#SIMEU16 Nuove prospettive per la medicina d’urgenza.

21 Nov SIMEU_congresso2016_Locandina_A3_logo_ESEC

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 Ott 4e193a6c-13de-44f2-aabe-2b095321f652_1-8a517f942153f96606ebbde8331f1dc8

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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How Ultrasound (really) improved my clinical practice

24 Ago echo for dum like me

Beyond theories and protocols, here we are three (real) clinical prehospital scenarios  in which without ultrasound my own practice would have been different with (probably!!!) some (bad!!) consequence on patients final outcome.

Case #1

 

 

pic 2

Apparently 45 yrs old female found unconscious in a secondary street by people accidentally passing by. No witness of the event. No other information on the patient.

When the first medical team arrived, the patient was unconscious with some non coordinated vocal response (if stimulated) and no finalized movements of the extremities; she was spontaneously breathing with an apparent good respiratory drive a RR of 24 and O2 sat of 98% on room air.  Good breath sounds were (apparently) bilaterally transmitted (not easy to appreciate when you perform auscultation of the chest on the roadside).

She had a good palpable radial pulse (bilaterally), the HR was 72 and her BP 110 over 70. To a quick external exam multiple minor signs of trauma where present on her face, forehead and left anterior chest wall. No sign of major external bleeding was present.

When we arrived the above clinical scenario was confirmed. The cops, on the scene, were investigating about what happened, but at the moment no other new information was available.

As first thing I was concerned, cause of the low level of consciousness, about patient’s competence to maintain airway patency , so I decided to protect the airways with tracheal intubation. 

But first to proceed to RSI, during the preox period and despite the apparent hemodynamic stability I decided to perform an extended FAST ultrasound exam; it takes 2 min, is safe and free.  The EFAST revealed a pneumothorax on the left, no abdominal bleeding, no pericardial fluid effusion. At this point we decide to open the chest (finger bougie tecnique, Ketamin pre-medication) before intubating the patient in prevision  of the mechanical positive pressure ventilation, and air transport.

The patient arrived well compensated (from both respiratory and hemodynamic point of view) at the trauma  center where was discharged 3 weeks later without major clinical consequences.

But what without ultrasound???

We don’t have a clinical guidance (and practice) to open the chest simply ‘cause of the presence of external sign of chest trauma when the patient is in a well compensated respiratory status and had a good hemodynamic balance.

In this case the chance to find clear US signs of penumothorax, prevented a possible worsening of respiratory and hemodynamic status  after intubation.  Intubation itself, PPV and high altiutde transport, are all factors that can precipitate a prior stable pneumothorax.

Case #2

pic 1

28 yrs male victim in a car accident extricated after several minutes by the firefighters. At the arrival of the fire crew he was still breathing but when the first medical crew arrived found him in CA. Advanced life support started and was ongoing when we arrived.

The patient was intubated on the field, two thoracic tubes were bilaterally placed (emo-thorax on the right side no pneumo bilaterally)  and a bolus of 2 liters of fluids administered via two large bore venous accesses.

He had an organized cardiac electric activity and an EtCO2 value of 35 mmHg (without chest compressions in place). The US of the heart shown some weak wall motion (coordinated with electric activity), so we decided to rapidly transport the patient to the nearest trauma center where he was reanimated for more than 1 hour and then called  without any evidence of possible cause of death.

In this case the presence of wall motion at the US exam (well supported from EtCO2 values and and by an organized cardiac electric activity) strongly influenced the decision to transport the patient in TCA to the hospital for definitive care.

Ultrasound can be a further hint in the decision to carry on the resuscitative efforts in patients in CA with PEA and no evidence of reversible causes on the field. It can be also the decisive tool in deciding  to transport those patients to the hospital for second level diagnostic assessment and advanced care.

Case #3

pic 3

24 yrs old pedestrian male hit by a motorbike while crossing the road. He was found unconscious by first responders. When we arrived the patient was lying down on the spinal board wearing a cervical collar with eyes closed but responsive when called and able to execute simple commands with no apparent deficit of the limbs. He suffered a severe facial trauma  with  avulsion of several frontal teeth and a profound total tickness wound to the superior lip with presence of a lot of blood in the mouth and  the first part of the airways; his breathing was laborious and noisy. Anyway  the patient was able to maintain an ox sat of 93% on room air (that easily improved to 98% with 2 liters of oxygen administered via simple O2 mask). 

The radial pulse was present at a rate of 90/min and the BP was 100 over 70. The rest of external exam highlighted a profound wound at the internal part of the calf with exposition of muscular plan and some hemorrhage well controlled with external manual compression.

We provided (with not much success due to the unstoppable bleeding) to clear the airways from blood and secretions, but still the respiration was difficult and noisy even if the ox sat was on a satisfying 98% on O2 non rebreather mask . In the meanwhile two large bore venous accesses were placed and some fluids keep going.

The EFAST exam revealed no signs of pneumo but presence of blood in the right and left upper quadrant of the abdomen.

We decided to do not insist further on airways control because at this point the control of abdominal bleeding became the first priority. After a rapid transport in ED the total body CT (he was still hemodynamically compensated)  confirmed the presence of internal bleeding and the patient proceeded straight to OR.

Often the suspect of internal bleeding is not clear just by considering clinical signs, especially when we have to deal with young patients who have a large compensation range. POCUS can give us the chance to see the presence of blood in the abdomen and to prioritize our clinical pathway pondering these findings.

Take home points

#1

Performing a chest US before intubating a even stable chest trauma patient, prevents possible  (pre, intra and post) intubation hemodynamic disasters.

#2

Prehospital arrested trauma patients with an organized electric activity and good EtCO2  might have some cardiac activity even in absence of palpable carotid or femoral pulse. They deserve a strong effort on addressing reversible causes and a rapid transport to a  trauma center for advanced in hospital care.

#3

The presence of internal bleeding (revealed by US) can revolve clinical priorities enabling a fast track toward the OR. This virtuous path can start from the prehospital environment.

Getting to the Start Line

18 Ago

The Collective

We can debate the value of this advanced team model vs that advanced team model. We can debate videolaryngoscopy vs direct laryngoscopy for days. People do. Its all chump change compared to the real challenge. Getting that team where they need to be. Dr Alan Garner and Dr Andrew Weatherall have a bit reviewing a paper they’ve just had published trying to add to this discussion. 

You may just have noticed that there are things happening in Brazil. They are called Olympics and they are a curious mix of inspiring feats of athleticism and cynical marketing exercise inflicted upon cities that can probably barely afford them and which will be scarred for a generation afterwards. I’d hashtag that but it turns out the IOC will take you on if you mess with their precious sponsor money.

Now, you might think the obvious segue from a mention of the Olympics at the…

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“Best Practice” preospedaliera: Arresto cardiaco da trauma

4 Ago img_2166

Tra tutte le “Best Practices”, quella che rappresenta più di tutte un cambio radicale di mentalità nell’approccio clinico e terapeutico, è la gestione dell’arresto cardiaco da causa traumatica. Vi prego quindi di leggere attentamente le raccomandzioni raccolte nel documento sottostante e di non esitare a esprimere le vostre riflessioni nei commenti.

Arresto cardiaco adulto traumatico

Chi è interessato ad approfondire il razionale che sta alla base  delle raccomandazioni può scaricare e leggere il documento completo: Arresto cardiaco nell’adulto da causa traumatica full text

 

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“Best Practice” preospedaliera: Arresto cardiaco nel neonato

29 Lug IMG_1655

Continua la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La quarta della serie riguarda l’arresto cardiaco nel neonato.

Potete scaricare il documento cliccando sull’icona sottostante.

Arresto cardiaco neonato

 

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“Best Practice” preospedaliera: Arresto cardiaco in età pediatrica

16 Lug Arresto cardiaco pediatrico

Continua la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La terza della serie riguarda l’arresto cardiaco in età pediatrica.

Potete scaricare il documento cliccando sull’icona sottostante.Arresto cardiaco pediatrico

 

 

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“Best Practice” preospedaliera: Arresto cardiaco in gravidanza

1 Lug Arresto cardiaco gravidanza_Page_1

Continua la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La seconda della serie riguarda l’arresto cardiaco in gravidanza.

Potete scaricare il documento cliccando sull’icona sottostante.

Arresto cardiaco gravidanza_Page_1

 

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“Best Practice” preospedaliera

25 Giu Arresto cardiaco adulto non traumatico_Page_1

Da oggi inizia la pubblicazione di una serie di monografie dedicate alle Best Practices per l’emergenza preospedaliera.

La prima riguarda l’arresto cardiaco nel paziente adulto da causa non traumatica.

Potete scaricare il documento cliccando sull’icona sottostante.

Arresto cardiaco adulto non traumatico_Page_1

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Emorragia post-traumatica

2 Giu DCR copy

References link:

https://drive.google.com/file/d/0B4F2UNmFsOSxUi16d3d0WDRGbkE/view?usp=sharing

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