Tag Archives: emergenza

“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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How a perfect ALS can kill: Pulseles Electric Activity a novel approach in medical cardiac arrest.

27 Ott

HOW PERFECT ALS CAN KILLHEMS arrives on a patients where ground medical service is conducting a perfect ALS.

The 50 years old pt is in PEA cardiac arrest (CA) (sinus bradycardia narrow QRS) airway secured with an 8 ET. The pt was still pulseless (double checked) after almost 20 min of CA, 6 mg of epi already administered and good quality chest compression was ongoing. EtCO2 was 35 (!!!!) even when chest compression were stopped for the pulse check(!!!).

Still no palpable pulse. At this point a 12 lead EKG was performed (against alla the ALS dogmas) with the patient still pulseless and the chest compressions were conseguently suspended (other ALS eresia) while placing the precordial leads and acquiring the EKG.

EKG result: Sinus Rithm 50 bpm. Inf+dx STEMI with reciprocal changes in lateral leads.

S…t she is alive!!! This is not PEA but profound cardiogenic shock.

 

Pulseles Electric Activity a novel approach in medical cardiac arrest

When classical ALS algorithm comes to non defib rithm says that asystole and PEA are the same and have to be equally treated.

There is not such a clinical and therapeutic mistake.

Cardiac stand still and contractile cardiac activity without a palpable central pulse are totally different issues.Pulseless electric activity in the majority of cases is more like a profound state of shock than an asystole, and like this has to be treated.

But let’s make just a step backword.

First cosideration is on the identification of pulseless patients.

At the moment official guidelines consider a pulseless patient based on the palpation of carotid pulse. ERC BLS 2010 official guidelines about carotid pulse palpation says: “Checking the carotid pulse (or any other pulse) is an inaccurate method of confirming the presence or absence of circulation, both for lay rescuers and for professionals” so is no long recommended.

So why if is no recommended for BLS is used in ALS guidelines to recognize pulseless patients and to treat them as an asystolic one? Is our finger a reliable instrument to decide beetwen life and death? Even the BLS guidelines give us the answer: NO.

Second consideration is the research of the underlyng causes of PEA.

The H’s and T’s classification is an etiologic definition and not a clinical one and is often impossible to use in emergency settings cause of the lack of clinicla informations.

Norman and Desbiensin their 2008 article Simplifying the diagnosis and management of pulseless electrical activity in adults: A qualitative review proposed a new classification based on a more clinical concept that is somehow useful for the emergency clinicians.

3 and 3 rule, even if still not validate, seems more helpful for clinicians working on the field or at least for quick use in emergency situation. On plus give us a guide for tretment according on patophisiologic origin of PEA.

3+3+3 rule

 

 

More recently Littmann, Bustin and Haley in the 2013 article “A Simplified and Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity” use EKG findings to guide the diagnosys of cause of PEA and to treat it. On the base of QRS duration they identify a possible origin, mechanical or metabolic, and accordingly propose the specific treatment.

PEA evaluation algo

 

 

 

 

 

 

 

 

PEA evaluation algo1PEA evaluation algo2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The introduction of point of care echo and EtCO2 in ED and on the field put a new brick in definition, diagnosys and treatment of PEA.

Ultrasonography give us the chance to expolore, confirming or excluding, most of the mechanical causes of PEA and EtCO2 is a more reliable indicator of perfusion than the subjective pulse palpation.

Regarding the tretment options, there are still no evidences in favour or against epinephrine administation and chest compression utility in patients pulseless with electric activity and no cardiac standstill.

The end of clinical case

After performing 12 leads EKG the patients was loaded on the helicopter and directed to the cat lab where the patients arrived still pulseless but with EtCO2 38. The angio, performed after an echo showing weak heart contractility with inferior wall ipokinesia, confirmed critical occlusion of the dx coronary artery. A medicated STENT was placed with good TIMI flow result.

The patient regained consciouness a couple of hours later, and was dismissed from the hospital afer 15 days with CPC 1 and 45% EF.

In this case the strict observance of ALS protocol would have conducted the medical team to continue CPR, despite the presence of a organized rythm, due to the absence of a palpable central pulse. Epinephrine would have been regularry administered (at CA doses) and chest compressions performed.

The decision to load and go to the PCI center gave the patient the chance to treat the underlyng cause of CA.

Not the same thing can be said about the ALS protocol.

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References:

Una voce fuori dal coro sull’utilità dell’Acido Tranexamico nel trauma.

4 Set

I risultati dello studio CRASH-2 hanno portato prepotentemente all’attenzione dei professinisti sanitari l’uso dell’acido Tranexamico nel paziente traumatizzato.

Anche MEDEST qualche mese fa ha pubblicato un articolo in proposito, in cui oltre ad evidenziare i risultati dello studio veniva caldeggiata l’ipotesi che tutti i sistemi d’emergenza prendessero in considerazione l’inserimento dell’Acido Tranexamico nei propri protocolli sul politrauma.

L’entusiasmo è generale e scorrendo la letteratura è molto difficile trovare voci meno che entusiastiche sul tema. Nessuna traccia di dissenso.

E’ quindi con favore che accogliamo ed ospitiamo questo recente editoriale pubblicato su “The Medical Journal of Australia” dal titolo “Trauma and tranexamic acid” ed a firma di Russell L Gruen, Ian G Jacobs a e Michael C Reade (credits).

In sostanza gli autori sottolineano alcuni dubbi sia sul metodo che sul merito. Vediamo quali:

  1. Solo il 2% dei pazienti arruolati da CRASH-2 sono assimilabili a quelli trattati nei moderni sistemi trauma (nonostante lo studio si sia svolto in luoghi che hanno trauma systems molto avanzati) in cui l’accesso ai prodotti ematici, alla radiologia interventistica, alla damage-control surgery ed in generale all’area intensiva sono routinariamente disponibili. La mortalità di base indicata nel lavoro infatti è molto superiore a quella dei sistema trauma più evoluti, e questo potrebbe aver condizionato la significatività statistica a favore della sopravvivenza.
  2. Sembra molto sotto-investigata la possibile interazione dell’Acido Tranexamico con altre terapie tese a contrastare il sanguinamento e le coagulopatie post-trauma. Lo stato ipercoagulativo indotto dall’Acido Tranexamico potrebbe infatti (teoricamente) favorire l’insorgenza di complicanze spesso fatali, come l’embolia polmonare e la trombosi venosa profonda, tipiche del paziente politraumatizzato. Queste complicanze che nel CRASH-2 sono molto rare, nello studio parallelo, condotto in ambito militare (MATTERs study), sono rispettivamente 9 e 12 volte maggiori nella popolazione trattata con Acido Tranexamico rispetto a quella di controllo.
  3. Alcuni dubbi inoltre sorgono sull’effetto biochimico dell’acido tranexamico che riducendo l’azione fibrinolitica della plasmina tende ad indurre una coagulopatia acuta post-traumatica (ATC). Questa complicanza è in effetti poco correlata con il trauma in se stesso (sol 1 paziente su 10 ne soffre), mentre sembra essere molto frequente (per circa il 50% dei casi) nei pazienti politraumatizzati che vengono massivamente trasfusi. E visto che l’acido Tranexamico è frequentemente parte dei protocolli in cui sono previsti alte dosi di emazie concentrate o di altri fattori ematici, il dubbio sorge spontaneo. Nel CRASH-2 questa possibile correlazione non viene adeguatamente indagata e smentita.

Sicuramente uno studio, anche se ben potenziato e condotto rigorosamente, non può essere conclusivo. I dubbi espressi nell’articolo menzionato sono legittimi sia dal punto di vista scientifico, che metodologico.

A tal proposito sono già in programma (negli USA ed in Australai) altri trial che prenderanno in considerazione, cercando di dargli una risposta, i  dubbi lasciati irrisolti da CRASH-2.

Attendiamo fiduciosi e vigiliamo su ogni possibile cambiamento.

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References:

Russell L Gruen, Ian G Jacobs and Michael C Reade. Trauma and tranexamic acid.

American Board of Emergency Physician certifica i primi specialisti in Emergenza Sanitaria preospedaliera.

27 Giu

Mentre da noi il 2014 darà il benvenuto ai primi medici con formazione universitaria in Medicina d’urgenza negli Stati Uniti, dove questa figura professionale è stabilmente presente da anni, con il nuovo anno arriveranno i primi medici con formazione specifica in Medicina d’urgenza preospedaliera. La disciplina è una sub-specialaizzazione nell’ambito del corso di Medicina d’urgenza è stata attivata nel Settembre 2010 dall’American Board of Medical Specialties ed è certificata dall’ American Board of Emergency Medicine.

Emergency Medical Services è una subspecialità medica i cui target formativi riguardano il trattamento preospedaliero dei pazienti. In particolare si occupa della stabilizzazione iniziale del paziente e del suo trasporto mediante mezzi attrezzati (ambulanza o elicottero) verso i presidi ospedalieri.

Il suo intento è di:

  • Standardizzare la formazione e i criteri certificativi dei medici che operano sul territorio
  • Aumentare la sicurezza dei pazienti
  • Incrementare la la qualità dei professionisti preospedalieri
  • Promuovere l’integrazione dei percorsi terapeutici dei pazienti tra ambito extra ed intraospedaliero

Scarica EMS Core Content con i contenuti dettagliati

Alcune considerazioni:

  • Per un paese come gli Stati Uniti in cui la medicalizzazione dell’emergenza preospedaliera è una percentuale minima la creazione di un percorso formativo specifico in questo senso è un segnale molto importante.
  • Una Nazione così evoluta dal punto di vista formativo e culturale, patria della Medicina d’Urgenza, riconosce che quella preospedaliera è talmente specifica da meritare una ultraspecializzazione.
  • In Italia dove esiste una radicatissima tradizione di medicalizzazione dell’emergenza sanitaria extraospedaliera con un patrimonio professionale immenso rispetto agli Stati Uniti ed una esperienza organizzativa decennale  dei sitemi di Emergenza Sanitaria Territoriale, il fatto che nessuno ci abbia pensato ci fa essere “leggermente” in controtendenza…

 118trash

 

Dolore epigastrico in diabetica

28 Mag

Download English transcript

rt-PA e Stroke: IST-3 l’analisi dei risultati

10 Apr

Stroke 3

L’analisi detagliata dei dati dello studio più potente e promettente sull’uso del trombolitico nello stroke ischemico chiude definitivamente la discussione su uno studio nato per essere conclusivo, ma che ottiene il risultato, non solo di suscitare molti (e decisivi) dubbi, ma anche di scalfire alcune ragionevoli certezze.

Scarica la trascrizione del podcast

Scarica la Cronostoria dei trials sulla trombolisi nello stroke ischemico

Guarda la cronistoria dei trials sulla trombolisi nell’ictus ischemico

Leggi il post sul “pubblication bias”

Referencs:
  1. IST 3 Study The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen
  2. IST 3 analysys 2013
  3. Bekelman JE, Li Y, Gross CP. Scope and impact of financial conflicts of interest in biomedical research: a systematic review.
    JAMA. 2003;289:454-469.
  4. Lexchin J, Bero LA, Djulbegovic B, et al. Pharmaceutical industry sponsorship and research outcome and quality: systematic review.
    BMJ. 2003;326:1167-1170
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