Tag Archives: medicina d’urgenza

La “constatazione” di decesso. Storia presunta e non-fondamento legislativo di una leggenda metropolitana.

27 Ago

La “constatazione del decesso” è stata in questi anni frequente motivo d’invio di mezzi medicalizzati (automedica o ambulanza medicalizzata) da parte della CO 118. 

La più o meno fondata convinzione che la diagnosi ed il successivo accertamento della morte è  prerogativa della sola professione medica ha spesso giustificato l’utilizzo in emergenza territoriale di tale figura professionale per “constatare” la morte anche di quei pazienti in cui, per vari motivi clinici ed etici, non esisteva alcuna indicazione alla  rianimazione cardiopolmonare

Facciamo chiarezza esaminando i riferimenti di legge disponibili.

L’accertamento di morte e’ prerogativa della professione medica

Il fondamento legislativo dell’accertamento di morte risale al Testo Unico delle Leggi Sanitarie (TULS) approvato con Regio Decreto nel 1934 che all’articolo 103 tra le prerogative delle professioni sanitari recita che “Gli esercenti la professione di medico-chirurgo, oltre a quanto e’ prescritto da altre disposizioni di legge, sono obbligati a denunziare al podestà le cause di morte entro ventiquattro ore dall’accertamento del decesso.”

In esso sia pur indirettamente la figura medica veniva individuata come unica responsabile dell’accertamento e della comunicazione della morte alle autorità.

In epoca più recente la legge n. 578 del 29 dicembre 1993 “Norme per l’accertamento e la certificazione di morte”all’articolo 1 comma 1 stabilisce che “La morte si identifica con la cessazione irreversibile di  tutte le funzioni dell’encefalo.

La morte dell’ encefalo a tutti i suoi livelli infatti determina l’irreversibile disgregazione funzionale del classico “tripode vitale di Bichat”, che consiste nella contemporanea presenza della funzionalità respiratoria, cardiocircolatoria e del sistema nervoso centrale.

La medesima legge infatti all’articolo 2 comma 1 chiarisce cheLa  morte  per  arresto  cardiaco si intende avvenuta quando la respirazione e la circolazione sono  cessate  per  un  intervallo  di tempo  tale  da  comportare  la  perdita  irreversibile  di  tutte le funzioni dell’encefalo e puo’ essere accertata con le modalita’ definite con decreto emanato dal Ministro della sanita’.

Per le modalità di accertamento si rimanda quindi al decreto n. 582 del 22 agosto 1994, “Regolamento recante le modalita’ per l’accertamento e la certificazione di morte.”  che all’articolo 1 comma 1 stabilisce:  “In conformita’ all’art. 2, comma  1,  della  legge  29  dicembre 1993,  n.  578,  l’accertamento della morte per arresto cardiaco puo’ essere effettuato da  un  medico  con  il  rilievo  grafico  continuo dell’elettrocardiogramma protratto per non meno di 20 minuti primi.

Ma allora cos’e’ la “constatazione di decesso”? 

In effetti tale termine non ha alcun riferimento nel complesso legislativo che regola l’accertamento e la certificazione della morte e  non compare in nessuna parte dei regolamenti di polizia mortuaria. E’ quindi un termine derivato dalla consuetudine operativa, si confonde con la diagnosi e l’accertamento di morte ed è stato alimentato dalla trasmissione aneddotica/orale con sporadico riscontro nei  regolamenti locali. 

Ma per capire che un paziente e’ in arresto cardiaco serve un medico?

Sulla “diagnosi” di arresto cardiaco il BLS e la comune pratica ci hanno da anni insegnato che essa è clinica e non strumentale e può essere effettuata anche da personale laico addestrato e non addestrato sia pure se guidato anche in modo remoto da un professionista sanitario. Questo estendere una “diagnosi” a personale non sanitario ha contribuito in modo fondamentale ai progressi in termini di sopravvivenza nei pazienti colpiti da morte improvvisa  diffondendo la cultura e delle rcp di base e della defibrillazione precoce.

Abbiamo quindi oramai universalmente stabilito che i laici possono  individuare la presenza di criteri clinici di arresto cardiaco tanto che essi sono autorizzati ad effettuare un massaggio cardiaco ed utilizzare un defibrillatore. 

L’arresto cardiaco nei pazienti in cui non e’ indicata la RCP

A maggior ragione tale “diagnosi” può essere effettuata da familiari o astanti in pazienti a fine vita, affetti da patologie in fase terminale  in cui sono esauriti i margini terapeutici ed in cui l’assistenza e la cura non sono oramai un’emergenza.

Riassumiamo

L’accertamento della morte non è una procedura d’emergenza-urgenza e può essere effettuata da un medico (in genere il necroscopo) mediante il rilievo per 20 minuti in continuo delle’ECG.

Nel complesso delle norme non viene mai nominata la “constatazione del decesso” essa è spesso utilizzata come sinonimo fuorviante di accertamento di morte o dichiarazione di arresto cardiaco/morte.

L’arresto cardiaco è un riscontro clinico e può essere fatta da chiunque se addestrato o sotto guida dell’infermiere di centrale.

C’è una categoria di pazienti per i quali esistono clinicamente (assenza di prospettive di buon outcome per la presenza di patologie croniche in fase terminale o neoplasie senza margine ulteriore di trattamento) ed eticamente (fine vita, dichiarate o manifeste disposizioni anticipate di trattamento) delle chiare controindicazioni alla pratica di manovre rianimatorie.

Sistema 118, diagnosi ed accertamento di morte

Il sottile limite concettuale e temporale tra le urgenti manovre di rianimazione cardiopolmonare e l’accertamento della morte ha portato in questi anni a confondere il ruolo del medico del 118 con quello del certificatore della morte.

Ma viste le premesse ed in un’ottica di ottimizzazione e razionalizzazione dell’utilizzo delle risorse dell’emergenza preospedaliera non ha senso né clinico né organizzativo inviare il medico a fare diagnosi di morte ed accertare e certificare il decesso in paziente in cui è chiaramente controindicata la RCP.

In un’ottica attuale e limitatamente ai casi in cui non sono indicate le manovre rianimatorie, il compito della certificazione della morte dovrebbe essere affidato ad altre figure professionali come il MMG, il medico di continuità assistenziale o il medico necroscopo.

In pratica in caso di chiamata per arresto cardiaco in cui appaia chiara la futilità delle manovre rianimatorie si dovrebbero attivare, da parte della CO 118, risorse mediche alternative e non urgenti per procedere alla certificazione della morte. 

Open Chest Wounds. The Prehospital Management

3 Ago

Is the flutter valve beneficial? Is the chest seal itself beneficial? Or, does it convert a sucking chest wound into a life-threatening tension pneumothorax? “Why do we treat a non-lethal condition (open pneumothorax) with an intervention that may result in a lethal condition (tension pneumothorax)?” If the size of the chest seal defect is larger than the diameter of the trachea, then air will preferentially move through the chest defect which can be fatal. Many of the chest seals are being placed on small defects which could lead to a tension pneumothorax.

It is unknown whether modifying the current practice of treating an open pneumothorax with an occlusive chest dressing might cause some of these injuries to then result in fatalities.

Saving Lives on the Battlefield
A Joint Trauma System Review of Pre-Hospital Trauma Care in Combined Joint Operating Area – Afghanistan (CJOA-A)
FINAL REPORT
30 January 2013
U.S. Central Command Pre-Hospital Trauma Care Assessment Team

The current guidelines indicates commercial chest seals both vent or non vent as a valid option to treat open chest wounds. In any case if a commercial chest seal is not available the 3 sided closed dressing is no longer recommended and a total occlusive medication is the current indication.

Commercial chest seal VS improvised 3 sided chest dressing

A chest dressing closed on 3 sides was the traditional option of treatment. They are often difficult to adhere, ineffective and difficult to improvise in time-critical scenarios. New and recent guidelines recommended an occlusive medication with strict surveillance and in case of signs of tension pneumothorax the dressing must be removed. If the patients does not improve after removing the seal open thoracostomy is indicated.

There is no clear evidence to suggest that the use of one-way chest seals would reduce the incidence of respiratory complications in patients with penetrating chest wounds. However, these seals may be easier to use and should be considered as part of the medical kit for out-of-hospital settings.

BET 3: In a penetrating chest wound is a three-sided dressing or a one-way chest seal better at preventing respiratory complications?

BET 3: In a penetrating chest wound is a three-sided dressing or a one-way chest seal better at preventing respiratory complications?

Major trauma: assessment and initial management. 1.3 Management of chest trauma in pre‑hospital settings

Vent vs Non Vent Chest Seal

A vent commercial chest seal is the first line option in prehospital setting.

Both vented and unvented CSs provided immediate improvements in breathing and blood oxygenation in our model of penetrating thoracic trauma. However, in the presence of ongoing intrapleural air accumulation, the unvented CS led to tension PTx, hypoxemia, and possible respiratory arrest, while the vented CS prevented these outcomes.

Vented versus unvented chest seals for treatment of pneumothorax and prevention of tension pneumothorax in a swine model

Vented versus unvented chest seals for treatment of pneumothorax and prevention of tension pneumothorax in a swine model

Treatment of Thoracic Trauma: Lessons From the Battlefield Adapted to All Austere Environments

In case vent chest seal is not available use non vent chest seal and if the patients develops hypotension, hypoxia, respiratory distress, remove the seal or performa an open thoracostomy.

So what to do?

First get an airway and put the lung on positive pressure ventilation (Volume or Pressure Targeted Ventilation) :

Positive pressure in the chest during the entire respiratory cycle and avoiding negative pressure during inspiration decreases the risk of tension pneumothorax

If you have the patient on a spinal board with a cervical collar the larynx is narrowed and when the patient is in spontaneous breathing the air preferentially enters from the chest wound. Placing an OT and positive pressure ventilation avoids this mechanism and prevents tension in the thorax.

Positive pressure ventilation re-inflates the collapsed lung and improve oxygenation (PEEP) and ventilation (Minute Ventilation).

Second close the wound with

Vent chest seal as first option

Non vent chest seal if vent is not available

Non commercial chest dressing closed on 3 sides is your last resort

Beyond Advanced Cardiac Life Support. Do we have to change our practice in COVID Era?

3 Mag

Main changes in recommendations

Personal Protective Equipment for Advanced Life Support interventions need to be at maximum level of protection of full body, eyes and airways.

CAT 3 level of protection 4 (at least) for the full body

FPP2/N95 airway filter for team members who are NOT directly involved in airway management, ventilation or manual chest compressions

FPP3/N99 airway filter for providers who are directly involved in airway management, ventilation and manual chest compressions.

Face shield and protective googles are strongly suggested

Mechanical Chest compressors devices are the gold standard to perform cardiac massage. They reduce contacts and contamination risk and team member exposure to contaminants.

Adhesive disposable pads are the only option to check rhythm and deliver shock. Dispose non-disposable, manual pads.

Passive O2 administration (via simple face mack at a rate of 15l/m) during chest compressions is the first option over bag mask ventilation when performing Basic Life Support waiting for advanced airway management.When using a Bag Valve Mask always put a HEPA/HME filter between Bag and mask to avoid contamination

Hold chest compressions when performing airway managment

Cover patient head with a transparent plastic foil to minimise virus spreading and contamination when performing airway management and bag mask ventilation

Tracheal intubation using a video laryngoscope is the first line option for advanced airway management to minimise contamination.

If video laryngoscope is not available Extraglottic devices are an acceptable first line option

Use all the implementation to improve intubation first passage success:

Video laringoscopy

Bougie

RAMP positioning

Suctioning (SALAD technique)

Use all the implementation to improve Extraglottic device placement

Laryngoscope for tongue displacement and mouth opening (DO NOT USE hands)

Deflate cuff

Lubrificate the device

Whatever plan you apply use an HEPA/HME filter immediately after the ventilation device

Use disposable cover and disposable gel to perform Ultrasound during chest compressions

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.

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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“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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