Phillip Hughes

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Phillip Hughes

Like many cricket lovers around the world, I had a soft spot for Phil Hughes. I can still remember the dread I felt as an England supporter watching him thrash a very good South African attack for back to back hundreds. What on earth would he do to our bowlers? Given that he was only 20, I thought we could have another 15 years of watching him put the best bowlers in the world to the sword. Sadly, this will never now come to pass.  Given he was only 25, I agreed with Alan Border – Hughes would still play a 100 tests. Sadly, I was wrong again.

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 A Rare Tragedy

An out of hospital cardiac arrest can be terrifying – many of us struggle outside of our comfort zone.  The idea that this could happen to a 25 year old in the prime of his sporting career is terrifying.  It has happened before (and been widely reported) but because it is relatively rare it is truly confronting.  We had all hoped for a similar outcome to that of Fabrice Muamba in the English Premier League in 2012 but tragically two days after being struck by the ball Phillip Hughes succumbed to his injuries.

Clearly, this injury (apparently a Verterbral Artery Dissection leading to Subarachnoid Haemorrhage) was absolutely catastrophic.  This terminal injury would have been fatal regardless of the available management at the scene or in the nearby hospital.  Having said this, like many others who have seen the news report’s footage I have several questions about the initial care provided.  When the dust settles, I think these things should be thought about because we can always try and do better.  Next time the sports person or crowd member may have a survivable injury that needs a rapid response.  So with this in mind perhaps we need to make some changes in the future not only in cricket but in all major sporting events…

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Reports of The Event

I am puzzled by some of the reporting in the Sydney Morning Herald (SMH) as it seems to be contradicted by the available footage of the tragedy.  The SMH’s claims such as “the team doctor who intubated him with oxygen from the ground’s new defibrillator” or “Watson and Haddin, …placed their former Blues teammate in the brace position”.  This narrative of the media as a whole seems to be the bystander medics at the game did exactly the right thing (despite apparently not providing compressions or ventilations) and that the ambulance service are the apparent villains for a delayed low priority response.   It all seems to be very shocking but from what I can deduce there was in fact a degree of disbelief and inaction on the part of bystanders until the terrible realisation that Phillip was not breathing became apparent.

For the moment, however, let’s acknowledge that all the Emergency Responders did their best at the time under very difficult circumstances and they gave Phil Hughes a “fighting chance” with minimal resources.  I’ve provided the links below so you can make up you own mind about the information reported:

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“Hands Only CPR”

If a player collapsed during a game in the local park, how many people present would know what to do? It is actually a concern that not enough people know how to (or are willing to) perform basic CPR.  And it is now so simplified. You don’t have to do mouth to mouth, you just do chest compressions – hard and fast – till the ambulance gets there. Forget about feeling for a pulse. If they are unresponsive and not breathing normally, call for an ambulance and start chest compressions. You won’t do any harm and you may save a life.  So what are the barriers?  Is it cultural? Or is it just disbelief that a young person can just collapse and stop breathing on the field of play?

This area is currently highly topical in the literature – just in September the EMJ published a study looking at (specific local) attitudes into providing bystander CPR:

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In both the United Kingdom and the United States there were television adds teaching “hands only CPR”

 

In 2013 The Australian Resuscitation Council had a YouTube CPR video competition to “to facilitate the mission of the Australian Resuscitation Council (ARC): that “any attempt at resuscitation is better than no attempt”. The results were brilliant:

I’m not sure if these videos were ever shown on TV but perhaps it is time that they were…

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Medical Help at Major Sporting Events

  • What should the role of the team doctor be?  
  • What help should be available at sporting events?
  • Is the team doctor there to treat minor sprains or fractures or is he there in case a player sustains a critical injury?

If one was to expect a plethora of critical illness at a game then the team doctor should be some-one whose day job involves the initial resuscitation of the critically ill; in other words, an ED doctor or anaesthetist.  However, these tragic events are really just so rare and low crowd numbers at State Level cricket are too small to justify the presence of medical team or ambulance to treat emergencies in the crowd.  Even in large sporting events a critical care practitioner would generally be redundant.  

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Why training and preparation are important?

From my understanding of the history of these type of tragic events even with large crowds and trained responders there is no guarantee of a rapid response.  Perhaps this is due to the disbelief that athletes in the prime of their fitness and ability could just drop on the field of play.  A classic example of this was Hank Gathers a college basketball player who died of a Cardiac Arrest on call in the 1990s:

CLICK HERE (warning – confronting footage)

Similar cases have been reported in many sporting areas leading to campaigns to have defibrillators at sporting events.  Organisations such as the Craig Hodgkinson trust advocate and fund defibrillators (AEDs) at all sporting events:

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For more on the Craig Hodgkinson Trust – CLICK HERE

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The Future

Perhaps the current role and training of the sporting team medical support staff should be looked at. Is the team doctor there to treat minor sprains or is he there in case a player has a critical injury?  The set-up of having a trained critical care doctor at every game is not practical in most circumstances so perhaps training the public and non specialised medical teams is the key.  The key components of training would include simplified first aid (basic life support) with a focus on “real life” practice, operation of AEDs and time spent in training sessions on the discussion of the barriers to responding. These changes would be a pertinent change to future practice and may save a life where there is a reversible pathology.

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REMI 2011. CMI para vancomicina y mortalidad en pacientes con bacteriemia por S. aureus





Artículo original: Association between vancomycin minimum inhibitory concentration and mortality among patients with Staphylococcus aureus bloodstream infections: a systematic review and meta-analysis. Kalil AC, Van Schooneveld TC, Fey PD, Rupp ME. JAMA 2014; 312(15): 1552-1564. [Resumen] [Artículos relacionados]
      
Introducción: Tras más de 50 años de uso, la concentración mínima inhibitoria (CMI) de la vancomicina para el Staphylococcus aureus (SA) se ha ido elevando. Según algunos estudios, las CMI más elevadas, aunque aún dentro de la susceptibilidad, se puede asociar con un aumento del fallo del tratamiento y de la mortalidad, lo que ha ocasionado que se empleen otros antibióticos en estos casos. Tres metanálisis previos muestran esta asociación, pero incluyen una población de pacientes muy heterogénea, diferentes sitios de infección y evalúan principalmente el fallo del tratamiento, que es un desenlace susceptible de sesgo. El objetivo de este nuevo metaanálisis es averiguar si una CMI elevada, aunque dentro del rango de la susceptibilidad, se asocia con mayor mortalidad o peores resultados en pacientes con bacteriemia por SA.
      
Resumen: Se buscaron en diversas bases de datos estudios que comunicaran mortalidad y CMI de vancomicina en pacientes con bacteriemia por SA hasta abril de 2014. Se definición como elevada una CMI > 1,5 mg/L. El desenlace principal fue la mortalidad de todas las causas y se usó un modelo de efectos aleatorios. Se encontraron 38 estudios que cumplían los criterios de inclusión, con 8.291 pacientes. La mortalidad global fue del 26,1%. La mortalidad estimada para los pacientes con CMI elevada fue del 26,8% y la de los pacientes con CMI baja de 25,8% (diferencia de riesgo DR ajustada 0,6%; IC 95% -2,3 a -5,6; P = 0,43). En los estudios de mayor calidad, la mortalidad estimada fue de 26,2% para los pacientes con CMI elevada y de 27,8% para los de CMI baja (DR ajustada 0,9%; IC 95% -2,9 a -4,6; P = 0,65). En los estudios que incluyeron solo SARM, las mortalidades fueron respectivamente de 27,6% y 27,4% (DR ajustada 1,6%; IC 95% -2,3 a -5,5; P = 0,41). Los resultados fueron semejantes cuando se valoraron diferentes puntos de corte para la CMI, el tipo de ensayo empleado, la presencia de heterorresistencia a la vancomicina, la presencia de endocarditis o la exposición previa a la vancomicina.
      
Comentario: Aunque estos hallazgos no pueden descartar definitivamente un aumento del riesgo de mortalidad, el gran tamaño de la muestra y el bajo grado de heterogeneicidad fortalecen los resultados de este metanálisis. Con ellos, una diferenciación rutinaria de valores de CMI de menor o mayor de 1 mg/L no parece necesaria. Debería valorarse más la evolución clínica, el control del foco o la búsqueda de fuentes ocultas de infección antes de cambiar a antibióticos alternativos a la vancomicina basándose en una CMI elevada aunque dentro del rango de sensibilidad. Tampoco se justifica el uso de un antibiótico alternativo en el caso de los SARM por una CMI ≤ 2 mg/L.
      
Ramón Díaz-Alersi
Hospital U. Puerto Real, Cádiz.
© REMI, http://medicina-intensiva.com. Noviembre 2014.
        
Enlaces
  1. The clinical significance of vancomycin minimum inhibitory concentration in Staphylococcus aureus infections: a systematic review and meta-analysis. van Hal SJ, Lodise TP, Paterson DL. Clin Infect Dis 2012; 54: 755-771. [PubMed] [Texto completo]
  2. Impact of vancomycin minimum inhibitory concentration on clinical outcomes of patients with vancomycin-susceptible Staphylococcus aureus infections: a meta-analysis and meta-regression.Mavros MN, Tansarli GS, Vardakas KZ, Rafailidis PI, Karageorgopoulos DE, Falagas ME. Int J Antimicrob Agents 2012; 40: 496-509. [PubMed
  3. High vancomycin minimum inhibitory concentration and clinical outcomes in adults with methicillin-resistant Staphylococcus aureus infections: a meta-analysis. Jacob JT, DiazGranados CA. Int J Infect Dis 2013; 17: e93-e100. [PubMed
Búsqueda en PubMed
  • Enunciado: estudios clínicos sobre la CMI de la vancomicina para el S. aureus 
  • Sintaxis: clinical trial AND vancomycin AND minimum inhibitory concentration AND Staphylococcus aureus 
  • [Resultados
      

PEA made simple

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PEA made simple

The way we learn to manage pulseless electrical activity (PEA) from the Advanced Cardiac Life Support course is a mockery wrapped up in a sham. The mnemonic is cumbersome and the treatment (such as CPR for all, empiric epinephrine) is not always appropriate for a patient with normal electrical activity and a pulse. Fear not, […]

ercast.org - Emergency medicine podcasts, reviews and curbside consults

Visualizing PPV for Intuitive Understanding and Application

Resus Review

A 1978 study by Casscells showed that physicians were dismal at using PPV test characteristic (positive predictive value, Bayes estimation) for assessing the value of a laboratory test. It was repeated this year with similar disappointing results. Both studies posed a simple question on application of laboratory test results given the test characteristics.

Here is the question both studies used.

“If a test with perfect sensitivity to detect a disease whose prevalence is 1/1000 has a false positive rate of 5%, what is the chance that a person found to have a positive result actually has the disease, assuming you know nothing about the person’s symptoms or signs?”

Only 25% got it right. The others were spectacularly wrong.

Using PPV and Bayes Formula

There are several ways to solve this problem. Shown below is how calculate the answer using PPV and Bayes formula.

PPV and Bayes formula solution for problem

Visualizing PPV

While understanding the math is important, you can develop a more intuitive understanding by visualizing the population (see figure below). If a draw a sample of 1000 patients from the population (all of the dots), only one will have the disease (red dot). Since the test has a 100% sensitivity, it will be a true positive. The remaining 999 patients do not have the disease, but 50 of them will test positive (blue dots), and the rest will test negative (black dots).

Notice that the false positive blue dots far out number the true positives. If this hypothetical example, those patients would be subjected to unnecessary further workup or treatment.

Visualization of sample population

Visualization of a sample population of 1000 patients. Red dots represent true positive patients, blue are false positives, and black are true negatives.

The solution to the posed question then is easy to see. If your patient has a positive test (which 51 out of 1000 would), only 1 actually have the disease. 1/51 is then calculated at 1.96%. PPV calculation done by visualization without any formula memorization.

References

  1. N Engl J Med 1978;299(18):999. Interpretation by physicians of clinical laboratory results.
  2. JAMA Internal Medicine 2014;174(6):991. Medicine’s Uncomfortable Relationship With Math: Calculating Positive Predictive Value.

Is PPV intuitive for you? Share your thoughts below.

Visualizing PPV for Intuitive Understanding and Application

20 year old woman with dizziness and hypotension

This is posted courtesy of Jaber Ibrahim Almajbri.  He posted it on Facebook EKG club and gave me permission to post it here.

This 20 year old has hypotension, 70/40.
What is it?























 It is irregularly irregular, so it is atrial fibrillation.  The QRS complexes are not all the same, so it is not just atrial fib with aberrancy (RBBB, LBBB, other IVCD).   Some R-R intervals are less than 160 ms, corresponding to a possible heart rate of almost 400.   The AV node cannot conduct this fast. These are conducting down an accessory pathway.

Thus, it is atrial fibrillation with WPW.

I doubt that one could really get a diastolic BP at this rate.  This case shows how fast the heart rate can be in this condition.

This can easily degenerate into ventricular fibrillation, especially if any AV nodal blocker is given.  This must be cardioverted immediately.

Then the patient will need ablation by an electrophysiologist.

A Young woman with chest pain: The Conclusion

Let’s welcome Dr. Shafer back to the blog.  Between being a chief resident and being accepted in to a critical care fellowship, she has another interesting case presentation for you.  Some really interesting learning points on this one.  Here is a link to the original post in case you missed it, and here is the answer…

-Bob

Diagnosis: Spontaneous LAD dissection

This is an unusual diagnosis that is mainly described as case reports in the literature.  In 1996 only 100 cases in the world had been identified (2). Of these reported cases, 75% were diagnosed at autopsy and the rest were diagnosed with coronary angiography (1). The majority of these cases (approximately 75%) were in women, and of these cases, 32% of the patients were pregnant, post-partum, or taking oral contraceptives (2). One study in 2009 observed that one out of ten women under the age of 50 who clinically presented with ACS instead had a coronary dissection on coronary angiography (3). 

LAD dissection is considered especially disastrous and results in malignant arrhythmias, severe CHF, extensive infarct and sudden death (2). The clinical presentation of coronary dissection is similar to that of a patient having an acute MI, but they are usually younger and without the cardiac risk factors.  It is important to note that spontaneous coronary dissection can be recurrent. The etiology of this disease is unclear, but some autopsies have demonstrated an eosinophilic penetration of the tunica adventitia and it is postulated that this subsequently causes damage to the collagen, elastin and smooth muscle wall (2). Treatment options for these patients include medical management only versus stenting versus bypass surgery. There is no treatment standard at this time and the prognosis of these patients who survive is unknown. However, the case reports overall seem to demonstrate that at least one year post-event survival rate is quite high. 

For our case presentation, the patient was emergently taken to the cath lab where her diagnosis of spontaneous LAD dissection was made. She was stented at this time and started on Aspirin, Metoprolol, and Effient.  She had a complicated hospital course, developing pericarditis, a small pericardial effusion,  and a new apical thrombus. Ultimately, however, after a week her symptoms had dramatically improved and she was discharged home. 

Spontaneous coronary dissection is a rare but rapidly fatal diagnosis that should be considered in the differential diagnosis of young patients who present with symptoms of ACS; it can be both diagnosed and treated in the cath lab.  Remember that diffuse ST segment elevation in the younger patient with chest pain will not always equate to a diagnosis of pericarditis.

  1. Spontaneous Coronary Artery Dissection, Aneurysms, and Pseudoaneurysms: A Review. Echocardiography. 2004: 21(2), 175-182.
  2. Zampieri et al. Follow up after spontaneous coronary artery dissection: a report of five case series; Heart.1996: 75, 206-209.
  3. Vanzetto, et al. Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: results from a database of 11,605 patients. European Journal of Cardio-thoracic Surgery. 2008: 35 (3), 205-254.