Table-of-Contents and FOAMcc in One Bolus


MattGreerMatt Greer placed a comment on my Path to Insanity Post:

I’m currently in my 3rd year of EM residency in California, and hoping to do a Critical Care fellowship in the future. I’ve drank the kool-aid and have tried to read at least the TOC from all these journals for the last few months and I love it!! Its like trying to drink from a fire-hose, but it’s really rewarding when an article that you happen to pick out of the massive flood of articles gets picked up and talked about on the various FOAM sites. The repetitiveness of the important things causes the info to really stick.

I’m a huge nerd and have created a feedly list which includes the TOC of all of your journals as well as a majority of the major EM / CC FOAM sites (in different sections of course). I have shared the opml file with my peers in residency and those that are into the FOAM stuff love it (it saves them from populating their feedly list from scratch). I figured I’d make it available to your readers .

Click Here and Find the Download Link at the Top of the Screen to get the OPML File on to your Computer

download image


Then you need to import the file into your RSS Reader (we all recommend Feedly)



To get the OPML file imported into feedly:

  1. Click the add content link
  2. Click the OPML icon

You can then remove feeds as you like, but it’ll start you off with a framework.


Thanks Matt!

Ebola Diagnosis and Treatment


Intensive Care Medicine Worth Knowing has a great post on how to manage Ebola–Just in case, you know…

Expert Commentary on EMCrit

from ALIEM

from ALIEM

A few months ago, my friend Michelle Lin instituted a few new features on the Academic Life in EM Blog (ALIEM). She and her crew of awesome editors added pre-publication critique as well as post-publication, expert peer review. I have debated on numerous occasions in the FOAMosphere all the reasons I find pre-publication peer review to be an unnecessary vestige of a flawed publishing paradigm. Smarter folks than me have said the same thing. On often-visited sites like EMCrit, post-publication peer review happens automatically and with a width and breadth that traditional journals can’t hope for (I love you commenters!).

But there are a few interviews I do for the podcast in which I am a well-informed user, but not an expert. For these ‘casts I am interviewing an expert, but I am giving you just that single practitioner’s viewpoint. It would be nice to balance these podcasts with a separate expert’s take. For these situations, I am taking a page from Michelle’s book. Next Monday, I will have a podcast on PE teams with Oren Friedman. I reached out expert-commentto Jeff Kline to provide expert commentary on this podcast and he was kind enough to oblige. I personally don’t consider this to be peer review and I am staying away from the term entirely. Instead, look for the “expert commentary” symbol on select future podcasts.

Are you Following Jeff Kline’s Twitter Account


If you care about pulmonary embolism (PE) and you are not following @klinelab, then you are missing out.

Here are some of the things I have learned so far:


  • Causes of False Negative D-Dimer: Symptoms>72 hrs, distal clots, lipemia with turbidimetric assays, and blocking proteins
  • Sudden onset of dyspnea or chest pain has zero predictive value for or against PE (Ann Emerg Med 2010;55:307)
  • Two point DVT may not be enough due to missed SFV Clots (J Thromb Thromb 2014;37(3):298)
  • Age <65, witnessed arrest and PEA as initial rhythm predicts >50% probability of PE as the cause of arrest in a small study (see Mike’s comments below) (PMID 15797276)

Evaluation of PE Patients

  • Thrombophilia testing is a waste of time (PMID 23235639)
  • The Daniel EKG Score can rule-in Severe Pulmonary Artery Hypertension (Chest 2001;120(2):474)
  • He uses Hestia to determine acceptably low risk for Out-Pt treatment, but not ones with pulmonary infarction (they bounce back secondary to pain)
  • A study shows high rates of Chronic ThromboEmbolic Pulmonary Hypertension in higher-risk PEs (Thromb Res 2011;127(4):303)


  • Patients with metabolic syndrome may have resistance to fibrinolysis with tPA


  • Any new onset hypoxemia must be explained clinically and in the chart
  • Must also explain signs of acute pulmonary hypertension on ecg (PMID 19766353)
  • Bronchitis doesn’t cause SOB unless there is bronchospasm

PEMED’s Resus Kit


andy-sloasRemember we did an episode with Keith Conover on creating resus resource packs for your body, car, and home? Well, Andrew Sloas of the PEMED podcast took the advice to heart. He created 3 identical kits, for his and his wife’s car and for his house. Crazy or Brilliant? Let us know in the comments section. Here’s Andrew:

PEMED’s Resus Kit

This list is designed to allow you to create a similar emergency resus kit, but saves you the painstaking hours that I spent considering not only how to get all this stuff into a trauma bag, but how to arrange it in the most functional manner.

Click Here for the Full Kit Contents and Where to Buy the Gear

The first column describes the item type and the second column the location of each item. I have also provided you with the merchant i used and a hyperlink to each item’s web-POS page. The price I paid is in the next column, but that will fluctuate. Some of the items must be purchased in bulk, but I try to only have 1-2 in my bag. As you can imagine, the bag is fairly heavy with one of each item. How often are you expecting to get two emergency out of hospital intubations on your family at the same time? Just stick with one item for most things.





Compartment 1 – The Main Compartment: This is where all the airway stuff is located (with the exception of the surgical airway kit). When things are really bad (let’s face it they’re really really bad if you ever have to use this kit) and you haven’t looked at the kit in over a year, you wont’ have to relearn where everything is located. Everything you need to intubate is in one space.



Compartment 2 – Fluids, Drugs, & Accessories: This section is color coded via the handy multicolor velcro packets that come with the trauma backpack. I labeled each packet with permanent ink to make it easy to find things during a code. Again, the last thing I want to do when I’m thinking about intubating a friend or family member is stop and search for things.



Compartment 3 - Central Line, gloves and face shields.



Side Pockets – For all the non-medical stuff or anything you can’t fit in the main compartments.


Kit tips:

  • Some of the items don’t have a merchant listed. Those items were obtained over years of teaching airway. Often your hospital will get rid of items, which would make a great addition to your bag, just because past their expiration date. Make friends with your supply tech.
  • Volume ordered = if I had to buy it in bulk it that is the minimum number you can buy for that price.
  • I keep a central line kit in the bag not because I’m planning on lining-up someone at Arby’s, but because it can be used for so many other things: the scalpel is great for procedures if the other scalpel is in use, the needle is great for thoracostomy, retrograde intubation, or cric.
  • A 10F peds stylet works with a 4.0ET and all adult ETs, so you don’t really need an adult ET stylet.
  • The M6 oxygen tank has a built in wrench, but it’s flimsy and the having an additional oxygen wrench is a necessary backup. Tape the wrench to your oxygen tank or you’ll never find it when you need it.
  • I have a simple CPR resus mask easily accessible in one of the side-pockets because my nanny can’t intubate, but she can use the mask
  • I chose ET sizes 4,5,6, 7 to make sure I have a tube for everyone. I omitted an 8 because I’m not planning on bronching anyone in the field. You could probably get buy with a just a 4, 5, and 6.
  • Super Glue = poor man’s Dermabond. Good for everything from gluing in an IV or chest tube, to repairing small lacerations. This is the item in my bag that I use the most…for lacerations, not chest tubes.
  • I only have an adult EpiPen (no EpiPen Jr in the bag), why no peds dosing, because an overdose of epi doesn’t make your head, heart, or lungs explode. 300-500 mcg ain’t going to hurt anyone (even a child). If they need epi they need epi so just give he adult dose….
  • Cric Kit, just bc I happen to have one and I like contingency plans, but for me I perform surgical airways with a bougie and scalpel.
  • Suction Tubing: Great tubing for Heimlich valve – thoracostomy tube also a good 2nd tourniquet
  • Why an 8F Thoracostomy tube: it has a needle-like trochar stylet, which makes it the most perfect device invented for needling a tension PTX in the field when there are no other options. Put it in the same place you’d put a chest tube; even with the nipple. Once your in, just slip the tube in over the trochar-stylet. I prefer the traditional surgical technique (no trochar) when in a controlled environment like the ED.
  • Write instructions on things you don’t use all the time (ie. “Blue goes toward the chest”on the Heimlich valve package).



Handwashing – Shakes and Bumps


Having just returned from SMACC, I’ve been thinking of all of the wonderful people with whom I got to interact. Always a delight is the inestimable Vic Brazil. I remember her gently mocking the EMCrit site for its absence of a single article on handwashing. While this is merely tangential, a search of the site for “handwashing” will now bring up this post saving me from any further shame:


Reducing pathogen transmission in a hospital setting. Handshake verses fist bump: a pilot study

Ghareeb PA1, Bourlai T, Dutton W, McClellan WT.

J Hosp Infect. 2013 Dec;85(4):321-3. doi: 10.1016/j.jhin.2013.08.010.


Handshaking is a known vector for bacterial transmission between individuals. Handwashing has become a major initiative throughout healthcare systems to reduce transmission rates, but as many as 80% of individuals retain some disease-causing bacteria after washing. The fist bump is an alternative to the handshake that has become popular. We have determined that implementing the fist bump in the healthcare setting may further reduce bacterial transmission between healthcare providers by reducing contact time and total surface area exposed when compared with the standard handshake.

PMID: 24144553 [PubMed - in process]


Has it always struck you as silly to mandate hand-washing prior to putting on gloves for simple exams? Well, your intuition is quite correct it seems:

Am J Infect Control. 2013 Nov;41(11):994-6. doi: 10.1016/j.ajic.2013.04.007. Epub 2013 Jul 24.


Here is a viewpoint on handshakes in the healthcare setting

Is hand hygiene before putting on nonsterile gloves in the intensive care unit a waste of health care worker time?–a randomized controlled trial.



Hand hygiene (HH) is recognized as a basic effective measure in prevention of nosocomial infections. However, the importance of HH before donning nonsterile gloves is unknown, and few published studies address this issue. Despite the lack of evidence, the World Health Organization and other leading bodies recommend this practice. The aim of this study was to assess the utility of HH before donning nonsterile gloves prior to patient contact.


A prospective, randomized, controlled trial of health care workers entering Contact Isolation rooms in intensive care units was performed. Baseline finger and palm prints were made from dominant hands onto agar plates. Health care workers were then randomized to directly don nonsterile gloves or perform HH and then don nonsterile gloves. Postgloving finger and palm prints were then made from the gloved hands. Plates were incubated and colony-forming units (CFU) of bacteria were counted.


Total bacterial colony counts of gloved hands did not differ between the 2 groups (6.9 vs 8.1 CFU, respectively, P = .52). Staphylococcus aureus was identified from gloves (once in “hand hygiene prior to gloving” group, twice in “direct gloving” group). All other organisms were expected commensal flora.


HH before donning nonsterile gloves does not decrease already low bacterial counts on gloves. The utility of HH before donning nonsterile gloves may be unnecessary.

Copyright © 2013 Association for Professionals in Infection Control and Epidemiology, Inc. Published by Mosby, Inc. All rights reserved.


Alcohol hand rub; Handwashing; Health care-associated infection; Infection control; Nosocomial infection

PMID: 23891455

EMCrit / ISMMS Conference 2014


Conference Recap

The site did a fantastic recap of the conference thereby saving me the trouble.

Live-Tweeting from the Conference

The Talks

The lectures will be posted on the EMCrit site in the coming weeks.

Proper Vancomycin Dosing


Bryan Hayes has a great post on ALIEM on proper dosing of vancomycin.

We are very bad at this in the ED

Proper Vancomycin Dosing

  • 15-20 mg/kg every 8-12 hours in patients with normal renal function [1]
  • In seriously ill patients (eg, sepsis, meningitis, infective endocarditis) with suspected MRSA infection, a loading dose of 25-30 mg/kg may be considered [3]
  • Actual body weight should be used
  • IDSA recommends a max dose of 2 gm
  • In adults, we round to the nearest 250 mg increment

See the post for more and all of the references

Another Comment from Our Semi-Retired Critical Care Doctor on Fluids and the Lymphatics


If you hadn’t already read John (Last Name Not Given), go immediately to this post and read it.

A physiology master comments on the sepsis talks

The comment was in response to the two podcasts on Dr. Paul Marik’s Fluids in Sepsis Talk

The Role of the Lymphatics

In the light of our ‘improved’ understanding of the capillary fluid dynamics of which lymphatics play a significant part (I know, I am sounding like a broken record when it comes to the role of lymphatics!), a few points need to be addressed…..

Optimal fluid resuscitation involves the maintenance of adequate microcirculatory flow coupled with prevention of development of interstitial edema. Edema develops when the capillary hydrostatic pressure increases, coupled with a reduction in removal of interstitial fluid. There is always a normal extravasation of fluid from the intracapillary space to the extracapillary (interstitial) space, otherwise the cells would starve. This extravasation happens along the entire length of the non-fenestrated, non-sinusoidal capillaries and not just at the arteriolar end, as previously thought ( Tom W’s fantastic article!!).

A normally functioning lymphatic system is crucial for returning this fluid back to the central circulation, otherwise edema would ensue.

Normal Lymphatic Function

Let us have a very brief outline of the normal lymphatic structure in this context. I find it useful to think about the arrangement as a kind of a bronchial tree in reverse ….

Initial lymphatics, rich in numbers and deeply embedded in tissue parenchyma, consist of pure endothelial channels without perivascular cells (e.g., pericytes) and smooth muscle cells. They have overlapping cell junctions forming primary valves in addition to traditional secondary lymph valves, and they rely on surrounding tissue motions to achieve periodic lymph channel expansion and compression for collection of interstitial fluid and fluid transport inside the lymphatics.
By contrast, the contractile lymphatics, (calcium dependant) are equipped with rows of bileaflet valves and contract by a specialized smooth muscle phenotype unique to the lymphatics to carry fluid from the initial lymphatics to the lymph nodes. Each pair of upstream and downstream valves in contractile lymphatics forms a lymphangion, facilitating unidirectional lymph fluid during periodic contraction. Contractile lymphatics have many of the vascular control mechanisms present in the arterioles, from classical myogenic contraction to neurogenic, purinergic, and endothelial-dependent and -independent controls.

The microenvironment surrounding collecting lymphatic vessels is a determinant of lymphatic function. Under physiological conditions, NO produced by eNOS in endothelial cells is required for periodic contraction and lymph flow; removing NO caused a reduction in contraction strength. Under inflammatory conditions, iNOS overproduces NO, overwhelms the subtle flow-dependent NO production from eNOS, and prevents contraction. At least in mouse models, higher levels of NO production stimulated by ACh evoked dilation, decreased tone, slowed contraction frequency and reduced fractional pump flow. The situation facilitates lymph edema, reduces antigen delivery into lymph nodes, and consequently, reduces antigen-presenting cells and T-cell activation. It is interesting to note that the effect of nitric oxide and therefore Nitroglycerin are completely different in normal circumstances and in inflammation!
Suppression of lymphatic function by CD11b-positive myeloid cells is a mechanism of self-protection from autoreactive responses during on-going inflammation. To initiate an immune response, antigen and antigen-presenting cells arrive in lymph nodes within hours on antigen encounter. Myeloid cells may accumulate at an inflammatory site and inhibit collecting lymphatic function, suppressing additional immune response to self-antigen by reducing antigen transport into the lymph node.

Some good references on this point are ..

Glycocalyx Protection

Now, on to the aspect of glycocalyx protection,

Injudicious fluid administration in resuscitation practices can cause edema to develop by a variety of mechanisms.
A rapid fluid bolus can cause significant shear stress on the delicate glycocalyx, disrupting it and breaking down the barriers to extravasation.

Colloids and hyperoncotic stuff can themselves cause dessication and compaction of the glycocalyx, by sucking up its water content.

Hypervolemia itself can cause atrial stretch, causing the release of ANP and BNP (evil twins of volume overload.) The actions of both peptides include natriuresis and diuresis, a decrease in systemic blood pressure, and inhibition of the renin–angiotensin–aldosterone system. Further, ANP and BNP elicit increases in blood microvessel permeability sufficient to cause protein and fluid extravasation into the interstitium to reduce the vascular volume. They have a rather differential action on the lymphatics, interms of altering either the permeability or the contractility. Notably, ANP abolishes spontaneous contraction amplitude while BNP augments both parameters by ?2-fold . In aggregate, the consensus is that an increase in collecting lymphatic permeability opposes the absorptive function of the lymphatic capillaries, and aids in the retention of protein and fluid in the interstitial space to counteract volume expansion. The works of Joshua P. Scallan, Michael J. Davis and Virginia H. Huxley, in this regard are noteworthy.

One can see the possible pitfalls of using Nitroglycerine at a micro-circulatory level….

One, by causing vasodilatation, it can aggravate edema..(increased capillary hydrostatic pressure)

Two, by knocking off lymphatics, (through the NO synthase mechanisms) it might perpetuate interstitial fluid retention.

Hope this helps.
“Semi retired critical care doc”.

It does indeed help, but…!

Now, an alternative view is to go to the actual clinical data (albeit preliminary), for instance

Spronk PE, Ince C, Gardien MJ, Mathura KR, Oudemans-van Straaten HM, Zandstra DF. Nitroglycerin in septic shock after intravascular volume resuscitation. Lancet. 2002 Nov 2;360(9343):1395-6.

His letter of response to questions also has additional references for the mode of action that may be beneficial

These two fantastic review articles on microcirculatory resuscitation are must reads:

  • Intensive Care Med 2002;28:1208
  • Critical Care 2006;10:221

What do you think?

Think You Understand Fluids–Cause I don’t have a grasp yet


John (I think he wants to remain somewhat anonymous) is a clinically-retired, still actively teaching intensivist in India. He left the following comment on my Marik Response Post:

In the last 5 years or so, we have had a better understanding of capillary fluid dynamics, particularly in conjunction with an appreciation of the glycocalyx. We now know that the glycocalyx normally ‘traps’ about a litre and half of plasma water in it (due to its hydrophilic chemical composition!) and that normally in the capillaries, there is a central moving layer of plasma and a relatively immobile layer closer to the endothelium….the bit that is bound to the glycocalyx. This explains the differences in measured capillary and venous hematocrit values, and also why Crystalloid : Colloid equivalence is 1.3 : 1 rather than 4: 1 as previously thought.

We have also acquired a better understanding of the mechanisms of edema formation in critical illness and more importantly, the magical phenomenon of improved diuresis that we have all marvelled at, during the recovery phase.

In short, we have kinda debunked the original Starling theory of fluid dynamics in the capillary.

We now know that the colloid osmotic pressure in the intravascular space will only oppose the outward movement of water, and increasing the colloid osmotic pressure by synthetic colloids will not reverse the flow and draw fluid from the interstitial to the intravascular space. ( Multiple trials , starting with the SAFE trial have proved the futility of using synthetic colloids !) What they end up doing is, probably drawing water from the glycocalyx in the intravascular space itself and dehydrating and then disintegrating this vital layer. As a result you will find a transient improvement in blood pressures, but afterwards, a lot of this fluid will track into the extravascular space. Any hyperosmolar solution can do this including Soda Bicarb….we have all seen the very transient increase in blood pressure after bicarb which has always been incorrectly attributed to ‘reversal of acidosis’…bah!!

Extravasation of fluid from the capillaries is predominantly dependant on capillary hydrostatic pressure and not on decreased intravascular colloid osmotic pressure— because we have realised that interstitial and intravascular colloid osmotic pressures are very close to each other.

The way to prevent overloading and thus extravasation would be to minimise rapid increases in capillary hydrostatic pressure. How can we do that? – By small volume crystalloid boluses and early use of alpha1 agonists—the latter work by afferent arteriolar constriction and thus minimising huge increases in capillary hydrostaic pressures. This is where Marik’s argument takes a strong foothold.

Albumin is needed for the integrity of glycocalyx, — explaining why albumin is making a comeback into our fluid armamentarium.

The lymphatics have assumed a pivotal role in the normal mechanisms that prevent edema formation. We have realised that they are a very active conduit to return of interstitial fluid to the central circulation, and they they have contractile collecting ducts and passages that are calcium dependant. They are inhibited by the terrible twins ANP and BNP—therefore shutting down in active sepsis, where the twins tend to dominate. (This also partly explains the peripheral edema commonly seen with Ca channel blockers when they are used as antihypertensives). Once the sepsis resolves, ANP and BNP levels drop and the lymphatics recover their contractile elements. All the interstitial fluid can now be returned to the central circulation causing an improved diuresis.

In any case, fluids should only be used as any other drug should be— only if needed. We need to realise that fluid requirement and fluid responsiveness are two completely different things and focus on appropriate fluid balance rather than branding it as either restrictive or liberal.

What do you think? One question that I had is are we not doing the same thing with pressors if their true first action is to add to stressed venous volume?

photo credit