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Beyond Guidelines: what’s new in OCHA management

6 Set

Chest compressions alternate to abdominal compression–decompression technique

Background

The abdominal compression–decompression technique is based on an “abdominal pump” model, which induces pressure changes within the abdominal cavity and promotes the return of blood from the abdominal cavity to fill the heart and be eventually pumped to the brain. A combination of abdominal compression–decompression and chest compression was previously shown to increase the venous refilling of the heart, which could generate increased coronary perfusion pressure and increase blood flow to vital organs . With this combination method, chest release during abdominal compression leads to increased venous return to the thorax by negative intrathoracic pressure. Moreover, abdominal decompression during chest compression may lead to increased blood flow via decreased afterload. In myocardial blood flow, a better 48-h outcome was documented with the combination method compared with STD-CPR

The study

Evaluation of abdominal compression– decompression combined with chest compression CP9R performed by a new device: Is the prognosis improved after this combination CPR technique?

This study was performed in China. It’s a single center, randomised, not blinded study.

The study aimed to compare the outcomes of standard cardiopulmonary resuscitation (STD- CPR) and combined chest compression and abdominal compression–decompression cardiopulmonary resuscitation (CO-CPR) following out-of-hospital cardiac arrest (OHCA).

Primary outcome ROSC. Secondary outcome hospital admission, hospital discharge and neurological outcome at hospital discharge.

Results

ROSC and survival to hospital admission: no statistical benefit

Survival at hospital discharge and neurological outcome: CO-CPR had statistical significant better outcome respect STD-CPR

Limitations

Single center, small sample size, no evaluation of possible abdominal injuries.

Bottom line

For prehospital use of combined chest compression and abdominal compression–decompression cardiopulmonary resuscitation we have first of all to account the need of an additional rescuer to perform abdominal compression-decompression. By the way the alternate chest/abdominal compression-decompression method is promising even if we need larger multicenter randomised trial for a more consistent evaluation of its efficacy.

Head and thorax elevation during cardiopulmonary resuscitation

Background

Gradual elevation of the head and thorax enhances venous return from the head and neck to the thorax and further lowers intracranial pressure. This automated controlled elevation (ACE) CPR strategy consists of: (1) manual active compression decompression (ACD)-CPR and/or suction cup-based automated (LUCAS 3) CPR; (2) an impedance threshold device (ITD); and (3) an automated controlled head and thorax patient positioning device (APPD).

The study

Head and thorax elevation during cardiopulmonary resuscitation using circulatory adjuncts is associated with improved survival

Observational, prospective study. The Objectives of the study was to assess the probability of OHCA survival to hospital discharge after ACE-CPR versus C-CPR. ACE-CPR data were collected from a dedicated registry implemented by 10 EMS Agencies. Conventional (C) CPR data were collected from 3 large historical randomized controlled OHCA resuscitation trials.

NB: for ACE-CPR only 6/10 agencies data were evaluated.

The primary outcome was survival to hospital discharge. Secondary outcomes included ROSC at any time, and survival to hospital dis- charge with favorable neurological function.

Results

Cumulative results on primary and secondary outcome before taking into consideration the time from 911 call to ACE-CPR were not statistically significative differences. The statistical significance of ACE-CPR was reached only when time from 911 call to ACE-CPR initiation was considered.

Limitations

Observational study. Participating personnel form EMS agencies were highly motivated about ACE-CPR. 165 patients excluded with no clear explanation (generally didn’t meet inclusion criteria) from 4 EMS participating agencies. Statistical significance on primary and secondary outcome was reached after surrogate secondary analysis that considered time form 911 call to ACE-CPR start.

Bottom line

There are still insufficient historical data to understand the benefit of automated controlled elevation (ACE) CPR and this study doesn’t clear any doubt about it’s efficacies on clinical oriented outcomes.

Aortic occlusion during cardiac arrest. Mechanical adrenaline?

Background

Thoracic aortic occlusion during chest compressions limits the vascular bed for the generated cardiac output. This may increase the aortic pressure and subsequently the coronary perfusion pressure (CPP).

The coronary perfusion pressure (CPP), the pressure gradient between the aorta and right atrium, is a major determinant of the myocardial blood flow. Consequently, generating a high CPP by providing high-quality chest compression during CPR is one of the most critical factors for achieving ROSC in cardiac arrest patients.

It is uncontroversial to state that the desired effect of adrenaline in CPR is the potential increase in CPP. The potential detrimental effects of adrenaline, such as decreased cerebral blood flow, increased myocardial oxygen consumption or recurrent ventricular tachycardias after ROSC, is yet to be found with REBOA. However, adverse effects of REBOA are not reported in the limited human data published, nor has this been an endpoint in the studies conducted so far.

The study

Resuscitative endovascular occlusion of the aorta (REBOA) as a mechanical method for increasing the coronary perfusion pressure in non-traumatic out-of-hospital cardiac arrest patients

This is a pilot study. The aim of the study was to calculate the CPP before and after REBOA balloon inflation. EtCO2 and median aortic pressure before and after balloon inflating were also measured.

Results

CPP, MAP and EtCO2 significative increased after REBOA placement in Zone 1 and balloon inflation

Limitations

Single center, small numbers, need of a large number of operators to insert the REBOA and to obtain the measurements.

Bottom line

REBOA in Cardiac Arrest is potentially useful to increase CPP and less dangerous than epinephrine administration.

It’s feasibility in emergency (in-hospital and out of hospital) settings in a timely manner and with a small number of medical personnel needs to be demonstrated.

By Mario Rugna

In case of oesophageal intubation

19 Ago

Just published Preventing unrecognised oesophageal intubation: a consensus guideline from the Project for Universal Management of Airways and international airway societies

Thanks to a prestigious panel of international authors. Great job and definitely solid indication about how to prevent and recognise accidental oesophageal intubation.

Just some of the key recommendations

  • Exhaled carbon dioxide monitoring and pulse oximetry should be available and used for all episodes of airway management.
  • Routine use of a videolaryngoscope is recommended whenever feasible.
  • Inability to detect sustained exhaled carbon dioxide requires oesophageal intubation to be actively excluded.
  • Tube removal should be undertaken if any of the following are true:
    • Oesophageal placement cannot be excluded
    • Sustained exhaled carbon dioxide cannot be restored
    • Oxygen saturation deteriorates at any point before restoring sustained exhaled carbon dioxide

Refer to the full text guidelines for more.
Here is the link to Safe Airway Society livestream event.
Must read, must follow. Free open access.

Let’s go outside

The following are personal considerations on peculiar aspects about management of accidental oesophageal intubation in prehospital environment and come from my personal clinical experience.

Beware they are just personal considerations and practical tricks and tips and are not intended to substitute the above guidelines. 

They are intended to suggest an alternative mental and technical approach when dealing with oesophageal intubation on uncontrolled patients in difficult environment.

Some general considerations

  1. Prehospital uncontrolled patients are not on empty stomach so are at high risk of regurgitation/inhalation
  2. Even few ventilation efforts in case of oesophageal intubation pone the patient at high risk of regurgitation/inhalation 
  3. Suctioning in prehospital setting is not always ready avalliate (mind your environment) or maximally performant (mind your equipment) 
  4. First attempt in prehospital setting must be always the best one. Think before trying a second attempt in case of failure. Implement your plan or change plan.
  5. Apply the Indication, Suitability, Feasibility approach while supporting oxygenation, ventilation and protection.

DO NOT REMOVE THE OT TUBE STRAIGHT FORWARD IN CASE OF ACCIDENTAL OESOPHAGEAL INTUBATION IN PREHOSPITAL ENVIRONMENT.

The way I like it. The way I do it.

  1. Live the “oesophageal” OT tube in (overcuffed) and if it’s possible apply a continuous suctioning to exclude the oesophagus and protect the airways 
  2. Place a SGA to restore oxygenation and ventilation (trough BMV or NIV)
  3. After restoring oxygenation (SaO2 >94%) and ventilation (EtCO2 40 mmHg) if suitable and feasible (see below) proceed to a second attempt of tracheal intubation (must be videolaryngoscope+bougie)
  4. If the second attempt succeeds remove the “oesophageal” OT
  5. If the second attempt is not suitable or feasible transport to nearest hospital (patient is well oxygenated and ventilated via SGA and protected via oesophageal exclusion) for further stabilisation (you can replace the oesophageal OT tube with a large bore oro-gastric tube or insert the orogastric tube trough the SGA dedicated channel)
  6. If you can’t restore oxygenation and ventilation via SGA or you can’t place a SGA remove the oesophageal OT tube and try to oxygenate and ventilate (remember patient is not protected) via BVM and NC (double oxygenation) 
  7. If even BVM fails declare CICO 
Suitability 
  • Do I have a plan to implement regarding the  first attempt
  • Can I improve my environment (Setting) moving the patient to a more comfortable place/position 
  • Is the time to nearest hospital short/long 
Feasibility 
  • Am I in the right mental mood after 1st attempt (me) to try a better second one
  • Is my team ready for a second attempt (team) 
  • Do I have the right equipment to implement my second attempt (Equipment)

The visual algorithm

The Video

By Mario Rugna

Pulseless electrical activity following traumatic cardiac arrest: Sign of life or death?

11 Giu

On May 2019 was published an article we review today, cause the authors conclusions are pretty astonishing and worth a deeper look.

Israr, S & Cook, AD & Chapple, KM & Jacobs, JV & McGeever, KP & Tiffany, BR & Schultz, SP & Petersen, SR & Weinberg, JA. (2019). Pulseless electrical activity following traumatic cardiac arrest: Sign of life or death?. Injury. 10.1016/j.injury.2019.05.025.

Authors Conclusions: Following pre-hospital traumatic cardiac arrest, PEA on arrival portends death. Although Cardiac Wall Motion (CWM) is associated with survival to admission, it is not associated with meaningful survival. Heroic resuscitative measures may be unwarranted for PEA following pre-hospital traumatic arrest, regardless of CWM.Trauma death 2.jpg

What kind of study is this?

retrospective, cohort study consisting of adult trauma patients (n. 277 patients ≥18 years of age) admitted to one of two American College of Surgeons verified level 1 trauma centers in Maricopa County, Arizona within the same hospital system between February 2013 to September 2017 and January 2015 to December 2017.

Pre-hospital management by emergency medical transport services was guided by advanced life support protocols. 

Both hospitals for management of Traumatic Cardiac Arrest (TCA) followed the Western Trauma Association Guidelines

The following variables were collected from each patient:

  • Age
  • Gender
  • Duration of pre-hospital CPR
  • Survival to admission vs. pronouncement of death in ED
  • Disposition at hospital discharge

Results

  • 277 trauma patients that underwent pre-hospital CPR for TCA
  • Mean patient age was 43.1
  • Mechanism of injury was penetrating in 99 patients (35.7%), the most common of which was due to ballistic injuries, the rest where blunt trauma.
  • 52.0% of the patients were intubated prior to hospital arrival
  • 235 patients received epinephrine in route (84.8%)
  • Pre-hospital resuscitation duration, 20.0 (15.0 – 25.0) minutes

Outcomes

20 patients were identified on arrival to have had ROSC. 18 of these patients survived to hospital admission and 4 of them were discharged alive from hospital

147 patients were identified on arrival in asystole. Among these patients none were discharged alive from hospital.

The remaining 110 patients presented with PEA. 10 patients survived to admission, 9.1%, but only one, 0.9% was discharged from alive from hospital.

P-FAST was performed in 79 of the 110 patients with PEA (71.8%)

Presence of CWM was significantly associated with survival to hospital admission (2 but not to hospital discharge (zero with or without CWM).

Authors conclusions

  • Resuscitative efforts are unlikely to reverse the course of this pathophysiology, warranting sound clinical judgement from the treating physician concerning the decision to continue or desist, relative to mechanism of injury and clinical presentation.
  • CWM (signifying a beating heart and thereby pseudo PEA) was not associated with meaningful survival.
  • Nonetheless, we conclude that P-FAST is a useful tool for distinguishing PEA with cardiac standstill, which is in all likelihood terminal (and continued resuscitation would become an attempt at reanimation), versus pseudo PEA, whereby the heart is actually still beating, representative of a veritable sign of life, and ongoing resuscitative attempts may be considered appropriate despite the unfavorable prognosis.

My considerations on methodology and results

  1. Conventional ACLS protocol, as performed in the study, IS NOT the standard of care in TCA.
  2. No clinical intervention to address reversible causes where performed (or mentioned) in the field.
  3. The only clinically oriented manoeuvre performed in the field was tracheal intubation in just half of the patients (52.0% of the patients were intubated).
  4. Prehospital resuscitation time (20 minutes mean time) was spent performing non useful and potentially  dangerous interventions (closed chest compressions, epinephrine administration) for TCA.
  5. Patients with PEA and documented CWM (but not only them) at their arrival in ED has been hypo perfused during the entire pre-hospital resuscitation time and lost most of their chances for good clinical outcome.

So in my opinion this study and it’s conclusions are biased by a wrong approach to Traumatica Cardiac Arrest in the prehospital phase.

Emergency providers, when treating patients in traumatic cardiac arrest, need to perform interventions addressing the possible REVERSIBLE causes:

  1. Exanguination/Massive Hemorrage (Pelvic Binding, TXA administration, Tourniquet or direct compression)
  2. Hypoxia (Tracheal Intubation)
  3. Tension Pneumo (Double Thoracostomy)
  4. Hypovolemia (Blood or fluid resuscitation)

Emergency providers need to rely on direct (central pulse palpation, Ultrasuond) or indirect (EtCO2, Plethysmography) signs of perfusion to guide their clinical interventions.

Resuscitation of Traumatic Cardiac Arrest patients in not futile just need to be performed in the right way.

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References

Israr, S & Cook, AD & Chapple, KM & Jacobs, JV & McGeever, KP & Tiffany, BR & Schultz, SP & Petersen, SR & Weinberg, JA. (2019). Pulseless electrical activity following traumatic cardiac arrest: Sign of life or death?. Injury. 10.1016/j.injury.2019.05.025.

 

 

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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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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Articles at the Top. Take home messages from 2017 (part 3). Trauma.

1 Mag

Welcome to our review of the best articles from the last year.

This will be a weekly (or so..) appointment with the top articles from 2017 divided by topic and chosen by me.

Here is the best about:

 Trauma

Traumatic Cardiac Arrest

Fluid Therapy

Spinal Immobilisation

Field Triage

Antifibrinolytics

Prehospital blood

Massive transfusion protocol

Traumatic Brain Injury

The rest

If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.

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Articles at the Top. Take home messages from 2017 (part 2).

19 Gen

Welcome to our annual review of the best articles from the finishing year.

This will be a weekly (or so..) appointment with the top (or so…) articles of 2017 divided by topic and chosen by me.

Here is the best (for me) about:

 Advanced Life Support

Here are the best 2017 articles:

My take home messages:

Pathophysiological bases in experimental swine models

  • In a swine model following primary cardiac arrest the respiration continues at least for 1 minute. and after that Gasping starts lasting for another minute.
  • In a swine model following primary cardiac arrest the blood shifts from high pressure compartment (arteries) to low pressure compartment (veins). 
  • In a swine model the PaO2 following primary cardiac untreated VF arrests PaO2 results 70 mmHg after 9 min with a saturation of 93% and decrease at 44 mmHg with a saturation of 61% after 14 min of CPR. In this period airway management with possible interruption of chest compressions and starting positive pressure ventilation (with decreased return to the thorax end depression of cardiac output) is not mandatory due to the low cost/beneficial ratio and the potential detrimental effect. 

Chest compressions

  • Chest compressione only CPR is associated with worst outcome in children under 8 yers. Always perform chest compression/ventilation (ratio 15:2) in children <8 years of age (only exception if the cardiac arrest is due to primitive cardiac causes). 
  • Chest compressione only CPR can be a valuable option in adult witnessed VF/pulseless VT primary cardiac arrest (delayed airway management and passive O2 administration is reasonable).
  • Mechanical chest compression (MCC) is the future of CPR. They still do not demonstrated evident superiority in terms of outcome respect to manual chest compressions, but are evidently not inferior with a similar rate of life treating lesions. For sure MCC avoid variability in quality and allows good quality CC during transport. 

Ventilation

  • Lower Tidal volumes following OHCA is independently associated with favourable neurocognitive outcome
  • Weak evidences demonstrate that the ideal rate for ventilation of intubated patients  during CPR is 10/min

Airway management

  • There is not beneficial effect on outcome with early intubation in Cardiac Arrest (CA)
  • Privilege High Quality CPR and Defibrillation (if needed).
  • Use Supraglottic Airway Devices (SAD) in first part (15 min) of resuscitation 
  • If Mechanical Chest Compressions is used, to optimise ventilation with SAD, use 30:2 ratio (because the intrathoracic pressure generated during MCC overrules that generated from SAD and impaires ventilation).
  • In prolonged Cardiac Arrest management converting SAD to Endotracheal Tube can be considered.
  • Experience provider only can perform endotracheal intubation in CA. They have a better chance of first passage rate, without interruption in chest compressions. First pass success rate is positively associated to survival and good neurological outcome.

Defibrillation

  • Escalating bilevel energy (150-200-360 Joule) is associated with more efficacy in termination of shock resistant VF/pulselessVT cardiac arrest
  • Dual Sequential Defibrillation is feasible and safe. Although the evidences on its beneficial effect on outcome are still lacking it has to be considered in case of CA with refractory shockable rhythm. 

Antiarrhythmics drugs

  • There has been no conclusive evidence that any antiarrhythmic agents improve rates of ROSC, survival to admission, survival to discharge or neurological outcomes.

Ultrasound

  • Ultrasound in PEA is a key tool to detect CA causes improving survivival.

Post Resuscitation Care

  • In post resuscitation phase avoid any arterial oxygen and carbon dioxide abnormality because are associated to increased mortality.
  • Centralisation of resuscitated patients toward an acute PCI/CABG capable Center  is associated to better outcome.

Targeted Temperature Management

  • Prehospital cooling does not improve faster in-hospital target temperature achieving and due to its costs is not recommended.
If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.

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Articles at the Top. Take home messages from 2017 (part 1).

25 Dic

Welcome to our annual review of the best articles from the past year.

This will be a weekly (or so..) appointment with the top (or so…) articles of 2017 divided by topic and chosen by me.

At the end of the post I will also mention some take home points as summary of the evidences emerged from the articles. 

And now here is the best (for me) about:

 Airway management

Here are the best articles of the past year about Airway Management:

My take home messages about airway management:

  1. Risk factors for intubation related cardiac arrest are: overweight or obesity, age more than 75 years old, low SBP prior to intubation, hypoxemia prior to intubation, and absence of preoxygenation before intubation procedure.
  2. Preoxygenation is crucial (at least 2 minutes), before paralysing, to extend safe apnea time.
  3. Use apneic oxygenation during intubation attempts.
  4. Tracheal intubation is good in the hands of very well skilled professionals. Otherwise can improve mortality rate.
  5. Supraglottic devices perform well in cardiac arrest and are a valuable option for airway management. 
  6. Videolaryngoscopy improve glottic view but need training to improve first pass success.
  7. Always use paralytics when intubating a non cardiac arrest patient. It improves the chances fo first pass success.
  8. Rocuronium and Succynocholine are both valuable options for paralysis in airway management. 
  9. Dose Succynocholine, and other depolarising neuromuscular blockade drugs, based on actual body weight. Dose Rocuronium or Vecuronium based on ideal body weight.
  10. Use cuffed tracheal tubes even in paediatric patients. They perform well and  complications rate is the same. 
  11. The difficult airway is a myth. It’s not  a matter of technique but of decision making.
If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.

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

25 Apr

HEMS

Take home points:

Speed

Mission Time

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

 

On scene time

 

  • –HEMS > GEMS

Severity

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

Trauma Center Access

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

Crew

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

Survival 

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

 

 

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Fluid resuscitation in bleeding trauma patient: are you aware of wich is the right fluid and the right strategy?

23 Apr

DCR copy

The fluids of choice in prehospital field are, in most cases, cristalloids (Norma Saline or Lactate Ringer).

But what is the physiological impact of saline solutions when administered in large amounts (as the latest ATLS guidelines indicates) to hypotensive trauma patients?

Is aggressive Fluid resuscitation the right strategy to be pursued?

The triad of post-trauma lethal evolution is:

  • Hypotermia
  • Acidosis
  • Coagulopathy

Aggressive fluid resuscitation with cristalloids, and saline solutions in particular, can be detrimental in many ways:

  1. Cristalloids tend to displace the already formed clots and improves bleeding
  2. Normal Saline produce hypercloremic acidosis worsening coagulation and precipitating renal and immune dysfunction
  3. Cristalloids diluts the coagulation factors and precipitate the coagulation system (dilution coagulopathy)
  4. Cristalloids rapidilly shift in intercellular space worsening SIRS process and interstitial edema (brain edema, bowel wall edema) with consequent compartment hypertension

So wich is the perfect fluid to infuse in trauma?

The perfect fluid doesn’t exists.

Balanced saline and Hypertonic saline are promisng prospective but there are still no good quality evidences about their benefit on clinical outcomes.

Colloids has no place in fluid resuscitation of trauma patients.

The fluid of choice, regarding the actual evidences and indications, is Lactate Ringer.

More than on the type of fluid the attention of researchers and clinicians is oriented on the strategy to pusue in those cases.

Hypotensive resuscitation, part of damage control resuscitation, is at the moment the strategy of choice in trauma bleeding patients.

Restrictive fluids administration is the way to achieve this goal.

The target systolic BP has to be diferentiated depending on the type of trauma

  • 60–70 mmHg for penetrating trauma
  • 80–90 mmHg for blunt trauma without TBI
  • 100–110 mmHg for blunt trauma with TBI.

More important do not delay definitive treatment.

ASAP give blood products (PRBC, FFP etc…) to contrast post-trauma coagulopathy and send the patients in OR to fix treatable causes of bleeding

The following are a collection of  un essentials resources on haemostatic resuscitation after trauma

 Logo MEDEST2

 

CriticalCareNow

A Site for Intensivists and Resuscitationists

ALL Ohio EM

Supporting ALL Ohio EM Residencies in the #FOAMed World

Triggerlab

Let's try to make it simple

thinking critical care

a blog for thinking docs: blending good evidence, physiology, common sense, and applying it at the bedside!

urgentcareultrasound

More definitive diagnosis, better patient care

Critical Care Northampton

Reviewing Critical Care, Journals and FOAMed

OHCA research

Prehospital critical care for out-of-hospital cardiac arrest

SonoStuff

Education and entertainment for the ultrasound enthusiast

phemcast

A UK PREHOSPITAL PODCAST

First10EM

Emergency medicine - When minutes matter...

Songs or Stories

Sharing the Science and Art of Paediatric Anaesthesia

airwayNautics

"Live as if you will die tomorrow; Learn as if you will live forever"

resusNautics

Navigating resuscitation

Life in the Fast Lane • LITFL

Emergency medicine and critical care education blog

emDOCs.net - Emergency Medicine Education

Our goal is to inform the global EM community with timely and high yield content about what providers like YOU are seeing and doing everyday in your local ED.

The Collective

A Hive Mind for Prehospital and Retrieval Med

Dave on Airways

Thoughts and opinions on airways and resuscitation science

FOAMcast

A Free Open Access Medical Education Emergency Medicine Core Content Mash Up

Broome Docs

Rural Generalist Doctors Education

St.Emlyn's

Emergency Medicine #FOAMed

"CardioOnline"Basic and Advanced Cardiovascular medicine" Cariology" concepts and Review -Dr.Nabil Paktin,MD.FACC.دکتـور نبــــیل "پاکطــــین

این سایت را به آن دکتوران و محصلین طب که شب و روز برای رفاه نوع انسان فداکاری می کنند ، جوانی و لذایذ زندگی را بدون چشمداشت به امتیاز و نفرین و آفرین قربان خدمت به بشر می کنند و بار سنگین خدمت و اصلاح را بدوش می کشند ، اهداء می کنم This site is dedicated to all Doctors and students that aver the great responsibility of People’s well-being upon their shoulders and carry on their onerous task with utmost dedication and Devotionاولین سایت و ژورنال انتــرنتی علـــمی ،تخـصصی ، پــژوهشــی و آمــوزشــی طبـــی در افغــانســـتان

EmergencyPedia

Free Open Access Medical Education

Little Medic

Learning everything I can from everywhere I can. This is my little blog to keep track of new things medical, paramedical and pre-hospital from a student's perspective.

Prehospital Emergency Medicine Blog

All you want to know about prehospital emergency medicine

Italy Customized Tour Operator in Florence

Creating seamless Travel experiences!

GoogleFOAM

The FOAM Search Engine

EM Lyceum

where everything is up for debate . . .

Pediatric EM Morsels

Pediatric Emergency Medicine Education

AmboFOAM

Free Open Access Medical Education for Paramedics

FOAM4GP

Free Open Access Meducation 4 General Practice

Rural Doctors Net

useful resources for rural clinicians

Auckland HEMS

Unofficial site for prehospital care providers of the Auckland HEMS service

ECHOARTE

L'ECOGRAFIA: ENTROPIA DELL'IMMAGINE

MEDEST

Prehospital Emergency Medicine

ruralflyingdoc

Just another WordPress.com site

EM Basic

Your Boot Camp Guide to Emergency Medicine

KI Doc

WE HAVE MOVED - VISIT WWW.KIDOCS.ORG FOR NEW CONTENT

Emergency Live

Prehospital Emergency Medicine

AMP EM

Academic Medicine Pearls in Emergency Medicine from THE Ohio State University Residency Program

Prehospital Emergency Medicine

 Academic Life in Emergency Medicine

Prehospital Emergency Medicine

Comments on: Homepage

Prehospital Emergency Medicine

Greater Sydney Area HEMS

The Pre-hospital & Retrieval Medicine Team of NSW Ambulance

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