#FOAMed Review 12th Edition

Welcome to the twelfth edition of the #FOAMed Review! The idea of the FOAMed review is to give you a digestible selection of reliable content from the online EM/CC world that you can fit into your busy weekly schedule. Each review will include highlights from the highest yield blog, podcast, video and web sources around. Over a year's span we will be sure to include topics from all core EM content areas...even the ones that may not be the coolest. Check out our indexing section #FOAMexplore which allows you to view previous #FOAMed review by edition or by selecting from CORD curriculum categories.


Onto the FOAMed.


LAMOTRIGINE IS KETAMINES BLACK SWAN [BLOG]: Interesting post on case report (and there are several others) on failure of ketamine sedation in lamotrigine overdose from Sydney HEMS. 

EVIDENCE FOR MIDLINE CATHETER INSERTION [BLOG]: Should we be optimizing our US guided peripheral venous cannulations with midline catheters instead of the usual equipment. Excellent case made by EM Nerd in his post, 'The Adventure of the Sussex Vampire.'

HYPERTROPHIC CARDIOMYOPATHY ON ECHO [BLOG]: A few evidence based tips and tricks to recognizing HCM on beside echo at Champagne Tap.

THE FALLACY OF HALOPERIDOL ALLERGY [BLOG]: "There are no reports of anaphylaxis, angioedema or cutaneous allergy from haloperidol." This explanation and more at Pulm Crit. 


More FOAMed.

Trauma

PERIPHERAL VASCULAR INJURY [BLOG]: Excellent and succinct review on diagnosis and management of traumatic peripheral vascular injury at EM Docs. 

Hand

HAND FOAMED [PODCAST]: How to perform a good hand neuro exam, Kanavel's signs for flexor tenosynovitis, finger amputations and more in this well versed podcast at Foamcast. 

ECG Interpretation 

The 360 Degree Heart  [BLOG]: Do you truly understand the hexaxial reference system? Highly recommended graphical representation and explanation of how the 12-lead ECG maps onto the hexaxial reference system. This is helpful with the concept of axis and reciprocal depressions in STEMI. Thank you EMS 12-lead. 

Thoracic & Respiratory Disorders 

CROUP [BLOG]: Wise words about managing the little one's that present to your ED with a barking cough, stridor and subcostal retractions at Don't Forget the Bubbles.


 

See you next week. 

#FOAMed review is brought to you by Michael Macias. If you want to recommend content you think should be added to our curriculum, send me an email, I would love to hear from you. 

 

Lombalgia e cortisone, la storia continua

In medicina, come nella vita, i corsi e i ricorsi storici si rincorrono.Farmaci o procedure prima esaltati poi messi in soffitta e poi nuovamente alla ribalta, grazie a nuovi studi. Questo il preambolo doveroso su un tema che molti riterranno desueto e persino noioso, ma che richiama grande interesse, soprattutto da parte dei pazienti, visto […]

The post Lombalgia e cortisone, la storia continua appeared first on EM Pills.

Inspired by curiosity

Bathyscaphe_Trieste

While driving home from a busy shift I recently listened to a new SMACC podcast Dangers of the Deep: Exploration Medicine by Dr. Glenn Singleman who recounts his his experiences as physician to James Cameron and his team who explored the depths of the Mariana trench.

Two great insights from Dr. Singleman were to consider how explorers are likely to die and how to mitigate this risk. He also suggested developing a detailed and logical plan of action that can be defended in the event of an accident. Great food for thought.

The podcast is available here: http://intensivecarenetwork.com/dangers-deep-exploration-medicine/

Also check out this video of James Cameron talking about how he inspires and motivates his teams.

http://www.theglobeandmail.com/report-on-business/video/james-cameron-explains-how-he-inspires-people-on-his-teams-to-bring-their-best-every-day/article20488814/?videoembed=true


Pneumothorax ex vacuo: Post-thoracentesis pneumothorax in the ultrasound era

CT showing pneumothorax ex vacuo due to trapped lung (Pereyra 2013)

Introduction

A recent review article by Wilcox in JAMA questions whether ultrasound guidance truly reduces the risk of pneumothorax.   Bedside ultrasound reduced pneumothorax (OR = 0.55) but this reduction was statistically insignificant due to a huge confidence interval of 0.06-5.3.   Another meta-analysis found a statistically significant reduction in pneumothorax with ultrasonography (OR = 0.3, CI 0.2 - 0.7; Gordon 2010).  

However, this post isn't about whether or not ultrasonography reduces the rate of pneumothorax.   Although I am enthusiastic about evidence-based medicine, this question is about as interesting as whether a parachute prevents death after jumping out of a helicopter (Smith 2003).   This post is about the changing significance of a post-procedure pneumothorax in the ultrasound era.

Different causes of post-thoracentesis pneumothorax

There are three causes of pneumothorax after thoracentesis.   The first and most obvious cause is lung laceration by the needle or plastic catheter.   This may occur if the operator inserts the needle into the lung.   Another way this could conceivably occur may be if the stiff plastic catheter is inserted in the middle of the thorax (rather than over the diaphragm), forcing the lung to re-expand around the catheter.   For a fragile lung with bullae, this could tear the lung as it re-inflates (figure below).   With ultrasound-guided placement, these problems should be rare.

The second cause of pneumothorax is air introduced into the thorax through the catheter inadvertently.   For example, if the catheter is opened to the air while the patient inspires, air would be pulled into the pleura.   Although this does indeed cause a pneumothorax, this pneumothorax is of no clinical significance.   It is impossible for this type of pneumothorax to expand or develop into a tension pneumothorax.   With good technique, this should be avoidable. 

The third cause is pneumothorax ex vacuo.    This occurs if the underlying lung is unable to expand, for example due to bronchial obstruction.   In this situation, the pleural effusion originallywas caused by lung collapse, leading to negative pressure in the pleura which gradually pulled in fluid.   The primary problem is not the pleural effusion, but rather the fact that the lung cannot expand.   Thoracentesis in this situation generates a low intrapleural pressure which transiently opens a tiny hole in the lung to allow air into the pleural space (alleviating the "vacuum").   Pneumothorax ex vacuo only occurs following therapeutic thoracentesis, not diagnostic thoracentesis.

The emergence of pneumothorax ex vacuo as an important clinical consideration

With ultrasound guidance and expert technique, lung laceration and introduction of air into the thorax are largely avoidable.   For example, the pneumothorax rate following diagnosticthoracentesis should be close to zero.   In expert hands, pneumothorax ex vacuoemerges as the most common cause of pneumothorax following therapeutic thoracentesis (Heidecker 2006).   Although pneumothorax ex vacuohas always occurred, its relative importance has increased as the other causes of post-procedure pneumothorax have become less common.

Pneumothorax ex vacuo usually doesn't require any immediate treatment

Pneumothorax ex vacuo is a benign phenomenon which rarely enlarges or leads to tension pneumothorax.   Patients are asymptomatic.   This should not be treated with a chest tube, because the primary problem is unexpandible lung and this will not respond to pleural drainage (Heidecker 2006; Huggins 2010).  

Management focuses on investigating and treating the underlying cause of the lung not expanding.   The occurrence of pneumothorax ex vacuo may be helpful because it redirects the diagnostic investigation (for example to evaluate for such entities as trapped lung or endobronchial obstruction).  

Should we limit all thoracenteses to under one liter in efforts to decrease in the rate of pneumothorax ex vacuo?  

Wilcox noted a small increase in the pneumothorax rate when over one liter of fluid was removed at thoracentesis (4.1% vs. 4.9%).   Although this difference is not statistically significant, it may relate in part to an increased risk of pneumothorax ex vacuo with larger volume thoracentesis.   On this basis, the authors suggested limiting thoracentesis volume to under one liter.

Pneumothorax ex vacuo is rare, benign, and potentially a useful diagnostic finding.   Avoiding pneumothorax ex vacuo could lead the clinician to continue futile efforts to drain the pleural effusion (i.e., with repeat thoracentesis or chest tube; Staes 2009).  For a patient with unexpandible lung, these procedures will be ineffective, as the effusion will recur until the underlying atelectasis is resolved.

The recommendation to limit the volume removed at thoracentesis in order to avoid pneumothorax may reflect a failure to appreciate the significance of pneumothorax ex vacuo.   Not all post-procedure pneumothorax is created equal.   

Take-home points
  • There are many mechanisms of post-thoracentesis pneumothorax.   With ultrasound guidance and excellent technique, most can be avoided except for pneumothorax ex vacuo.   In expert hands, this becomes the most common cause of pneumothorax after therapeutic thoracentesis.
  • Pneumothorax ex vacuo is important to recognize as a possible cause of pneumothorax following therapeutic thoracentesis.   This is a benign entity which doesn't benefit from chest tube placement and can usually be observed.  
  • Although pneumothorax ex vacuo may possibly be avoided by performing small-volume thoracentesis, its unclear that this is a beneficial approach as it may leave the underlying problem (unexpandible lung) obscured.  

This is the first part of a two-part series on thoracentesis.   We're only getting warmed up... stay tuned for next week's post.      




Two (apparent wide complex) Rhythms in One Patient: First is at rate of 300, second at Rate of 180

A middle-aged patient with no known significant past medical history had sudden onset of  palpitations, diaphoresis, dyspnea. This lasted for roughly 30 seconds.  EMS was called and he had palpitations again and had this monitor strip (labeled as leads I, II, and III):
There is a wide complex tachycardia at a rate of 302.  There is a narrow spike at the top of each wave, suggesting rapid conduction to the ventricle.  Perhaps it is actually a narrow complex?

He was awake with a normal blood pressure and no shock.

A rate of 302 is very fast for any tachycardia in an adult, but is particularly fast for ventricular tachycardia.  The narrow spike at the beginning of each QRS suggests that the ventricle is activated through the fast conducting Purkinje system, and is probably a supraventricular rhythm.  One typical SVT that occurs at a rate of 300 is atrial flutter.  It is unusual, however, for the AV node to conduct at this rate.

No matter what the source, it is very fast.

Before this could be electrically cardioverted, the patient spontaneously converted to sinus rhythm (again, leads I, II, and III):
This shows sinus rhythm.  There is a wide complex with a deep S-wave in lead I, strongly suggesting right bundle branch block.

He arrived in the ED and had this 12-lead ECG:
Again, sinus rhythm, and with confirmation of RBBB.  No ischemia.

That the patient tolerated his rhythm of 300 is very re-assuring and makes this rhythm much less life-threatening than if he had been syncopal, hypotensive, or in shock.  It also suggests a structurally normal heart.  A patient with cardiomyopathy would not tolerate this rate.  He remained stable in the ED.

K was 3.6 mEq/L.  Mg was 1.6 mEq/L.

Thinking the patient had suffered from VT, he was started on amiodarone.

Because of worry about primary ischemia as the underlying etiology, he went to the cath lab and coronaries were normal.

An echocardiogram showed normal anatomy and function.

While in the hospital, he again had symptoms and had another ECG recorded:
This is very different from the first. 
It shows a regular wide complex tachycardia, with a left bundle branch block pattern and an inferior axis.  The rate is 180.  There are no P-waves.  The QRS duration is only 120 ms, which is quite narrow for VT.
Considerations in the diagnosis:

The electrophysiologist noted A-V dissociation in lead-II (which is nearly diagnostic of ventricular tachycardia).  I am unable to recognize it in this tracing.

An LBBB pattern by itself strongly suggests an SVT with LBBB-type aberrancy, as does the QRS duration of 120 ms.  Most typical VT (but certainly not all) has a QRS duration of  > 140.  Few typical (i.e., not fascicular) VT have a QRS as short as 120 ms.

However, the fact that the patient has RBBB at baseline, and this ECG has LBBB, makes SVT (sinus, PSVT, flutter) with LBBB-aberrancy virtually impossible.

So now we know that it is wide, LBBB, not SVT with aberrancy, and not a typical VT.  The ultrasound showing a structurally normal heart also makes typical VT unlikely. 

If you can see A-V dissociaton as the electrophysiologist did, that clinches the diagnosis of VT.  

This leaves us with the "idiopathic" ventricular tachycardias: probably fascicular VT or right ventricular outflow tract VT.  These are "idiopathic"  VT's which occur in an otherwise normal heart, and are, compared to typical VT, relatively narrow.  See these cases for a more detailed explanation of fascicular VT.

Subsequent events;

For the second rhythm, the electrophysiologist suspected right bundle branch fascicular re-entry (I had not heard of it before) because of the presence of baseline RBBB when in sinus.  

For the first rhythm, he suspected atrial flutter with 1:1 conduction.

At EP study, he was right on both counts, and underwent ablation of fascicular VT as well as cavo-tricuspid isthmus ablation to eliminate the atrial flutter loop.

The patient did very well.

Final Diagnosis:

1. Atrial Flutter at rate of 302 with 1:1 conduction and ventricular rate of 302 with RBBB.
2. Right Bundle Fascicular Re-entrant Tachycardia.