Tag Archives: emergency medicine

Prehospital Emergency Procedures: Scalpel, Finger, Bougie. That’s all you need!

13 Lug

In Emergency Medicine “Simplicity” is synonymous of efficiency, efficacy and reproducibility.

More the time frame is stressful more we need procedures that are efficient, efficacious and standardised, in one word SIMPLE.

Critcothyrodotomy and chest drain are procedures usually performed in high stressing scenarios and more simply they are more chance of success they have.

I don’t like complicate kits. They need training of course but even a calm and protected environment, and the middle of a street or a busy ER room aren’t nothing like that. 

I don’t like blindly performed procedures but prefer trusting my own senses and sensibility when performing high invasive procedures that, mostly of the times, are a lifesaving last chance.

So this is the best way I know to perform a surgical access to the airway and to drain a highly unstable tense pneumo: using simple instruments, always present in every emergency pack, and trusting my own tactile sensitivity.

surgical-airway-sfb

In those following videos you can see live records of the procedures. They were captured during a recent cadaver lab where I had the honour to join Jim DuCanto, Yen Chow, Carmine Della Vella and Fabrizio Tarchi in teaching airway management and clinical emergency procedures.

Hope you enjoy.

 

 

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Prehospital POCUS: Why I love it! Real Clinical Scenario.

10 Lug

73 yrs old male found unconscious by his wife. CPR started by a neighbour with pre arrival CPR instructions provided by dispatcher. We found him in asystolic cardiac arrest. Established mechanical chest compressions (MCC), ventilated through an 8.0 ET tube, placed an intraosseus access, 10 min of ALS and 2 mg of epinephrine later, on the monitor appears an organised rhythm at 40 bpm (narrow junctional shape), NO CENTRAL PULSE. After 2 min (CPR still going) same rhythm stil NO CENTRAL PULSE but this time, during the MCC pause, a subcostal view of the heart was obtained (sorry for the quality of the images but were recorded during the code and I’m not an expert but just an ultrasound user) 

As you can see the heart is moving and the right ventricle is almost the double of the left one. Due also to the clinical history of a recent surgical knee replacement the most probable origine of the cardiac arrest is PE. We decided to continue chest compressions, but to stop epinephrine at 1 mg dose, starting push doses of 0,1 mg till the return of a central pulse. After 5 min a strong carotid pulse appeared and this is the ultrasound view of the heart at that moment

  

The patient arrived to the hospital sedated and paralysed in assisted pressure control ventilation. You can see on the monitor the rest of vital signs.

No follow up yet.

You can read more about PEA and Pseudo-PEA on MEDEST

Forget ACLS guidelines if you are dealing with Pulseless Electric Activity. Part 1.

Forget ALS Guidelines when dealing with PEA. Part 2.

HEMS vs GEMS: by ground or by air, which is the best way to take care of traumatized patients

25 Apr

HEMS

Take home points:

Speed

Mission Time

  • –In case of simultaneous activation HEMS is competitive for distance >10 miles from Trauma Center
  • In case of non simultaneous activation HEMS is faster  for distances >45 miles from Trauma Center

 

On scene time

 

  • –HEMS > GEMS

Severity

  • –HEMS patients are generally more severely injured than GEMS patients

Trauma Center Access

  • –HEMS transported patients have more chances to be referred to a level I Trauma Center

Crew

  • –More time on scene (beyond the golden hour)
  • –More procedures performed
  • –The accuracy of prehospital documented diagnoses was not increased in HEMS compared to GEMS rescue

Survival 

  • –No definitive evidences on HEMS benefits on survival rate
  • –Recent literature points on a trend toward an increased chances of survival in some categories of trauma patients transported by HEMS

 

 

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

5 Ott

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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“Best Practice” preospedaliera: Arresto cardiaco da trauma

4 Ago

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

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

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

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

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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2016 NICE Major Trauma Guidelines. The pre-hospital recommendations.

21 Feb

NICE released the 2016 Major trauma Guidelines.

Many interesting recommendations where made for pre-hospital and in hospital providers about several topics

  • Airway management

  • Chest trauma

  • Haemorrage control

  • Circulatory access

  • Volume resuscitation

  • Fluid replacement

  • Pain management

  • Documentation

  • Training

Here is the Excerpt regarding the pre-hospital settings

Download the full guidelines for in-hospital recommendations and full description of Guidelines process and rationale behind every single recommendation

Download the full Guidelines at:

Major trauma: assessment and initial management

NICE guidelines [NG39] Published date: February 2016

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