Vocal cord dysfunction

An asthma mimic.

Atrial appendage exclusion for stroke prevention in atrial fibrillation: is it ready for prime time?

Here's the current status.

Acute kidney injury (AKI)

Lots of good stuff in this review.

Some take home points:

The cornerstone of assessment and management is volume.

Assess volume and volume responsiveness (which can be a little tricky, and how you do that depends on the resources where you practice) and replete as indicated.

Low FeNa does not always mean volume responsive. Exceptions are listed and discussed.

Though aggressive volume resuscitation is indicated in early septic shock and often early AKI a price is often paid later in terms of organ congestion (lungs, kidneys, skin, abdominal compartment) such that less may be more in the later stages.

Diuretics have not been proven to lead to improvement in hard clinical outcomes although there may be some benefit in mitigating volume overload and hyperkalemia in those patients capable of responding.

Atrial fibrillation in young and old patients

A review.

Lectures in pulmonary pathophysiology

From UCSD.

Insulin resistance syndromes

This review is one of the best discussions I've seen on the various insulin resistance syndromes. It centers around a case report of a patient with type 2 DM who developed DKA and extreme insulin resistance in the face of acute MI.

The case in question raises several discussion points. This is a case of DKA which, in defiance of the usual rule, developed in a patient with DM type 2. Traditional teaching holds that DKA is associated with DM 1. DM 1 strictly defined, however, is that type of DM in which DKA predictably develops spontaneously, in deprivation of administered insulin, in the basal state. This patient had acute MI and was therefore not in a basal state. But to further complicate matters this patient, being Hispanic, could have had ketosis prone type 2 diabetes, a syndrome in which patients seemingly flip-flop between type 1 and type 2 phenotypes. This is a condition of intermittent beta cell fatigue which may have rendered the patient more prone to glucose toxicity which the authors speculate was a factor. This patient's insulin resistance was not defined by the presence of DKA but rather by the amount of administered insulin it took to achieve glycemic control.

The activation of counter regulatory (stress) hormones by the AMI, and perhaps inflammatory cytokines, could explain the development of DKA but, in the opinion of the authors, probably not this degree of insulin resistance (extreme insulin resistance). While AMI has been cited as a situation causing extreme insulin resistance, it appears to do so by multiple and poorly understood mechanisms.

Bell's palsy

Quick reference via Academic Life in Emergency Medicine.

Coffitivity gets the creative juices flowing

Atmosphere for the blogging cave!

HT to Academic Life in Emergency Medicine.

Precedex for ethanol withdrawal??

Here's a nice reference.

A few observations:

It is supported only by low level evidence.

It is off label.

It appears to be safe and is gaining popularity.

It harks back to the old trick of adjunctive use of clonidine (it's a central alpha2 agonist).

It is physiologically very appealing in those patients with hypertension and tachycardia.

Medicine and basic science videos

Browse here. 

Lytics for submassive PE: Is the controversy any closer to being resolved?

No, despite two recently completed trials, one recently published and one just presented in abstract form at ACC.  The former study, published in the American Journal of Cardiology, using half dose TPA, showed good safety (no major bleeding) but improvement in only soft endpoints attributable to TPA.  The study presented at ACC showed improvement mainly in soft endpoints and a concerning increase in major bleeding attributable to thrombolysis.  So read the studies and opine as you will but my bottom line remains that thrombolysis for submassive PE is not well supported.

There is a nice summary on this topic over at Academic Life in Emergency Medicine.

Professor Fink's lectures

In physiology and other topics.

Human physiology lectures

Slide sets.

Mastocytosis: cutaneous and systemic

A review.  Multiple variants of the disease exist and the protean manifestations can be attributed to the vast array of mediators secreted from the mast cell.

Video lecture on blood gas analysis in critical care

FDA clarifies the mechanism of cardiovascular death associated with azithromycin

It can prolong the QT and lead to Torsades.  The original report linking it to cardiovascular death was in NEJM last year.

We can add it to the list of antibiotics capable of doing this.

Is pacing effective in vasovagal syncope?

It's no cure but it has a role and patient selection is important.  The pendulum has swung back and forth on this topic.  The Vasovagal Pacemaker Study of some years ago failed to show a benefit when patient selection was based on tilt testing.  But an abstract just presented at ACC showed benefit after careful patient selection based on evaluation via an implanted event monitor.

Is it the end of the line for niacin?

No, but a new study presented at ACC raises concerns.  Before jumping to conclusions about niacin note the following:

The results do not permit a distinction between niacin and the antiflushing agent laropiprant in attribution of the negative outcomes.

The patients were studied without regard to LDL particle density, ignoring previous findings that niacin has a powerful niche in patients with low LDL particle density (LDL pattern B).

In the trial, niacin was combined with a statin with a higher toxicity profile.

In the Coronary Drug Project, an example of comparative effectiveness research done decades before the term was co-opted for political ends, niacin was the first lipid modifying agent found to favorably impact significant clinical outcomes.

Respiratory physiology lectures

From UCSD.

I love posting these educational resources.  Remember a couple of RW's rules for learning:  The better you understand physiology the less stuff you'll have to memorize (or look up) AND the quickest way to get smart is to realize you're a dumb s...

Learners TV

For lectures on just about everything.  Lots of basic science and medical stuff.  

Aldosterone receptor antagonism (Inspra) in the first 24 hours of STEMI?

Benefit was shown in a trial presented at ACC but the composite endpoint was driven mainly by a surrogate marker (BNP/proBNP).   So....hypothesis generating and not ready for prime time pending further study.  Via Medpage Today.

Physiochemical analysis and strong ion difference: another method of acid-base analysis

Not for sissies. Watch this when you're well rested and well fed.

Questionable treatment shamefully promoted

---at respected national meetings.  The trial in question (TACT) was hopelessly flawed in my opinion and that of others.  

Spironolactone in diastolic heart failure

Pathophysiologic rationale and surrogate endpoints look promising but that's as far as we've come so far.  A long journey awaits.  The latest study in JAMA.

RW's Tweets

OK, so I've stepped into the 21st century and am finally tweeting.  But I need some followers.

Medical education resources on YouTube

Here are some I've found recently:

COMLEX USMLE review.

Medical Sciences Animated Videos.

Eric's Medical Lectures.

MedCram.

The Southern diet as a risk factor for stroke

Presented at the International Stroke Conference.

Via Medpage Today.

Initial sedation intensity in mechanically ventilated patients: go easy

From this study recently published in the blue journal:

Measurements and Main Results: We studied 251 patients (mean age, 61.7 ± 15.9 yr; mean Acute Physiology and Chronic Health Evaluation [APACHE] II score, 20.8 ± 7.8), with 21.1% (53) hospital and 25.8% (64) 180-day mortality. Over 2,678 study days, we completed 14,736 RASS assessments. Deep sedation occurred in 191 (76.1%) patients within 4 hours of commencing ventilation and in 171 (68%) patients at 48 hours. Delirium occurred in 111 (50.7%) patients with median (interquartile range) duration of 2 (1–4) days. After adjusting for diagnosis, age, sex, APACHE II, operative, elective, hospital type, early use of vasopressors, and dialysis, early deep sedation was an independent predictor of time to extubation (hazard ratio [HR], 0.90; 95% confidence interval [CI], 0.87–0.94; P less than 0.001), hospital death (HR, 1.11; 95% CI, 1.02–1.20; P = 0.01), and 180-day mortality (HR, 1.08; 95% CI, 1.01–1.16; P = 0.026) but not delirium occurring after 48 hours (P = 0.19).

Conclusions: Early sedation depth independently predicts delayed extubation and increased mortality, making it a potential target for interventional studies.

Which antidepressants prolong the QT interval?

According to a BMJ study:

Results Dose-response association with QTc prolongation was identified for citalopram (adjusted beta 0.10 (SE 0.04), P less than 0.01), escitalopram (adjusted beta 0.58 (0.15), P less than 0.001), and amitriptyline (adjusted beta 0.11 (0.03), P less than 0.001), but not for other antidepressants examined. An association with QTc shortening was identified for bupropion (adjusted beta 0.02 (0.01) P less than 0.05). Within-subject paired observations supported the QTc prolonging effect of citalopram (10 mg to 20 mg, mean QTc increase 7.8 (SE 3.6) ms, adjusted P less than 0.05; and 20 mg to 40 mg, mean QTc increase 10.3 (4.0) ms, adjusted P less than 0.01).

Obesity associated severe asthma

Obesity may be associated with a distinct phenotype of severe asthma according to this paper.

Prehospital advanced airway management associated with more than double the risk of bad neurological outcome

----in this analysis.

This adds support for the arguments Gordon Ewy and his group at Arizona have been making for years, as I have posted here many times.