak evidence for mild improvement in delayed neurologic sequelae at 6 weeks is not a strong enough motivator for me to be enthusiastic about subjecting someone to the risks of HBO therapy.  I'd love to see more data.


"Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning."
www.ncbi.nlm.nih.gov/pubmed/12362006


"Hyperbaric Therapy for Acute Domestic Carbon Monoxide Poisoning: Two Randomized Controlled Trials."
www.ncbi.nlm.nih.gov/pubmed/21125215


"Hyperbaric Oxygen for Carbon Monoxide Poisoning (Review)."
www.ncbi.nlm.nih.gov/pubmed/21491385

Thursday, September 22, 2011

We're Covered in Filth

This is not the first study showing physician white coats and nursing uniforms are colonized with bacteria, nor that may of those bacteria are pathogenic and multi-drug resistant.  In the past, this has been used as a call for the abolishment of physician white coats, ties, and all long-sleeved apparel.

This study, however, shows that short-sleeved nursing uniforms were just as likely to be coated with bacteria - 49% to 54%.  Interestingly, even "changing uniform daily" still resulted in colonization with pathogenic bacteria.  The authors speculate the main issues are that all textiles easily transmit bacteria, and that hand hygiene might be more critical than uniforms in prevent transmission from patients to physician clothing.

This study also, like the many before it, doesn't demonstrate anything but colonization - not documented patient-to-patient transmission via healthcare worker clothing or any specific outcome measures.  However, I am a believer that white coats are fomites and medical relics that should go the way of bloodletting and golden elixirs. The studies in support of white coats cite patient satisfaction and ease of identification of roles - which, while important, could be mitigated by new interventions for identification of healthcare providers.  Even though we yet have no evidence of harms from this colonization with pathogenic bacteria, it's essentially a zero-cost intervention to stop wearing white coats and ties - so even if the number needed to treat to prevent a transmissible infection is immense, it's a free way to protect our patients as best we can.

"Nursing and Physician Attire as Possible Source of Nosocomial Infections."
www.ncbi.nlm.nih.gov/pubmed/21864762

Tuesday, September 20, 2011

CMS ED Quality Measures Are Coming

When the government is the largest healthcare payor, you pay attention when they start measuring "quality" - because it's usually not long after that payments are tied to "quality".

This is an Annals study looking at the pilot reporting program from CMS, which includes seven metrics that hospitals are going to have report in the next two years.  These metrics are:
 - Throughput time for admitted patients.
 - Throughput time for discharged patients.
 - Admit order to bed placement for admitted patients.
 - Time to pain management for long bone fractures (discharged and admitted)
 - Time to chest x-ray after order placed (discharged and admitted)

I love the pain management metric.  The literature that supports how poorly ED physicians manage pain is extensive.  Not a day goes by where have a resident trying to give a 2 milligram dose of morphine to treat acute pain.  The other metrics - well, so, faster is more and more is better, so therefore more, faster is "quality", right?  Well, there are some studies that show improved outcomes when patients reach the floor more rapidly, so, perhaps that's what they're getting at.  I don't know if we'll ever really know how improving these measures affects quality, because there are so many other confounding variables affecting these issues.

What is good about these metrics is that it should make a lot of EDs re-examine their processes and see how they can maximize the resources they have.  But, after the low-hanging fruit, you run up against issues of physical and financial resources - many of which are hospital-wide issues.  It will be interesting to see how our workplace changes in response to this.  Unsurprisingly, academic centers and busy EDs had the worst throughput statistics; not sure about magical solutions there.

"A Field-Test of Time-Based Emergency Department Quality Measures."
www.ncbi.nlm.nih.gov/pubmed/21868129

Monday, September 19, 2011

How Do We Miss Aortic Dissection?

This is a retrospective look at 109 cases eventually diagnosed with aortic dissection - with a focus on the differentiating clinical features present in the 17 cases where the diagnosis was initially missed in the Emergency Department.

Confounding clinical attributes that were associated with a missed diagnosis were walk-in vs. ambulance arrival and presence of anterior chest pain.  Chest x-rays lacking a wide mediastinum were nonsignificantly associated with missed aortic dissection, and with only 55% of their diagnosis cohort having a wide mediastinum vs. 25% of their misdiagnosis cohort.  Interestingly, over 75% of each group received a d-Dimer and they were all positive in the misdiagnosis group as well as all but one in the diagnosis group.  It would seem that they order so many d-Dimers that they've become fatigued to its clinical usefulness due to its poor specificity.

The good news is the patients who were initially misdiagnosed had similar mortality (18% vs. 15%) - despite 7 of the 17 being treated with antithrombotic agents.  Most of the missed diagnoses were classified as undifferentiated possible ischemic chest pain, but two were diagnosed with renal colic.

As always, the main problem with missed-diagnosis literature is there's no guarantee the authors didn't miss another set of cases themselves.

"Factors leading to failure to diagnose acute aortic dissection in the emergency room."
www.ncbi.nlm.nih.gov/pubmed/21889877