Parachute use to prevent death and major trauma in gravitional accidentes: the first randomized controlled double blind trial!

3 Feb

© Copyright 2012 CorbisCorporationBusinessman falling in city center

Following the recent article published the on B.M.J. “Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials“ and its conclusions “We were unable to identify any randomized controlled trials of parachute intervention” so “the effectiveness of parachutes has not been subjected to rigorous evaluation by using randomised controlled trials”,
MEDEST proposes the first ever randomized controlled double blind  trial on:

Parachute use to prevent death and major trauma in gravitational accidents.

  • Study design: Double blinded, randomized controlled trial
  • Randomization: the enrolled participants (also called “precipitants”) will all precipitated from a 800 meters height. They will be blindly randomized in two groups:
  1. Precipitants with parachute
  2. Precipitants without parachute (control group)
The precipitants and the investigators will be both blinded for humanitarian reasons.
  • Major end-points: surviving rate at 5, 10, 30 minutes from the impact.
Enrolled starts as soon as resolved some minor ethical issues.
Scarica la traduzione in italiano del post.

It could be me!

24 Jan
A  Rescue Helicopter suffered a fatal crash in L’Aquila, Abruzzo, Italy. Six person died in the crash. Doctor, Nurse, Pilot, HHO, Mountain rescue expert, patient. linea_a_lutto_by_gigicave
The helicopter crashed during a routine HEMS mission.
The five people of the crew and the patient all died.

When something like that happens the first thought for an HEMS professional is:

IT COULD BE ME!

Then you start to rationalise the situation, mostly in a technical and non emotional way, and arrive at the conclusion:

NEVER WOULD HAPPEN TO ME. 

There are many reason, in my opinion, why we arrive at that. 

We all have family and friends to care about and who take care of us. And we can’t even imagine them devastated by grief.

Our major concern is about patients health and not about our safety. 

And finally, we are humans and human being self-protect their inner fragility, avoiding to hurt themselves thinking about death, especially their own .

But I know, and always will. that IT COULD HAVE BE ME despite any protection and self-lie.

Cause even the 6 persons  who died in the crash had family and friends that now live in a devastating grief.

Even them were taking care of patients over they own safety.

And also them were humans, like me. 

So WAS ME! 

Today a part of me ideally died in that crash.

Tomorrow a new day will begin, but from now on things will look different.

Logo MEDEST2

 

 

Sepsis: Sepsis 3, Surviving Sepsis Campaign what now?

23 Jan

From a practical clinical point of view, after the 2016 update of the SSC (Surviving Sepsis Campaign) guidelines we have two references when comes to deal with a potential septic patient. Question Marks Sphere Ball Many Questions Asked

2016 Sepsis 3 definition and early management.

2016 Surviving Sepsis Campaign

Let’s see how to treat, based on top evidences, a real patient in the the pre-hospital and emergency department time window. 

But, first of all,  the definitions:

  • Definitions

Both the guidelines now agree that:

“Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection“

“Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) despite adequate volume resuscitation”

  • Early identification

    1. SIRS criteria. The new 2016 SSC guidelines do not indicate any criteria for early identification of sepsis, so SIRS criteria no longer exists.
    2. qSOFA score (G.C.S. of 13 or less, SBP of 100 mm Hg or less, and RR 22/min or greater): Good negative and positive prediction value(similar to that sepsiscouchof the full SOFA score outside the ICU). Non specific for sepsis. It’s the actual early identification tool for sepsis to use out-of-hospital end in emergency department. It performs quite good to identify patients at risk of negative evolution. A qSOFA score ≥2 indicates a high mortality risk comparing to a qSOFA ≤1.
      sofa-score-1024x743
    3. SOFA score: indicates organ disfunction (when the score is >2 points) consequent to the infection and defines sepsis. Is a validated ICU tool to asses risk and mortality chance. Is not a tool to use out-of-hospital or in ED.
    4. The Pre-hospital Sepsis Score (PSS) or Miami Sepsis Score: As out-of-hospital professional I love pre-hospital early warning tools.I like to mention PSS cause is well validated to early recognise sepsis in the field. PSS includes Shock Index (HR/SBP) that is really sensible to identify critical evolution chance, RR that is included in qSOFA and other sepsis score plus body temperature (obligatory) that identifies an infection. Is for me the good compromise, in the field, between good positive and negative predictive value. A PSS of 1 point identifies a low risk patient, 2 points moderate risk, 3-4 points high risk patients.pss

  • Early management

    1. Early goal directed therapy: no longer recommended. CVP is no longer required and fluid response to initial volemic reanimation has to be clinically and dynamically assessed (passive leg raise, fluid challenges)
    2. Fluid resuscitation: 30 ml/Kg(in the first 3 hrs) to restore normal emodynamics values (MAP >65 mmHg). Lactate is a risk assessment tool (>2 mmol/L) and is no longer recommended to guide resuscitation efforts. Crystalloids are the fluids of choice. 
    3. Vasopressors: indicated if initial fluid resuscitation doesn’t reach the target. Norepinephrine is the pressor of choice. Epinephrine the second line agent in case Norepinephrine is not sufficiente to reach the target.Stop giving Dopamine.
    4. Bloodcultures: immediately and preferably before starting antibiotics but without delaying  antibacterial therapy. 
    5. Antibiotics: no double cover routinely but broad spectrum mono therapy is the recommended choice.
    6. Corticosteroids: consider just if patient is fully volume resuscitated and vasopressors are unsuccessful to maintain emodynamic stability.

Take home points for early phase management

Early Identification
Use either:
  • qSOFA (preferred in ED) cut off ≥2 points
  • PSS (preferred in the field) cut off ≥2 points.
Initial Management (target to a MAP >65)
  • Emodynamic stabilisation
    • 1st Fluid 30 ml/Kg of crystalloids.
    • 2nd Norepinephrine up to 35-90 μg/min (if 1st step failed).
    • Add Epinephrine up to 20-50 μg/min to achieve MAP target (if first 2 step failed).
  • Take blood cultures (if feasible before antibiotics but without delaying antibiotics).
  • Do not delay early broad spectrum antibiotic mono therapy.

 

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References 

 

 

 

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My favourite EM articles of 2016. Part 1.

19 Jan

Here are some articles that influenced my clinical practice and my clinical thinking during the last year.

They are not probably the best of all but are my choice, and are all free full text.

So read carefully the full article and judge yourself if worth  or not the mention.

Good reading to everyone. 

The state of the art: Moderate to high quality evidence suggests that compared with medical care alone in a selected group of patients endovascular thrombectomy as add-on to intravenous thrombolysis performed within six to eight hours after large vessel ischaemic stroke in the anterior circulation provides beneficial functional outcomes, without increased detrimental effects.

A radical change in definition and concepts of Sepsis and sepsis management . From SSC to Sepsis 3. Not a worldwide accepted change in clinical practice. If you are interested in more about go to Sepsis folder

A complete guide to approach at children with decreased level of consciounes is for me a constant friend in my clinical practice.

Less is better when comes to Oxygen therapy. This very well done Italian study despite his early unplanned termination (cause of a earthquake that hitted the centre of Italy) confirm the trend toward reduced mortality in conservative targeted oxygen administration versus conventional liberal therapy.

Hypoxic lactic production is a mantra in both patho-physiology and clinical practice. In this article the author gives different interpretation of the phenomena. One of my favourite. 

This systematic review and meta-analysis clearly demonstrate how in both cases CA and CS, ECMO support improve mortality compared with standard techniques. Every emergency system has to consider this option.

Rare but dramatic condition among all the epileptics status need the best of EB treatment. Here is the latest reference guidelines released by one of the most important international scientific society. Must read.

Traditional performance measures and a proposal for a new more complete model for Clinical Performance Benchmarking. An efficiency and quality assessment method that prehospital systems need to acquire. 

Debating about with model of EMS is the more efficient in performing out of hospital CPR? This systematic review and meta-analysis  affirm that physician based models have better performances than non physician based ones.

HEMS vs GEMS. Ground or air transport in traumatized patients? This article is not the end of the story, but pose a good base on how HEMS can be a better alternative to rescue and transport trauma patients.

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2016 in Review

12 Jan

MEDEST-review

2016 has been a great year for Emergency Medicine.
MEDEST on a daily base, via Twitter or Facebook, shared the best (for us) Emergency Medicine articles coming from the net.
At the beginning of a new year we would like to share a collection of those articles (all free full text) organised by topics.
You can browse freely for research or educational proposal
I hope you’ll enjoy.

2016 Review by topic

You can also find articles from previous years on this page

MEDEST Review’s

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2017

31 Dec

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Was one of my first shift as pre-hospital emergency physician in an ambulance, when I was called on a basketball field where a young man collapsed during a match.

He was in cardiac arrest and I was panicking.  At that time there were small evidences on almost everything, but I grabbed the paddles and defibrillated him. BOOM he had a ROSC. I did it!.

When we arrived at the hospital and old nurse came to me, and tapping on my shoulder said “well done ‘dottorino’ (cute young doctor) but next time don’t forget to put gel on the pads!” Looking at the guy I noticed two circled rush on the chest right in the place where I defibrillated him. At that exact time I realized that even if you fell like a god you have always something to learn, even from the last person you can imagine.

That ‘dottorino’ grown up and experienced a bit now but never stopped studying and learning from everyone, and this is my wish for 2017, to every professional who works in emergency medicine:

Never stop studying  even if you feel to be “the best”.
Never stop listening to everyone, they can have something useful to say.
Open your mind to innovation and be ready to change everyday.
Be ready to start again even in the worst moments of your career; every start is the beginning of a better life.
You can look at the future just if you have a steady past.

Good 2017 to all MEDEST friends and followers.

Mario

Fluid responsiveness…will your echo help?! #FOAMed #FOAMcc #POCUS

10 Dec

Great summary about fluid responsiveness and ultrasound evaluation through caval index (IVC collapse). Must read.

Epinephrine (Adrenaline) in cardiac arrest: the glorious past, the (in)famous present and the possible future.

6 Dec

The glorious past.

adrenaline2

In 1901 Jokichi Takamine (1854-1922) isolated the pure form of adrenaline, also known as epinephrine.

In 1893, George Oliver (1841– 1915), using his own instruments, studied the impact of glycerol extracts on arteries.

Routine use of adrenaline for cardiac arrest was first proposed in the 1960’s. Its inclusion within cardiac arrest management was based upon an understanding of the physiological role of adrenaline, and experimental data from animal research which showed that ROSC was more likely when the drug was used. It was not included on the basis of evidence of benefit in humans, but has remained, since today, a significant component of advanced life support despite minimal human data indicating beneficial effect .

The (in)famous present

aha-advanced-cardiac-life-support-acls-initial-certification-classes-50

The original rationale for use of epinephrine in cardiac arrest was that, in animal studies, increases aortic blood pressure and thus coronary perfusion pressure during chest compressions.
Many and strong recent evidences demonstrates that “Among patients with OHCA in Japan, use of prehospital epinephrine was significantly associated with increased chance of return of spontaneous circulation before hospital arrival but decreased chance of survival and good functional outcomes 1 month after the event” as Hagihara A, Hasegawa M, et al. concluded in their 2012 article “Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest” published in JAMA.

A recent review article “Adrenaline for out-of-hospital cardiac arrest resuscitation: A systematic review and meta-analysis of randomized controlled trials” published on Resuscitation in 2014, also concluded “There was no benefit of adrenaline in survival to discharge or neurological outcomes. There were improved rates of survival to admission and ROSC with SDA over placebo and HDA over SDA”.

 

Let’s review some physiology about aortic pressure and coronary perfusion.

  • Coronary vessels are contained in epicardium and their flow is possible in the diastole when they are not compressed by myocardium during systolic contraction.
  • coro-vessels

    Coronary flow depends from the gradient between aortic diastolic (Ao) pressure and diastolic left ventricular (LV) pressure.

acls3_3-1
  • Higher is the coronary pressure perfusion (CPP), greater is the chance of ROSC.

circ1

  • The cut off value for ROSC is 15 mmHg of CPP, but more is better.
  • Epinephrine is a key determinant factor in maintaining diastolic aortic pressure in cardiac arrest; thanks to its interaction with alpha receptors, located on the endothelium of the arteries, produce generalized peripheral arterial vasoconstriction maintaining aortic diastolic pressure to a high level even during chest compressions.

So why epinephrine doesn’t work and can be detrimental on long term outcome

mp-5744_3_wrong_landingpage1_8

I think there are two key factors, in the actual way to use Epinephrine,cwho determine its failure:

The wrong administration route

When epinephrine is administered intravenously in a low flow state patient (as is a patient during cardiac arrest, even if proper chest compressions are performed), the amount of drug that arrives to perform the “local” alpha effect on arteries is just a minimal quantity of the (high!!!) dose. The major part rely in the venous circulation and is mobilized in great quantity only when ROSC happens determining a widespread vasoconstriction and a consequent “overdose” effect (think just at the “stunned” myocardium that has to overwhelm such ha great post-load).

The wrong dose to the wrong patient

From the coronary perfusion pressure (CPP) point of view, every cardiac arrest patient is different: some patients have a (relative) good aortic pressure and a (relative) good  coronary perfusione comparing to others.

When we administer the same amount of epinephrine to each of them this takes to an underdose in some patients (with low flow state) and an overdose in others (with good or high flow state).

The possible future

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The right administration route

Probably the best route to administer epinephrine is not the vein but the artery.

It allows, even in a low flow state patient, a better chance to reach the vasoconstrictor effect maintaining a good aortic diastolic pressure and a consequent good coronary flow.

Nowdays (the era of REBOA, open thoracotomy and more) the chance to use ultrasound make this skill easier than before and definitively possible even in prehospital settings.

The right dose to the right patient

Giving epinephrine (standard dose) to a patient who has a low flow state (patients who need it more) make epinephrine usefulness (underdose) because just a little part of it circulate.

Giving  epinephrine to patients in a good or high flow state (patients that need it less or don’t need epi at all) is detrimental and can cause overdose effect.

We need to know wich is the circulatory state of the patients to administer the right dose avoiding the “overdose” effect.

The only way to do this is monitoring aortic diastolic pressure through an arterial catheter. We can target Epinephrine dosage to reach a good aortic pressure maintaining a good CPP (achieving ROSC) and avoiding overdose.

Take home points for future improvement.evolution

  1. Train to reach an US guided arterial line in cardiac arrest

  2. Check aortic pressure via peripheral or central (femoral) arterial line

  3. Give Adrenaline intrarterially

  4. Target Adrenaline doses to maintain a good aortic pressure

Tanks to Jim Manning who inspired this post with his talk Rethinking Adrenaline in Cardiac Arrest

References

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#SIMEU16 Nuove prospettive per la medicina d’urgenza.

21 Nov

Si è appena concluso il decimo congresso nazionale SIMEU che è già tempo di bilanci e conclusioni.

Io non sono in grado di farlo, conosco pochissimo il mondo SIMEU, come purtroppo la maggior parte dei medici d’emergenza che lavorano in ambito preospedaliero. Ma anche SIMEU conosce pochissimo il mio mondo.

Quest’anno però è successo qualcosa di nuovo.

Mi sono avvicinato, timidamente con le mie certezze e qualche pregiudizio, al mondo SIMEU ed ho tenuto due relazioni, una nella (unica a parte qualche altro spot sparso) sessione dedicata al setting preospedaliero, l’altra nella sessione dedicata all’arresto cardiaco.

Ma SIMEU cosa ha fatto per me.

Secondo me moltissimo.

Mi ha fatto capire che nel suo mondo, tra i suoi uomini e le sue donne c’è già il seme del nuovo medico di medicina d’urgenza.

Un medico che ha competenza e capacità per accompagnare il paziente da casa o dalla strada al ricovero in reparto passando per la stabilizzazione preospedaliera a quella in DEU. Un medico che ha capacità per affrontare scelte cliniche e terapeutiche complesse ed attuare le tecniche che permettono di raggiungerle in tutti i setting dell’emergenza.

Ma sopratuttto un medico che ha un’umanità sconfinata, un professionista che si realizza nell’assistenza delle persone prima che dei pazienti, nella cura dell’anima prima che del corpo.

Tutto questo ho visto nelle persone con cui ho parlato e con cui ho sognato un futuro entusiasmante per tutti noi.

Federica, Matteo, Giacomo, Efrem (e non cito altri perchè non ricordo i nomi ma solo le bellissime facce) sono già così: competenti, umani e pieni d’entusiasmo.

Sono stati Alessandro, Mario, Fabio, Carlo e tanti altri ad ispirarli, e loro sono già pronti.

Saranno Mario, Alessandro, Fabio, Carlo a guidarli, ma loro sono il futuro.

Buongiorno Medicina d’Emergenza Urgenza!

“Humans Are Not Yeast”: (almost) everything we believe about lactate is a myth. 

5 Oct

4e193a6c-13de-44f2-aabe-2b095321f652_1-8a517f942153f96606ebbde8331f1dc8On September issue of Emergency Medicine News, Paul Marik wrote an article entitled “Humans are not yeast”. 

This is a game changer article about the current concepts on lactic acid and its clinical meaning in emergency medicine.

The author illustrate simple but well established concepts about lactic acid metabolism that revert most of the common conceptions about its significance in clincal medicine.  

I will resume below some of the most relevant concepts expressed in the article. The italic bullet point text is from the original article.

I really encourage all of you to read the full text of original article to completely understand the whole rationale behind those statements and to access the complete list of references.

It is free open access.

Let’s start with some biochemistry.  

Piruvate, the product of glycolysis, can enter in Krebs cicle to produce energy through aerobic (oxygen driven) process or can take a shorter and faster (x100 times) way to produce energy when is transformed to lactate (the basis of lactic acid) using NADH (so reduced to NAD+ and ready to take another H+) and H+.

  • No hydrogen ions are present in glycolysis. In fact, the conversion of pyruvate to lactate consumes hydrogen ions. It is actually a lactic alkalosis. (J Mol Cell Cardiol 1997;9[11]:867.)
  • Increased lactate may simply occur because of increased production of pyruvate due to in- creased glycolysis there is no oxygen debt. We spoke about the muscles exporting lactate; the same thing happens in shock: lactate is used as a fuel for oxidative metabolism. Lactate is transported into the mitochondrion through specific transport proteins, and then is converted to pyruvate in the mitochondrial intermembrane space. Pyruvate then moves into the mitochondrial matrix and undergoes oxidative metabolism.
    Lactate is, therefore, a fuel for oxidative metabolism. It’s consumed by the brain and heart, and that is absolutely vital to survival when someone is in shock    .
So why is lactate produced and used for?
Lactate is aerobically producted by muscle and is a more efficient source of energy for the brain and the heart.
  • Lactate is a much more efficient bioenergetic fuel than glucose so as someone exercises, the muscles make lactate to fuel the heart. The heart works much more efficiently with lactate. What happens to the brain? The exact same thing. As someone exercises, brain lactate goes up, and the brain starts using lactate preferentially as a source of fuel. This is a brilliant design: Muscles make lactate aerobically as a source of energy for the brain and heart.
Lactic metabolic acidosis is a biochemical myth! It’s more a lactic alkalosis.
  • The lactic acidosis explanation of metabolic acidosis is not supported by fundamental biochemistry, and has no research basis. Acidosis is caused by reactions other than lactate production.  
  • No hydrogen ions are present in glycolysis. In fact, the conversion of pyruvate to lactate consumes hydrogen ions. It is actually a lactic alkalosis. (J Mol Cell Cardiol 1997;9[11]:867.)
Hypoxia does not induce lactate serum level elevation, and in sepsis oxygen cellular level is not decreased. 
  • There is this pervasive idea that people with sepsis have cellular hypoxia and bioenergetic failure, but this concept was debunked in 1992. Compared with limited infection, the muscle O2 goes up in patients with severe sepsis.
  • Increased lactate may simply occur because of increased production of pyruvate due to increased glycolysis there is no oxygen debt. We spoke about the muscles exporting lactate; the same thing happens in shock: lactate is used as a fuel for oxidative metabolism. Lactate is, therefore, a fuel for oxidative metabolism. It’s consumed by the brain and heart, and that is absolutely vital to survival when someone is in shock. The body makes lactate, which is then used as a metabolic fuel.
Iperlactic state is generated, by epinephrine and not by hypoxia, in case of extreme physiological stress as protective mechanism.
  • The clinical plausibility was that lactate increases during adrenergic states and in the absence of an oxygen debt. Lactate increases with epinephrine infusion; lactate increases with hyperdynamic sepsis. All of the states have a high cardiac output, high oxygen delivery, and not a single trace of hypoxia. It’s driven by epinephrine, not by hypoxia.
  • We do know that lactate is associated with increased mortality because the sicker a patient is, the higher his epinephrine levels. It’s a protective mechanism. The association is related to the fact that lactate is a biomarker of physiological stress. And clearly the greater the physiological stress, the greater the risk of death. But lactate itself is a survival advantage, and it’s not an evolutionary accident that we make lactate.

Credits:

Thanks to the author and to Aidan Baron who originally shared the article.

Reference:

  1. The Science of Emergency Medicine: Humans Are Not Yeast. Emergency Medicine News: September 2016 – Volume 38 – Issue 9 – pp 1,29–30 doi:10.1097/01.EEM.0000499522.28133.48

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