Tag Archives: medicina d’urgenza preospedaliera

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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Only Evidenced Based Medicine? Evidently……not!

4 Feb
man-jumping_logoThe modern emergency medicine based most of his clinical practice on evidence-based trials. 
But really all that is not coming from randomized controlled trials does not exist?

The paradox of the demonstration of the effectiveness of the parachute with randomized controlled trials, in accordance with the method EBM (The Parachute trial), provocatively poses a fundamental question:

If the scientific basis of any therapeutic intervention are already strong, and the benefit for the population is large, is ethically correct to wait large-scale trial to implement it, delaying its potential benefits?

A 2006 article published in the BMJ Controversy Parachute approach to evidence based medicine brilliantly responded to this question.

It contains some examples of very common diseases in developing countries (HIV, dehydration in children, postpartum hemorrhage) whose remedies, implemented previously than results of relative trials where available, have saved thousands of lives.

The authors conclude that:

1. Randomised controlled trials are usually required before new interventions are implemented

2. If other evidence of effectiveness is good, and potential benefits large, the resultant delays may be unethical

3. Examples from poor countries show the price of delaying interventions

The triad of decision-making at the base of the construction of Evidenced Based Medicine provides an integrated approach between explicit data (scientific evidence derived from trials of good quality) and tacit data(clinical expertise and the patient’s needs).

MedInfo_EBMtriadImage

The clinical decision is derived from the combination of these three factors:
• Scientific evidence
• Clinical Experience

• Needs of the patient

But when defining the level of quality of evidence those derived from clinical practice and experience are relegated to the base (lower level) of the pyramid whose apex (higher degree) are the evidence derived from studies on large patient populations.

ebp_pyramid

Randomisation and de-personalization of scientific research, while eliminates everything that is “non-evident” in medical research, and is well suited to a concept of public health, on the other hand maintains an unbridgeable gap with daily clinical practice that is focused on the care of the individuals.

But in practice what we can do:

  • Integration of explicit data, result of the evidence, with the “tacit knowing” that is generated only from the direct doctor-patient relationship is desirable.
  • The “tacit knowing” is the basis of our medical education, such as learning the language is to pre-school children: it does not need structured teaching but it is learned from direct experience.
  • The “tacit-knowing”, often reduced to subjective data and therefore of lesser dignity, is in fact, just because “innate”, less prone to the common bias of explicit data;
  • We must recognize equal dignity to both those data “explicits” and “tacits.”
  • We must take into account both explicit and tacit elements in the formulation of the hypothesis and the resulting diagnostic therapeutic strategy.

We can and we must go beyond the exclusive use of EBM in medical research and clinical practice.

The adoption of an integrated approach between the explicit scientific evidence derived from clinical trials (EBM) and a “patient- centered approach” derived from the clinical experience, should be a stimulus and an intent to the future development of our approach to the critically ill patient.

It must always be clear in the mind of the emergency medicine professionals which treatment is scientifically more correct for a given disease, but he must contextualise, and implement it for the particular patient who is dealing with at that time

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Italian transcript

References:

“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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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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The 3-3-2 rule. A pratical tool for predicting the difficult airway on the field

31 Mag

3_3_2_ruleThe 3-3-2 rule is part of the evaluation in a patient for a predicted difficult airway. This evaluation can be done on an unconscious patient in supine position and is reliable tool for the anticipation of a difficult BVM ventilation and intubation out of the hospital.

In the video you can see the 3-3-2- rule application on a patient with a predicted difficult airway. .

This patient was difficult to BVM ventilate (cause of the “sloopy” chin) and was intubated in VL with the aid of a bougie.
In this case the predicted difficulty of the airway, determined the choice of VL bougie aided intubation as first choice for the airway management, avoiding so multiple attempts. This choice was of more importance view the difficulty of BVM ventilation that would have conducted to a critical desaturation during the intubation attempts.

The invasive airway management is a critical skill in out of hospital emergency medicine and, when indicated, not avoidable. Predicting in advance the difficulty is important to choose the right plan and avoiding multiple attempts.

View in Prezi.com

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My favourite VL view to increase first pass intubation

8 Feb

A debate is ongoing among #FOAMED social media about increasing first passage rate in tracheal intubation and some difficulties when using VL.

At the beginning of my experience with VL I experienced some difficulties, but with a radical change in technical approach I reached a good security on first pass success.

Here are my consideration and I hope will be useful for anyone is starting using VL

 

There are some fundamental differences in VL technique respect to DL, that makes the DL more easy and intuitive to pass the tube trough the cords.

3axys

The 3 axys theory for airway management

“Sniffing position” align the pharyngeal axis with the laryngeal one

Sniffing position

Sniffing position

Perfoming Direct Laryngoscopy with the laryngoscope we align the mouth axis to have a direct view of the cords.

DL view

DL VIEW

 

 

 

 

 

 

 

 

 

 

This view coincide with the route for passing the tube, making this step intuitive and easy.

 

When using a Video Laryngoscope we take our eyes right in front of the larynx, having a perfect “video” view of the vocal cords, but also minimally modifying the axis of the mouth.

Visione in videolaringoscopia

VL VIEW

This difference makes the act of passing the tube not so easy and not so intuitive, cause of the contrast between the perfect video laryngeal view and the not easy passage of the tube trough the cords.

In those cases the stylet, the Bougie/Froban or the external glottic maneuvers, are useful to facilitate the video-intubation.

tubo stylet

Golf stick shape of the tube+stylet

But the first goal is to reach this view on the screen of the videolaryngoscope.

IMG_1278

I want to have the epiglottis right at the center of the screen and this comes prior of a good view of the larynx.

Epiglottoscopy is the key point of my management of the airways in general and when prforming VL in particular.

Having the epiglottis in central position on the screen allow to:

  • lower the glottic plane facilitating intubation
  • decrease  the force to apply on the airways minimizing traumatism and neck movement in case of trauma.
  • fits all the difficult airway situations because a poor view of the cords is what you are looking for!

If you agree, memorize my favorite view and reach for it when using a video device to mange the airways.

All comments are welcome so please let me know your thoughts.

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Settaggio iniziale del ventilatore polmonare.

27 Ago

Uno degli skill importanti per la gestione del paziente critico in emergenza è il settaggio e la gestione del ventilatore polmonare.

La scelta della modalità di ventilazione ed il settaggio consapevole dei parametri ventilatori spesso scoraggia l’uso di uno strumento fondamentale, per chi fin dalla fase preospedaliera deve gestire il malato critico che necessita di assistenza ventilatoria.

La familiarità con concetti base, ma non per questo scontati, di fisiopatologia polmonare, ma anche un piano operativo predefinito da applicare ed adattare volta per volta alle varie situazioni cliniche, sono di basilare importanza per il settaggio in emergenza del ventilatore.

Recenti concetti come la Lung Protective Ventialtion, hanno inoltre reso necessaria una rivoluzione critica di quelli che erano i vecchi cardini della ventialzione meccanica.

Sono liberamente disponibili in rete risorse preziose che illustrano in modo chiaro ed autorevole questi nuovi concetti.

Mechanical Ventilation Protocol Summary

Sono inoltre disponibili alcuni simulatori e tutorial molto utili per poter interagire e settare in modo virtuale, ma anche realistico, il ventilatore polmonare e comprendere la ventilazione polmonare.

Questo modulo che presentiamo di seguito fa parte del corso Prehospital Airway Management (PHAM) e spero sia utile per la comprensione dei settaggi di base per tutti coloro che non hanno una pratica quotidiana con il ventilatore ma che necessitano di usarlo in emergenza sia fuori che dentro l’ospedale.

Settaggio di base del ventilatore polmonare

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Why the VideoLarygoscopy don’t gonna kill the DirectLaryngoscopy (at least in the near future)

17 Ago

A novel publication goes to enrich the long-living debate on direct laryngoscopy (DL) vs video laryngoscopy (VL) efficacy in emergency intubation.

The recent article, pubblished on JEMS and titled  “Deploying the Video Laryngoscope into a Ground EMS System” ,compares the success rate beetwen DL vs VL in a ground EMS Service. The device used was the King Vision with channeled blade. The partecipants had a prior training on the divide, consisting in didactic orientation and practical skills on manikins.

The result of the study shown that “Within the first 100 days of the study, the video laryngoscope utilizing the channeled blade has shown to be at least as effective as DL in relation to first-attempt success” and considering that “the mean experience in our group with DL is nine years, yet the success rate remains unacceptable” “It’s time to consider transition from a skill that’s difficult to obtain and maintain to one that appears to have a quicker learning curve and will likely result in decreased episodes of multiple attempts at intubation and associated complications.”

So is direct laryngoscopy dead?( Or will be so in a few years)

Laryndo dead

Here are some considerations

There are some fundamental differences in  VL tecnique respect the DL tecnique, that makes the DL more intuitive to pass the tube trough the cords.

We have basically 3 main axis in the airways

3axys

When we manage the airways we first put the head in “sniffing position” aligning the pharyngeal axis with the laryngeal one

Sniffing position

Then we use the laryngoscope to align the mouth axis having so a direct view of the cords. This view coincide with the way to pass the tube, making this step intitive and easy.

DL view

 

 

 

 

 

 

 

 

 

 

 

 

 

When using the videolaryngoscope we take our eyes right in front of the larynx, having a perfect “video” view of the vocal cords, but also minimally modifying the axis of the mouth.

Visione in videolaringoscopia

For this reason passing the OTT is not straight forward, so we need the stylet, the Bougie/Froban or the external glottic maneuvers, to facilitate the intubation.

tubo stylet

Bougie

This difference in tecnique makes the VL not so intuitive  due to the contrast between the perfect laryngeal view and the not  intuitive passage of the tube trough the cords.

In fact the available evidences almost accordingly demonstrate an equivalent success first pass rate beetwen traditional laryngoscope an video but a prolonged intubation time in VL groups.

As the previously cited article demonstrate the learning curve for VL is short and easy to perform, and this make this tecnique surely suitable for emergency intubation.

But for emergency professionals well trained and familiar with DL I think this has to be the first choice approach when managing an emergent airway.

Emergency field is not the place to make trianing or experience with novel devices or drugs.

The still not widely availability of video-laryngoscope makes this device a perfect alternative in all the casess when is not possible to obtain a good laryngela view with DL, but still not the gold standard tecnique.

In the future the increasingly diffusion of videoleryngoscopes (due mostly to more affordable prices), will chenge the airway management scenario. Novel emergency medicine operators will grown up parallel experience wid DL and VL so the latter will be more suitable as first choice device.

Bottom line

Wich way you prefer to go home?

The quickest and the shorter one for sure!

Do you use the GPS to go home?

Agree, me neither!

And when you use it?

lost

Right! When you are lost!

So that’s why Direct Laryngoscope il still my Plan A

My straight way home!

straight road

Prehospital Airway Management Action Plan

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2013 in Review

2 Gen

Cari lettori di MEDEST,

nell’augurarvi un felicissimo 2014 MEDEST ha il piacere di rendervi partecipi del grande successo che il Blog ha avuto quest’anno.

Abbiamo pubblicato 79 nuovi post.

Abbiamo ricevuto un totale di 32,00 visite da 84 paesi nel mondo.

Cliccate il link per vedere il report completo e rileggere, se mai ve li foste persi, i post più popolari pubblicati nel 2013

Click here to see the complete report.

Grazie ancora a tutti voi.

Ci prepariamo ad un 2014 che speriamo sia ricco di soddisfazioni per tutti.

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Intossicazione da CO sul territorio

27 Dic

CO-decal

La diagnosi di intossicazione da CO (monossido di carbonio) è clinica. La definizione classica prevede la presenza della triade:

  • Storia di esposizione a CO
  • Sintomi compatibili con intossicazione da CO
  • Elevati livelli di CO nel sangue

Non esiste alcun sintomo patognomonico per intossicazione da CO nonostante la diagnosi clinica ne preveda la presenza.

I sintomi più comunemente associati all’esposizione acuta sono cefalea, nausea/vomito, ipostenia, dolore toracico, dispnea e sincope. Quello forse più comune è la cefalea, anche se non ha una clinica tipica. Non esistono inoltre combinazioni sintomatologiche tali da poter confermare o escludere la diagnosi d’intossicazione da CO. Storicamente è stato indicato il colore “rosso ciliegia” della cute come indicatore vagamente patognomonico della patologia. In realtà, tale segno è sia raro che tardivo, e quando presente indica uno stato molto avanzato caratterizzato da livelli ematici pressoché letali di CO.

La diagnosi clinica necessita comunque di conferma strumentale che dimostri la presenza di livelli elevati di CO ematica.

Valori superiori al 3-4% nei non fumatori e superiori al 10% nei fumatori devono essere considerati valori eccedenti la fisiologica quantità di carbossiemoglobina.

Si parla di:

  • Intossicazione lieve:con valoro di CO >10% senza segni clinici
  • Intossicazione moderata: con valoro di CO >10% con segni e sintomi minori (cefalea, letargia, astenia)
  • Intossicazione severa: con valoro di CO >20-25% con perdita di conoscenza, confusione mentale, segni d’ischemia miocardica

La misurazione non invasiva della Carbossiemoglobina attraverso apparecchi che sfruttano l’assorbimento della lunghezza d’onda pulsata è controversa in termini di affidabilità e va comunque sempre confermata attraverso la misurazione mediante prelievo ematico (venoso o arterioso).

La rilevazione della SaO2 nei pazienti con sospetta intossicazione da CO non è indicativa dell’effettivo stato d’ossigenazione del sangue periferico. Lo spettro di assorbimento della carbossiemoglobina infatti è molto vicino a quello dell’emoglobina ridotta ed i normali saturimetri per tale motivo non sono in grado di discriminare tra quella effettivamente legata all’O2 e quella legata al CO.

La rilevazione di bassi livelli ambientali di CO in presenza di storia di esposizione acuta al tossico non esclude la possibile intossicazione delle persone coinvolte. Al momento della misurazione infatti i valori rilevati potrebbero essere falsati dalla precedente apertura di porte o finestre.

La rilevazione di alti livelli ambientali di CO di contro rende mandatoria la valutazione  clinico strumentale dei pazienti convolti ed il loro trattamento d’emergenza in caso di sospetto clinico.

L’O2 normobarico ad alti flussi somministrato via maschera facciale o tubo orotracheale è il trattamento di prima linea per l’intossicazione da CO (nonostante non esistano trial adeguati che ne dimostrino la reale efficacia).

Non esistono evidenze di livello A che indichino l’utilizzo mandatorio dell’ossigeno iperbarico nei pazienti intossicati da CO.

Non esistono segni o sintomi che indichino l’utilizzo dell’ossigeno iperbarico.

La terapia con O2 iperbarico  può essere considerata (secondo il parere di alcuni esperti Livello C) nei seguenti casi:

  • Coma
  • Transitoria perdita di conoscenza
  • Alterazione del comportamento
  • Cefalea
  • Nausea o vomito
  • Vertigini
  • Dolore toracico o segni ECG di ischemia
  • Aritmie
  • Gravidanza
  • Bambini inferiori a 6 mesi d’età (per la presenza di Hb fetale)
  • Esposizione a CO accertata ≥24 hours

La terapia con O2 iperbarico è controindicata nei seguenti casi:

  • Pnx non drenato,
  • Crisi comiziali,
  • Claustrofobia accertata

Tutti i mezzi di soccorso dovrebbero essere dotati di rilevatore di CO. L’unità di misura in cui tale dispositivo visualizza i livelli misurati è il ppm (parti per milione).

Il professionista sul territorio in caso di sospetto clinico di intossicazione da CO

  • Allontana il paziente dalla fonte di CO
  • Inizia il trattamento con O2 ad alti flussis
  • Sostiene i parametri vitali
  • Centralizza il paziente al DEA dell’ospedale dove è presente il servizio d’urgenza per il trattamento con O2 iperbarico

References:

  1. Kao LW, Nanagas KA, Carbon monoxide poisonin. Emerg Clin N Am. 2004 Nov;22(4):985-1018.
  2. Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ, Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011 Apr 13;(4):CD002041.
  3. Wolf SJ, Lavonas EJ, Sloan EP, Jagoda AS; American College of Emergency Physicians. Clinical Policy- Critical Issues in the Management of Adult Patients Presenting to the Emergency Department with Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2008 Feb;51(2):138-52.
  4. Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med. 2009 Mar 19;360(12):1217-25.

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