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"

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.


"Analysis of 22,655 presentations with back pain to Perth emergency departments over five years"

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"

"Intubating ICU patients with ketamine: adverse effects that can occur."

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."

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."

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."

"Hyperbaric Therapy for Acute Domestic Carbon Monoxide Poisoning: Two Randomized Controlled Trials."

"Hyperbaric Oxygen for Carbon Monoxide Poisoning (Review)."

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."

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."

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."

Saturday, September 17, 2011

Ondansetron, Just Like Droperidol

Droperidol used to be one of the most widely used anti-nausea medications, particularly in the peri-operative period.  Now, none of my residents are familiar with it because it's rarely used since the FDA gave it a black box warning for its QT-prolonging effects.  We have largely and copiously replaced it with ondansetron, the supposedly safe alternative.

Now, the FDA is asking GlaxoSmithKline to go back and look at the safety profile for ondansetron...due to QT-prolonging effects:  They are already changing the labels to reflect cardiovascular risk in the meantime.

It should be interesting to see the results.  It is fairly clear that ondansetron prolongs the QT interval probably nearly, but not quite, as much as droperidol.  The droperidol black box was based on cardiovascular events including only a mere 10 patients receiving doses in the therapeutic range of 0.625mg to 1.25mg, and those events had multiple confounding factors or drug co-administrations.  It would not surprise me if ample, if equally flimsy, evidence exists implicating ondansetron as well.

"Food and drug administration black box warning on the perioperative use of droperidol: a review of the cases."

"Droperidol and ondansetron-induced QT interval prolongation: a clinical drug interaction study."

"The effects of droperidol and ondansetron on dispersion of myocardial repolarization in children."

Friday, September 16, 2011

Putting Acetylcysteine To Rest

Essentially, another study to nail the coffin shut for using n-acetylcysteine to prevent contrast-induced acute kidney injury.

Over 1000 patients each in the acetylcysteine and placebo groups, this study showed exactly equal 12.7% chance of acute kidney injury resulting from contrast exposure during cardiac catheterization.  In addition, the 30-day mortality was nearly identical at 2.2% for acetylcysteine and 2.3% for placebo, and only 3 patients in each group required dialysis within 30 days.

Perplexingly enough, the only advantage acetylcysteine had was a lower incidence in adverse effects versus placebo, 2.2% vs. 1.3%.  They do not mention what formulation their placebo formulation was, but apparently it caused more nausea & vomiting.

The authors also do a mini meta-analysis to evaluate why previous studies showed a benefit, and they additionally find that studies that had appropriately blinded allocation showed identical outcomes while patients with inadequate blinding demonstrated an acetylcysteine advantage.

"Acetylcysteine for Prevention of Renal Outcomes in Patients Undergoing Coronary and Peripheral Vascular Angiography."

Wednesday, September 14, 2011

Rivaroxaban Can Be Reversed, But Not Dabigatran

We all hate coumadin - difficult to control levels and causes life-threatening bleeding, but at least we can measure its activity and reverse it in a straightforward manner.  However, coumadin's days are at an end with the approval of the new oral anticoagulants - and the two most extensively evaluated are dabigatran (direct thrombin inhibitor) and rivaroxaban (factor Xa inhibitor).

This is a randomized, placebo-controlled trial of the reversal of dabigatran and rivaroxaban using prothrombin complexe concentrates - which, most importantly, have been theorized to be the only used agent for dabigatran.  Their results - in groups of 12 healthy volunteers - is that PCCs have no effect on any of the laboratory clotting parameters for dabigatran, but fully reverse rivaroxaban.

So, while there are no studies as of yet describing the acute reversal of either of these agents in a clinical situation, this is definitely concerning that we still have no theoretical way to treat life-threatening bleeding with dabigatran.

"Reversal of Rivaroxaban and Dabigatran by Prothrombin Complex Concentrate."

Tuesday, September 13, 2011

Predicting Poor-Performing Residents

This is an entertaining look into the residency training experience in the United States, which is renowned for its brutality in certain specialities.  As far as sleep-deprivation goes, it ranks right up there with some of the lowest quality of life professional jobs.

This is, basically, the quality-of-life information from the Internal Medicine in-service training examination, as reported in JAMA.  The authors have linked it to in-training examination results for the, probably predictable, association of poor work/life balance and poor in-training scores.

Interesting tidbits I noticed:
 - 15.3% of residents stated that life was as good as it could be.
 - PGY-1 and PGY-2 residents had nearly equal poor quality-of-life and work/life balance - which improves significantly PGY-3.
 - Over 40% of residents have >$100,000 in debts - and that was associated with poorer quality-of-life scores.
 - Improvements in quality-of-life for PGY-3 was mirrored by a corresponding increase in depersonalization.

Not a healthy experience, by a longshot.  Pity those whose residencies are longer than the bare minimum of 3 years.

"Quality of Life, Burnout, Educational Debt, and Medical Knowledge Among Internal Medicine Residents."

Sunday, September 11, 2011

More Platelets In Massive Transfusion

Where are we going to get all these blood products?  The rapidly growing body of literature backing early transfusion of FFP and platelets in massive transfusion protocols continues to tilt towards the 1:1:1 ratio.

This is a retrospective review of whether platelet transfusion impacts survival in trauma.  They identify three categories of ratios of platelets to RBCs (>1:20, 1:2, and 1:1) and measure a variety of different outcomes.  Briefly, more platelets helped with survival to 24 hours, but more platelets also increased multi-organ failure.  In the end, the initial survival differences were great enough that they outweighed the additional multi-organ failure for a significant survival benefit (52% vs. 57% vs. 70%).

They exclude 25 patients who died within an hour in an effort to mitigate survival bias.  However, looking at the breakdown of survival times, it looks as though almost all the mortality benefit to increased platelet ratios was realized in the first 6 hours - and then the mortality numbers worsen in tandem after that.  The authors state they were unable to truly quantify retrospectively whether the patients survived because they received more platelets vs. whether patients surviving longer were able to receive more platelets, and note that prospective trials will need to be performed.

I would also note that a significant portion of their high ratio patients also received Factor VII, for whatever that's worth.

So, we continue to await high quality prospective trials that specifically address the impact of survival bias.

"Increased Platelet:RBC Ratios Are Associated With Improved Survival After Massive Transfusion."

Saturday, September 10, 2011

Impedance Threshold Devices Are Useless

So, supposedly, impedance threshold devices installed inline for ventilation during CPR potentially improve hemodynamics via negative intrathoracic pressure.  This is a prospective, randomized, multi-center, placebo-controlled sham study that really meets a very high standard for internal validity.  Over 4000 patients in the ITD group, the sham ITD group, and the not-enrolled comparison cohort.

Short summary:
 - Minimal differences between groups.
 - 27.8% sham vs. 27.1% active device ROSC in the ED.
 - 8.2% sham vs. 8.2% active device discharge from the hospital.
 - No apparent harms from the ITD device, but no benefits either.

The most important point from this article is that we have gotten sloppy in our rush to implement supposedly new and beneficial therapies in medicine.  Hypothermia, TPA for stroke, Factor VIIa, direct thrombin inhibitors, etc. and we should add impedance threshold devices to the list.  The AHA has had ITD as a class IIa recommendation to improve hemodynamics since 2005 - six years of useless therapy and costs based solely on a theoretical model without proof of improved outcomes.  Hammering this point home never gets old.

"A Trial of an Impedance Threshold Device in Out-of-Hospital Cardiac Arrest."

Friday, September 9, 2011

More Mistakes In An Unfamiliar System

Probably tells us what we already know - and likely underestimates the problem.

These authors take a retrospective look at all the reported medication errors between 2000 and 2005, and then try to associate increased errors with the involvement of a temporary staff member.  The problem is, they don't actually have staffing documents that report which employees are temporary - they rely on the population of a QA field listing "contributing factors", under which temporary staff is an option.  So, you can dismiss this as a bit of garbage-in/garbage-out depending on how accurate the reporting is - but, I figure, if anything, people will forget to implicate temporary staffing more frequently than not.

More interesting - and potentially confounding re: temporary vs. permanent - are the perceived reported reasons behind the medication error.  Temporary staff were more likely to be reported to have knowledge deficits, performance deficits, and fail to follow appropriate procedures.  I might read into that data that it's easier for an unfamiliar temp to appear knowledge-deficient, although that's just my own imagination.

From a risk management standpoint, the solution seems to be: whatever the retention costs of your permanent staff members, they are almost assuredly lower than the costs associated with the errors inflicted upon patients by temps.

"Are Temporary Staff Associated with More Severe Emergency Department Medication Errors?"

Wednesday, September 7, 2011

Epinephrine Neither Wins Nor Fails

The crux of the problem - epinephrine continues to improve short-term ROSC with uncertain long-term outcome improvement.

This is a prospective out-of-hospital arrest study from Australia in which epinephrine or saline placebo was given to patients during resuscitation by EMS.  And, like many studies before it, it fails to show a meaningful difference between patients receiving epinephrine and patients receiving placebo.  Rather, their primary outcome of survival to hospital discharge had 1.9% with placebo and 4.0% with epinephrine - but this result was not statistically significant with a p-value of 0.15.

Of course, what the lack of statistical significance means in this case is that this difference could have occurred by chance 15 times out of 100 times they performed this study - which, while not meeting the gold standard of 5 out of 100, is still a reasonably interesting clinical trend.  Like all studies before it, the short-term endpoints met statistical significance, including ROSC of 8.4% for placebo and 23.5% for epinephrine.  There are a few confounding differences between groups: more placebo patients had witnessed arrest, although the number with bystander CPR was the same; more placebo patients were endotracheally intubated in the field, which usually confers a survival disadvantage; and more epinephrine patients were ultimately transported to the hospital from the field.

So, there's two ways to look at it: 1) epinephrine works, and we just need to figure out how to salvage more of those ROSC or 2) epinephrine is flogging far too great a number of lost husks back to life that will go on to consume ICU resources and expire regardless.

But, if we're not going to give epinephrine, how do we otherwise look busy during a code?  And, what happens downstream to our epinephrine ROSC that fail to leave the hospital or the ER, and can we prevent it?

I am still not sure what the right answer is - like many diseases, cardiac arrest patients are a heterogenous group in which there is almost certainly a subset of patients that benefits from epinephrine, but we don't yet know who that might be.

"Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial."

Thanks to @cliffreid of Resus M.E! for first noting this article.

Tuesday, September 6, 2011

Sternal IO is the Best IO

All our cardiac arrest patients roll in these days with an IO in place - and we are full proponents of rapid, successful access in the uncontrolled field environment.  But, how effective is it really in the CPR situation?

So, this is an animal study that tries to address the theoretical efficacy of intraosseous access versus central venous access.  They use injection of dye tracers into Yorkshire swine for a comparison between intraosseous sternal, intraosseous tibial, and external jugular central venous cannulation.

Unfortunately, this is a good news/bad news study.  The good news - peak concentrations were achieved only slightly more slowly in the arterial circulation following sternal intraosseus injection than the gold standard central venous injection.  And, the peak concentrations were nearly identical.  Bad news, the tibial IO was half the speed and half the arterial peak concentration of the sternal IO.

In theory, this is of relative importance depending on which medication you're using - presumably the speed of administration matters in CPR and peak concentration may matter as well.  Of course, this is limited as 1) pigs and 2) efficacy vs. effectiveness, because they're not measuring clinical outcomes.

But it's interesting to worry about.  Too bad it's hard to do chest compressions with your access point where your hands are supposed to go.  It would be interesting to compare this result to a humeral head IO.

"Pharmacokinetics of Intraosseous and Central Venous Drug Delivery During Cardiopulmonary Resuscitation."

Sunday, September 4, 2011

New Pediatrics UTI Guidelines

For children between 2 and 24 months of age, the relevant high points for EM:
 - Don't use bag urines.  Catheterization or suprapubic aspiration is the only acceptable way to make a diagnosis.  However, if you're stuck, and you have to use a bag, a completely normal bag urine is diagnostic.
 - Send a culture to definitively establish the diagnosis based on pyuria and/or bacteruria and the presence of at least 50,000 CFU/mL of a uropathogen.
 - Oral antibiotic recommendations listed include amoxicillin-clavulanate, trimethoprim-sulfamethoxazole, and a range of oral cephalosporins for at least 7 days.  They do not have any evidence to compare 7, 10, and 14 day courses.  Nitrofurantoin is not appropriate.

Nothing terribly earthshaking - seems all pretty reasonable.

"Urinary Tract Infection: Clinical Practice Guideline for the Diagnosis and Management of the Initial UTI in Febrile Infants and Children 2 to 24 Months."