Concussions: Tough Love

by Nicholas Otts, MD

edited by Gal Altberg, MD

A Common Problem:

16 y F presents with headaches, nausea, cloudy mentation, and irritability a day after heading a ball during a soccer game. You diagnose a concussion. Parents want to know when she should start exercising again and when she can go back to school?                          

 Two female soccer players competing for the ball, aerial view.

A Small Dose of EBM:

Many physicians commonly advocate for both physical and mental rest following concussion, but the evidence for that practice is lacking.  Let’s break it down into two areas, PHYSICAL and MENTAL.

**PHYSICAL **

Evidence for physical rest post concussion is based on old small observational studies, animal models, and “expert consensus” opinions, which in the EBM world is the same thing as letting the patient’s Mother and Google decide what is best.

Evidence that does exist suggests aerobic physical activity is beneficial in the initial week post concussion.

A prospective, multicenter cohort study showed physical activity within a week (versus no physical activity) was associated with reduced risk of persistent postconcussive symptoms a month later (1). A prospective randomized control trial showed similar benefit (2). Further, another study suggested that patients that had prolonged symptoms a week after the initial event, aerobic physical activity improved symptoms and was beneficial to recovery (3).

(*Important caveat: these studies refer to aerobic physical activity that does not risk further head injury. This does not mean the patient can return to whatever exercise activity he or she wants.)


Thus, the tough love advice of getting the athlete back on the exercise bike (but off the football field) is probably the better approach than nurturing them on the couch with Netflix and pizza.

**MENTAL**

The current approach is to suggest “mental rest,” until the patient has no further symptoms, which includes a prescription for staying home from school, avoid reading or writing, and “stimulating” video games.

The evidence for this approach is based on expert consensus and observational studies, which, again, is not ideal for clinical decision making (4,5,6).

1107_gsoccer1 01 1107_gsoccer1 01

A prospective trial previously mentioned (2) actually suggested that cognitive rest lengthened duration of post concussive symptoms.

Bottom line, if you prescribe cognitive rest or cognitive activity as tolerated, the evidence so far will not back you either way.  But I think it reasonable to suggest that children attempt as much mental activity as they can tolerate without worsening symptoms. Thus, the tough love approach in this scenario may also be best.

References:

1 Grool AM, Aglipay M, Momoli F, et al. Association Between Early Participation in Physical Activity Following Acute Concussion and Persistent Postconcussive Symptoms in Children and Adolescents. JAMA 2016; 316:2504.

2 Thomas DG, Apps JN, Hoffmann RG, et. al. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics 2015; 135:213.

3 Leddy JJ, Kozlowski K, Donnelly JP, et al. A preliminary study of subsymptom threshold exercise training for refractory post-concussion syndrome. Clin J Sport Med 2010; 20:21.

4 Brown NJ, Mannix RC, O’Brien MJ, et. al. Effect of cognitive activity level on duration of post concussive symptoms. Pediatrics 2014; 133: e299.

5 Sady MD, Vaughan CG, Gioia GA. School and concussed youth: recommendations for concussion education and management. Phys Med Rehabil Clin N Am 2011; 22:701.

6 Howell D, Osternig L, Van Donkelaar P, et. al. Effects of concussion on attention and executive function in adolescents. Med Sci Spots Exerc 2013; 45: 1030.

 

This EKG comes courtesy of Paramedic Guttman!

67 y/o male with a history of MS c/o chest pain and weakness.
The following rhythm strips are obtained.

1. How would you describe this rhythm?
2. How would you manage this patient?

 

ANSWER:

The rhythm strip begins with an escape rhythm (likely junctional) followed by a very long pause with complete AV block and no escape rhythm. It then converts back to a junctional escape rhythm.

The patient should be treated with pacing if they are symptomatic or if the escape rhythm does not return.

 

The rhythm begins with a wide complex rhythm at a rate of 60 with absent P waves.

Escape rhythms can be junctional or ventricular. Junctional rhythms are usually at a rate of 45-60. They usually have a narrow QRS complex unless the patient has an underlying bundle branch block. Ventricular escape rhythms are usually at a rate of 30-45 with a wide QRS complex. Our patient has an underlying bundle branch block. The initial rhythm likely represents a junctional escape rhythm.

After the first four beats there is a long pause. Pauses on EKG can be caused by: 1) non-conducted PAC’s (most common cause); 2) sinus node disease (Sinus arrest or SA block); 3) AV block.

In a non-conducted PAC, you will see a P wave that comes earlier than expected with no QRS complex following it. This happens because the PAC occurs so early that when it hits the AV node, it is still refractory. The P wave may come so early that it is buried in the preceding T wave just before the pause. Look back at the last T wave before the pause and see if it looks different than the other T waves on the strip. If it looks different, it might be because there is a P wave buried in that T wave. An example is below.

In sinus node disease, you will see a pause with no P waves. In sinus arrest, the SA node takes a little vacation and doesn’t fire. So there will be a pause with no P waves and the length of the pause will be random. In SA block, the SA node continues to fire but can’t depolarize the atrium. So, again there are absent P waves, however the length of the pause will be a multiple of the normal P-P length. Meaning, if you make believe a P wave happened during the pause at it’s expected location, the next P wave will come on time. An example is attached.

Finally, if the pause is due to AV block (2nd or 3rd degree), there will be P waves coming on time with no QRS complex following. Differentiate 2nd degree from 3rd degree and 2nd degree type I from type II the same way you would in any other AV block.

The following algorithm is useful in diagnosing pauses:

In our patient, there is a long pause. There are P waves present and they do not come earlier than expected. So, they are not PAC’s. Since there are P waves present during the pause, it is not sinus arrest or SA block. So, we are dealing with an AV block. In this case there are P waves only with no QRS complexes at all. So, there is no conduction to the ventricles at all so we are dealing with a 3rd degree AV block. Usually a 3rd degree AV block is accompanied by an escape rhythm. During this long pause, there is no escape rhythm that kicks in. Later on the strip (b), the junctional escape rhythm returns.

Patients with long pauses that are symptomatic or unstable should be treated with transcutaneous (pre-hospital) or transvenous (in-hospital) pacing.

Our patient had a cardiac cath which showed clean coronaries. He then had a permanent pacemaker placed.

Double Sequential Defibrillation

Double Sequential External Defibrillation for Refractory Ventricular Fibrillation

Ilya Litvak, DO             Mikhail Podlog, DO            Anna Van Tuyl, MD

 

Ventricular fibrillation (VF) is the most common initial dysrhythmia after out-of-hospital cardiac arrest(OHCA) occurring in approximately 70 % of the cases.  VF  is also considered the rhythm with the highest likelihood of neurologically intact survival (1). Unfortunately, there is a subset of patients who do not respond to standard ACLS algorithm for VF and are termed to have refractory ventricular fibrillation (RVF).

 

What is refractory ventricular fibrillation?

The exact definition of RVF is subject of debate. However, the literature in the past has used persistent VF without response to at least five single defibrillations (including AED) as the definition of RVF.  One intervention that has been reported to terminate RVF is double sequential defibrillation (DSD).

 

What factors affect successful defibrillation?

Successful defibrillation depends on several variables, including pad placement, total energy used, length of stay in VF, and patient’s body habitus (2). Zhang et al. demonstrated in swine models that body mass had inverse relationship with the success of defibrillation (3).  Other studies have shown lower success rates in cardioversion of atrial fibrillation in patients with BMI >25 (4).

The amount of energy is also an important factor in successful defibrillation. Although there are concerns that higher energy may result in myocardial injury or chest wall trauma, several studies have shown safety of high energy defibrillation in humans. For example, Stiell et al. found no deleteriouseffects of biphasic defibrillation up to 360 J (5).  Multiple other studies have found no deleterious effects in subjects cardioverted for atrial fibrillation with energy levels of up to 720 J monophasic. 

 

What is Double Sequential Defibrillation?

Double sequential external defibrillation refers to the use of two simultaneous defibrillator pads to deliver the shock. In addition, to increased energy, another theory behind this set-up is that the addition of a second pair of defibrillator pads allows for two alternative vectors of energy delivered to fibrillating myocytes. This allows the energy to overcome limiting factors, such as poorly placed electrodes and the air in the lungs, which otherwise divert the vectors from fibrillating myocardium.(6). Yet another theory postulates that the first defibrillation serves to lower the threshold for successful shock with the second defibrillation (7).

 

How should the pads be positioned?

There is no clear evidence on which pad placement is ideal. Two sets of pads can be placed in anterior-posterior (AP) orientation, antero-lateral (AL) or AP/AL orientation. 

 

Evidence

The first report of DSD in VF patient was described in 1994 by Hoch et al. in the electrophysiology literature (8). This case series paper described 5 patients with WPW or other cardiomyopathies undergoing routine studies in the electrophysiology lab. All five subjects had VF intentionally induced as part of their evaluation. In this study, patients failed to convert to normal sinus rhythm with monophasic energies ranging from 200-360 J, but all of them responded to double shock with a total of 720 J. However, until recently there has been paucity of data (limited mostly to case reports) supporting the use of DSD in the Emergency Department or OHCA. 

One recent paper in Resuscitation by Cortez et. Al from August 2016 shows promising evidence for the use of DSD for RVF in OHCA  (9).  In this retrospective chart review, 2428 OHCA events were reviewed with 12 patients treated with DSD. Nine patients out of twelve were successfully converted out of ventricular fibrillation. Of the patients treated with DSD, three patients survived to hospital discharge with good neurologic function.

Also important to note is that the median time to DSD was 27 minutes in the above study. This is significantly shorter than reported values in other papers. This may mean that DSD maybe more effective when incorporated earlier in resuscitation efforts of VF arrest.

Although the above paper provides promising evidence for DSD it has several important limitations including small sample size and retrospective case series nature of the study. Unfortunately, to date there are no double blind randomized control studies on DSD to determine its efficacy.

 

Conclusion

Management of RFV remains challenging and when standard ACLS measures have failed DSD may be another tool that can be utilized to achieve ROSC in RVF patients.

 

____________________________________________________

1 Holmberg M. Holmberg S. Herlitz J. Incidence, duration and survival of ventricular fibrillation in out-of-hospital cardiac arrest patients in Sweden. Resuscitation 2000.44:7-17

2 Morrison LJ, Dorian P, Long J. et al Out- of- hospital cardiac arrest rectilinear biphasic to mopnophasic damped sine defibrillation waveforms with advanced life support intervention trial (ORBIT). Resuscitation 2005; 66 :149-57

3 Zhang Y, Clark CB, Davies LR, Karlsson G, Zimmerman MB, Kerber R. Body weight is a predictor of biphasic shock success for low energy thranthorasic defibrillation. Resuscitation 2002; 54:281-7.

4 Glover BM, Walsh SJ, McCann CJ, et al. Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. The BEST AF Trial. Heart 2008;94:884-7

5 Stiell IG, Walker RG, Nesbitt LP, et al, BIPHASIC Trial: a randomized comparison of fixed lower versus escalating higher energy levels for defibrillation in out-of-hospital cardiac arrest. Circulation 2007;115:1511-7

6 Ristagno G, Yu T, Quan W, Freeman G, Li Y. Comparison of defibrillation efficacy between two pads placements in a pediatric porcine model of cardiac arrest. Resuscitation 2012;83:755-9

7 Kerber RE. Indications and techniques of electrical defibrillation and cardioversion. In: Fuster V, Walsh R, Harrington RA, editor. Hurst's the heart. 13th ed. New York, New York: McGraw-Hill; 2011

8 Hoch DH, Batsford WP, Greenberg SM, et al Double sequential external shocks for refractory ventricular fibrillation. J Am Coll Cardiol 1994;23:1141-5

9 Cortez E et al. Use of Double Sequential External Defibrillation for Refractory Ventricular Fibrillation During Out-of-Hospital Cardiac Arrest. Resuscitation 2016. S0300-9572(16): 30398 – 7.

 

EKG of the Week 2017 2-19

A 52 y/o male with history of hypertension, smoker, presents to the ED complaining of chest pain and SOB. His vital signs are normal. His EKG is below.

1.    What does the EKG show?

2.    How would you manage this patient?

 

ANSWER:

The EKG shows a posterior wall MI

This patient should be treated like a STEMI. He should go emergently to the cath lab for PCI or receive tPA.

 

The EKG shows R waves with ST depressions in leads V1-V3 (as well as V4-V6, I and aVL). R waves with ST depressions in leads V1-V3 is consistent with a posterior wall MI.

Remember that the heart is a 3 dimensional structure. That means that it has an entire posterior side as well. Just as the anterior wall, the lateral wall, and the inferior wall can infarct, the posterior wall can infarct as well. Most of the time, the posterior wall does not infarct by itself. It usually occurs together with an inferior wall or infero-lateral MI. However, infarctions of the posterior wall alone can occur in up to 4% of MI’s. In these cases, the other walls of the heart will be normal. None of the standard 12 leads look directly at the posterior wall. So, how can we recognize a posterior wall MI on a 12 lead EKG? We have to infer the presence of a posterior wall MI based on reciprocal changes.

ST depressions can be a sign of primary ischemia, or they can be a reciprocal change of ST elevations in the opposite wall of the heart. Reciprocal ST depressions occur in the leads opposite the wall with the ST elevations. ST depressions in leads V1-V3 are a reciprocal change of ST elevations in the “opposite wall”. The opposite wall of the antero-septum is the posterior wall. ST depressions with R waves in leads V1-V3 are seen in a posterior wall MI.

Imagine a mirror situated between the posterior wall and the anterior wall. If an acute MI occurs in the posterior wall, it would cause ST elevations and Q waves.  Since we can’t see the posterior wall on a standard 12 lead EKG, we can only see the “mirror image” of the posterior wall in the antero-septal leads. The mirror image of ST elevations and Q waves is ST depressions and R waves. So, when we see ST depressions and R waves in leads V1-V3, that indicates a posterior wall MI.

Some people will actually take this EKG and turn it upside down and backwards, and look at leads V1-V3 through the back of the page. If you do that, you will see ST elevations and Q waves.

To confirm a posterior wall MI, you can do posterior leads. Place leads V8 and V9 on the left back. They are placed at the same intercostal space as lead V6. Lead V8 is placed in the midscapular line. Lead V9 is placed at the left spinal border. Now run the EKG again and look for ST elevations in leads V8 and V9. If they are present, that is diagnostic of a posterior wall MI. The EKG below demonstrates posterior leads.