Endovascular for Stroke – Even Better than the Evidence

What happens when you let Medtronic, et al, author an article on endovascular therapy in The Lancet:  exactly what you'd expect.

We are, in principle, fans of endovascular therapy for acute stroke as presented in the major trials: ESCAPE, EXTEND-IA, and SWIFT-PRIME.  These trials carefully selected eligible patients by use of advanced perfusion imaging and demonstrated high rates of revascularization.  Viable brain plus restored flow has face validity for improved outcomes.

However, these sponsored authors use the meta-analysis for its most nefarious purpose: to obfuscate the important subtleties and eligibility criteria of its included trials.  These authors pool the aforementioned trials, along with MR CLEAN and REVASCAT to provide the following conclusion:
“Endovascular thrombectomy is of benefit to most patients with acute ischaemic stroke caused by occlusion of the proximal anterior circulation, irrespective of patient characteristics or geographical location.”(emphasis mine)
The authors also provide a staggering number-needed-to-treat for endovascular therapy of 2.6.

But, of course, this was written to shock and awe the lay press and general medicine community, rather than edify the astute clinician.  Their NNT is not based on the typical dichotomous cut-off used in stroke trials of mRS 0-1 or 0-2 – but rather the hopelessly flawed ordinal shift analysis.  As the decades turn, apparently, we have forgotten why this approach was frowned upon from the start: it is not appropriate to equate the outcome value difference between mRS 5 and 4 with the difference between mRS 3 and 2, and the limitations in inter-rater reliability in the mRS introduce a vast additional amount of measurement error.  Then, by burying any mention of the strict imaging criteria responsible for the bulk of benefit seen in these trials, they mislead the reader into considering this therapy appropriate for all-comers.

Is there any value to these data as presented?  A little.  There is hypothesis generating evidence that tPA prior to endovascular therapy provides no additive benefit.  There is also evidence that increasingly distal sites of occlusion may not benefit from intervention.

Unfortunately, the flaws in this article outweigh the few potentially usable insights.  This is just yet another piece of direct-to-physician marketing masquerading as scientific evidence.

“Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials”
https://www.ncbi.nlm.nih.gov/pubmed/26898852

REMI 2126. El daño alveolar agudo se asocia a un aumento de mortalidad en pacientes con síndrome de distrés respiratorio agudo

ARTÍCULO ORIGINAL: The presence of diffuse alveolar damage on open lung biopsy is associated with mortality in patients with acute respiratory distress syndrome: a systematic review and meta-analysis. Cardinal-Fernández P, Bajwa EK, Dominguez-Calvo A, Menéndez JM, Papazian L, Thompson BT. Chest 2016. [Resumen] [Artículos relacionados]
    
INTRODUCCIÓN: La relación entre el síndrome de distrés respiratorio agudo (SDRA) y el daño alveolar difuso (DAD) ha sido postulada desde hace años; sin embargo su significado ha sido muy controvertido dado que 1) la correlación entre SDRA y DAD es moderada [1]; 2) realizar el diagnóstico de DAD en la práctica clínica es un gran desafío, pues no existen biomarcadores subrogados de DAD y todos los procedimientos para obtener tejido pulmonar son invasivos y asociados a efectos adversos [2], y 3) se desconocía el efecto del DAD sobre el SDRA [3]. En el año 2015, en un grupo de 149 autopsias de pacientes con SDRA se demostró por primera vez que la presencia de DAD se asocia a una evolución clínica y analítica diferente de la del resto de los pacientes (edad, puntuación en la escala SOFA, índice PaO2/FiO2, distensibilidad pulmonar, INR y causa de muerte) [4]. Adicionalmente se desarrolló un modelo predictivo para DAD basándose en 3 variables (edad, PaO2/FiO2 y distensibilidad pulmonar), medidas en el momento de diagnosticar el SDRA, cuya capacidad discriminativa, objetivada mediante el área baja la curva ROC, fue de 0,74 (en la cohorte internacional de validación fue de 0,73).
   
RESUMEN: En el presente metaanálisis se evalúo específicamente el efecto del DAD en pacienteS con SDRA. Se incluyeron 8 estudios con 350 pacientes en total. Los hallazgos más relevantes fueron: (a) que la proporción de DAD es del 45% (IC 95%: 35-56%), y (b) que el DAD se asocia con un aumento en la mortalidad (OR 1,81; IC 95% 1,14-2,80).
  
COMENTARIO: Estos resultados demuestran que el SDRA y el DAD constituyen una entidad clínico-patológica específica y distinta del SDRA sin DAD. Esta demostración no es un simple ejercicio académico, pues: (a) determina que debamos reinterpretar gran parte del conocimiento clínico respecto al SDRA, especialmente todo aquel derivado de estudios en los cuales no se consideró la histología, (b) influirá dramáticamente en el diseño de futuras investigaciones clínicas y translacionales. Por ejemplo, es posible que al ensayar un fármaco para el SDRA se deba identificar a los pacientes con el patrón de oro y no tan solo con el SDRA como hasta ahora. Por todo lo cual, identificar biomarcadores subrogados de DAD en pacientes con SDRA constituye una de las principales prioridades que debemos afrontar [5].
   
Cardinal-Fernandez P.
Hospital Universitario HM Sanchinarro, Madrid.
Department of Genetic Medicine - Weill Cornell Medical College, New York.
pablocardinal@hotmail.com
© REMI, http://medicina-intensiva.com. Abril 2016.

ENLACES:
  1. Comparison of the Berlin definition for acute respiratory distress syndrome with autopsy. Thille AW, Esteban A, Fernández-Segoviano P, Rodriguez JM, Aramburu JA, Peñuelas O, Cortés-Puch I, Cardinal-Fernández P, Lorente JA, Frutos-Vivar F. Am J Respir Crit Care Med 2013; 187: 761-767. [PubMed]
  2. Acute Respiratory Distress: from syndrome to disease. Cardinal-Fernández P, Correger E, Villanueva J, Rios F. Med Intensiva 2016; 40: 169-175. [PubMed]
  3. ARDS: lessons learned from the heart. Cardinal-Fernández P, Esteban A, Thompson BT, Lorente JA. Chest 2015; 147: 7-8. [PubMed]
  4. Acute respiratory distress syndrome in patients with and without diffuse alveolar damage: an autopsy study. Lorente JA, Cardinal-Fernández P, Muñoz D, Frutos-Vivar F, Thille AW, Jaramillo C, Ballén-Barragán A, Rodríguez JM, Peñuelas O, Ortiz G, Blanco J, Pinheiro BV, Nin N, del Carmen Marin M, Esteban A, Thompson TB. Intensive Care Med 2015; 41: 1921-1930. [PubMed]
  5. ARDS: Time to “separate the wheat from the chaff”. Cardinal-Fernández P, Pey C, Kao KC. J Crit Care 2016. [PubMed (pendiente)]
BÚSQUEDA EN PUBMED:
  • Enunciado: Histología del daño alveolar difuso en el SDRA
  • Sintaxis: "Acute respiratory distress syndrome" AND "diffuse alveolar damage" AND histology 
  • [Resultados]
[https://www.facebook.com/medicina.intensiva2.0] [https://www.facebook.com/groups/forodeuci/]
    

EKGs you don’t know: de Winter’s waves

winter waves2

Chest pain: the bread and butter of emergency medicine. We see so many of these that it can be mind-numbing, and for EXACTLY that reason it’s critical to recognize those weird EKGs that aren’t an obvious STEMI but can signal a coronary occlusion.

One of the less-talked-about danger signs on EKG is “de Winter’s waves“, which is thought to represent acute LAD occlusion (similar to the more commonly known Wellen’s criteria):

  •  Tall, symmetric T waves in precordial leads
  • Upsloping ST segment depression in precordial leads (no ST elevation)
  • May have subtle ST elevation in aVR
  • T waves are often taller than the QRS

These waves can look similar to the peaked T waves seen in hyperkalemia, but are typically isolated to the precordial leads, and that’s the tipoff.

de Winter’s waves should be considered a STEMI equivalent, and the patient should be taken for urgent cath or considered for thrombolysis if cath is not available.

Take a look at several examples below. Would you recognize these as a STEMI?

Example 1

dewinter t waves 1

Example 2

deWinter t waves 2

And this last is a particularly subtle (likely) example from Dr. Smith’s ECG Blog (hqmeded-ecg.blogspot.com/). Note the sagging T waves in v3 and v4, and tall T waves in v2/3 are clearly visible that outsize the associated QRS. This patient was unfortunately discharged after one negative troponin and was found dead 12 hours later. Read the full case here.

Example 3

Adapted from Life in the Fast Lane and Dr. Smith’s ECG Blog.

 

The Impact Of Radiographic Image Sharing Systems On Trauma Transfers

There has been a big push to implement systems of trauma centers across the US, primarily at the state level. This move to get the right patient to the right hospital has resulted in an increased number of transfers, and rightly so. However, the referring hospital frequently performs some radiographic imaging before transfer

So it is critical that both the patient and their imaging get to the receiving hospital for good continuity of care. Failure to do so results in re-imaging, additional exposure to radiation, delays in care, and potentially increased costs. Radiologists may be reluctant to read outside images because they generally will not get paid for it.

Unfortunately, there are lots of barriers to getting those images to the receiving trauma center. They may forget to send a disc. The disc may not work on the receiving hospital’s computers. A direct connection between PACS systems may be lacking, or may not work. In any case, patient care may suffer.

Cloud solutions using web-based software and an intermediary for image storage and delivery have been around for years. Their use is inconsistent around the US, mainly because they cost money. A group in Ohio looked at the impact of implementing one of these system on the incidence of cost of re-imaging at their Level I trauma center. Four years of patient transfer data were reviewed for imaging at the first hospital, re-imaging at the trauma center, and charges. The authors compared re-imaging rates before and after the availability of the cloud sharing system.

Here are the factoids:

  • 1,081 transfers occurred during the study period, and 639 (59%) had at least one CT prior to transfer
  • 345 repeat scans were performed on 222 patients (35%)
  • The most common repeats were head CT (32%) and cervical spine (23%)
  • The overall re-scan rate was significantly higher before the cloud service was available (38%) vs after (28%)
  • If patient data was available from the cloud service, the re-scan rate dropped to 23% (??!)
  • Mean hospital charges for re-CT dropped from $1046 to $589

Bottom line: This study is interesting, but could use some improvement. It is older data (2009-2012), from the early days of these cloud services. Centers were a little less facile using them, which may have contributed to some of the soft numbers above. And the use of charge data rather than costs is old-school. 

Re-scanning a quarter of the patients, even when cloud images were available, is just not acceptable. However, this paper does suggest that there are real benefits, as re-scan rates and (presumably) costs should decrease. Radiation exposure would definitely drop, too.

The key to making a cloud sharing system work, or any other system for that matter (VPN, optical discs, etc), is to make it part of your PI program. Every transfer in needs to be scrutinized, and if an image transfer issue is found, quick feedback to the referring hospital needs to occur to ensure that it doesn’t happen again.

Related posts:

Reference: Implementation of an image sharing system significantly reduced repeat computed tomographic imaging in a regional trauma system. J Trauma 80(1):51-56, 2016.