Do we really need Lights and Sirens when transporting a patient?

16 Apr

For who has a multiyear experience in prehospital emergency medicine and deals everyday with emergency transportation of critical patients the sensation is that the use of emergency warning systems are, mostly of times, useless and doesn’t really have any impact on clinical outcomes. 

aditya-vyas-1390338-unsplash-e1554782919903.jpg

But beyond any subjective thought, do we have any evidence on that?

My analysis starts from this article published in 2018 on Annals of Emergency Medicine

by Brooke L. Watanabe, MD et al. and entitled  “Is Use of Warning Lights and Sirens Associated With Increased Risk of Ambulance Crashes? A Contemporary Analysis Using National EMS Information System (NEMSIS) Data”. The authors conclusion says that Ambulance use of lights and sirens is associated with increased risk of ambulance crashes. The association is greatest during the transport phase. EMS providers should weigh these risks against any potential time savings associated with lights and sirens use.

Curbside to Beside blog published an interesting post about this topic and resumed the data in this incredibly intuitive infographic

Lights-and-Sirens-Graphic-Red-Ambo

Data extrapolated from
Wantabe et al. (2018)

While ambulances crash rate when using L&S (light and sirens) in the response phase is slightly increased  (7.0 vs 5.4) in the transportation phase the amount of crashes associated with L&S use is significatively higher (17.1 vs 7.0). 

So L&S transportation increases the odd of crash (and this is intuitive) but, on the other side, is there any evidence that use of L&S increases response time and improve clinical outcome?

Fast is Time????

Fabrice Dami et al in an article entitled Use of lights and siren: is there room for improvement?” found that the time saved with L&S transport was 1.75 min (105 s; P<0.001) in day time and 0.17 min (10.2 s; P=0.27) night-time.

So evidently fast is time, but is a gain of less than 2 min a clinical significative time?

Time is Life???

In 2010 in the article “Emergency Medical Services Intervals and Survival in Trauma:Assessment of the “Golden Hour” in a North AmericanProspective Cohort” concluded that there was no association between EMS intervals and mortality among injured patients with physiologic abnormality in the field”.

Anderson et al in a 2014 article “Preventable deaths following emergency medical dispatch – an audit study” demonstrated how just 0,2% of the 94.488 “non L&S” dispatched emergencies died in the first 24 hours from the call.  Of those just 0.02% of total “non L&S” emergencies were considered “potentially preventable if the dispatcher had assessed the call as more urgent and this had led to an ambulance dispatch with a shorter response time and possible rendezvous with a physician-staffed mobile emergency care unit”

So mostly of the emergencies are not time sensitive and the clinical outcome does not differ if the transport time is shorter.

Take home messages for our system and for clinical practice

Maybe we need lights and sirens in response phase, cause slightly increase in accident risk corresponds to  some gain in arriving time on the scene.

Maybe we don’t need lights and sirens in transportation phase  cause a great increase in risk of crash do not correspond to a clinical sensitive time gain.

camilo-jimenez-1499711-unsplash

For sure when using L&S we need to be aware that the risk doesn’t worth the price, and even if we use L&S in the varies phases of emergencies pushing the threshold of                security too forward increases the risks and don’t improve clinical benefits for the transported patients.

Clinicians need to be more concerned about performing the right procedures to stabilise patients on pre-hospital phase more than hurrying  with unstable patients toward an unreal Eldorado and risking their own and patients lives

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Syncope. We need a prehospital pathway.

18 Feb

Non traumatic Transitory Lost Of Consciousness (TLOC) is a common cause of medical emergency call. Among TLOC Syncope is the most common cause. So the first challenge for an emergency professional is discerning from Syncope and non syncope situations (seizures, psychogenic, other rare causes).

Screenshot 2019-02-09 at 11.33.01

2018 ESC Guidelines for the diagnosis and management of syncope

Syncope according to 2018 Guidelines definition is a “TLOC due to cerebral hypoperfusion, characterised by a rapid onset, short duration, and spontaneous complete recovery”. 

Among Syncope the causes can be found in vagal reflex (Reflex syncope), a drop in blood pressure due to a deficiency of compensation in a standing position (Orthostatic syncope) and a cardiac cause of syncope (Cardiac syncope)

Screenshot 2019-02-17 at 17.44.17

2018 ESC Guidelines for the diagnosis and management of syncope

But what is the role and what can and must be done on the prehospital field to understand treat and risk stratify a Syncope?

Anamnesis

Is a fundamental step to understand and risk stratify a syncope episode. It has to be targeted to collect all the important informations and to don’t loose precious time.

We can divide the information we collect in two categories.

The first kind of information we area going to ask (to bystanders and patients) is about the syncope event.

  • How much the lost of consciousness lasted
  • How it happened (standing, sitting or laying)
  • What was the patient doing (resting or during exercise)
  • What the patient felt before the syncope (palpitations, chest pain, dyspnea, dizziness, other)
  • What happened during or immediately after the syncope (seizures, other)

Second step is collecting informations about the patient medical conditions. We have to focus on

  • What medical condition he actually suffers or suffered in the past
  • Which kind of drugs he is actually doing

After a focus anamnesis the second step is about the physical exam of the patient.

Diagnostic tests

During physical exam a rapid general neurologic and cardiac examination has to be completed, but two additional steps need to be done in a syncope patients

  • Orthostatic challenge in active standin position
  • Carotid sinus massage (CSM) in patients aged >40 years.

Orthostatic challenge:  Standing BP evaluation has to be done after 3 minutes of active standing position with the patient fully monitored, and “abnormal BP fall is defined as a progressive and sustained fall in systolic BP from baseline value >_20 mmHg or diastolic BP >_10 mmHg, or a decrease in systolic BP to <90 mmHg” (European Society of Cardiology 2018 ESC Guidelines for the diagnosis and management of syncope).

Carotid sinus massage: A ventricular pause lasting >3 s and/or a fall in systolic BP of >50mmHg is known as carotid sinus hypersensitivity. “Carotid sinus syndrome (CSS) There is strong consensus that the diagnosis of CSS requires both the reproduction of spontaneous symptoms during CSM and clinical features of spontaneous syncope compatible with a reflex mechanism.” (European Society of Cardiology 2018 ESC Guidelines for the diagnosis and management of syncope)

12 leads EKG

It’s a fundamental diagnostic tool and has to be performed in all syncope patients.

What are the risky features we have to consider when looking to ann EKG of a syncope patients:

At least 6:

  1. Ischemia
  2. Arrithmia
  3. Pre-excitation/WPW
  4. Brugada pattern
  5. Hypertrophic cardiomyopathy
  6. Arrhythmogenic Right Ventricular Cardiomyopathy

POCUS

Is there a role for Point of Care Ultrasound in differential diagnosis and risk stratification of syncope.

Probably yes cause we can look at:

  • Aorta for dissection
  • VD/VS ratio for PE
  • Pericardium for effusion
  • EF for cardiac function evaluation
High risk VS non high risk syncope

At the end of those steps the prehospital professional has two chances.

  1. There is a likely cause of syncope
  2. The syncope is of unknown cause
Screenshot 2019-02-17 at 18.52.22

2018 ESC Guidelines for the diagnosis and management of syncope

If the cause is known or very likely we have to follow the specific pathway.

In the unknown syncope we have to stratify the risk.

In prehospital field is important to look for high risk features of syncope:

  • History of heart failure or other cardiac conditions
  • Syncvope in supine position
  • Syncope during excercise
  • Dyspnea before or immediately following syncope
  • Palpitations before syncope episode
  • EKG abnormalities
  • Persisting low blood pressure (SBP<90 mmHg) in supine positi
  • Orthostatic Hypotension

Each one of those is indicative of high risk prehospital features and the patient need further ED examination.

In all other cases the clinician can decide case by case if the patient can be treated out of the hospital or need admission to ED.

Syncope.001

References :

Michele Brignole, Angel Moya et al. European Society of Cardiology 2018 ESC Guidelines for the diagnosis and management of syncope

 

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1 Year in Review. Trauma papers.

3 Gen

Third step of 1 YEAR IN REVIEW, the classical end of year MEDEST appointment with all that matter in emergency medicine literature.

In this post we review the 2018 Trauma papers divided by topic.

So let’s start

  • Traumatic Brain Injury

Effect of Early Sustained Prophylactic Hypothermia on Neurologic Outcomes Among Patients With Severe Traumatic Brain Injury. The POLAR Randomized Clinical Trial.

Rapid Sequence Intubation in Traumatic Brain-injured Adults

Brain Oxygenation Optimization After Severe Traumatic Brain Injury: An Ode to Preventing Brain Hypoxia

Management of traumatic brain injury patients

Efficacy of pre-hospital rapid sequence intubation in paediatric traumatic brain injury: A 9-year observational study

Pediatric traumatic brain injury—a review of management strategies

  • Traumatic cardiac arrest

Traumatic arrest & the HOTTT Drill

EMERGENCY MEDICAL SERVICES SIMPLE THORACOSTOMY FOR TRAUMATIC CARDIAC ARREST: POSTIMPLEMENTATION EXPERIENCE IN A GROUND-BASED SUBURBAN/RURAL EMERGENCY MEDICAL SERVICES AGENCY

  • Hemorrhagic shock

Plasma-first resuscitation to treat haemorrhagic shock during emergency ground transportation in an urban area: a randomised trial.

Prehospital Plasma during Air Medical Transport in Trauma Patients at Risk for Hemorrhagic Shock

What fluids are given during air ambulance treatment of patients with trauma in the UK, and what might this mean for the future? Results from the RESCUER observational cohort study

Evaluation of tranexamic acid in trauma patients: A retrospective quantitative analysis

Efficacy of prehospital administration of tranexamic acid in trauma patients: A meta analysis of the randomized controlled trials

Prehospital haemostatic dressings for trauma: a systematic review

Resuscitative endovascular balloon occlusion of the aorta performed by emergency physicians for traumatic hemorrhagic shock: a case series from Japanese emergency rooms

Resuscitative Endovascular Balloon Occlusion of the Aorta and Resuscitative Thoracotomy in Select Patients with Hemorrhagic Shock: Early Results from the American Association for the Surgery of Trauma Aortic Occlusion in Resuscitation for Trauma and Acute Care Surgery Registry

Permissive Hypotension vs. Conventional Resuscitation Strategies in Adult Trauma Patients with Hemorrhagic Shock: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

Trauma ‘Code Crimson’ Pathway. Streamlining access to definitive intervention for patients with life-threatening haemorrhage

  • Pediatric

Pediatric airway management devices: an update on recent advances and future directions

Cricoid Pressure During Induction for Tracheal Intubation in Critically Ill Children: A Report From National Emergency Airway Registry for Children

  • The rest

Pre-hospital emergency anaesthesia in awake hypotensive trauma patients: beneficial or detrimental?

Circulation first – the time has come to question the sequencing of care in the ABCs of trauma; an American Association for the Surgery of Trauma multicenter trial

Damage Control for Vascular Trauma from the Prehospital to the Operating Room Setting

Ultrasonography Assessments of Optic Nerve Sheath Diameter as a Noninvasive and Dynamic Method of Detecting Changes in Intracranial Pressure

Issues and challenges for research in major trauma

Effect of hypoxia on mortality and disability in traumatic brain injury according to shock status: A cross-sectional analysis

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1 Year in Review. Airway management.

27 Dic

Second step of 1 YEAR IN REVIEW, the classical end of year MEDEST appointment with all that matter in emergency medicine literature.

In this post we review the 2018 Airway management literature of note divided by topic.

So let’s start

  • Bag mask ventilation

Effect of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation on Neurological Outcome After Out-of-Hospital Cardiorespiratory Arrest. A Randomized Clinical Trial

  • Extraglottic Devices

Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest. A Randomized Clinical Trial.

Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of Hospital Cardiac Arrest on Functional Outcome. The AIRWAYS-2 Randomized Clinical Trial.

Preliminary Report: Comparing Aspiration Rates between Prehospital Patients Managed with Extraglottic Airway Devices and Endotracheal Intubation.

Pre-hospital i-gel blind intubation for trauma: a simulation study.

Supraglottic airway devices: indications, contraindications and management.

Laryngeal mask airway versus bag-mask ventilation or endotracheal intubation for neonatal resuscitation.

Self-pressurized air-Q intubating laryngeal airway versus the LMA ClassicTM: a randomized clinical trial.

  • Intubation, Direct Laryngoscopy, Airway management

Endotracheal Intubation for Traumatic Cardiac Arrest by an Australian Air Medical Service.

Effect of Cricoid Pressure Compared With a Sham Procedure in the Rapid Sequence Induction of Anesthesia. The IRIS Randomized Clinical Trial.

Effect of Use of a Bougie vs Endotracheal Tube and Stylet on First-Attempt Intubation Success Among Patients With Difficult Airways Undergoing Emergency Intubation. A Randomized Clinical Trial.

Cardiac Arrest and Mortality Related to Intubation Procedure in Critically Ill Adult Patients: A Multicenter Cohort Study.

Tracheal intubation in critically ill patients: a comprehensive systematic review of randomized trials.

Cardiac Arrest and Mortality Related to Intubation Procedure in Critically Ill Adult Patients: A Multicenter Cohort Study.

Airway Management During Out-of-Hospital Cardiac Arrest

Assessing Advanced Airway Management Performance in a National Cohort of Emergency Medical Services Agencies

  • Video Laringoscopy, VL vs DL

Comparison of video laryngoscopy versus direct laryngoscopy for intubation in emergency department patients with cardiac arrest: A multicentre study.

First attempt success with a Macintosh-style video laryngoscope is high whether or not the video screen is viewed.

Should the Glidescope video laryngoscope be used first line for all oral intubations or only in those with a difficult airway? A review of current literature.

Comparison of King Vision video laryngoscope and Macintosh laryngoscope: a prospective randomized controlled clinical trial.

Interpreting the Cormack and Lehane classification during videolaryngoscopy.

Intubation with cervical spine immobilisation: a comparison between the KingVision videolaryngoscope and the Macintosh laryngoscope. A randomised controlled trial.

Videolaryngoscopy versus direct laryngoscopy for emergency orotracheal intubation outside the operating room: a systematic review and metaanalysis

  • Guidelines, clinical policies and more

Guidelines for the management of tracheal intubation in critically ill adults.

Airway Management for Trauma Patients

Pragmatic Airway Management in Out-of-Hospital Cardiac Arrest

Implementation of a Clinical Bundle to Reduce Out-of-Hospital Peri-intubation Hypoxia

The Vortex model: A different approach to the difficult airway

Airway management in critical illness: practice implications of new Difficult Airway Society guidelines

Airway Management Practice in Adults With an Unstable Cervical Spine: The Harborview Medical Center Experience

Defining the criteria for intubation of the patient with thermal burns

Shifting Priorities from Intubation to Circulation First in Hypotensive Trauma Patients

Airway and ventilation management strategies for haemorrhagic shock. To tube, or not to tube, that is the question!

Advanced airway management in hoist and longline operations in mountain HEMS. Considerations in austere environments: a narrative review This review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM)

  • Pediatric

Pediatric airway management devices: an update on recent advances and future directions

Cricoid Pressure During Induction for Tracheal Intubation in Critically Ill Children: A Report From National Emergency Airway Registry for Children

  • Drugs

Emergency Department Intubation Success With Succinylcholine Versus Rocuronium: A National Emergency Airway Registry Study

Rapid Sequence Intubation in Traumatic Brain-injured Adults

  • The rest

How much experience do rescuers require to achieve successful tracheal intubation during cardiopulmonary resuscitation?

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Clinal Myths and Scientific Truth about heart failure/pulmonary edema management in prehospital setting.

18 Dic

Clinical Myth #1. All heart failure/cardiogenic pulmonary edema (HF/CPE) patients are fluid overladed .

Scientific Truth #1: Just a small part of heart failure/ cariogenic pulmonary edema (HF/CPE) patients are fluid overloaded. Most (>50%) patients are redistributed (from splanchnic circulation and lover limb to pulmonary circle). Use your clinical judgement (poor sensitivity and specificity) or ultrasound (lung US for the presence of ≥3 B lines in ≥2 bilateral thoracic lung zones is reliable and sensitive for pulmonary edema) to establish which kind of patient you are dealing with: Overloaded or Redistributed. That makes the difference.

Clinical Myth #2. All HF/CP patients benefit from diuretic ( Furosemide or other diuretics) therapy.

Scientific Truth #2: Just normotensive overloaded HF/CPE patients can benefit from diuretic ( Furosemide or other diuretics) therapy.

Furosemide can be detrimental on short and long term outcome because:

  • decreases LV function, increasing ventricular filling pressure 

  • increases systemic vascular resistance through activation of the renin-angiothensyn system

  • decreases glomerular filtration rate

Clinical Myth #3. Nitrates small doses continuous infusion is the right strategy in HF/CP patients.

Scientific Truth #3: Nitrates and Non Invasive Positive Pressure Ventilation are effective first line interventions in hypertensive HF/CPE patients.

High doses Nitrates administration is safe. 2 mg bolus of nitrates every 3 min in hypertensive patients (with close blood pressure check) are safe and faster in achieving clinical targets and symptoms relief. 

Clinical Myth #4. Morphine is safe and effective in HF/CP patients because relief anxiety and reduce preload, and has to be part of first line interventions.

Scientific Truth #4: Morphine administration has no evidences of clinical benefit in HF/CPE patients and is not part of first line treatment for HF/CPE patients. Low quality evidence suggests that morphine is associated with worse outcomes when compared to patients not receiving opioids.

Clinical Myth #5. In hypotensive (cariogenic shock) HF/CP patients Dopamine is the first choice vasopressor.

Scientific Truth #5: Norepinephrine is the first line medication to reach target mean arterial pressure and achieve organ perfusion, rather than Dopamine. Evidence suggests that norepinephrine is associated with improved outcomes including
lower mortality and lower risk of dysrhythmia when compared with Dopamine.

Bottom Line Clinical Pearl: Use ultrasound during every step of your clinical pathway in HF/CPE patients.

  • US detection of B-lines for diagnosis in undifferentiated dyspneic patients

  • US of IVC to discriminate between fluid overloaded or redistributed patients

  • Pump/Tank/Pipes US approach for differential diagnosis in undifferentiated shock patients

 

Liberally adapted from:

Brit Long MD, Alex Koyfman, MD,  Eric J. Chin, MD. Misconceptions in acute heart failure diagnosis and Management in theEmergency Department. American Journal of Emergency Medicine. 2018 Sep;36(9):1666-1673. doi: 10.1016/j.ajem.2018.05.077. Epub 2018 Jun 1

References:

Myth #1

  • Fallick C, Sobotka PA, Dunlap ME. Sympathetically mediated changes in capacitance: redistribution of the venous reservoir as a cause of decompensation. Circ Heart Fail 2011;4:669–75.
  • Zile MR, Bennett TD, St John Sutton M, et al. Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures. Circulation 2008 Sep 30;118 (14):1433–41.
  • Chaudhry SI,Wang Y, Concato J, Gill TM, Krumholz HM. Patterns of weight change preceding hospitalization for heart failure. Circulation 2007;116:1549–54
  • Viau DM, Sala-Mercado JA, Spranger MD, et al. The pathophysiology of hypertensive acute heart failure. Heart 2015;101:1861–7.
  • Jambrik Z, Monti S, Coppola V, et al. Usefulness of ultrasound lung comets as a non radiologic sign of extravascular lung water. Am J Cardiol 2004;93(10):1265–70.
  • Mallamaci F, Benedetto FA, Tripepi R, et al. Detection of pulmonary congestion by chest ultrasound in dialysis patients. JACC Cardiovasc Imaging 2010;3(6):586–94.
  • Anderson KL, Fields JM, Panebianco NL, et al. Inter-rater reliability of quantifying pleural B-lines using multiple counting methods. J Ultrasound Med 2013;32(1):115-20.

Myth #2

  • Francis GS, Siegel RM, Goldsmith SR, et al. Acute vasoconstrictor response to intravenous furosemide in patients with chronic congestive heart failure. Ann Intern Med 1985;103(1):1–6.
  • Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990;98:124–8.

Myth #3

  • Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998;351:389–93.
  • Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.
  • Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate i safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.

Myth #4

  • Sosnowski MA. Review article: lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema. Emerg Med Australas 2008;20:384–90.
  • Vasko JS, Henney RP, Oldham HN. Mechanisms of action of morphine in the treatment of experimental pulmonary edema. Am J Cardiol 1966;18:876–83.
  • Kaye AD, Hoover JM, Kaye AJ, et al. Morphine, opioids, and the feline pulmonary vascular bed. Acta Anaesthesiol Scand 2008;52:931–7.
  • Riggs TR, Yano Y, Vargish T. Morphine depression of myocardial function. Circ Shock 1986;19:31–8.
  • Miró Ò, Gil V,Martín-Sánchez  FJ, et al.Morphine use in the ED and outcomes of patients with acute heart failure: a propensity score-matching analysis based on the EAHFE registry. Chest 2017 Oct;152(4):821–32.

Myth #5

  • Rui Q, Jiang Y, Chen M, et al. Dopamine versus norepinephrine in the treatment of cardiogenic shock: a PRISMA-compliant meta-analysis. Medicine 2017;96(43):e8402.

IMG_1655

 

1 Year in Review. 2018 Guidelines you must know.

13 Dic

So 2018 is at the end and we give, as every year, a look back to literature and articles of this finishing year.

This is the first step of 1 YEAR IN REVIEW the classical MEDEST appointment with all that matter in emergency medicine literature.

So let’s start with Guidelines but first I want to cite an important point of view about Clinical practice Guidelines and they future development:

Clinical practice guidelines will remain an important part of medicine. Trustworthy guidelines not only contain an important review and assessment of the medical literature but establish norms of practice. Ensuring that guidelines are up-to-date and that the development process minimizes the risk of bias are critical to their validity. Reconciling the differences in major guidelines is an important unresolved challenge.”

Paul G. Shekelle, MD, PhD. Clinical Practice Guidelines What’s Next?

And now here it is, divided by topics, the most important new 2018 Guidelines. Click on the link to read more.
  • Airway management

Guidelines for the management of tracheal intubation in critically ill adults
Guidelines for the management of tracheal intubation in critically ill adults PP presentation

  • Trauma

Management of severe traumatic brain injury (first 24 hours)
Spinal Motion Restriction in the Trauma Patient –A Joint Position Statement
Guidelines for Prehospital Fluid Resuscitation in the Injured Patient
Re-thinking resuscitation: leaving blood pressure cosmetics behind and moving forward to permissive hypotension and a tissue perfusion-based approach
  • Cardiac

2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay

  •  Stroke

2018 Guidelines for the Early Management of Patients with acute ischemic stroke.A Guideline for Healthcare Professionals From the American HeartAssociation/American Stroke Association

  • Others

Health Professions Council of South Africa. Clinical Practice Guidelines

 

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Social media & aggiornamento. Dacci il tuo parere!

18 Ott

banner survey SoMe

Medici e infermieri d’emergenza-urgenza e area critica, come usate i #SocialMedia per aggiornarvi?

Rispondi a questa breve survey ➡️ bit.ly/2yiVXXI ⬅️per contribuire a delineare la realta’ italiana #FOAMed #FOANed #FOAMcc #AreaCritica #Emergenza

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CPR in TCA: A TLA PSA

12 Ott

Should we withhold chest compressions in traumatic cardiac arrest. A (very) reasonable poin of view.

The Collective

‘Don’t compress the chest in traumatic arrest…’ That’s the narrative. But Alan Garner has questions.

Do you do chest compressions in traumatic cardiac arrest (TCA)?

Don’t be dopey, right? Compressions are not important compared with seeking and correcting reversible causes. Indeed you can just omit the compressions altogether and transport the patient without them as they are detrimental in hypovolaemia and obstructive causes of arrest, right?

I would like to work through the logic of this.  I think the nidus of an idea got dropped into a super saturated FOAMEd solution and Milton the Monster* precipitated out.  The end result might be an approach that got extrapolated way beyond the biologically plausible.

The Starting Point

First let’s try to step slowly through the logic…

  1. In hypovolaemia or obstructive causes of shock that are likely in the trauma patient (tension and tamponade) and where the patient is in PEA (preferably with good…

View original post 1.100 altre parole

The Never Ending Debate. Airway management in cardiac arrest.

22 Set

Yes we are talking about airway management in cardiac arrest.

Yes this is another blog post on that topic, and if you are leaving the blog cause you had enough of that topic you have all my comprehension!

Still there?

I ask you just a few minutes of your time and attention to review two new studies that are making so much noise in the FOAMED world.

Here is the first trial:

Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of-Hospital Cardiac Arrest on Functional Outcome. The AIRWAYS-2 Randomized Clinical Trial.

Jonathan R. Benger, MD1; Kim Kirby, MRes1,2; Sarah Black, DClinRes2; et al

What kind of study is this:

This is a multicenter, cluster randomized clinical trial of paramedics from 4 ambulance services in England.

Inclusion criteria

  • 18 years or older
  • Non-traumatic OHCA

Exclusion criteria

  • Detained by Her Majesty’s Prison Service
  • Previously recruited to the trial (determined retrospectively);
  • Resuscitation deemed inappropriate (using guidelines from the Joint Royal Colleges Ambulance Liaison Committee)
  • Advanced airway already in place (inserted by another paramedic, physician, or nurse) when a paramedic participating in the trial arrived at the patient’s side;
  • Known to be enrolled in another prehospital RCT
  • The patient’s mouth opened less than 2 cm

Intervention

  • Insertion of a second-generation supraglottic airway device with a soft non inflatable cuff (i-gel; Intersurgical) (759 paramedics)

Control

  • Tracheal intubation using direct laryngoscopy (764 paramedics)

Main Outcome

  • Modified Rankin Scale score at hospital discharge or 30 days after out-of-hospital cardiac arrest
  • Secondary outcomes included ventilation success, regurgitation, and aspiration.

Results

Sample population

  • 1523 paramedics involved
  • 95 hospitals
  • 13462 potentially eligible patients
  • 4166 (31%)excluded
  • 9296(69%) enrolled

Primary outcome

  • The primary outcome was available for 9289 of 9296 patients (99.9%).
  • In the supraglottic airway device group, 311 of 4882 patients (6.4%) had a good outcome (modified Rankin Scale score range, 0-3)
  • In the TI group 300 of 4407 patients (6.8% adjusted OR, 0.92 [95%CI, 0.77 to 1.09];

Secondary outcomes

  • The supraglottic airway device treatment strategy was significantly more successful in achieving ventilation after up to 2 attempts with tracheal intubation
  • Two of the secondary outcomes, regurgitation and aspiration, were not significantly different between groups
  • The median time to death was not significantly different between the groups
  • The compression fraction was not significantly different between the group but in a very small sample of 66 patients

Conclusions

Among patients with out-of-hospital cardiac arrest, randomization to a strategy of advanced airway management with a supraglottic airway device compared with tracheal intubation did not result in a favorable functional outcome at 30days.

And here is the second trial:

Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest. A Randomized Clinical Trial

Henry E. Wang, MD, MS1,2; Robert H. Schmicker, MS3; Mohamud R. Daya, MD, MS4; et al

What kind of study is this:

Multicenter pragmatic cluster-crossover clinical trial involving 37 EMS agencies from the Resuscitation Outcomes Consortium Paramedics where Randomized in 13 clusters. Crossover of clusters to the alternate strategy at 3- to 5-month intervals.

Inclusion criteria:

Adults with OHCA and anticipated need for advanced airway management

Intervention

  • LT insertion (n = 1505 patients)

Control

  • ETI (n = 1499 patients)

Main Outcome

  • 72-hour survival

Secondary outcomes

  • Return of spontaneous circulation
  • Survival to hospital discharge
    Favorable neurological status at hospital discharge (Modified Rankin Scale score3)
  • Key adverse events

Results

Population

  • 3004 enrolled patients

Rates of initial airway success

  • 90.3%with LT
  • 51.6%with ET

Primary Outcome

  • Seventy-two hour survival was 18.3%in the LT group vs 15.4%in the ETI group

Secondary Outcomes

  • Return of spontaneous circulation in the LT group 27.9% vs 24.3% in ETI group
  • Hospital survival LT group 10.8%vs 8.1% in ET group
  • Favorable neurological status at discharge 7.1% in LT group vs 5.0% in ET group
  • No significant differences in oropharyngeal or hypopharyngeal injury airway swelling or pneumonia or pneumonitis

Conclusions

Among adults with OHCA, a strategy of initial LT insertion was associated with significantly greater 72-hour survival compared with a strategy of initial ETI. These findings suggest that LT insertion may be considered as an initial airway management strategy in patients with OHCA,

Strength:

This is a well conducted study with a large population that investigated a relevant clinical  topic.

Limitations:

In the TI group the first passage success rate is particularly low (51%) and there is no mention on the percentage of reintubation. This makes the neurologic outcome of this group particularly subject to procedural bias.

In general there is no mention of the post resuscitation care protocol and we know how this period is important on neurological outcome and individual variation makes bias very likely on this particular end point.

Take home messages Airway.001Take home messages Airway.002Take home messages Airway.003Take home messages Airway.004

References: 

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Epinephrine in cardiac arrest: the past, the present and the (im)possible future. Reflections after PARAMEDIC 2 trial.

23 Lug

The past (a brief history of epinephrine use in cardiac arrest)

19489_eb_adrenaline_molecule

In 1901 Jokichi Takamine (1854-1922) isolated the pure form of adrenaline, also known as epinephrine.

Routine use of adrenaline for cardiac arrest was first proposed in the 1960’s. Its inclusion within cardiac arrest management was based upon an understanding of the physiological role of adrenaline, and experimental data from animal research which showed that ROSC was more likely when the drug was used.

Epinephrine was not included in cardiac arrest protocols on the basis of evidence of benefit in humans.

Epinephrine remained, since today, a significant component of advanced life support despite minimal human data indicating beneficial effect .

The rationale for use of epinephrine in cardiac arrest was that, in animal studies, increases aortic blood pressure and thus coronary perfusion pressure during chest compressions.

IMPORTANT, brief reminder on epinephrine effect and Coronary Perfusion Pressure.
  • Coronary vessels are contained in epicardium and their flow is possible in the diastole when they are not compressed by myocardium during systolic contraction.coro-vessels
  • Coronary flow depends from the gradient between aortic diastolic (Ao) pressure and diastolic left ventricular (LV) pressure.acls3_3-1
  • Higher is the coronary pressure perfusion (CPP), greater is the chance of ROSC.

circ1

  • Epinephrine is a key determinant factor in maintaining diastolic aortic pressure in cardiac arrest; thanks to its interaction with alpha receptors, located on the endothelium of the arteries, produce generalized peripheral arterial vasoconstriction maintaining aortic diastolic pressure to a high level even during chest compressions.
  • The cut off value for ROSC is 15 mmHg of CPP, but more is better (at least 40 mmHg9.

Many and strong recent evidences demonstrates that “Among patients with OHCA, use of prehospital epinephrine was significantly associated with increased chance of return of spontaneous circulation before hospital arrival but decreased chance of survival and good functional outcomes Screen-Shot-2015-03-11-at-8.38.35-PM

The Present: PARAMEDIC 2 trial.

G.D. Perkins, C. Ji, C.D. Deakin, et al. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. 

What kind of study is this:

Randomized, double-blind, multicentric.

Population

8014 patients with out-of-hospital cardiac arrest in the United Kingdom

  • Inclusion Criteria

Adult (>16 years) patients, transported by five National Health Service ambulance services in the United Kingdom, who had sustained an out-of-hospital cardiac arrest for which advanced life support was provided by trial-trained paramedics.

  • Exclusion criteria

Apparent pregnancy, age of less than 16 years, cardiac arrest from anaphylaxis or asthma, administration of epinephrine before the arrival of the trial-trained paramedic.

Intervention

Paramedics administered either IV epinephrine 1mg every 3 – 5min + standard care  or IV 0.9% normal saline bolus + standard care.

Comparison

Placebo (IV 0.9% normal saline bolus) + standard care

Outcome

Primary outcome:
  • Rate of survival at 30 days.
Secondary outcomes:
  • Rate of survival until hospital discharge with a favorable neurologic outcome, as indicated by a score of 3 or less on the modified Rankin scale. 
  • Lengths of stay in the hospital and in the intensive care unit
  • Rates of survival at hospital discharge and at 3 months
  • Neurologic outcomes at hospital discharge and at 3 months
Description-of-the-modified-Rankin-Scale.ppm

Results

  • Patients who received epinephrine had a higher rate of 30-day survival than those who received placebo.
  • No clear improvement in functional recovery among the survivors in the epinephrine group.
  • The proportion of survivors with severe neurologic impairment was higher in the epinephrine group (31.0% vs. 17.8%)
  • Epinephrine NNT of 112 patients to prevent 1 death at 30-days (Early defibrillation NNT = 5, CPR performed by a bystander NNT = 15 )

PARAMEDIC-2-Results-1024x255

Image attribution: REBEL Cast Ep56 – PARAMEDIC-2: Time to Abandon Epinephrine in OHCA?

Conclusions

In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.

Strengths

  • Randomized, multicenter, double blind, placebo controlled
  • 8014 patients randomised.
  • Well balanced characteristics at baseline of the two groups
  • Concurrent treatments were similar
  • Median time from the emergency call to ambulance arrival was 6.6 minutes
  • Patient oriented outcomes

Paramedic

Limitations

  • Overall survival rate in this trial was disappointingly small (3.2% and 2.4%, respectively)
    • 615 patients where excluded because had return of spontaneous circulation before paramedics can open the trial pack. Of these 615 patients of which we don’t know the clinical outcome but including the survivors overall survival rate is similar to other EMS in Europe.
  • Median time from the emergency call until administration of the trial agent 21 min and we know (according the other studies) that cardiac arrest has 3 phases (Electrical Phase, first 5 min (Defib), Circulatory Phase next 10 – 15min (Chest compressions), Metabolic Phase 10-20min) and epinephrin is effective if administered in the first 20 min of the cardiac arrest.
  • Information about the quality of CPR was limited to the first 5 minutes of cardiac arrest and involved <5% of enrolled patients 
  • The protocol neither controlled nor measured in-hospital treatments and we know that the most common cause of in-hospital death is iatrogenic limitation of life support, which may result in the death of potentially viable patients.

What we know till today

  • Epinephrine in cardiac arrest improve ROSC and patients alive.
  • The improved survival is mostly due to patients with bad (<3 MRS) neurological outcome.

What that means

  • Administering the current recommended dose of Epinephrine we have to choose between numbers and quality of life.
  • Patients clearly said quality of life is more important
  • Epinephrine is anyway important because having bigger numbers of ROSC give the chance to improve neurological outcomes.

Future challenges

  • Understanding why epinephrine doesn’t work and can be detrimental on long term neurological outcome.
  • Obtaining more ROSC and better neurological outcomes in Cardiac Arrest

The (im)possible future

I think there are two key factors, in the actual way to use Epinephrine, that determine its failure:

The wrong administration route

When epinephrine is administered intravenously in a low flow state patient (as is a patient during cardiac arrest, even if proper chest compressions are performed), the amount of drug that arrives to perform the “local” alpha effect on arteries is just a minimal quantity of the (high!!!) dose. The major part rely in the venous circulation and is mobilized in great quantity only when ROSC happens determining a widespread vasoconstriction and a consequent “overdose” effect (think just at the “stunned” myocardium that has to overwhelm such ha great post-load work).

The wrong dose to the wrong patient

From the coronary perfusion pressure (CPP) point of view, every cardiac arrest patient is different: some patients have a (relative) good aortic pressure and a (relative) good  coronary perfusione comparing to others.

When we administer the same amount of epinephrine to each of them this takes to an underdose in some patients (with low flow state) and an overdose in others (with good or high flow state).

So now what?

The right administration route

Probably the best route to administer epinephrine is not the vein but the artery.

It allows, even in a low flow state patient, a better chance to reach the vasoconstrictor effect maintaining a good aortic diastolic pressure and a consequent good coronary flow.

The right dose to the right patient

Giving epinephrine (standard dose) to a patient who has a low flow state (patients who need it more) make epinephrine usefulness (underdose) because just a little part of it circulate.

Giving  epinephrine to patients in a good or high flow state (patients that need it less or don’t need epi at all) is detrimental and can cause overdose effect.

We need to know wich is the circulatory state of the patients to administer the right dose avoiding the “overdose” effect.

The only way to do this is monitoring aortic diastolic pressure through an arterial catheter. We can target Epinephrine dosage to reach a good aortic pressure maintaining a good CPP (achieving ROSC) and avoiding overdose.

evolution

Take home messages for future improvements in cardiac arrest management 

  1. Obtain an arterial line

  2. Give Adrenaline intrarterially

  3. Check blood pressure via arterial line

  4. Target Adrenaline (doses and times) to maintain at least 40 mmHg of diastolic arterial pressure

References

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