Gone fishin’

The weather is finally starting to warm up and the fish are biting.  Unfortunately, amateur and pro fishermen alike will also either catch themselves or their friend while out on the waterways this summer.  While a small fishhook lodged in a finger may seem trivial compared to some of the more traumatic injuries we see, the process of removing a fishhook can still be challenging and time consuming.  In this month’s issue of ACEP Now we published four different ways of removing these pesty hooks. Check it out here. 

Post by: Terrance McGovern DO MPH (@drtmcg13)

Fat embolism syndrome

Typically when we start talking about anything related to fat embolisms our minds go immediately to trauma and long bone fractures as the cause, but this isn’t always the case. The constellation of signs and symptoms of respiratory insufficiency, neurologic dysfunction and petechial rash which are typically associated with fat embolism syndrome can also be caused by pancreatitis, sickle cell disease and liposuction; all of which show up regularly in the Emergency Department. With mortality rates as high as 20%, despite the fact that FES usually doesn’t present for at least 12 hours after the initial event, it should be something that we are aware of.

There are two competing theories as what causes FES. Some believe more in the mechanical-obstruction theory where the fat globules act similarly as other embolic events, showering throughout the end organs and wreaking havoc by those means. The new challenger to this theory is the biochemical theory where proponents support the notion that the fat is broken down into free fatty acids and the damage is caused by the endothelial damage and subsequent increased vascular permeability. No matter which theory you support, the clinical diagnosis is going to be equally as challenging. There are a few criteria/scores that have been developed in the past that are non-specific diagnostic tools to identify patients with FES, but they have not been compared head-to-head in their accuracy. In the Emergency Department we are limited with the tests that we can routinely order. Unfortunately, CXRs are going to be essentially useless in diagnosing FES, but MRI may hold more promise. The starfield pattern seen on MRI is not specific to FES, but has been seen routinely in patients who have disease processes associated with FES along with neurologic symptoms. Otherwise, in the ED this is going to essentially be a clinical diagnosis with a good history and a little bit of luck. There is some evidence that earlier fixation and specific orthopedic surgery techniques may decrease the rate of FES, but from an EM point-of-view it is essentially supportive care. Research seems to be lacking into the non-trauma causes of FES, so maybe there is somewhere for us to intervene in those patients…

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Time for Terlipressin?

Correct, we don’t have terlipressin in the US, yet… Hopefully, sometime in the not so far off future we’ll have the chance to play around with it. Essentially it’s a synthetic analog of vasopressin which we are more familiar with. There’s some written about its use in variceal bleeds and here is a cool little study from Egypt using it for refractory septic shock.

They enrolled 80 ICU patients that were in refractory septic shock; meaning that they had to meet sepsis criteria and have the following three criteria:

  1. SBP < 90mm Hg or MAP < 70
  2. Received at least 1000ml of IVF or CVP 8-12cmH2O
  3. Necessitated more than 0.5 mcg/kg/min of norepinephrine

The 80 adult patients were split into two, pretty well matched groups, of 40. One group received adrenaline (0.2ug/kg/min) as their second-line vasopressor and the other group received a continuous infusion of terlipressin (1.3ug/kg/hr). This study was interesting because it only lasted for the next 6 hours after the second vasopressor was started. Unfortunately, they really didn’t look at patient related outcomes, but instead their primary endpoints were:

  1. MAP > 65 mmHg
  2. Systemic vascular resistance index > 1300 dynes s/cm5/m2
  3. Cardiac index > 4 L/min/m2
  4. Oxygen delivery index (DO2I) > 550 ml/min/m2

From an Emergency Medicine point-of-view the MAP is probably what we are most familiar with and is an easy enough measure to monitor in the ED.  After initially starting with a statistically equivalent MAP before the start of the second vasopressor, to having a statistically significant difference (p<0.001) after the 6 hours is hard to ignore despite the lack of reported clinical outcomes. This was in addition to showing improved hemodynamic measures and decreased doses of norepinephrine needed in the terlipressin group. This by no means is the do-all and end-all for terlipressin, and doesn’t mean we start throwing it at everything with hypotension when it gets approved in the US. Might as well get familiar with it now though, so when it does show up there are no surprises.

Post by: Terrance McGovern DO, MPH (@drtmcg13)