EMS MEd Blog

Feel The Heat: Managing Exertional Heat Stroke

by Mark Liao, MD, NRP (@EMSDocMark)

Expert Peer Review by Dorothy Habrat, MD (@EMSDrDorothy)

Clinical Scenario

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A 25-year-old male is brought to your Finish Line medical station. Bystanders noted that he was unsteady on his feet while running a half-marathon before he collapsed. The outside conditions are notable for an air temperature of 22.7 °C (73 °F) and a humidity of 45%, which subjectively feels quite mild to you. The patient does not respond to questions properly, is pale and diaphoretic. Once inside the medical station tent, his skin does not feel hot when his forehead is touched and is otherwise moist. A tympanic membrane thermometer registers an aural temperature of 36.7 °C (98 °F). The patient is persistently confused and a rectal thermometer is subsequently utilized, which registers 41.1 °C (106 °F).

Review

Exertional Heat Stroke (EHS) is an environmental medical emergency from excessively high body core temperature due to physical exertion. National surveillance data for annual prevalence is difficult as these cases are included with classic heatstroke seen in the elderly [1] or reported alongside other types of exertional heat illness such as heat exhaustion [2,3]. Typical risk groups for EHS include athletes (particularly high school football players [4]) and military personnel. In 2018, the US Armed Forces experienced 578 cases of EHS for soldiers on Active Duty during global operations and training [5] . EHS is also a particular concern for medical planners involved in large sporting events: an 8-year study at the Indianapolis Mini Marathon identified 32 cases of EHS among over 235,000 combined participants [6]. Recognizing the need for early and aggressive treatment of EHS, the National Association of EMS Physicians published an important consensus statement in 2018 that outlines the identification and management of EHS in the pre-hospital setting which will be reviewed here [7].   

Identification of EHS

While Exertional Heat Stroke is typically associated with hot conditions, it can still occur in cooler climates.

While Exertional Heat Stroke is typically associated with hot conditions, it can still occur in cooler climates.

EHS should be considered if an individual has been performing physical activity and experiences central nervous system disturbance. This can range from irritability or confusion to decreased level of consciousness. Delays in EHS recognition are multifactorial. Counterintuitively, EHS can still occur in cooler weather despite its association with hot climates [8]. It is a common misconception that EHS patients will have stopped sweating.   Patients, when touched, may not always feel warm and may even feel cool with skin moisture present.

Waiting for the development of profound central nervous system dysfunction such as obtundation or unconsciousness may result in delayed treatment and underscores the importance for maintaining a high level of suspicion during athletic events [9].

 

 Inaccurate Equipment Can Result in Misidentification 

Rectal thermometers, such as the one seen here, are the only way of getting an accurate rectal temperature to recognize EHS.

Rectal thermometers, such as the one seen here, are the only way of getting an accurate rectal temperature to recognize EHS.

The only accurate and practical prehospital method of core body temperature evaluation for EHS is to use a rectal thermometer, placed at a depth of 15 centimeters (about 6 inches) [10]. The National Athletic Trainers’ Association (NATA), like NAEMSP, similarly recommends that rectal thermometers be considered the gold standard for EHS assessment and therefore should be part of the EHS emergency treatment plan for athletic programs [11] . As such, EMS providers should be educated on these thermometers being used prior to ambulance arrival. Once inserted, the rectal thermometer should be left in place for continuous monitoring during cooling efforts and transport. Many rectal thermometers used in the hospital setting are only inserted 1.5 centimeters into the rectum and therefore are not accurate enough for EHS assessment [12]. Temporal artery thermometers, ear/tympanic membrane thermometers, and oral thermometers are not accurate in the detection of EHS and should not be used [13-15].

(A)  Hospital thermometers probes (left) generally are unable to be inserted into the recommended depth of 15cm (B) Clockwise from left: Temporal artery surface thermometer, oral digital thermometer, tympanic membrane thermometer and forehead infrared thermometer. These devices should not used in the evaluation of EHS due to problems with accuracy.

(A) Hospital thermometers probes (left) generally are unable to be inserted into the recommended depth of 15cm (B) Clockwise from left: Temporal artery surface thermometer, oral digital thermometer, tympanic membrane thermometer and forehead infrared thermometer. These devices should not used in the evaluation of EHS due to problems with accuracy.

 Strategies for Rapid Cooling

This 50 Gallon tub is used at the Indianapolis Mini Marathon for Cold Water Immersion

This 50 Gallon tub is used at the Indianapolis Mini Marathon for Cold Water Immersion

Rapid cooling is the key management step of EHS. Rapid cooling should begin when the patient is symptomatic.  Based on expert consensus, if the rectal  temperature is greater than 40.5 °C (104.9 °F), Cold Water Immersion cooling should occur when available (see algorithm below), as it most expeditiously accomplishes rapid cooling.  This involves placing the patient into a tub of ice water (with enough ice to maintain a water temperature of 10 °C / 50 °F  ) and the body immersed in water from the neck down. Tubs of approximately 50-gallon capacity are generally sufficient for this task, though some programs prefer tubs of 150-gallon capacity [16]. Proper cooling techniques should result in a reduction of rectal temperature to less than 38.6 °C (101.5 °F) within 30 minutes.

 

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Other alternatives include the use of a tarp (“tarp assisted cooling”), also filled with ice water, while the water is agitated continuously by responders to keep the cold water moving [17]. A similar technique involves using a fluid impervious body bag filled with ice water, which may be helpful in the hospital setting if no tub or tarp is available.

Other field methods of cooling

The use of ice packs placed close to arteries (neck, axilla, groin) has been taught for many years and may be one of the few practical options in an ambulance. However, this technique appears to have marginal cooling benefit when used alone and should not be used as the primary method of cooling whenever possible[18].

The US Army Training and Doctrine Command is a proponent of ice sheets as part of heat casualty response plan for trainees, which utilizes cotton sheets soaked in ice water and stored in coolers [19]. This requires placement of sheets onto as much bare skin as possible except for the face, and rotated with fresh sheets when the placed sheets start to feel warm. The technique is not as effective as cold water immersion [20].

Recommended rectal temperature thresholds to start and stop Cold Water Immersion

Recommended rectal temperature thresholds to start and stop Cold Water Immersion

Evaporative cooling, such as fanning a patient or even using the rotor wash from a helicopter, appears to be significantly slower than cold water immersion in reducing body temperature [21-22]. Evaporative cooling may also be less effective in high humidity situations.

While it may seem intuitive that chilled intravenous fluids would be helpful for rapid cooling, research in this area is limited. In a small study of healthy human volunteers, chilled saline of 4 °C (39.2 °F) decreased core body temperature by only 1 °C  (1.8 °F) after 30 minutes [23]. Though using cold saline infusion in combination with other cooling modalities may improve patient outcomes [7].

 

Prehospital Protocol Considerations

Given the importance of rapid cooling in the setting of EHS, EMS protocols should consider prioritizing cold water immersion over transport if the equipment is available onsite; NAEMSP and NATA both recommend a “cool first, transport second” approach. Communication with the receiving hospital is essential, particularly if onsite cooling is unavailable as Emergency Departments may need to initiate cooling in non-traditional care areas such as a decontamination room. EMS providers should be reminded to consider other causes of collapse and confusion, including hypoglycemia and hyponatremia.

Prevention

Monitoring Wet Bulb Globe Temperature provides a real-time assessment of heat risk

Monitoring Wet Bulb Globe Temperature provides a real-time assessment of heat risk

The risk of EHS is increased in the setting of hot, humid conditions. Providers working at mass gathering or athletic events should evaluate event policies regarding adjustments to work/rest cycles, safety messaging, rest/sleeping facilities, provision of cooling devices (such as arm immersion cooling systems) and ensure appropriate EHS response equipment is available [24]. The Heat Index or Wet Bulb Globe Temperature are tools that are useful in developing an understanding of current or projected risk of heat related illness [25].

 


Conclusion

EHS can be effectively managed in the prehospital environment when recognized in a timely fashion. A high index of suspicion is needed anytime an athlete experiences CNS disturbance after doing physical activity: responders can be falsely reassured when the climate does not appear too warm, CNS disturbance is only mild or if the patient’s skin is not hot to the touch. A multidisciplinary approach should be taken to incorporate on-site medical personnel, such as athletic trainers, in developing protocols to ensure the coordinated management of EHS. Finally, EMS agencies should take steps to ensure the availability of equipment such as rectal thermometers and cold-water immersion supplies at local athletic centers, sporting events and military training venues.

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 References

1.     Choudhary, E., & Vaidyanathan, A. (2014, December 12). Heat Stress Illness Hospitalizations — Environmental Public Health Tracking Program, 20 States, 2001–2010. Retrieved from https://www.cdc.gov/mmwr/preview/mmwrhtml/ss6313a1.htm

2.     Yeargin, S. W., Kerr, Z. Y., Casa, D. J., Djoko, A., Hayden, R., Parsons, J. T., & Dompier, T. P. (2016). Epidemiology of Exertional Heat Illnesses in Youth, High School, and College Football. Medicine & Science in Sports & Exercise48(8), 1523-1529. doi:10.1249/mss.0000000000000934

3.     Yeargin, S. W., Dompier, T. P., Casa, D. J., Hirschhorn, R. M., & Kerr, Z. Y. (2019). Epidemiology of Exertional Heat Illnesses in National Collegiate Athletic Association Athletes During the 2009–2010 Through 2014–2015 Academic Years. Journal of Athletic Training, 54(1), 55-63. doi:10.4085/1062-6050-504-17

4.     Centers for Disease Control and Prevention. (2010, August 20). Heat Illness Among High School Athletes --- United States, 2005--2009. Retrieved from https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5932a1.htm

5.     Armed Forces Health Surveillance Branch. (2019, April 1). Update: Heat Illness, Active Component, U.S. Armed Forces, 2018. Retrieved from https://www.health.mil/News/Articles/2019/04/01/Update-Heat-Illness

6.     Sloan, B. K., Kraft, E. M., Clark, D., Schmeissing, S. W., Byrne, B. C., & Rusyniak, D. E. (2015). On-site treatment of exertional heat stroke. Am J Sports Med, 43(4), 823-9. doi:10.1177/0363546514566194

7.     Belval, L. N., Casa, D. J., Adams, W. M., Chiampas, G. T., Holschen, J. C., Hosokawa, Y., … Stearns, R. L. (2018). Consensus Statement- Prehospital Care of Exertional Heat Stroke. Prehospital Emergency Care, 22(3), 392-397. doi:10.1080/10903127.2017.1392666

8.     Roberts, W. O. (2006). Exertional Heat Stroke during a Cool Weather Marathon. Medicine & Science in Sports & Exercise, 38(7), 1197-1203. doi:10.1249/01.mss.0000227302.80783.0f

9.     Hostler, D., Franco, V., Martin-Gill, C., & Roth, R. N. (2014). Recognition and Treatment of Exertional Heat Illness at a Marathon Race. Prehospital Emergency Care, 18(3), 456-459. doi:10.3109/10903127.2013.864357

10.  Miller, K. C., Hughes, L. E., Long, B. C., Adams, W. M., & Casa, D. J. (2017). Validity of Core Temperature Measurements at 3 Rectal Depths During Rest, Exercise, Cold-Water Immersion, and Recovery. Journal of Athletic Training, 52(4), 332-338. doi:10.4085/1062-6050-52.2.10

11.  Casa, D. J., DeMartini, J. K., Bergeron, M. F., Csillan, D., Eichner, E. R., Lopez, R. M., … Yeargin, S. W. (2015). National Athletic Trainers' Association Position Statement: Exertional Heat Illnesses. Journal of Athletic Training. doi:10.4085/1062-6050-50-9-07

12.  Welch Allyn. (2018). Capturing Rectal Temperature. Retrieved from https://www.welchallyn.com/content/dam/welchallyn/documents/sap-documents/MRC/80022/80022620MRCPDF.pdf

13.  Ronneberg, K., Roberts, W. O., McBean, A. D., & Center, B. A. (2008). Temporal Artery Temperature Measurements Do Not Detect Hyperthermic Marathon Runners. Medicine & Science in Sports & Exercise, 40(8), 1373-1375. doi:10.1249/mss.0b013e31816d65bb

14.  Huggins, R., Glaviano, N., Negishi, N., Casa, D. J., & Hertel, J. (2012). Comparison of Rectal and Aural Core Body Temperature Thermometry in Hyperthermic, Exercising Individuals: A Meta-Analysis. Journal of Athletic Training, 47(3), 329-338. doi:10.4085/1062-6050-47.3.09

15.  Mazerolle, S. M., Ganio, M. S., Casa, D. J., Vingren, J., & Klau, J. (2011). Is Oral Temperature an Accurate Measurement of Deep Body Temperature? A Systematic Review. Journal of Athletic Training, 46(5), 566-573. doi:10.4085/1062-6050-46.5.566

16.  Zhang, Y., Davis, J., Casa, D. J., & Bishop, P. A. (2015). Optimizing Cold Water Immersion for Exercise-Induced Hyperthermia. Medicine & Science in Sports & Exercise, 47(11), 2464-2472. doi:10.1249/mss.0000000000000693

17.  Hosokawa, Y., Adams, W. M., Belval, L. N., Vandermark, L. W., & Casa, D. J. (2017). Tarp-Assisted Cooling as a Method of Whole-Body Cooling in Hyperthermic Individuals. Annals of Emergency Medicine, 69(3), 347-352. doi:10.1016/j.annemergmed.2016.08.428

18.  Gaudio, F. G., & Grissom, C. K. (2016). Cooling Methods in Heat Stroke. The Journal of Emergency Medicine, 50(4), 607-616. doi:10.1016/j.jemermed.2015.09.014

19.  Training and Doctrine Command. (n.d.). Prevent of heat and cold casualties (TRADOC Regulation 350-29). Retrieved from Department of the Army website: https://adminpubs.tradoc.army.mil/regulations/TR350-29.pdf

20.  Nye, E. A., Eberman, L. E., Games, K. E., & Carriker, C. (2017). Comparison of Whole-Body Cooling Techniques for Athletes and Military Personnel. Int J Exerc Sci, 10(2), 294-300. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5360373/

21.  Armstrong, L. E., Crago, A. E., Adams, R., Roberts, W. O., & Maresh, C. M. (1996). Whole-body cooling of hyperthermic runners: Comparison of two field therapies. The American Journal of Emergency Medicine, 14(4), 355-358. doi:10.1016/s0735-6757(96)90048-0

22.  Poulton, T. J., & Walker, R. A. (1987). Helicopter cooling of heatstroke victims. Aviat Space Environ Med, 58(4), 358-61.

23.  Moore, T. M., Callaway, C. W., & Hostler, D. (2008). Core Temperature Cooling in Healthy Volunteers After Rapid Intravenous Infusion of Cold and Room Temperature Saline Solution. Annals of Emergency Medicine, 51(2), 153-159. doi:10.1016/j.annemergmed.2007.07.012

24.   DeGroot, D. W., Kenefick, R. W., & Sawka, M. N. (2015). Impact of Arm Immersion Cooling During Ranger Training on Exertional Heat Illness and Treatment Costs. Military Medicine, 180(11), 1178-1183. doi:10.7205/milmed-d-14-00727

25.  Casa, D. J., DeMartini, J. K., Bergeron, M. F., Csillan, D., Eichner, E. R., Lopez, R. M., … Yeargin, S. W. (2015). National Athletic Trainers' Association Position Statement: Exertional Heat Illnesses. Journal of Athletic Training. doi:10.4085/1062-6050-50-9-07

EMS MEd Editor : Maia Dorsett, MD PhD (@maiadorsett)

Trouble in Thin Air: Responding to Inflight Medical Emergencies

By Mark Liao, MD, NRP (@EMSFellowMark)

Peer Reviewed by Jeremiah Escajeda, MD (@JerEscajeda)

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Clinical Scenario:

As you settle into your seat on a cross-country airline flight to yet another Emergency Medicine conference, you hear the familiar Hi-Low tone signaling an announcement. Suddenly a pressured, yet professional, voice booms overhead: “If there is a medical professional on board the aircraft, would you please contact a member of the cabin crew?”  You pause for a moment and do a mental size up – what exactly would I be able to provide? Am I protected legally? What equipment is on board? The uncomfortable realization that you may be on your own – at 35,000 feet – quickly settles in as you unbuckle your seat belt and walk to the nearby galley.

Review:

Legacy Emergency Medical Kit prior to the 1998 Aviation Medical Assistance Act

Legacy Emergency Medical Kit prior to the 1998 Aviation Medical Assistance Act

Medical professionals such as EMS providers and physicians have always been aware that they may be called upon to respond as Good Samaritans in the event of an off-duty emergency. Aviation in-flight medical emergencies are uncommon events, with estimates ranging widely from 1 event every 40 flights to 604 flights or up to 10-40 events every 100,000 passengers [1-3]. The variation in estimates are due to the lack of a central registry with most studies relying on proprietary company data from either the airlines or a ground-based aeromedical consultation service.  Common in-flight medical events include syncope/near-syncope, GI complaints, respiratory problems and cardiovascular emergencies. Cardiac arrest is rare, with one review showing it represented only 0.3% of all inflight medical events [4].

Fortunately for potential first responders, the United States 1998 Aviation Medical Assistance Act provides generous legal protections for American air carriers:

Current emergency Medical Kit that meets minimum FAA Part 121 EMK requirements

Current emergency Medical Kit that meets minimum FAA Part 121 EMK requirements

An individual shall not be liable for damages in any action brought in a Federal or State court arising out of the acts or omissions of the individual in providing or attempting to provide assistance in the case of an in-flight medical emergency unless the individual, while rendering such assistance, is guilty of gross negligence or willful misconduct [5].

 The same law also updated required equipment on board commercial civil aviation aircraft in the United States. A scheduled air carrier – which the FAA calls a Part 121 Operator – is what most passengers fly in the United States. If a Part 121 aircraft has at least one flight attendant on board, the aircraft is required to have an Emergency Medical Kit (EMK), Automated External Defibrillator (AED), general first aid kit, bloodborne pathogen spill equipment and oxygen for first aid (if the aircraft operates above 10,000 feet) [6]. All Part 121 cabin crew in the United States are required to receive first aid and CPR/AED training, with demonstration of CPR/AED skills every 2 years, in addition to being familiar with the location of equipment on board the aircraft [7]. However, cabin crew education on obtaining vital signs or performing a physical exam is not required by regulations.   

 

Preparing to Respond

Above: An example of an in-flight patient care form

Above: An example of an in-flight patient care form

Each airline dictates their own policy on identifying potential medical volunteers and may request professional identification. Some international airlines – such as Japan Airlines, Lufthansa, SWISS and Austrian Airlines – maintain a registry of physician passengers who can be called on to render assistance if needed [8,9]. Medical volunteers, such as physicians who choose to respond should not have consumed alcohol prior to rendering care or otherwise be impaired [10]. Many airlines across the globe are contracted with an aeromedical ground support service, such as MedLink (located in Arizona) or Stat-MD (located in Pennsylvania) that provides physician consultation and helps the flight crew determine if diversion is necessary and assists cabin crew and volunteers with passenger medical care. They also perform ground based medical evaluations of patients if there is a concern that arises as to whether the patient is medically suitable to fly on a commercial flight. The ultimate decision for diversion rests with the pilot-in-command who will use the ground-based physician service and possibly inflight medical volunteers to assist in making the decision. Diversion is very costly and airlines attempt to avoid medically unnecessary diversions. Given the unique considerations of the aeromedical setting, suitable airports and local available services, medical volunteers should defer to the recommendations of the ground physician. Communication with the ground physician may take place with in-cabin headsets, telemedicine equipment or relayed through the flight deck.  Some airlines – particularly those flying long-haul routes – have also elected to equip their aircraft with patient monitors that integrate voice communication, video, EKG, pulse oximetry, temperature and other parameters that can be transmitted to the ground physician, though these are rare to find on domestic US operations [11]. Airlines will ask that volunteer help complete documentation for care that is rendered.

 

Vital Signs

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The only FAA required vital signs equipment in an EMK is a stethoscope and blood pressure cuff. Auscultation of breath sounds and blood pressure can be challenging due to engine noise and vibration. As such, blood pressures may need to be palpated. Pulse oximeters, while not required by regulations, are sometimes added to EMKs, although providers should be aware that the effects of altitude may cause normal changes in oxygen saturation. While oxygen saturation at sea level is approximately 97%, decreased oxygen tension at altitude will reduce this saturation value. Most civilian airlines are pressurized to maintain a cabin altitude of approximately of 6,000 to 8,000 feet: at 8,000 feet a normal oxygen saturation will be approximately 93% [12]. 

 

IV and Medication Administration

 

Figure5.jpg

The EMK is required to stock a limited amount of parental medication equipment and includes one IV tubing set with Y-connectors, 500cc of normal saline, 5cc and 10 cc syringes in addition to medication needles. As many EMKs utilize vial or ampoule epinephrine instead of an epinephrine autoinjector, 1cc syringes are also included. Curiously, the FAA did not specify the type or quantity of intravenous catheters to be equipped, thus leaving the decision up to the airlines or their EMK vendor. The author has seen as few as two 16-gauge IV catheters to a more generous set of one 18, 20 and 22 gauge IV catheters.

 

Airway and Ventilation Support

Figure6.jpg

 Basic airway adjuncts are included in the kit and at a minimum must include a bag-valve resuscitator (regulations do not specify what size), 3 sizes of oral airways and masks (pediatric, small adult, large adult) and CPR masks of equivalent sizes. The EMK presented above met these requirements by providing three mask sizes that could be either used with the adult bag mask resuscitator or a one-way CPR valve. Oddly, there is no requirement for the equipped bag-valve resuscitator to have oxygen tubing that is compatible with the aircraft portable oxygen bottle outlets.

 

Portable aircraft oxygen bottles, unlike those found in medical settings, are generally equipped with only two settings, low (2 liters per minute) and high (4 liters per minute). For these types of bottles, applying the mask adapter into the appropriate rate connection outlet will determine the flow rate.

A bronchodilator is also required as part of the EMK. A spacer, which is not required to be equipped, may need to be improvised using a toilet paper roll, rolled-up magazine or plastic bottle when treating children [13].

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Syncope

Based on previous literature, near-syncope and syncope comprise the majority of inflight medical emergencies. This condition, although frightening to the crew and other passengers, rarely requires IV administration or diversion. Simple maneuvers such as laying the patient supine, with legs elevated and applying oxygen, for the most part, are all that is required [2,4].

 Nausea/Vomiting

 Antiemetics are not required to be equipped in the EMK despite nausea and vomiting being a common inflight medical event. Although carrying antiemetics while traveling is advisable, it should be noted that serotonin receptor antagonists, such as ondansetron, are not effective for motion sickness [14]. Alternatively, the EMK does carry diphenhydramine which can be used off-label as an antiemetic. It is also reasonable to request if other passengers may be carrying over the counter antiemetic medications. 

 Cardiac Emergencies

Figure10.jpg

The EMK provides four 325mg of aspirin and at least 10 tablets of nitroglycerin. There is no requirement to include a single or 3-lead EKG as part of the equipment, though some airlines include this as a stand-alone device or optional attachment to the on-board AED [15].

 


Cardiac Arrest and Resuscitation Management

Figure11.jpg

In addition to the on-board Automated External Defibrillator, the EMK provides two doses each of 1mg atropine and 1mg epinephrine. A total of 200 mg of lidocaine is also required. Despite the provision of antiarrhythmics, there is no requirement for airlines to ensure that the equipped AED has a screen that permits the user to see the underlying cardiac rhythm.  Due to space constraints within the cabin, patients in cardiac arrest may need to be moved or dragged to the galley or a bulkhead row to ensure enough space is provided to render effective CPR. Ending resuscitation can be challenging and consultation with the ground physician is advisable.

 Allergic Reactions and Anaphylaxis

Figure12.jpg

 Diphenhydramine in both oral and injectable forms are provided in the EMK, with four 25mg tablets and two 50mg vials.  Two ampoules of epinephrine 1mg/mL (1:1000) must also be equipped. Some airlines have included epinephrine autoinjectors as part of their EMKs, but this is not required by regulations.

 



Diabetic Emergencies

Figure_13.jpg

A total of 25 grams of injectable dextrose is equipped in the EMK, though there is no requirement for a glucometer or lancets. If a glucometer is needed, one option is to ask the cabin crew to make a public address announcement to see if another passenger may be willing to volunteer a personal one. An alternative is to assume the blood sugar is low (particularly in a syncopal event) and to provide an oral dextrose source such as orange juice if the passenger is able to drink.

 

 Upcoming Developments

 The EMK was primarily designed for adult medical emergencies and lacks pediatric appropriate supplies and equipment. In 2018, the FAA Reauthorization Bill was passed which included verbiage from the Airplane Kids in Transit Safety Act and directed the FAA to revise the EMK to meet the needs of children [16]. The FAA has yet to provide guidance in response to this bill.


 International Regulations and Equipment

 

Figure 14

An EMK that meets European AMC1 CAT.IDE.A.225 regulatory requirements

An EMK that meets European AMC1 CAT.IDE.A.225 regulatory requirements

Internationally, wide variations exist for on-board medical equipment. In Canada, an AED is not required by regulations and an EMK is only required on civil aircraft carrying more than 100 passengers [17, 18].  In Europe, defibrillators are not required, although are recommended if an aircraft has 30 or more passengers with at least one member of cabin crew [19].  One 2014 paper found that many German airlines did not carry AEDs and one carrier did not have any CPR equipment on board [20]. In contrast, some airlines on their own initiative, such as British Airways, far exceed these requirements, carrying an extensive array of medications and equipment including benzodiazepines, buprenorphine, antibiotics and suture equipment [21]. These optional enhancements have led to several remarkable stories of innovation and improvisation, including a 1995 case in which a physician volunteer improvised a chest tube for a passenger suffering from a tension pneumothorax using a urinary catheter found in the British Airways medical kit [22].

 Conclusion

 Despite the perceived austere clinical environment a commercial aircraft might present, US airline carriers are equipped with emergency medical supplies that a physician volunteer can effectively utilize. Whenever possible, the medical volunteer should consult with ground based medical support.  Familiarity with what and what is not carried will enhance a volunteer provider’s ability to respond to in-flight emergencies. For further information, an excellent review in JAMA is published at https://jamanetwork.com/journals/jama/article-abstract/2719313

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References

[1] Epstein, Catherine R, et al. “Frequency and Clinical Spectrum of in-Flight Medical Incidents during Domestic and International Flights.” Anaesthesia and Intensive Care, vol. 47, no. 1, 13 Feb. 2019, pp. 16–22., doi:10.1177/0310057x18811748.

[2] Peterson, D. C., Martin-Gill, et al.  (2013). Outcomes of Medical Emergencies on Commercial Airline Flights. New England Journal of Medicine, 368(22), 2075-2083. doi:10.1056/nejmoa1212052

[3] Kesapli, Mustafa, et al. “Inflight Emergencies During Eurasian Flights.” Journal of Travel Medicine, vol. 22, no. 6, 2015, pp. 361–367., doi:10.1111/jtm.12230.

[4] Martin-Gill, C., Doyle, T. J., & Yealy, D. M. (2018). In-flight medical emergencies. JAMA, 320(24), 2580-2590. doi:10.1001/jama.2018.19842

[5] U.S. G.P.O. Public Law 105 - 170 - Aviation Medical Assistance Act of 1998 (1998) (enacted).

[6] FAA. (2006). Emergency medical equipment (121-33B). Retrieved from

https://www.faa.gov/documentLibrary/media/Advisory_Circular/AC121-33B.pdf

[7] FAA. (2006). Emergency medical equipment training (121-34B). Retrieved from https://www.faa.gov/documentLibrary/media/Advisory_Circular/AC121-34B.pdf

[8] JAL. (n.d.). JAL DOCTOR Registration System. Retrieved from https://www.jal.co.jp/en/jmb/doctor/

[9] Lufthansa. (n.d.). Doctor on Board. Retrieved from https://www.lufthansa.com/de/en/doctor-on-board

[10] Nable, J. V., Tupe, C. L., Gehle, B. D., & Brady, W. J. (2015). In-Flight Medical Emergencies during Commercial Travel. New England Journal of Medicine, 373(10), 939-945. doi:10.1056/nejmra1409213

[11] Doyle, A. (2010, December 7). MEBA: RDT demonstrates Tempus IC telemedicine system. Retrieved from https://www.flightglobal.com/news/articles/meba-rdt-demonstrates-tempus-ic-telemedicine-system-350616/

[12] Gradwell, D., & Rainford, D. (2016). Hypoxia and hyperventilation. In Ernsting's Aviation and Space Medicine 5E (pp. 55-56). Boca Raton, FL: CRC Press.

[13] Zar, H. (2000). Are spacers made from sealed cold-drink bottles as effective as conventional spacers? Western Journal of Medicine173(4), 253-253. doi:10.1136/ewjm.173.4.253

[14] Gradwell, D., & Rainford, D. (2016).Motion Sickness. In Ernsting's Aviation and Space Medicine 5E (pp. 794-795). Boca Raton, FL: CRC Press.

[15] JAL. (n.d.). Medical Supplies and Equipment on Board. Retrieved from https://www.jal.co.jp/en/health/medicines/

[16] Kraft, C. (2018, October 3). AAP Applauds Passage of Bill That Will Keep Children Safe During Air Travel. Retrieved from https://www.aap.org/en-us/about-the-aap/aap-press-room/Pages/AAPStatementAirplaneKiTSAct.aspx

[17] Transport Canada. (2018, April 5). Advisory Circular (AC) No. 705-010. Retrieved from http://www.tc.gc.ca/en/services/aviation/reference-centre/advisory-circulars/ac-705-010.html

[18] Transport Canada. (2019, March 18). Part VII - Commercial Air Services. Retrieved from https://www.tc.gc.ca/eng/civilaviation/regserv/cars/part7-standards-725-2173.htm#725_90

[19] EASA. (2018). Carriage and use of Automatic External Defibrillators (2018-03). Retrieved from https://ad.easa.europa.eu/blob/EASA_SIB_2018_03.pdf/SIB_2018-03_1

[20] Hinkelbein, J., Neuhaus, C., Wetsch, W. A., Spelten, O., Picker, S., Böttiger, B. W., & Gathof, B. S. (2014). Emergency Medical Equipment On Board German Airliners. Journal of Travel Medicine, 21(5), 318-323. doi:10.1111/jtm.12138

[21] British Airways. (n.d.). BA Medical Kit. Retrieved from https://www.britishairways.com/health/docs/during/Aircraft_Medical_Kit.pdf

[22] Wallace, W. A. (1995). Managing in flight emergencies. BMJ, 311(7001), 374-375. doi:10.1136/bmj.311.7001.374

 

 

Not Your Typical Wake Up: A review of opioid related noncardiogenic pulmonary edema

by Aaron Farney MD

 Clinical Scenario

 You are called for a 25-year-old male, possible overdose, unknown if breathing.  On arrival, the patient is unresponsive on his bathroom floor.  Family reports they found him on the floor not breathing just prior to calling 911.  They had last seen him well 15 minutes prior.  He has a known history of heroin use, and you notice an empty syringe next to him.  On exam, he is unresponsive, cyanotic, with agonal respirations and has a pulse of 40. 

 You immediately commence resuscitative measures.  The airway is positioned, a nasopharyngeal airway is inserted, and positive pressure ventilations are initiated via a bag-valve mask connected to high-flow oxygen, with resultant resolution of cyanosis.  Four milligrams intranasal naloxone is administered.  About three minutes later, the patient wakes and you start to notice copious pink, frothy secretions.  You suction, but it continues, and even seems to increase.  The patient is now alert, complaining of shortness of breath and hypoxic to 78% despite a non-rebreather mask flowing at 15 liters/minute.  Your partner asks you “did he aspirate…?” 

 

What is happening, and what is the correct management?

 The phenomenon of opioid-related noncardiogenic pulmonary edema (NCPE) is not widely known in the prehospital realm.  As we are in the midst of an opioid crisis, the odds that the average field provider will encounter opioid-related NCPE is increasing.  The ability to recognize this phenomenon and knowing what to do will make all the difference to your patient.

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Background & Prevalence

The physician William Osler first described narcotic-related pulmonary edema during an autopsy in 1880 [1,2].  Its presentation and clinical course was not appreciated until the 1950s-60s.  The prevalence of opioid-related NCPE is about 2-10% of heroin overdoses [1,2].  It is most commonly seen in heroin overdose but has been reported with other opioids.

 Presentation & Clinical Course

Opioid-related NCPE typically presents as dyspnea accompanied by development of pink, frothy pulmonary secretions associated with ongoing hypoxia despite reversal of respiratory depression with an opioid antagonist (i.e. naloxone).  It often presents immediately after reversal but can be slightly delayed, up to four hours [1].  Most cases will resolve within 24-36 hours, but up to one-third of cases will require aggressive respiratory support [1,2].  If left untreated, it can progress to complete hypoxic respiratory failure, hypoxic end-organ injury, and cardiac arrest. 

Pathophysiology

The mechanism of opioid-related NCPE is poorly understood, in part because there are a variety of drugs involved, including the opioid antagonist naloxone.  There are several published theories.  Perhaps the most popular theory is increased pulmonary capillary permeability related to hypoxia and/or histamine release [1,2].  Heroin in particular is prone to causing excessive histamine release, causing leaky pulmonary vasculature.  Morphine is another drug known to do this. 

Other theories blame naloxone.  A patient who is opioid dependent, overdoses, and who is rapidly reversed with a high dose of naloxone subsequently experiences a catecholamine surge, particularly in those with concomitant cocaine use. [2] A second theory blaming naloxone is that following a prolonged period of near or complete apnea, reversal that results in inspiratory effort prior to complete opening of the glottis can result in excessive negative pressure within the lung, drawing in fluid from the pulmonary vasculature.  Administering positive pressure ventilation prior to naloxone therapy may mitigate this.  It is likely that opioid-related NCPE is multifactorial, with both the opioid agent and naloxone contributing.  Regardless of the underlying etiology, treatment remains the same.

 Management

The treatment of opioid-related NCPE is supportive and focused on correcting hypoxemia.  Initial measures include application of supplemental oxygen, preferably via a non-rebreather mask.  Patients with hypoxia refractory to high flow O2 warrant assisted ventilations.  Paramedics should have a low threshold for initiating CPAP therapy in the patient experiencing opioid-related pulmonary edema.  Hypoxemia or distress refractory to CPAP therapy may warrant endotracheal intubation and invasive ventilation to correct hypoxemia.  There has been no identified role for nitroglycerin or other medications in treating opioid-related NCPE.

 Back to the case:

The medic recognizes that this patient is experiencing opioid-related NCPE.  Only 8 minutes from the nearest emergency department, RSI is deferred in favor of immediate transport.  CPAP is placed onto the patient at a pressure of 5 cm H20.   The patient tolerates CPAP well, and oxygenation is improved to 90% on arrival at the emergency department, where care is transferred.  The patient continues to improve on CPAP and is admitted for further monitoring.

 Take-home points:

  • EMS should administer only the amount of naloxone required to reverse respiratory depression, not mental status.  Higher doses may increase risk of NCPE.

  • Opioid-related NCPE occurs in about 2-10% of opioid overdoses

  • Patients may complain of shortness of breath and will develop pink, frothy pulmonary secretions and hypoxia despite opioid reversal

  • Treatment is focused on correcting hypoxemia with supplemental oxygen and CPAP 

  • Cases refractory to CPAP may require invasive ventilation

  • All patients with opioid-related NCPE warrant transport.

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References

1.     Sporer KA & Dorn E. Heroin-Related Noncardiogenic Pulmonary Edema: A Case Series.  Chest 2001; 5:1628-1632.

2.     Sterrett et al. Patterns of Presentation in Heroin Overdose Resulting in Pulmonary Edema. American Journal of Emergency Medicine 2003; 21:32-34.

3.     Grosheider T & Sheperd SM. Chapter 296: Injection Drug Users.  Tintinalli’s Emergency Medicine 8th ed. 2016.

Can you leave them be? A Review of The Recommendations of Hypoglycemia Treat and Release Protocols

by David Ismael Arbona Calderón, MD

Case Scenario:

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A 48 y/o unconscious male presented with dizziness and weakness in his office. On arrival of paramedics, patient is diaphoretic and unresponsive, but with pulse and spontaneous respirations. Initial assessment reveals a glucose level of 23 mg/dL. Paramedics find the patients current medication list in the patient’s wallet. Patient is given IV dextrose and regains consciousness. After returning to baseline the patient is refusing transport and further treatment. How do you proceed?

Literature Review:

Diabetes is one of the most common chronic disease, with estimated diagnosis of 23.1 million people in the United States and another 84.1 million adults with prediabetes.[1] As diabetes continues to increase in our population, hypoglycemic events are rising secondary to the use of insulin and oral hypoglycemic agents. Insulin management has been related to the most serious cases of hypoglycemia, either due to strict goals of keeping normal glucose levels or due to confusion between dosing and type of insulin medication. Other diabetes medications like sulfonylureas have been linked to episodes of hypoglycemia and accidental ingestion in the pediatric population. Although hypoglycemia is more common in type 1 diabetes (T1DM), patients with type 2 diabetes (T2DM) experience a similar frequency of these events as they require more aggressive treatment.

The National Electronic Injury Surveillance System-Cooperative Adverse Drug Event Surveillance (NEISS-CADES) has estimated that around 97,648 ED visits occur annually due to insulin-related hypoglycemia and errors related to diabetes management. It has been accounted that around 10% of ED visits are considered under Adverse Drug Events (ADEs) occur annually.[2]

Around 95% of hypoglycemic events occur outside of medical settings, requiring assistance by family members, other caregivers, or emergency medical services (EMS)  personnel.[3] Patients with diabetes might not understand when hospital evaluation is needed for proper management of low blood sugars. EMS personnel carry most of the weight of identifying red flags of hypoglycemic episodes that require further workup as some cases can be fatal. There is a continuous debate in the ambulance service as to whether patients suffering from hypoglycemia need to be transported to the hospital after examination and treatment in the field.[4] While some studies have referred that most cases of hypoglycemia can be successfully treated at the scene, conflictive results have been reported in other cases with complications days later.[5]

On 1991, Thompson et al produced one of the earliest studies of treat and release protocols proposed five criteria that should be met before being released form prehospital care without the need for further treatment:

1.    History of either T1DM or T2DM

2.    Pretreatment blood sugar of less than 4.4 mmol/L or 80mg/dL

3.    Post-treatment blood sugar equal or greater to 4.4 mmol/L or 80mg/dL

4.    Return to normal mental status within 10 minutes of treatment

5.    Absence of complicating factors that require ED evaluation, such as renal dialysis, chest pain, alcohol, dyspnea, of falls.

Clinical manifestations of hypoglycemia are nonspecific, and can be divided into neurogenic and neuroglycopenic symptoms.[6] 

 

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As reported by NEISS-CADES, patients over 80 years old have a higher risk of being hospitalized due to hypoglycemic events since neuroglycopenic symptoms can mimic other cardiovascular and neurologic conditions.

Other studies regarding younger groups, involving T2DM and over the age of 50 and glycated hemoglobin (HbA1c), suggest that both extreme hyperglycemia and hypoglycemia contribute to poor outcomes when encountering a hypoglycemic event.[7] This can also be applicable for patients with Diabetes Type 1 with extreme values of HbA1c, as recurrent episodes of hypoglycemia and impaired awareness during these episodes are known major risk factors for these events.

Concerns about inappropriate use of sulfonylureas in the elderly and hospitalization rates due to hypoglycemic episodes have been studied.[8] Around one-third of hypoglycemic episodes in the ED were exclusively related to sulfonylurea treatment as they had more prolonged hypoglycemia. Hospital admission of all patients under sulfonylurea treatment with hypoglycemia has been strongly recommended, arguing that regardless resolution of hypoglycemia was done in the ED, observation was needed.  Moreover, treatment of hypoglycemia due to sulfonylurea includes octreotide administration. [9]

The National Model EMS Clinical Guidelines (NASEMSO Model) published on 2017, facilitated hypoglycemia protocol.[10] Treatment is focused on level of consciousness and patient disposition will also rely on initial neurological presentation. In a nutshell, a conscious patient with a patent airway can obtain oral glucose, with adults receiving approximately 25 grams of dextrose (at a concentration of 10-50%) and pediatric patients receiving 0.5-1g/kg (at a concentration of 10-25%).

Under NASEMSO Model, an unconscious patient will require Dextrose IV with or without use of Glucagon. A maximum of 25g of 10-50% dextrose IV was determined for adults and for children the 0.5-1g/kg of 10-25% dextrose IV. Patient is in need of transport if hypoglycemic symptoms continue or if patient had a seizure at any point of the episode. Release without transport should only be considered if patient meets all of the following:

  1. Repeat glucose measurement over than 80mg/dL
  2. Patient takes insulin or metformin to control diabetes
  3. Patient returns to normal mental status, with no focal neurologic signs or symptoms after receiving glucose/dextrose
  4. Patient can promptly obtain and will eat a carbohydrate meal
  5. Patient or legal guardian refuses transport and EMS providers agree transport not indicated
  6. A reliable adult will be staying with patient
  7. No major co-morbid symptoms occur, such as chest pain, shortness of breath, seizures, intoxication
  8. A clear cause of the hypoglycemia is identified (e.g. skipped meal)

Regardless of National EMS guidelines established for hypoglycemia, there is still variability in EMS protocols throughout the United States. [10-12] Further studies are required to determine the reasons underlying these variations and patient outcome.

Case Scenario Follow-Up:

Patient was given an early lunch at the office, had normal vital signs, and normal EKG. On further questioning patient refers he did not eat breakfast because he was running late for work but did administer his insulin. Patient denied any other symptoms and a coworker is able to stay and watch after the patient. Paramedics used their well person protocol to determine if any abnormalities warranted further intervention. Assessed patient for capacity and oriented the patient about the need for close follow up. Patient indicated he understood all orientations and refused further care.

Take Home:

 Any patient with seizures, persistent symptoms of hypoglycemia, and that does not comply with the NASEMSO Model for release without transport criteria should be taken to the emergency department for further evaluation.

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References:

[1] Centers for Disease Control and Prevention. National diabetes statistics report: Estimates of diabetes and its burden in the United States, 2017. Atlanta, GA: US Department of Health and Human Services. 2017.  https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf

[2] Geller AI, Shehab N, Lovegrove MC, et al. National Estimates of Insulin-Related Hypoglycemia and Errors Leading to Emergency Department Visits and Hospitalizations. JAMA Intern Med. 2014;174(5):678–686. doi:10.1001/jamainternmed.2014.136

[3] Lipska, K. J. et al. "Hba1c And Risk Of Severe Hypoglycemia In Type 2 Diabetes: The Diabetes And Aging Study." Diabetes Care 36.11 (2013): 3535-3542. Web. 9 May 2018.  https://doi.org/10.2337/dc13-0610

[4] Roberts, K., and A. Smith. “Outcome of diabetic patients treated in the prehospital arena after a hypoglycemic episode, and an exploration of treat and release protocols: a review of the literature. (Prehospital Medicine).“ Emergency Medicine Journal, May 2003, p. 274+. Health Reference Center Academic. http://link.galegroup.com.ezproxyhost.library.tmc.edu/apps/doc/A102769958/HRCA?u=txshracd2509&sid=HRCA&xid=14527de1

[5] Tohira, H., Fatovich, D., Williams, T. A., Bremner, A., Arendts, G., Rogers, I. R., . . . Finn, J. (2016). Paramedic checklists do not accurately identify post-ictal or hypoglycaemic patients suitable for discharge at the scene. Prehospital and Disaster Medicine, 31(3), 282-293. doi:http://dx.doi.org/10.1017/S1049023X16000248

[6] Hepburn, D. A. et al. "Symptoms Of Acute Insulin-Induced Hypoglycemia In Humans With And Without IDDM: Factor-Analysis Approach." Diabetes Care 14.11 (1991): 949-957. Web. 9 May 2018.

[7] Moheet, Amir, and Elizabeth R. Seaquist. "Hypoglycaemia, Emergency Care And Diabetes Mellitus." Nature. N.p., 2014. Web. 9 May 2018.doi:10.1038/nrendo.2014.67

[8] Rajendran R, Hodgkinson D, Rayman G. Patients with diabetes requiring emergency department care for hypoglycaemia: characteristics and long-term outcomes determined from multiple data sources. Postgraduate Medical Journal 2015;91:65-71. doi:10.1136/postgradmedj-2014-132926

[9] McLaughlin, S. A., Crandall, C. S., & McKinney, P. E. (2000). Octreotide: an antidote for sulfonylurea-induced hypoglycemia. Annals of emergency medicine36(2), 133-138.

[10] "National Model EMS Clinical Guidelines". Nasemso.Org, 2017, http://www.nasemso.org/documents/National-Model-EMS-Clinical-Guidelines-2017-Distribution-Version-05Oct2017.pdf. Accessed 20 May 2018.

[10] Paul Rostykus, Jamie Kennel, Kristian Adair, Micah Fillinger, Ryan Palmberg, Amy Quinn, Jonathan Ripley & Mohamud Daya (2016) Variability in the Treatment of Prehospital Hypoglycemia: A Structured Review of EMS Protocols in the United States, Prehospital Emergency Care, 20:4, 524-530, doi: 10.3109/10903127.2015.1128031

[11] Howard H. Moffet, E. Margaret Warton, Lee Siegel, Karl Sporer, Kasia J. Lipska & Andrew J. Karter (2017) Hypoglycemia Patients and Transport by EMS in Alameda County, 2013–15, Prehospital Emergency Care, 21:6, 767-772, doi: 10.1080/10903127.2017.1321707

[12] Khunti, K., Fisher, H., Paul, S., Iqbal, M., Davies, M. J., Siriwardena, A. N. Severe hypoglycemia requiring emergency medical assistance by ambulance services in the East Midlands: A retrospective study. Primary Care Diabetes.2013; (7):159-165.

The Arresting LVAD patient: A Review of the Updated Recommendations

by Stephanie Louka, MD

Case Scenario:

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Paramedics are called to the home of a 59 year old male patient with an LVAD who was found unconscious and unresponsive by family members.  He was last seen 2 hours earlier acting normally. There is no evidence of trauma. Family members are unaware of any recent illness or mechanical issues with his LVAD.  Your assessment is notable for warm but pale skin, lack of palpable pulses, LVAD with “low-flow” alarm but audible hum and apneic respirations. After intubation, end-tidal CO2 shows no wave form.  How should paramedics proceed?

Literature Review:

The 2015 ACLS guidelines do not address assessment and treatment of an unresponsive patient with a mechanical assist device such as an LVAD.[1]  While there has never been a reported case of LVAD dislodgement resulting from chest compressions, for years, VAD manufacturers advised against routine use of chest compressions on these patients for fear of device dislodgement and rupture of the left ventricle.  Despite a lack of evidence of dislodgment, many hospitals and EMS systems adopted this advice in management of VAD patients and withheld chest compressions even in the setting of true cardiac arrest.[2,3] Alternatively, with the risk of dislodgement theoretical and death eminent, some institutions opted to go against the manufacturer recommendation and administer chest compressions in this setting.

In 2017, the AHA published its Scientific Statement on Cardiopulmonary Resuscitation in Adults and Children with Mechanical Circulatory Support in the journal Circulation offering the first evidence-based, consensus approach to management for unconscious and/or arresting patients with mechanical assist devices.

Relying heavily on physical exam and waveform capnography for assessment, the algorithm provides a systematic approach to management of LVAD patients.  Trouble-shooting the LVAD with family members and/or LVAD coordinators is still recommended, but if the LVAD cannot be restarted or is not functioning adequately (MAP ≤ 50 mmHg and/or end-tidal CO2 ≤ 20 mmHg), external chest compressions are now recommended. 

While this AHA position was published in 2017, many EMS agencies are behind in adopting this change.  As this policy makes its way into the ACLS Provider course curriculum and manual and EMS personnel take their ACLS recertification courses, we should see broader adoption of this approach to the arresting LVAD patient.

Case Scenario Follow-up:

The Paramedic in charge contacted the regional VAD center and received online medical direction from the EMS Physician on duty who instructed the crew to administer chest compressions and transport the patient to his facility.  Firefighters on scene initiated chest compressions which resulted in a notable and sustained increase in end-tidal CO2 levels. 

The patient was transported to the Emergency Department where ROSC was obtained, and he was admitted to the ICU for continuing care.

Take Home:

Per the American Heart Association (AHA), chest compressions are now the standard of care in arresting patients with mechanical circulatory support devices (e.g. LVAD), and end-tidal CO2 <20 for whom device troubleshooting was ineffective.

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Additional LVAD resources:

Make sure to review the EMS Field Guides provided at www.mylvad.com

Some additional LVAD Resources:

LVAD Management in the ED on the NUEM Blog

ALiEM PV Card on LVAD Management in the ED

 

References:

[1] American Heart Association (AHA). Advanced Cardiovascular Life Support (ACLS) Provider Manual, 16th edition. 2016.

[2] Shinar Z, Bellezo J, Stahovich M, Cheskes S, Chillcott S, Dembitsky W. Chest compressions may be safe in arresting aptients with left ventricular assist devices (LVADs). Resuscitation. 2014 May; 85(5):702-4.

[3] Mabvuure NT, Rodrigues JN. External cardiac compression during cardiopulmonary resuscitation of patients with left ventricular assist devices. Interactive CardiVascular and Thoracic Surgery. 2014 Aug; 19(2):286-289.

[4] Peberdy MA, Gluck JA, Ornato JP, et al. Cardiopulmonary Resuscitation in Adults and Children with Mechanical Circulatory Support. Circulation. 2017 Jun 13;135(24):e1115-e1134.

Tranexamic Acid: Does it Have A Role In Prehospital Management of Trauma Patients?

by Carly Loner, MD

Case Scenario:

EMS is called to the scene of a motorcycle accident involving a 42 year old male.  The patient was helmeted and his head is atraumatic, but he is confused.  Breath sounds are equal bilaterally. The patient’s abdomen is diffusely tender and he has an open left femur fracture that is bleeding profusely.  A tourniquet is applied to the left proximal thigh with control of active bleeding and a pelvic binder is placed. Initial vitals are HR 132, BP 85/60, RR 28.  The patient is loaded into the ambulance and they depart towards the Level One trauma center 35 minutes away.  The ground team does not carry blood, but they have been considering adding TXA for situations such as this…

Literature Review:

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Tranexamic acid (TXA) is a synthetic analog of the amino acid lysine that stabilizes clot formation by binding to lysine receptor sites on plasmin, thus preventing it from binding to and degrading fibrin.  It has been used in the medical arena for many years for the treatment of bleeding.  TXA is approved by the US Food and Drug Administration (FDA) only for use in heavy menstrual bleeding and for patients with hemophilia undergoing procedures, but it has a long history of off label use in the elective surgery setting [1]. More recently, it has been utilized as a therapy for the prevention and treatment of hemorrhagic shock.    TXA use to treat traumatic hemorrhagic shock became more widespread following publication of the Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage-2 (CRASH-2) trial [2].  This study showed that administration of TXA within 3 hours of injury reduced mortality, but had increased mortality if given after the 3 hours time-point.  The results of CRASH-2 were substantiated by the military application of tranexamic acid in trauma emergency resuscitation (MATTERs) study.  This retrospective study of a UK combat hospital found that subjects (combat casualties receiving 1 L or more of RBCs) had improved survival due to TXA versus placebo, and this benefit was increased in patients requiring massive transfusion [3].  Another study by Gayet-Ageron et al. sought to quantify the effects of treatment delay on TXA.  Simulated models determined that the benefit of TXA decreased by 10% for every 15 min of treatment delay until the 3 hour mark, after which there was no longer a benefit of TXA administration [4].  The literature supporting the use of TXA has continued to develop and the Department of Defense’s Committee on Tactical Combat Casualty Care (CoTCCC), American college of Surgeons Committee on Trauma, European Task Force for Advance bleeding Care in Trauma all recommend administering TXA to hospitalized trauma patients as soon as possible [5, 6].

The time-dependent benefit for TXA may be due to the pathophysiology of trauma-induced coagulopathy.  Massive bleeding within trauma patients has been shown to have distinct phases.  The fibrinolytic phase shows these patient are prone to acute blood loss not only from hypovolemia but also from coagulopathy resulting from acidemia, hypothermia, shock, and hemodilution [1].    The coagulation cascade is activated immediately after a trauma with increased tissue factor and thrombin production and activation [1].  Tissue hypoxia due to hemorrhagic shock causes release of tissue-plasminogen factor [1].  The early phase of response to trauma is a fibrinolytic coagulopathy and studies have shown that this is where TXA may be most beneficial [2-4].  If given at a later stage of post-trauma coagulopathy, the fibrinolytic shut-down phase,  TXA could enhance the pro-thrombotic state and increase multi-organ dysfunction secondary to vascular microvascular occlusion [1, 11].  The coagulation/fibrinolysis states of the patient may be important for determining benefit versus detriment of administering TXA. 

There are multiple mechanisms by which TXA is thought to contribute to improved outcomes in trauma patients.  In addition to its anti-fibrinolytic role in preventing fibrin breakdown, TXA prevents trauma- induced coagulopathy by preserving the endothelial glycocalyx and thereby reducing vascular permeability and intervascular hypovolemia contributing to shock [1,6,7].  TXA also has anti-inflammatory effects that reduces post-ischemic neutropenic and mast cell activation which protects lung tissue, reduces vasopressor requirements, and reduces chest tube output [8-10].

However, prehospital TXA administration remains controversial.

On the positive side, TXA administration has a time-dependent effect on mortality reduction:  a post-hoc analysis of the CRASH-2 data suggests that the mortality benefit is achieved by administration within one hour of injury [12].  Several studies have found benefits of prehospital TXA administration. A UK prospective analysis studied the effects of prehospital administration of 1 g TXA in patients with concern of hemorrhagic shock. This study found that reduced multi-organ failure (OR 0.27, 95% CI 0.10 – 0.73) and reduced mortality (OR 0.16, 95% CI 0.03 – 0.86) in patients with shock when TXA was given by prehospital providers [13].   A more recent retrospective, propensity-matched German study of trauma patients transported by helicopter found significantly reduced 24 hr mortality (5.8 %  with TXA vs. 12.4 % without TXA), but no significant difference in overall mortality (14.7% with TXA vs. 16.3 % without).  TXA was found to prolong time to death (8.8 +/- 13.4 days vs. 3.6 +/- 4 days) [14].  Preliminary evidence from the  Cal-Pat Study suggests a non-significant trend towards decreased 24 hr, 48 hr and 28 day mortality in patients receiving prehospital TXA [15].  In Israel, TXA is given at the point of injury in both civilian and military settings [16]. In the pediatric population, Eckert et al. studied the effects of TXA in pediatric patients  injured in a combat setting in Afghanistan and found reduced mortality [18].  Multiple studies of prehospital TXA use in trauma are ongoing, including the Study of TXA During Air and Ground Medical Prehospital Transport Trial (STAAMP Trial) is a US multicenter randomized control trial investigating TXA on US Helicopter EMS services and is expected to be completed in March 2018 [17]. 

On the opposite side, TXA use is associated with side effects induce GI pain, joint pain, fatigue, visual disturbances, and of greatest concern, thromboembolic events.  However, the CRASH-2 trial found no significant difference in vascular occlusive events between TXA group and controls, but did contribute thromboembolic events with delayed administration during fibrinolytic shut down phase [2].  Multiple other studies have found no significant increase in occurrence of thromboembolic events [4, 15].    However, in the UK prospective analysis, while favorable of TXA administration did find 4-fold increase of thromboembolic events in the shock group which received TXA [13].  TXA has not been found to increase thromboembolic events in the elective setting and thromboembolic events in the setting of trauma may be due to additional factors such as stasis and surgery [3].   

Given concern for increased coagulopathy and incidence of multi-organ failure if TXA is administered during the fibrinolytic shutdown phase, some argue that TXA should be withheld until coagulation testing can be done which demonstrates hyperfibrinolysis [5,19]. However, awaiting for this testing delays time to administration and puts patients closer to the fibrinolytic shut down phase of trauma- induced coagulopathy.  A study by Stein et al. compared coagulation studies both on scene and upon arrival to the hospital between patients administered TXA versus placebo.  On-scene samples showed no significant difference but coagulation studies of the TXA group on hospital arrival demonstrated reduced hyperfibrinolysis and preserved fibrinogen levels [20].  

A 2017 review of the literature of prehospital TXA administration recommends an intermediate approach where the 1 g initial bolus of TXA is given in the field with further administration of TXA only given after coagulation testing at the hospital demonstrates continued hyperfibrinolysis [6].  There is no current evidence to support this two-step approach,  bringing up the ever-important point that prehospital and in-hospital trauma care are two points on the same continuum.  Regardless of location, prehospital implementation of a TXA protocol requires a collaborative effort with hospital emergency department and trauma services to ensure that care that is initiated is continued.  

Take Home: The use of TXA within trauma is controversial and still developing as literature expands.  However, studies do indicate that there is greater benefit to early administration of TXA versus delayed administration.  The negative effects of TXA may also be decreased if given early in the course of hemorrhagic shock.  There is growing evidence demonstrating reduced morbidity and mortality with prehospital TXA administration.  The role of TXA will likely continue to expand and it has potential to be employed in the prehospital setting to improve survival of patients in hemorrhagic shock.  

EMS MEd Editors Maia Dorsett, MD PhD (@maiadorsett) & Jeremiah Escajeda (@jerescajeda)

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Additional Resources:

Current clinical prehospital trials of TXA use in Trauma at ClinicalTrials.gov

Enthusiasm for prehospital TXA use may be premature (JEMS)

Tranexamic acid's potentially bright future relies on collaborative data (JEMS)

Trending: More EMS Agencies administering TXA (EMS1)

 

References

1.         Nishida, T., T. Kinoshita, and K. Yamakawa, Tranexamic acid and trauma-induced coagulopathy. J Intensive Care, 2017. 5: p. 5.

2.         Roberts, I., et al., The CRASH-2 trial: a randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess, 2013. 17(10): p. 1-79.

3.         Morrison, J.J., et al., Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg, 2012. 147(2): p. 113-9.

4.         Gayet-Ageron, A., et al., Effect of treatment delay on the effectiveness and safety of antifibrinolytics in acute severe haemorrhage: a meta-analysis of individual patient-level data from 40 138 bleeding patients. Lancet, 2017.

5.         Chang, R., B.J. Eastridge, and J.B. Holcomb, Remote Damage Control Resuscitation in Austere Environments. Wilderness Environ Med, 2017. 28(2s): p. S124-s134.

6.         Huebner, B.R., W.C. Dorlac, and C. Cribari, Tranexamic Acid Use in Prehospital Uncontrolled Hemorrhage. Wilderness Environ Med, 2017. 28(2s): p. S50-s60.

7.         Diebel, M.E., et al., The temporal response and mechanism of action of tranexamic acid in endothelial glycocalyx degradation. J Trauma Acute Care Surg, 2018. 84(1): p. 75-80.

8.         Jimenez, J.J., et al., Safety and effectiveness of two treatment regimes with tranexamic acid to minimize inflammatory response in elective cardiopulmonary bypass patients: a randomized double-blind, dose-dependent, phase IV clinical trial. J Cardiothorac Surg, 2011. 6: p. 138.

9.         Peng, Z., et al., Intraluminal tranexamic acid inhibits intestinal sheddases and mitigates gut and lung injury and inflammation in a rodent model of hemorrhagic shock. J Trauma Acute Care Surg, 2016. 81(2): p. 358-65.

10.      Reichel, C.A., et al., Plasmin inhibitors prevent leukocyte accumulation and remodeling events in the postischemic microvasculature. PLoS One, 2011. 6(2): p. e17229.

11.         Moore, E.E., et al., Postinjury fibrinolysis shutdown: Rationale for selective tranexamic acid. J Trauma Acute Care Surg, 2015. 78(6 Suppl 1): p. S65-9.

12.         Crash-2 Collaborators. (2011). The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. The Lancet, 377(9771), 1096-1101.

13.         Cole, E., et al., Tranexamic acid use in severely injured civilian patients and the effects on outcomes: a prospective cohort study. Ann Surg, 2015. 261(2): p. 390-4.

14.         Wafaisade, A., Lefering, R., Bouillon, B., Böhmer, A. B., Gäßler, M., & Ruppert, M. (2016). Prehospital administration of tranexamic acid in trauma patients. Critical Care, 20(1), 143.

15.         Neeki, M.M., et al., Efficacy and Safety of Tranexamic Acid in Prehospital Traumatic Hemorrhagic Shock: Outcomes of the Cal-PAT Study. West J Emerg Med, 2017. 18(4): p. 673-683.

16.        Nadler, R., Gendler, S., Benov, A., Strugo, R., Abramovich, A., & Glassberg, E. (2014). Tranexamic acid at the point of injury: the Israeli combined civilian and military experience. Journal of Trauma and Acute Care Surgery, 77(3), S146-S150.

17.        https://clinicaltrials.gov/ct2/show/NCT02086500

18.         Eckert, M.J., et al., Tranexamic acid administration to pediatric trauma patients in a combat setting: the pediatric trauma and tranexamic acid study (PED-TRAX). J Trauma Acute Care Surg, 2014. 77(6): p. 852-8; discussion 858.

19.        La Rochelle, P., Prehospital transfer strategies and tranexamic acid during major trauma. The Lancet. 389(10079): p. 1604-1605.

20.      Stein, P., et al., The Impact of Prehospital Tranexamic Acid on Blood Coagulation in Trauma Patients. Anesth Analg, 2017.

Challenging the Dogma of “All Clear”: Is Hands-On Defibrillation the Next Step in Reducing the Peri-shock Pause?

by Brandon Bleess, MD EMT-T and Jeremy Cushman, MD, MS, EMT-P, FACEP, FAEMS

Case:

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A 54-year-old male is working in his yard when he collapses to the ground and his wife calls 911.  The call is dispatched as a cardiac arrest and the patient's wife is instructed to perform CPR per pre-arrival instructions.  Upon EMS arrival, the patient is found to be  apneic and pulseless.  EMS relieves the patient’s wife and compressions are continued while the patient is connected to the monitor.  The monitor is charged prior to the next pulse check where the patient is noted to be in ventricular fibrillation.  Everyone takes the time to drop contact with the patient as the operator declares “everyone clear” before shocking and resuming compressions and ventilation.   

When debriefing the case, one of the paramedics brings up the idea of hands-on defibrillation that he attended a lecture on at a recent conference.  Is it safe to defibrillate a patient while CPR is actively being performed?

The Evidence For:

There is little question that high quality, continuous compressions improve neurologic outcomes in patients with out-of-hospital cardiac arrest.  The choice of outcome here is important: compressions are really to maintain some oxygenated blood flow to the brain in order to keep it alive long enough to get the heart started again.  All too often, ROSC is achieved but the patient has anoxic brain injury which can be a result of extended down time or ineffective compressions. 

Thus the goal in performing compressions is to minimize interruptions, for every time compressions are stopped it takes a significantly longer time to return to the flow state that existed just prior to stopping them [1-5].  With the goal of increasing compression fraction and thus improving neurologic outcomes,  the American Heart Association (AHA) began recommending charging the defibrillator during chest compressions in 2005 [6].  Multiple studies have since demonstrated that charging during compressions decreases both post- and peri-shock pauses [7-9].  These included the Resuscitation Outcomes Consortium (ROC) PRIMED trial which found that the median peri-shock pause was reduced from 21 seconds to 9 seconds with compressions during charging. This reduction in peri-shock pause lead to a significant increase in mean chest compression fraction  (0.77 vs 0.70, 95% CI: 0.03-0.11), an independent factor in increasing survival [9, 10, 11].  Thus, the traditional analyze – charge - shock pattern should be changed to charge – analyze- shock.

But can we go one step further and continue CPR during defibrillation?  After decades of “I’m clear, you’re clear, we’re all clear,” it might be time to let that go the way of the backboard in the closet of EMS dogma.  Traditionally, external defibrillation has been considered a safety hazard to rescuers and clearing the patient is an almost universal practice, but there is little data to support this notion in the age of adherent defibrillation pads [12].  Indeed, there is now evidence to suggest that hands-on defibrillation is actually safe.

How much energy is potentially transferred to the compressor during hands-on defibrillation? Defibrillators generally deliver 30-40 A of current with each shock, and the threshold for perception is 2.5-4.0 mA, and exposure becomes painful at 6-10 mA.  In healthy adults 200-500 mA of current is thought to be needed to induce ventricular fibrillation with incidence correlating linearly to increasing current [12].

Lloyd et. al. found that the amount of "leakage" (the amount of current going to the provider) in an ideal setting (outpatient cardiac electrophysiology evaluations) was well below the allowable minimum [13].  Keep in mind, this study was looking at microamps of current.  The allowable being 3,500 microamps and the leakage was an order of magnitude less than that.  To put this into further perspective, when pacing patients with transcutaneous pacing generally 60-80 mA is required for capture.  Compared to the study’s mean leakage of 283 µA or 0.28 mA, transcutaneous pacing uses over 200 times the amperage to create capture.

Neumann et al. in 2012 followed up this study by inducing ventricular fibrillation in a swine model and comparing hands-on versus hands-off defibrillation.  They found that in the hands-on group, chest compressions were interrupted for 0.8% versus 8.2% of the total CPR time (P=0.0003) and coronary perfusion pressure was restored earlier to its pre-interruption level (P=0.0205). They also found that not only was the defibrillation shock imperceptible, but the compressor wearing a cardiac monitor had no arrhythmias noted [14].

Insulating the provider from current leakage is probably one of the easiest ways to protect the compressor from harm.  This was studied by Deakin et al. in 2015 using Class 1 electrical insulating gloves while simulating hands-on defibrillation.  They found that the median current leakage was 20 μA from the 61 shocks studied, and even at 360 J the median current leakage was 27 μA.  The highest recorded leakage was 28 μA, all below the 1 mA threshold they set [15].  More recently in 2016, Wampler et al. published a study looking at perception of shocks using multiple insulating barriers, including nitrile gloves, firefighting gloves, a neoprene pad, and a manual compression/decompression device.  Out of the 100 shocks with no barrier device, all but 1 shock was not detected.  Out of 500 shocks, only 5 were detected by the compressor - none causing harm, and most importantly the CPR puck prevented any detection [16].  

The Evidence Against:

Closer evaluation of these studies may give some rescuers pause.  In the 2008 Lloyd study, 8 of the 72 phases (36 shocks, 11.1%) exceeded the 500 µA threshold [13].  In the Neumann study of 2012, the compressors wore 2 pairs of polyethylene gloves which is outside the standard practice of many providers [14]. While Deakin’s study presents some very convincing data in relation to the safety, the compressor was wearing Class 1 electrical insulating gloves.  According to the Occupational Safety and Health Administration (OSHA) regulation 29 CFR 1910.137, Class 1 gloves are rated for a maximum usage of 7500 V AC and are proof tested to 10,000 VAC and 40,000 VDC [18].  Defibrillators typically fall well below this at around 2700 V for a biphasic defibrillator. 

In 2014, Lemkin et. al. published a cadaver study where they measured the differential of the voltages at various points on the body with several skin preparations (bare, water, saline, ultrasound gel).  This allowed them to collect the resistance and exposure voltage in relation to anatomic landmarks to create a map of the providers’ exposure.  From there, they derived a formula to measure the rescuer-received dose (RRD) to represent the proportion of energy the rescuer could receive from a shock to a patient.  Their results demonstrated the rescuer-exposure could exceed 1 J in any location at some energy level, and reached as high as 9.4J on the anterior chest wall [17].  The argument made is that 1 J could potentially cause a provider to be shocked into ventricular fibrillation themselves.  Since this does not include any barriers, it would apply if there was a large tear in the glove or the rescuer was contacting the patient without any gloves.

Conclusion:

While the literature suggests that hands-on defibrillation is safe, it should occur at the discretion of the compressor who should consider wearing two pairs of gloves or utilize both gloves and a CPR-feedback device if performing the procedure.  There are no studies that have measured the effect of this on clinical outcome, although it is postulated that increased compression fraction is a useful surrogate.  At minimum, the charge-analyze-shock method should be used during every defibrillation to minimize the hands-off time and increase the compression fraction.

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For additional Resources, REBEL EM published the following review of Hands-On-Defibrillation: CPR Hands-On or Hands-Off Defibrillation

EMS MEd Editor:  Maia Dorsett (@maiadorsett)

References:

1.     Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation. 2001 Nov 13;104(20):2465-70.

2.     Cunningham LM, Mattu A, O’Connor RE, Brady WJ. Cardiopulmonary resuscitation for cardiac arrest: the importance of uninterrupted chest compressions and cardiac arrest resuscitation. Am J Emerg Med. 2012 Oct;30(8):1630-8.

3.     Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA. 1990 Feb 23;263(8):1106-13

4.     Hazinski MF, Nolan JP, Aicken R, et al. Part 1: executive summary: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2015;132(16)(suppl 1).

5.     Neumar RW, Shuster M, Callaway CW, et al. Part 1: executive summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132(18)(suppl 2).

6.     2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005;112:IV1–IV203.

7.     Perkins GD, Davies RP, Soar J, Thickett DR. The impact of manual defibrillation technique on no-flow time during simulated cardiopulmonary resuscitation. Resuscitation. 2007;73:109–114.

8.     Edelson DP, Robertson-Dick BJ, Yuen TC, et al. Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study. Resuscitation. 2010;81(11), 1521-1526.

9.     Cheskes S, Schmicker RH, Verbeek PR, Salcido DD, Brown SP, Brooks S, Menegazzi JJ, Vaillancourt C, Powell J, May S, et al. The impact of peri-shock pause on survival from out-of-hospital shockable cardiac arrest during the Resuscitation Outcomes Consortium PRIMED trial. Resuscitation. 2014 Mar; 85(3):336-42.

10.  Christenson J, Andrusiek D, Everson-Stewart S, et al. Chest compression fraction determines survival in patients with out-of-hospital ventricular fibrillation. Circulation. 120 (2009), pp. 1241-1247.

11.  Cheskes S, Schmicker RH, Christenson J, et al. Peri-shock pause: an independent predictor of survival from out-of-hospital shockable cardiac arrest. Circulation. 124 (2011), pp. 58-66.

12.  Brady W, Berlat JA. Hands-on defibrillation during active chest compressions: eliminating another interruption. Am J Emerg Med. 2016 Nov;34(11):2172-2176.

13.  Lloyd MS, Heeke B, Walter PF, Langberg JJ.  Hands-on defibrillation: an analysis of electoral current flor through rescuers in direct contact with patients during biphasic external defibrillation. Circulation. 2008 May 13;117(19):2510-4.

14.  Neumann T, Gruenewald M, Lauenstein C, Drews T, Iden T, Meybohm P. Hands-on defibrillation has the potential to improve the quality of cardiopulmonary resuscitation and is safe for rescuers—a preclinical study. J Am Heart Assoc. 2012 Oct;1(5):e001313.

15.  Deakin CD, Thomsen JE, Løfgren B, Petley GW. Achieving safe hands-on defibrillation using electrical safety gloves—a clinical evaluation. Resuscitation. 2015 May;90:163-7.

16.  Wampler D, Kharod C, Bolleter S, Burkett A, Gabehart C, Manifold C. A randomized control hands-on defibrillation study- Barrier use evaluation. Resuscitation. 2016 Jun;103:37-40.

17.  Lemkin DL, Witting MD, Allison MG, Farzad A, Bond MC, Lemkin MA.  Electrical exposure risk associated with hands-on defibrillation. Resuscitation. 2014 Oct;85(10):1330-6

18.  https://www.grainger.com/content/qt-electrical-safety-gloves-inspection-262

 

When it’s more complicated than a tweet: Door-to-Furosemide and EMS

by Sahar Morkos El-Hayek, MD

EMS MEd Editor Maia Dorsett, MD PhD (@maiadorsett)

This past summer, the results of the REALTY-AHF (Registry Focused on Very Early Presentation and Treatment in Emergency Department of Acute Heart Failure) study, a prospective observational cohort study of the management of patients presenting to the emergency for acute heart failure was published [1].   The one-liner conclusion – as summarized by tweets and online articles – was that early furosemide saves lives:

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If early furosemide saves lives, why aren’t we giving it prehospital?

Because it doesn’t necessarily help and it has the potential to cause harm.

The REALITY- AHF was a prospective observational study that examined the association between door to furosemide (D2F) and all-cause-in-hospital-mortality.  To be included in the study, patients had to be diagnosed with acute heart failure within their first three hours of admission to the ED.  Patients who received furosemide within 60 minutes of arrival were assigned to the early treatment group.  “Non-early” treatment was defined as furosemide administration at any time beyond the first hour.  A total of 1291 patients met the inclusion criteria. 481 patients (37.3%) were classified as the early treatment group and 810 (62.7%) composed the non-early treatment group. Overall, the authors found a decrease in both in-hospital and 30-day mortality for patients who received furosemide within the first 60 minutes, (OR 0.36, 95% CI 0.19-0.71 and OR 0.52, 95% CI 0.28-0.96) respectively.    Since the trial was not randomized, the authors attempted to control for confounding variables using propensity score matching and found similar results (OR 0.41, 95% CI 0.18-0.89 for in hospital mortality).  The authors accounted for many variables - demographics, lab values – but not whether patients concurrently received therapies with proven outcome benefits such as nitroglycerin and ACE-inhibtors or Noninvasive Positive Pressure Ventilation( NIPPV )[2-5].

Variables accounted for in the Propensity Analysis by Matsue et. al. (Reference 1).

Variables accounted for in the Propensity Analysis by Matsue et. al. (Reference 1).

Patients who received earlier treatment were more likely to arrive by ambulance, had a more rapid onset of symptoms, and more severe congestive symptoms.  As no other key interventions were examined – i.e. preload and afterload reduction – it is unclear whether “door-to-furosemide” time is simply a surrogate for the “door-to-rapid-recognition-and-treatment-of-acute-heart-failure” time. 

The patients we care for in EMS are fundamentally different from the patients included in the REALTY-AHF study in one important way:  they are undifferentiated.  We care for patients with respiratory distress and shortness of breath, not an unequivocal diagnosis of acute heart failure.  This is also true of the initial part of a patient’s stay in the emergency department. It is not always obvious at the time of presentation whether the etiology is acute heart failure, or rather a pulmonary embolism, Chronic Obstructive Pulmonary Disease (COPD), volume overload due to renal failure, sepsis from pneumonia or some combination of the above.  Moreover, acute heart failure itself is not a homogenous disease.  Most commonly heart failure is left-sided, but even then, it may be due to the heart’s decreased ability to pump blood into circulation (systolic heart failure) or incomplete filling during diastole [i.e diastolic heart failure or heart failure with preserved ejection fraction (HFpEF)].  Most emergency department patients with acute decompensated heart failure have preserved systolic function and are not overloaded in terms of total body volume [5].   Rather, these patients have a fundamentally vascular problem – one of an abrupt increase in afterload that results in acute decompensation.  More importantly, although hypertensive, these patients may be euvolemic or even hypovolemic.  In these cases, the treatment focuses on managing the flow of blood through system rather than eliminating fluid from the system.  This is accomplished by NIPPV in the form of CPAP or BiPAP, high dose nitroglycerin, and ACE inhibitors [2-5].

Since many EMS and ED patients with acute decompensated heart failure are not volume overloaded, liberal use of diuretics may not be helpful and has the potential to be harmful [5].  Several studies have been published regarding prehospital furosemide administration, mainly examining the accuracy of paramedics’ working diagnosis of acute decompensated heart failure by comparing it to the final hospital diagnosis and studying the side effect profile and potential harm.

Jerome Hoffman and Susan Reynolds published a study in 1987 that evaluated the effect of prehospital furosemide on patient outcomes [6].  At the time of the study, paramedics in LA County were instructed to administer furosemide and morphine +/- nitroglycerin to patients with a clinical presentation consistent with pulmonary edema.   Through clinical experience, the authors became concerned that morphine and furosemide led to clinically harmful respiratory depression and dehydration.  They carried out a prospective sequential trial of therapies which included patients with shortness of breath as a presenting symptom and paramedic clinical suspicion for pulmonary edema and a SBP > 120.  Patients received one of four treatment cocktails:

                  Group A: Sublingual nitroglycerin + 40 mg IV furosemide

                  Group B: 3 mg IV morphine + 40 mg IV furosemide

                  Group C: Sublingual nitroglycerin + 3 mg IV morphine + 40 mg IV furosemide

                  Group D: Sublingual nitroglycerin + 3 mg IV morphine [FUROSEMIDE-FREE]

Table 7 from Hoffman and Reynolds (Reference 6) . Group D represents the "Furosemide-free" group.

Table 7 from Hoffman and Reynolds (Reference 6) . Group D represents the "Furosemide-free" group.

Each therapy could be repeated up to three times and there were 15 patients in each group.  As this was not an intention-to-treat analysis, 2 patients were excluded who did not receive the prescribed treatment.  Patients were evaluated for clinical deterioration or improvement in the prehospital arena, in the emergency department, and 12 hours into their admission.  The study found that only 77% of patients had pulmonary edema in the emergency department with the most common alternative diagnosis being COPD exacerbation.  They also found that excluding nitroglycerin and administering morphine increased intubation rates.  Finally, their data suggested that prehospital furosemide administration lead to complications including arrhythmias due to hypokalemia, hypotension, increased tachycardia and need for fluid administration without clear evidence of benefit. The authors concluded that prehospital pharmacologic treatment of respiratory distress due to pulmonary edema should be limited to nitroglycerin.

In contrast, a multi-center retrospective study by Pan et. al. (2014) failed to identify an association between prehospital furosemide administration and serious adverse events (acute renal failure, intubation, vasopressors or death) [7].  The study included acutely ill patients 50 years and older with dyspnea who were diagnosed with acute heart failure in either the prehospital or hospital record.  330 patients were subdivided into three categories: Furosemide without heart failure (N=58), furosemide with heart failure (N=110), and no furosemide with heart failure (N = 162).   They performed a linear regression to identify whether there was an association between furosemide use and outcome.  The adjusted odds ratio for serious adverse event for patients receiving furosemide was 0.62 (95% CI 0.33 – 1.43) for patients with heart failure and 1.14 (95% CI 0.58-2.23) in those without.  Similar to the REALTY-AHF study, the adjustments accounted for historical factors, but not differences in use of NIPPV or nitroglycerin which differed significantly between the groups (see Table).

Pan et. al. Table 3 [Reference 7]

Pan et. al. Table 3 [Reference 7]

34.8% of patients who received furosemide did not have a final ED diagnosis of acute heart failure. Other studies have found this proportion to vary anywhere between 15 – 36% [6-9].  This level of diagnostic accuracy is similar to emergency department physicians [10].  These represent a substantial proportion of critically ill patients who may be harmed by furosemide administration [9].

 

Take Home Points:

EMS cares for undifferentiated patients with shortness of breath.  While expeditious furosemide therapy may benefit patients with acute heart failure due to volume overload, it may cause harm to the 15-36% of patients who are miscategorized as having acute decompensated CHF.  EMS should continue to focus on appropriate use of therapies with significant benefit towards patient-centered outcomes, such as NIPPV, and leave consideration of door-to-furosemide time out of our protocols.  

Sahar.001.jpeg

References

1.     Matsue Y, Damman K, Voors A.A, et al. Time-to-Furosemide Treatment and Mortality in Patients Hospitalized With Acute Heart Failure. Journal of the American College of Cardiology Jun 2017, 69 (25) 3042-3051; DOI: 10.1016/j.jacc.2017.04.042

2.     Sacchetti, A., Ramoska, E., Moakes, M. E., McDermott, P., & Moyer, V. (1999). Effect of ED management on ICU use in acute pulmonary edema. The American journal of emergency medicine, 17(6), 571-574.

3.     Vital, F. M., Saconato, H., Ladeira, M. T., Sen, A., Hawkes, C. A., Soares, B., ... & Atallah, Á. N. (2008). Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database Syst Rev3(3).

4.     Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A., Penugonda, N., ... & Zalenski, R. (2007). Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis. Annals of emergency medicine50(2), 144-152.

5.     Scott, M. C., & Winters, M. E. (2015). Congestive heart failure. Emergency Medicine Clinics33(3), 553-562.

6.     Hoffman, J. R., & Reynolds, S. (1987). Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema. Chest92(4), 586-593.

7.     Pan, A., Stiell, I. G., Dionne, R., & Maloney, J. (2014). Prehospital use of furosemide for the treatment of heart failure. Emerg Med J, emermed-2013.

8.     Dobson, T., Jensen, J., Karim, S., & Travers, A. (2014). Correlation of paramedic administration of furosemide with emergency physician diagnosis of congestive heart failure.. Australasian Journal of Paramedicine, 7(3).

9.     Wuerz, R. C., & Meador, S. A. (1992). Effects of prehospital medications on mortality and length of stay in congestive heart failure. Annals of emergency medicine21(6), 669-674.

10.  Ackerman, R., & Waldron, R. L. (2006). Difficulty Breathing: Agreement of Paramedic andEmergency Physician Diagnoses. Prehospital Emergency Care10(1), 77-80.

 

 

Screening & Treating: EMS and the Sepsis Care Continuum

by Elizabeth Odom, MD MPH

EMS MEd editor: Maia Dorsett MD PhD (@maiadorsett)

Case Scenario

It’s a hot summer day and EMS is dispatched to an old farmhouse on the edge of the town for a patient who has been ”generally weak” and now unable to get out of bed.  Upon arrival, paramedics find a previously healthy 65 year old female who has had a productive cough for a week.  She has had little oral intake for 3 days and her urine has been dark and low in volume. Her husband called EMS because she has become progressively more confused over the course of the day. Her vital signs are T 38.1 HR 96 BP 115/80 RR 23 O2 Sat 91%. 

The patient is quickly loaded into the ambulance.  An IV is placed and fluid bolus is initiated. Fingerstick blood sugar is within normal limits and an ECG demonstrates sinus rhythm.  Given the semi-rural location, transport to the hospital will exceed 30 minutes.

The paramedic suspects sepsis.  What is the role of EMS in sepsis screening and treatment? How should we best screen for sepsis in the prehospital environment? Beyond IV fluids, should EMS administer antibiotics?

Literature Review

Sepsis is a Time-Critical Diagnosis

Advancements in protocols for STEMI and trauma patients have drastically improved early identification and treatment [1,2].  Like STEMI and Trauma, sepsis is a time-critical diagnosis where early screening and intervention can impact outcome [3-6].  With a mortality rate of 18-50% depending on other risk factors, severe sepsis should be acted on as quickly as possible [7]. Septic patients who are transported by EMS are sicker and have a higher mortality than those who arrive via other means, so the effect of any delay in antibiotic administration in this population may be amplified [8].  Delays in care of even 1 hour after first medical contact have been shown to increase mortality in patients with severe sepsis [9-12] while antibiotic therapy within the first hour of severe sepsis recognition contributed to an 80% survival [13].  The rapid administration of broad spectrum IV antibiotics may save more lives than the administration of aspirin in acute MI and epinephrine in anaphylaxis [14].

Current literature suggests that sepsis is both underrecognized and undertreated in the prehospital setting [15-16].  The reasons are likely multi-factorial, but include knowledge gaps as well as  poor prehospital performance of sepsis screening tools.  A recently published survey study from Atlanta found that 24% of paramedics were unaware of evidence supporting early sepsis treatment [17]. Moreover, 73% of participating Emergency Physicians reported caring for patients with sepsis almost every shift, while 62% of EMS providers reported caring for patients with sepsis no more than occasionally.  While there are multiple sets of criteria for diagnosing sepsis, sepsis screening tools have variable performance in the prehospital setting. MEWS (Modified Early Warning Score) and BAS 90-30-90 scores were 74% and 62% sensitive, while the Robson score has been found to be 75-90% sensitive [18-21].  The PRESS (prehospital severe sepsis) score to identify severe sepsis also has a sensitivity near 90%, but is rather complicated for prehospital use [22].  qSOFA was developed as a  simple tool to prompt clinicians to consider sepsis and escalate therapy as appropriate [23,24].  However, recent studies have demonstrated that although very specific, it has extremely poor sensitivity for severe sepsis in the prehospital setting, predominantly due to absence of hypotension until after ED admission [25,26].  SIRS itself lacks specificity in the prehospital setting.  Moreover, in the hospital, 12.1% of patients with documented severe infection causing end-organ dysfunction are SIRS-negative [27].

Some services have successfully introduced lactate meters to detect occult hypoperfusion to enable hospital notification of a need for early, aggressive intervention [6].  As lactate meters are cost-prohibitive for many services, an important alternative to is end-tidal capnography, which is more widely available and has increasing applications in the prehospital setting.   More recently, end-tidal CO2 levels were found to correlate with lactate levels and mortality in the ED setting [28].  Incorporation of end-tidal capnography into a SIRS-based prehospital sepsis alert protocol had a sensitivity of 90% (95% CI 81-95%), a specificity of 58% (95% CI 52-65%), and a negative predictive value of 93% (95% CI 87-97%) for sepsis and severe sepsis [29] .

EMS Interventions and Antibiotic Administration

Although decreased time to from first medical contact to antibiotic administration has the potential to impact mortality for patients with severe sepsis and septic shock, few EMS systems have initiated the administration of antibiotics to septic patients in the prehospital setting.  This is due to a number of complexities.  First, as discussed above, sepsis may be difficult to diagnose, despite the numerous algorithms that have been presented.  Second, blood cultures allow for targeted antimicrobial therapy and these should typically be drawn prior to antibiotic administration, which may be subject to contamination or be difficult to obtain in the prehospital setting.  Third, logistics and costs behind carrying and administering antibiotic agents on ambulances limits feasibility without substantial evidence behind the routine administration of antibiotics in the field.  

Some EMS systems have standardized sepsis protocols based on one or a combination of scales references above. The mainstay of these protocols is fluid resuscitation and prehospital notification [6].  A small number of EMS systems have begun to introduce antibiotic administration into their protocols for patients with severe sepsis.  This has reduced time to antibiotic from an average of 131 minutes after first contact to 69 minutes [30].  Even with short transport times, antibiotics may be initiated prior to arrival, eliminating the wait time for a bed, to see a physician, to receive the drug from pharmacy, and for a nurse to administer it. In South Carolina, EMS has treated 650 septic patients according to this protocol and 59% have received antibiotics [31]. Patients with > 2 SIRS criteria and a Point of Care Lactate  >2.2mmol/L were treated with IV or interosseous ceftriaxone 1 g is in cases of suspected pneumonia or  piperacillin/tazobactam 4.5 g following obtainment of blood cultures.  Contamination rate for EMS-obtained blood cultures was <6%.  Preliminary data showing a reduction from 25.6% mortality vs 9.3% mortality for patients with sepsis within the hospital system.  In Australia and New Zealand, the PASS (Paramedic Antibiotics for Severe Sepsis) study, a randomized trial in which paramedics following a similar protocol is underway [32].

One of the most commonly cited fears regarding prehospital antibiotic administration is that it will cause an in antibiotic resistance.  Inappropriately prescribed antibiotics do indeed increase resistance [33].   “Inappropriate” antibiotic use in an undifferentiated patient is not straightforward to define.  Programs will have to fairly be compared to ED-administered antibiotics (rather than hospital final-diagnosis) and the impact on patient-centered outcomes measured prospectively. Empiric antibiotics provided are consistent with those recommended by local agencies for bacterial sensitivity resistance patterns for each area [34].  Ideally, a randomized-controlled trial will be conducted as the true risks-benefits of EMS-initiated antibiotics is unclear.

Take Home

Sepsis is a time-critical diagnosis and EMS can play a key role in reducing time to intervention and impacting patient-centered outcomes.  Currently, sepsis remains underrecognized and undertreated in the prehospital setting, largely due to knowledge gaps and poor performance of screening methods.  Recently, end-tidal capnography has emerged as a tool to enhance prehospital sepsis screening.  Some EMS agencies have introduced paramedic-initiated antibiotics with some success.  Further research is needed to fully understand the risks and benefits of this approach, which may vary regionally due to transport times and subsequent hospital-based patient management.  

References

1.    Mehta RH, Montoye CK, Gallogly M, et al., for the GAP Steering Committee of the American College of Cardiology. Improving quality of care for acute myocardial infarction: The Guidelines Applied in Practice (GAP) Initiative. JAMA. 2002; 287: 1269–1276.
2.    Demetriades D, Martin M, Salim A, Rhee P, Brown C, Chan L. The Effect of Trauma Center Designation and Trauma Volume on Outcome in Specific Severe Injuries. Annals of Surgery. 2005;242(4):512-519.
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Synthetic Opioid Overdose: Practical Considerations for Emergency Medical Services

by Aurora Lybeck, MD and M. Riccardo Colella, DO

Abstract: First responders, including Emergency Medical Services (EMS), fire departments, and law enforcement officers (LEOs), are often the first to respond to suspected opioid overdoses. The heroin epidemic has been worsening throughout the US and Canada, from coast to coast and in every state and province. The recent increase in synthetic opioid abuse and heroin contaminants can raises additional safety concerns for first responders and strains local resources. We suggest an emphasis on provider safety including personal protective equipment (PPE) and awareness of potential first responder exposure. Patient care for suspected overdoses should focus on respiratory support, transporting patients refractory to initial scene care, and ensuring appropriate naloxone dosage and adequate supply on each responding unit. Synthetic opioids in a local area can create a surge in overdose calls that has the potential to overwhelm available emergency resources and supplies, akin to a mass casualty event. EMS systems may mitigate potential strain on local resources by awareness and monitoring of local epidemiologic patterns, preparation, and collaboration with local agencies.  

Background: The number of heroin related deaths and overdoses have significantly increased over the past decade. Overdose deaths involving heroin more than tripled in the US from 2010 to 2014, and are anticipated to be even higher given the rapidly changing epidemic [1, 2, 3]. Numerous federal organizations such as The Center for Disease Control (CDC), Drug Enforcement Administration (DEA), National Drug Early Warning System (NDEWS), and the Canadian Centre on Substance Abuse (CCSA), continue to gather and report on these data as this epidemic burgeons. In 2016, the DEA declared prescription drugs, heroin, and synthetic opioids, such as fentanyl, the most significant drug related threat to the US.. Outbreaks of fentanyl and other synthetic opioids have contributed to surges in overdoses rates and deaths. In 2016 and early 2017, several EMS agencies experienced significant increases in overdose related call volumes. Multiple cities have witnessed overdose “outbreaks” which can overwhelm local EMS resources, akin to a mass causality event. For instance, in February 2017, EMS agencies in Louisville, Kentucky received 151 overdose calls within four days, with 52 of those calls occurring within 32 hours. [4] Medical examiner data from similarly affected areas reflects similar surges in overdose deaths, raising suspicion that fentanyl and other synthetic opioids may be at least partially to blame. [5, 6].  High-potency opiates require higher doses of naloxone for reversal.  A retrospective study of NEMSIS data from 2012-2015 found that among patients receiving prehospital naloxone, the percent of patients receiving multiple doses increased from 14.5% in 2012 to 18.2 % in 2015, anoverall increase of 25.8 % suggesting increased infiltration of the opiod market by high-potency synthetics [7].

Fentanyl is considered 100 times more potent than morphine and 600 times more lipid soluble, subsequently increasing brain absorption. Illicitly produced synthetic opioids include non-pharmaceutical fentanyl, fentanyl analogs, and novel synthetic opioids [8]. Synthetic opioid overdose outbreaks have occurred historically on a smaller scale, as evidenced by the China White (3-methylfentanyl) in the US in the 1980’s [9] and several hundred fentanyl deaths across the US in the mid 2000’s [10,11]. The CDC reports a marked increase in deaths involving synthetic opioids since 2013 [2, 12]. Since Pharmaceutical fentanyl prescription rates (primarily fentanyl patches) remained relatively stable in comparison, the etiology of this surge is not prescription fentanyl. [12, 13]. Synthetic opioids are often found as a heroin contaminant or are sold in pill form [14, 15]. Hundreds of thousands of counterfeit pills have been entering the US and Canadian drug market, many of which contain fentanyl and other synthetic opioids, some at lethal doses in a single pill [12-18].

The fentanyl analog carfentanil is considered 10,000 times more potent than morphine and 100 times more potent than fentanyl [5, 6, 19], and is reported in medical examiner overdoses cases across the US and Canada. In 2002, an unknown aerosolized “gas” was used by Russian special operations forces in an attempt to rescue 800 hostages held in a theater by Chechnan rebels. Sadly, at least 125 hostages were killed, and years later carfentanil and remifentanil were positively identified as likely agents in post-mortem samples [20]. Other synthetic opioids including various fentanyl analogs, (such as MT-45, AH-7921 and an isomer U-47700) are present in the illicit marketplace and have all been confirmed in deaths in the US, Canada, and Europe [21-24]. Once novel synthetic drugs appear in the market, there is often a significant time delay to the development of an assay for identification in post-mortem samples. By the time the chemical is identified with reliability, either from post mortem samples or seized drug samples, the synthetic drug manufacturers often have already flooded the market with a new compound. Consequently, first responders may encounter either an affected patient or a drug exposure in the field before it has been identified.

Provider Safety and Personal protective equipment (PPE)

The most commonly used PPE for first responders includes nitrile gloves and occasionally eye protection, escalating to other types of PPE as situationally indicated. In a 2017 descriptive surveillance study, data collected from 572 EMS workers who sought treatment in emergency departments (EDs) between 2010-2014 demonstrated that exposures to harmful substances were the second leading occupational injury (behind strains and sprains). The authors recommended new and enhanced efforts to prevent EMS worker injuries and exposures to harmful substances [25]. The concept of evolving and improving our use of PPE is not new to healthcare providers. Diseases such as Ebola and SARS have spurred additional training and use of PPE, and the use of PPE should be continually readdressed in the face of new threats to provider safety.

The DEA released a warning in June 2016 to the police and public regarding fentanyl exposures after two law enforcement officers (LEOs) experienced overdose symptoms after exposure to airborne particulate from a “tiny amount” of white powder. This warning was later expanded to include all first responders, with a guide for prehospital providers released in Jun 2017 [26, 27]. Heroin found in the white powder form (predominantly, with some regional variability) and is visually indistinguishable from most synthetic opioids (1). Fentanyl and other synthetic opioids in the white powder form may put first responders at risk by mucous membrane contact, inhalation of airborne particulate, and potentially skin contact. Toxic doses of carfentanil in particular pose a significant risk to first responders in small amounts, some as little as a few grains of salt. The Acting DEA Administrator stated in reference to synthetic opioids: “I hope our first responders- and the public- will read and heed our health and safety warning. These men and women have remarkably difficult jobs and we need them to be well and healthy” [19].

With increasing concern for first responder safety and exposures, the Justice Institute of British Colombia, in conjunction with the Royal Canadian Mounted Police (RCMP), British Colombia Emergency Health services, and Vancouver Fire Rescue services, and other collaborating services created an innovative website at www.fentanylsafety.com. Included are resources for all levels of first responders outlining specific considerations for LEOs, firefighters, EMS, and Hazmat personnel. Within the EMS recommendations is a guide specific for fentanyl/synthetic overdose education, treatment guidelines, field risk assessment, donning and doffing PPE including N95 masks, and protocol recommendations for self-administration of naloxone in the event of symptomatic exposure. NIOSH, the National Institute for Occupational Safety and Health, provides similar PPE recommendations for first responders, found at www.cdc.gov/niosh/topics/fentanyl/risk.html. Though exposures may be uncommon, the prehospital environment can be unpredictable and providers may unintentionally encounter substances while caring for patients. First responders should be intimately aware of risk for contact with, disturbing, or aerosolizing any powders on patients, their clothing, and surroundings. If such substances are on or near the patient, first responders should at minimum add respiratory precautions such as facemasks to routine PPE, and consider NIOSH recommendations for full PPE. As always, scene safety remains paramount.

Respiratory support

Synthetic opioids overdoses should be treated initially the same as all patients with respiratory failure and/or suspected opioid overdoses with a pulse, primarily with effective Bag-Valve-Mask (BVM) ventilations. Ensuring an open airway, providing respiratory support, and monitoring circulation remain cornerstones of patient care for all levels of EMS providers. Nasal or oral airway adjuncts and oxygen administration to correct hypoxemia should also be used when indicated.  Almost one quarter of synthetic opioid overdose patients described in one hospital based case series required advanced respiratory support for persistent hypoxemia despite high doses of naloxone, and repeat respiratory arrest after cessation of naloxone infusion [14]. While the current focus for lay persons and law enforcement is rapid naloxone administration for suspected opioid overdoses, EMS providers are experts in the “ABCs”. A full patient assessment, high quality basic skills such as use of airway adjuncts, BVM, and respiratory support is imperative.

Naloxone

Naloxone is a high affinity mu-opioid receptor antagonist which acts on the central nervous system. It can be given to suspected opioid overdoses to reverse respiratory depression in the prehospital setting. For routine suspected opioid overdose, there are no definitive studies that have determined the optimal dose of naloxone to administer. Recommendations for initial dose can vary 10-fold based on reference and medical specialty. In general, emergency medicine and anesthesia references suggest higher doses (0.4mg) while medical toxicology and general medicine references suggest lower doses (0.04mg) [28]. The naloxone nasal atomizer devices currently in use by most first responders and bystanders is delivered in either 2mg or 4mg single dose sprays. Intranasal (IN) naloxone has an approximate bioavailability of only 4%, significantly lower than intramuscular (IM) and intravenous (IV) naloxone [29].  One prehospital study found that 2mg IN naloxone was not inferior to 0.4mg IV naloxone at reversing opioid induced apnea or hypopnea [30].

There is some concern that following naloxone administration and reversal of opioid overdose, patients may have adverse events such as pulmonary edema, precipitation of withdrawal symptoms, vomiting, or aspiration pneumonitis. In a one year prospective study in Norway, EMS witnessed vomiting in only 9% of patients who received prehospital naloxone [31]. A retrospective study in Pittsburgh found a lower rate of adverse events following naloxone administration with vomiting in only 0.2% of patients [32]. Novel synthetic opioid overdose cases have demonstrated a variety of adverse events during or after naloxone administration, including pulmonary edema and diffuse alveolar hemorrhage [14, 21], though the exact incidence is not known. EMS and first responders should also be aware of the potential safety risk of unmasking of other drug intoxications (methamphetamine, cocaine, or other stimulants) leading to behavioral disturbances. LEO training in naloxone administration has been generally well received and initial studies also report low rates of adverse events [33-35]. Overall, prehospital naloxone administration for suspected opioid overdose is considered safe, though the impact of synthetic opioids on the safety profile is unknown.

Naloxone administered to patients with synthetic opioid overdoses may require multiple doses. During known fentanyl overdose outbreaks, patients have required up to 14mg of naloxone to reverse respiratory and CNS depression [10, 36, 37]. In the prehospital environment, resources can be limited, and a single responding unit or even an entire region may not regularly stock large quantities of naloxone for single patient use. Naloxone supply can be particularly strained during events such as multiple overdose calls for a single responding unit or a multi-day drug overdose outbreak within a single system or area. In a case series of 18 patients, many of whom required naloxone infusions after exposure to fentanyl-adulterated pills, an entire hospital supply of naloxone was depleted and required emergency delivery to replete supply. 83% of patients who had either witnessed or themselves overdosed in the preceding six months reported that two or more doses of naloxone (most commonly used 2mg IN) were required before any response in suspected fentanyl overdoses [38]. Since novel synthetic opioids may have varied street concentrations, potencies, and receptor affinities, the actual dosage of naloxone that may be required to restore adequate spontaneous respirations may be unpredictable. This further emphasizes the role of respiratory support and transport particularly for patients who do not respond adequately to initial attempts at reversal on scene.

Transport

While some studies have failed to demonstrate increased mortality after opioid overdose reversal in the field [39, 40], those who may have overdosed with known or suspected long acting opioids, synthetic opioids, or those requiring repeated doses of naloxone benefit from transport to the nearest emergency department [8, 14]. The safety of refusal of transport after a suspected synthetic opioid overdose has not been established. If spontaneous respiratory drive has not returned after initial resuscitation attempts, EMS should consider transport rather than staying for extended scene times to administer repeated doses of naloxone. En route patient care should include continued reassessment, monitoring, and ongoing respiratory support with repeated administration of naloxone titrated to return of adequate spontaneous respirations, per local protocols.

Awareness of local patterns, collaboration, and community engagement

Synthetic opioids have the potential to overwhelm available emergency resources and supplies, akin to a mass casualty event. EMS systems may mitigate potential strain on local resources by monitoring local epidemiologic patterns, preparing for outbreaks, and collaborating with local agencies, including call centers, law enforcement agencies, EMS/fire departments and EDs. EMS data is particularly well suited for surveillance of suspected overdose patterns as it is geographically indexed and can be collected in near real time [41, 42]. Initial suspicion and tracking of synthetic opioid patterns can involve local EDs, medical examiners, toxicologists, and law enforcement. By sharing knowledge of local trends, all collaborators can stay abreast of the epidemic.

EMS and other first responders are well positioned for a critical role in intervention and prevention, and can provide a unique perspective for community engagement. On-scene interaction with the patient and/or family provides a potentially impactful opportunity to provide resources and support. EMS systems should consider novel strategies for combating the underlying opioid epidemic, including providing on-scene resources, take home naloxone rescue kits, encouraging any local resource utilization including medication assisted treatment (MAT), role of community paramedicine, and other opioid reduction programs.
 

Additional Resources:

The DEA video with LEO personal accounts of their exposure

Canada's fentanyl safety website

NIOSH recommendations for prehospital PPE

DEA: "Fentanyl, a briefing guide for first responders"

 

Special thanks to Brooke Lerner, PhD and Jill Theobald, MD

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40.   Kolinsky D, Keim SM, Cohn BG, Schwarz ES, Yealy DM. Is a prehospital treat and release protocol for opioid overdose safe? The Journal of Emergency Medicine. 2017;52(1):52-58.

41.   Garza, A and Dyer, S. EMS Data Can Help Stop the Opioid Epidemic. JEMS, Nov 2016. Accessed Feb 25, 2017.

42.   Moore, PQ, Weber J, Cina S, Aks S. Syndrome surveillance of fentanyl-laced heroin outbreaks: Utilization of EMS, Medical Examiner, and Poison Center databases. Am J Emerg Med 2017 May 8

 

 

California’s Quest for Evidence-Based EMS Protocols: Chest Pain

by P. Brian Savino, MD; Melody Glenn, MD; Karl A. Sporer, MD

Paramedics respond the scene of a 65-year-old male complaining of chest pain. EKG is suspicious for STEMI. They give an aspirin and start to administer oxygen, even though the patient’s SpO2 is 97%. Based on their county protocols, medics transport the patient to the nearest STEMI receiving center, bypassing the nearest hospital. The patient receives emergency PCI within 60 minutes.

Meanwhile, another set of paramedics are also responding to a 65-year-old male, also complaining of chest pain. They give nitrates, decide not to perform an EKG, and transport the patient to the nearest hospital. The physician performs an EKG and sees that it is concerning for STEMI.  The patient is then transferred to a STEMI receiving center, but doesn’t receive his PCI until 120 minutes later. 

 

Who is providing better care? Although certain practices are considered commonplace in the prehospital management of chest pain, are they based on evidence? Or is it just dogma?

A team from California sought to find out. They modified the process that the American College of Emergency Physicians (ACEP) uses to create their clinical policies in order to assign levels of evidence and grade the strength of their recommendations. The California team reviewed relevant studies (summarized in an electronic appendix) and assigned LOE based on the study design, including features such as data collection methods, randomization, blinding, outcome measures and generalizability. LOE I consisted of randomized, controlled trials, prospective cohort studies, meta-analysis of randomized trials or prospective studies, or clinical guidelines/comprehensive review. LOE II consisted of nonrandomized trials and retrospective studies. LOE III consisted of case series, case reports, and expert consensus.

SUPPLEMENTAL OXYGEN THERAPY

Case: Paramedics respond the scene of a 65-year-old male complaining of chest pain. EKG is suspicious for STEMI. They start to administer oxygen, even though the patient’s SpO2 is 97%.

Clinical Question: Does giving oxygen to every patient with chest pain, even if they are not hypoxic, improve outcomes?

Summary of Current Evidence: There have been few randomized controlled studies that have attempted to answer this question. A study in 1976 by Rawles et al. randomized patients to oxygen or air and found more deaths in the oxygen group, although not clinically significant [1].  A more recent trial addressing this question was in 2012 by Ranchord et al. showing no difference in mortality between a titrated oxygen group and a high-flow oxygen group, but with a very small sample size [2].  The ILCOR ACS guidelines in 2010 do not find sufficient evidence to support the use of oxygen in suspected ACS, but do not find evidence of harm [3].  A meta-analysis by Cochrane review (updated in 2013) showed no evidence of benefit and, in fact, showed possible harm with routine oxygen administration in suspected ACS, but noted that the analysis lacked the power to substantiate or refute the use of oxygen in these cases [4]. A recent multicenter, prospective, randomized, controlled trial compared prehospital oxygen (8L/min) with no supplemental oxygen in patients with ST segment myocardial infarction (STEMI) and oxygen saturation of 94% or greater [5]. The authors demonstrated that supplemental oxygen in this group increased early myocardial injury and was associated with larger myocardial infarct size and a higher rate of re-infarction. The DETO2X-AMI trial is ongoing and will examine this question among patients with suspected ACS and should be adequately powered to address this question [6].

Conclusion: Routine oxygen administration to patients with chest pain who are not hypoxic does not improve outcomes. In fact, patients who are experiencing a true cardiac event could even be harmed by excess oxygen. Based on the level of evidence, a Level A recommendation can be made against routine oxygen use for chest pain patients who are not hypoxic. However, if a patient is hypoxic or shows sign of shock, oxygen is recommended.

In your system’s chest pain protocol, do you have maximum SpO2 level over which O2 CANNOT be administered? *
Profession

 

NITRATES

Case: Paramedics respond the scene of a 65-year-old male complaining of chest pain. EKG is suspicious for STEMI. They start to administer oxygen, even though the patient’s SpO2 is 97%. They give nitrates and ASA and transport to a STEMI center.

Clinical Question: Does giving nitrates such as sublingual nitroglycerin, topical nitroglycerin or nitroglycerin spray improve outcomes in prehospital patients with chest pain?

Summary of Current Evidence: There have been no trials to specifically evaluate the usefulness of nitrates in the field or in the emergency department (ED) among patients with chest pain of suspected ACS [3].  A reduction in infarct size (using creatinine kinase as a surrogate measure) was noted in those treated within three hours of symptoms in three studies of intensive care unit patients [12-14].  There have been two trials showing that combined treatment with nitroglycerin and fibrinolytics may have a detrimental effect on reperfusion [15,16].  There is currently not enough evidence to suggest clinical benefit or harm of nitroglycerin use in the prehospital setting.

Conclusion: There is not sufficient evidence to either support or refute the use of nitroglycerin in chest pain. A level C recommendation can be given that if nitroglycerin is used, contraindications should include erectile dysfunction medications, hypotension and inferior/right sided infarct.

In your system's chest pain protocol, do you advise administering Nitroglycerin? *
If so, does your protocol include any contraindications to administration? *
Profession

 

ASPIRIN

Case: Paramedics respond the scene of a 65-year-old male complaining of chest pain. EKG is suspicious for STEMI. They give an aspirin and transport to the nearest hospital.

Clinical Question: Does giving Aspirin to patients with chest pain improve outcomes?

Summary of Current evidence: There is high-quality evidence demonstrating benefit of aspirin administration (162.5mg) in improving mortality among patients with an acute myocardial infarction (MI) [3-9]. This reduction in long-term mortality is greatest when the aspirin is administered early [10,11].

Conclusion: Unsurprisingly, a Level A recommendation was given to early aspirin administration in the field. There is extensive literature praising its beneficial effects on morbidity and mortality in ACS. 

In your system’s chest pain protocol, do you require ASA administration? *
If you require ASA administration, are there contraindications for its use?
Profession

 

12-LEAD ECG

Case:  Paramedics respond the scene of a 65-year-old male complaining of chest pain. EKG is suspicious for STEMI, but they don’t have a way to transmit it to the ED.

Clinical Question: Does using prehospital ECG for patients with chest pain increase the ability to recognize patients with STEMI in the field?

Summary of Current Evidence

Several studies have demonstrated that prehospital 12-lead ECGs can improve the recognition of STEMI with reasonable sensitivity and specificity [17-23].  Repeat prehospital or ED 12-lead ECGs may be helpful [18,24].  The timely notification of the STEMI center is helpful in reducing door-to-intervention times [25].  The research on computer-interpreted electrocardiography has been mixed but seems to be generally accurate and had a greater influence on non-expert performance [3,26].  There has been limited research in the effectiveness of transmission of the 12-lead ECG [27].

Summary: The literature clearly supports the use of ECG in the field; a level A recommendation of benefit was assigned. Level B recommendations were added to repeat prehospital 12-lead ECG’s to improve diagnostic accuracy of STEMI and to notify receiving centers of potential STEMI, as this has been shown to potentially decrease door-to-intervention time [4,16,24].

In your system’s chest pain protocol, do you require a prehospital EKG? *
Do you have a way to transmit an EKG to any ED?
Do you have a way to transmit it to all of the STEMI receiving centers?
Profession

 

REGIONALIZATION OF STEMI CARE

Case: Paramedics respond the scene of a 65-year-old male complaining of chest pain. EKG is suspicious for STEMI. They give an aspirin and transport the patient to the nearest STEMI receiving center, bypassing the nearest hospital. The patient receives emergency PCI within 60 minutes.

Clinical Question: Does the development of STEMI regionalization (bypassing basic hospitals to approved STEMI receiving centers) lead to decreased times to cardiac catheterization and improved patient outcomes in patients with STEMI?

Summary of Current Evidence

It has been shown in multiple studies that primary PCI is the ideal method of reperfusion in patients presenting with STEMI [28]. Timely PCI leads to decreased morbidity and mortality in this patient population [29,30].  Current AHA recommendations call for a first medical contact to intervention time of less than 90 minutes and additionally note that the EMS system can play a large role in decreasing not only D2B time, but “total ischemic time,” as well [9,31,32]. The AHA also recognizes that PCI is not always available and in these cases thrombolytics may be required [9].  Regionalization of STEMI care does lead to decreased door-to-intervention times [33,34].  The evidence for improvements in mortality and other clinical outcomes among STEMI patients are less well studied.

Rapid inter-facility transfers of patients with STEMI presenting to a non-PCI hospital can reduce time to treatment. STEMI systems should include an organized inter-facility transfer process that includes inter-hospital agreements and ambulance dispatch protocols designed to minimize transfer time.

Conclusion: A level A recommendation was given in favor of STEMI regionalization, as research shows a benefit in decreasing door-to-intervention times. A level A recommendation was also given to transporting patients to centers capable of cardiac catheterization unless this service is not available within 90 minutes.  Current research has not yet demonstrated improved mortality or morbidity from regionalization.

In your system’s chest pain protocol, do you have designated STEMI centers? *
Do you allow ED bypass in order to go to a STEMI center? *
Profession

The above evidence-based guidelines and explanations were initially published in the following article:

Savino, P. B., Sporer, K. A., Barger, J. A., Brown, J. F., Gilbert, G. H., Koenig, K. L., ... & Salvucci, A. A. (2015). Chest Pain of Suspected Cardiac Origin: Current Evidence-based Recommendations for Prehospital Care. Western Journal of Emergency Medicine, 16(7), 983.

References:

1. Rawles JM, Kenmure AC. Controlled trial of oxygen in uncomplicated myocardial infarction. Br Med J. 1976;1(6018):1121–3. [PMC free article] [PubMed]

2. Ranchord AM, Argyle R, Beynon R, et al. High-concentration versus titrated oxygen therapy in ST-elevation myocardial infarction: a pilot randomized controlled trial. Am Heart J. 2012;163(2):168–75.[PubMed]

3. O’Connor RE, Bossaert L, Arntz HR, et al. Part 9: Acute coronary syndromes: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2010;122:S422–65. [PubMed]

4. Cabello JB, Burls A, Emparanza JI, et al. Oxygen therapy for acute myocardial infarction. Cochrane Database Syst Rev. 2010;(6):CD007160. [PubMed]

5. Stub D, Smith K, Bernard S, et al. Air Versus Oxygen in ST-Segment Elevation Myocardial Infarction. Circulation. 2015 [PubMed]

6. Hofmann R, James SK, Svensson L, et al. Determination of the role of oxygen in suspected acute myocardial infarction trial. Am Heart J. 2014;167:322–8. [PubMed]

7. Bosson N, Gausche-Hill M, Koenig W. Implementation of a titrated oxygen protocol in the out-of-hospital setting. Prehosp Disaster Med. 2014;29:403–8. [PubMed]

8. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet. 1988;2:349–60. [PubMed]

9. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:529–55.[PubMed]

10. Freimark D, Matetzky S, Leor J, et al. Timing of aspirin administration as a determinant of survival of patients with acute myocardial infarction treated with thrombolysis. Am J Cardiol. 2002;89:381–5.[PubMed]

11. Barbash I, Freimark D, Gottlieb S, et al. Outcome of myocardial infarction in patients treated with aspirin is enhanced by pre-hospital administration. Cardiology. 2002;98:141–7. [PubMed]

12. Bussmann WD, Passek D, Seidel W, et al. Reduction of CK and CK-MB indexes of infarct size by intravenous nitroglycerin. Circulation. 1981;63:615–22. [PubMed]

13. Charvat J, Kuruvilla T, al Amad H. Beneficial effect of intravenous nitroglycerin in patients with non-Q myocardial infarction. Cardiology. 1990;35:49–54. [PubMed]

14. Jugdutt BI, Warnica JW. Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location. Circulation. 1988;78:906–19. [PubMed]

15. Ohlin H, Pavlidis N, Ohlin AK. Effect of intravenous nitroglycerin on lipid peroxidation after thrombolytic therapy for acute myocardial infarction. Am J Cardiol. 1998;82:1463–7. [PubMed]

16. Nicolini FA, Ferrini D, Ottani F, et al. Concurrent nitroglycerin therapy impairs tissue-type plasminogen activator-induced thrombolysis in patients with acute myocardial infarction. Am J Cardiol. 1994;74:662–6. [PubMed]

17. Ioannidis JP, Salem D, Chew PW, et al. Accuracy and clinical effect of out-of-hospital electrocardiography in the diagnosis of acute cardiac ischemia: a meta-analysis. Ann Emerg Med. 2001;37:461–70. [PubMed]

18. Kudenchuk PJ, Maynard C, Cobb LA, et al. Utility of the prehospital electrocardiogram in diagnosing acute coronary syndromes: the Myocardial Infarction Triage and Intervention (MITI) Project. J Am Coll Cardiol. 1998;32:17–27. [PubMed]

19. Feldman JA, Brinsfield K, Bernard S, et al. Real-time paramedic compared with blinded physician identification of ST-segment elevation myocardial infarction: results of an observational study. Am J Emerg Med. 2005;23:443–8. [PubMed]

20. Le May MR, Dionne R, Maloney J, et al. Diagnostic performance and potential clinical impact of advanced care paramedic interpretation of ST-segment elevation myocardial infarction in the field. CJEM. 2006;8:401–7. [PubMed]

21. van ‘t Hof AW, Rasoul S, van de Wetering H, et al. Feasibility and benefit of prehospital diagnosis, triage, and therapy by paramedics only in patients who are candidates for primary angioplasty for acute myocardial infarction. Am Heart J. 2006;151:1255.e1–5. [PubMed]

22. Foster DB, Dufendach JH, Barkdoll CM, et al. Prehospital recognition of AMI using independent nurse/paramedic 12-lead ECG evaluation: impact on in-hospital times to thrombolysis in a rural community hospital. Am J Emerg Med. 1994;12:25–31. [PubMed]

23. Millar-Craig MW, Joy AV, Adamowicz M, et al. Reduction in treatment delay by paramedic ECG diagnosis of myocardial infarction with direct CCU admission. Heart. 1997;78:456–61. [PMC free article][PubMed]

24. Verbeek PR, Ryan D, Turner L, et al. Serial prehospital 12-lead electrocardiograms increase identification of ST-segment elevation myocardial infarction. Prehosp Emerg Care. 2012;16:109–14.[PubMed]

25. Bradley EH, Herrin J, Wang Y, et al. Strategies for reducing the door-to-balloon time in acute myocardial infarction. New Eng J Med. 2006;355:2308–20. [PubMed]

26. Kudenchuk PJ, Ho MT, Weaver WD, et al. Accuracy of computer-interpreted electrocardiography in selecting patients for thrombolytic therapy. MITI Project Investigators. J Am Coll Cardiol. 1991;17:1486–91. [PubMed]

27. Dhruva VN, Abdelhadi SI, Anis A, et al. ST-Segment Analysis Using Wireless Technology in Acute Myocardial Infarction (STAT-MI) trial. J Am Coll Cardiol. 2007;50:509–13. [PubMed]

28. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361:13–20.[PubMed]

29. McNamara RL, Wang Y, Herrin J, et al. Effect of door-to-balloon time on mortality in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2006;47:2180–6. [PubMed]

30. Nallamothu BK, Foxx KAA, Kennelly BM. Relationship of treatment delays and mortality in patients undergoing fibrinolysis and primary percutaneous coronary intervention. The Global Registry of Acute Coronary Events. Heart. 2007;93:1552–5. [PMC free article] [PubMed]

31. Armstrong PW, Boden WE. Reperfusion paradox in ST-segment elevation myocardial infarction. Ann Intern Med. 2011;155:389–91. [PubMed]

32. Bates ER, Nallamothu BK. Commentary: the role of percutaneous coronary intervention in ST-segment-elevation myocardial infarction. Circulation. 2008;118:567–73. [PubMed]

33. Langabeer JR, 2nd, Dellifraine J, Fowler R, et al. Emergency medical services as a strategy for improving ST-elevation myocardial infarction system treatment times. J Emerg Med. 2014;46:355–62.[PubMed]

34. Horvath SA, Xu K, Nwanyanwu F, et al. Impact of the prehospital activation strategy in patients with ST-elevation myocardial infarction undergoing primary percutaneous revascularization: a single center community hospital experience. Crit Pathw Cardiol. 2012;11:186–92. [PubMed]

 

 

 

 

 

 

 

Be All End-Tidal: The Expanding Role of Capnography in Prehospital Care

by Adam Rieves, MD (@AdamRieves) and Brandon Bleess, MD (@BBBleess)

EMS MEd Editor: Maia Dorsett (@maiadorsett)

Clinical Scenario: EMS is called to the home of an elderly gentleman with altered mental status.  On arrival, they find an elderly male who is muttering to himself.  Per his daughter, he has had decreased oral intake and confusion over the last day.  His vital signs include a heart rate of 95, blood pressure of 96/40, RR of 32 and an oxygen saturation of 89% on room air.   His finger stick blood sugar is 178.   The paramedics suspect severe sepsis.  Since sepsis is a time-sensitive diagnosis, they wonder whether capnography would be helpful in the care for their patient now and subsequently in the hospital.

Literature Review:  The capnograph represents continuous monitoring of the partial pressure of CO2 in a circuit and has four main phases [1]. The first phase (phase 1) represents the end of a breath; this is dead-space ventilation, meaning air that did not participate in gas exchange is cleared from the airways. Phase 2 is a rapid up-tick in the amount of CO2 measured which represents the first gas that is being sampled from the alveoli, i.e. initial exhalation.  Phase 3 is known as the “alveolar plateau”. It represents the amount of CO2 in all the alveoli, on average. This plateau should have a slightly positive inclination due to the continuous excretion of CO2 into the alveoli becoming progressively smaller and the late emptying alveoli with a low V/Q ratio containing a relatively higher concentration of CO2.  The value displayed on the monitor is equal to the end-tidal CO2 measured at the end of Phase 3. This is when the CO2 concentration reaches a maximum at the end of exhalation and reflects the CO2 concentration of the alveoli emptying last.  The last phase (phase 0) of the waveform represents inhalation.  Given the change in flow and there is minimal CO2 in the ambient air, the level measured by the detector quickly falls to near zero. 

Similar to the role of pulse oximetry in guiding the prehospital provider through both management decisions and differential diagnosis, end-tidal capnography can provide invaluable physiologic information that can be used to enhance prehospital patient care in both intubated and non-intubated patients. .

ETT Placement & Integrity of the Respiratory Circuit

Capnography is the most reliable method to confirm endotracheal tube placement in the pre-hospital setting.  In a 2001 study of 345 intubations, capnography had a sensitivity and specificity of 100% for correct placement.  It was also found to be better than capnometry (qualitative) given that capnometry had a sensitivity of only 88% in cardiac arrest [3]. This was again demonstrated in a 2005 study of 153 patients intubated in the pre-hospital setting; the incidence of unrecognized esophageal intubations was 0% in patients with continuous EtCO2 monitoring versus 23.3% when continuous EtCO2 monitoring was not used [4].  

Beyond initial confirmation of correct placement, capnography provides a continuous assurance of functional tube placement.  After initial placement, loss of the waveform can indicate movement of the tube, possible esophageal placement or circuit disconnection.  EtCO2 monitoring will also recognize dislodgement or apnea immediately compared to several minutes for the pulse oximeter to recognize desaturation.  Given that endotracheal tubes can move upwards of 3 cm with neck extension, patient movement alone can cause tube dislodgement which could go unidentified without continuous EtCO2 monitoring [2].  Therefore, continuous waveform capnography for all patients with an advanced airway can be viewed as standard of care.

Uses in Cardiac Arrest

Because EtCO2 is a surrogate for perfusion, capnography can be used during CPR to monitor the effectiveness of resuscitative efforts.  Continuous EtCO2 during resuscitation is associated with an improved rate of ROSC compared to no reported physiologic monitoring [12].  Furthermore, EtCO2>10 mmHg during CPRis associated with improved rates of patient survival to hospital discharge and survival with favorable neurological outcome [12].  A recent meta-analysis of 20 studies determined the average EtCO2 values of patients with ROSC versus those without.  This study demonstrated that the mean EtCO2 in participants with ROSC was 25.8 ± 9.8 mmHg versus 13.1 ± 8.2 mmHg in those without ROSC. The mean difference in EtCO2 between those patients who achieved ROSC and those that did not was 12.7 mmHg (95% confidence interval: 10.3-15.1), suggesting that the AHA guidelines of a threshold of 10 to 20 mm Hg during resuscitation may need to be higher [13]. 

Moreover, EtCO2 is useful in guiding when resuscitative efforts are unlikely to be successful.  In 1997 Levine et al. found that in patients with CPR duration > 20 minutes, EtCO2 averaged 4.4 ± 2.9 mmHg  (Range 0-10) in non-survivors and 32.8 ± 7.4 mmHg (Range 18-58) in survivors to hospital admission. They also found that a 20-minute EtCO2 value of < 10 mm Hg successfully discriminated between patients who survived to hospital admission and non-survivors.  In fact, the sensitivity, specificity, positive predictive value, and negative predictive value were all 100% [8].  This was duplicated in a pre-hospital study by Kolar et al. in 2008 which found thatafter 20 minutes of advanced life support, EtCO2 averaged 6.9 mmHg in patients who did not achieve ROSC and 32.8 mmHg in those who did.  A 20-minute EtCO2 value of ≤14.3 mmHg successfully discriminated between ROSC and no ROSC with a sensitivity, specificity, positive predictive value, and negative predictive value of 100% [9].  Reflective of this, the current American Heart Association Guidelines state that, “In intubated patients, failure to achieve an ETCO2 of greater than 10 mm Hg by waveform capnography after 20 minutes of CPR may be considered as one component of a multimodal approach to decide when to end resuscitative efforts but should not be used in isolation.” [10,11] 

Metabolic Derangements

DKA

End-tidal capnography has demonstrated great promise for assessment of metabolic derangements.  A 2015 research study evaluated end-tidal CO2 as a screening tool for diabetic ketoacidosis (DKA). [14]  Among patients presenting to the emergency department with a glucose greater than 550 mg/dL, an EtCO2 ≤ 21 mmHg was 100% specific for DKA.   Moreover, an EtCO2 ≥ 35 mmHg allowed DKA to be ruled out with a sensitivity of 100 %. [14]  In 2013, Soleimanpour et al.  demonstrated that EtCO2 values more than 24.5 mmHg could rule out the DKA diagnosis with a sensitivity and specificity of 90% in patients with a glucose greater than 250 mg/dL [15].  A 2002 study evaluated the usefulness of EtCO2 for identifying acidosis in pediatric patients with hyperglycemia.  It demonstrated that EtCO2 is linearly related to HCO3 and is significantly lower in children with DKA.  An EtCO2 cut-point of <29 mmHg demonstrated a sensitivity and specificity of 83% and 100% respectively for DKA while an EtCO2 of ≥36 mmHg effectively ruled out DKA. [16]            

Severe Sepsis

Severe sepsis and septic shock are time-critical diagnoses.  Prehospital activation of a Code Sepsis Alert for patients with severe sepsis has been shown to improve mortality. [17]  Severe sepsis is infection with associated end-organ dysfunction – of which one measure of is lactic acidosis due to anaerobic metabolism in the context of poor end-organ perfusion.   Several prehospital screens have utilized prehospital lactate, but the lack of availability and prohibitive cost of lactate meters have prevented this from being widely available.

Figures. From Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis.&nbsp; American Journal of Emergency Medicine . 2013 Jan; 31(1):64-71.

Figures. From Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. American Journal of Emergency Medicine. 2013 Jan; 31(1):64-71.

EtCO2 monitoring may serve as a useful surrogate for lactate measurement as it can evaluate for the respiratory compensation in response to the metabolic acidosis.  In a 2013 study, Hunter et al. demonstrated that EtCO2 concentration may perform similarly to lactate levels as a predictor for mortality in patients with suspected sepsis [18].  They found an inverse relationship between exhaled EtCO2 levels and serum lactate levels; non-survivors had lower EtCO2 on arrival (26 mmHg) compared to survivors (30 mmHg) [18].

As a follow-up, in 2016 Hunter et al. published a study that evaluated EtCO2 as a component of a prehospital screening tool for sepsis, severe sepsis, or septic shock patients.  If the patient met the following criteria: 1. Suspected infection, 2. Two or more of the SIRS criteria (Temperature not between 36°C and 38°C, respiratory rate > 20, heart rate greater than 90) and 3. EtCO2 < 25 mmHg, the ED was notified of a “Sepsis Alert.” This protocol was 90% sensitive, 58% specific and had a negative predictive value of 93% for severe sepsis.  Among all prehospital variables, low EtCO2 levels were the strongest predictor of sepsis, severe sepsis, and mortality. There were significant associations between prehospital EtCO2 and serum bicarbonate levels, anion gap, and lactate [19].

MCI Triage

Since the terrorist attacks of September 11, 2001, emergency medical services systems have had continued focus in preparation for a terrorism event causing an MCI.  Capnography is a single monitoring modality that can provide assessment of the ABCs in less than 15 seconds. The presence of a normal waveform allows the provider to know that the patient is breathing and the airway is patent.  A normal EtCO2 level (35-45 mm Hg) signifies adequate ventilation and perfusion.   Furthermore, capnography can allow for rapid assessment of common complications of chemical agents including: apnea, upper airway obstruction, laryngospasm, bronchospasm, and respiratory failure. The absence of the capnogram, in association with the presence or absence of chest wall movement, distinguishes apnea from upper airway obstruction and laryngospasm. Response to airway alignment maneuvers (chin lift, jaw thrust) can further distinguish upper airway obstruction from laryngospasm [6].  Given its usefulness in rapid assessment of the ABCs and ability to identify common complications of chemical terrorism, “EMS systems should consider adding capnography to their triage and patient assessment toolbox and emphasize its use during educational programs and MCI drills.”[7]

Limitations

End-tidal CO2 levels do not necessarily correspond to paCO2 levels obtained on an arterial blood gas. In patients that have abnormal lung function, the gradient will widen depending on the severity of the lung disease.  EtCO2 in patients with lung disease, such as an obstructive lung disease, is only useful for trending ventilatory status over time; not as a single number spot check that may or may not correlate with the pCO2 [20,21].

Conclusions

Capnography in EMS has evolved substantially from its origins as a qualitative color change pH indicator to identify successful endotracheal intubation.  What once was a tool just for anesthesia in the Operating Room has become a transformative tool in the pre-hospital setting.  Uses have evolved to include early recognition of respiratory inadequacy and failure, integrity of the ventilator circuit, identification of a dangerous inhalation and triage, adequacy of resuscitation during cardiac arrest including detection of ROSC, prediction of diabetic ketoacidosis and early identification and treatment sepsis.  Given this, capnography has the opportunity to become as indispensable as the cardiac monitor in the pre-hospital management of many conditions.

References

1.     Bhavani-Shankar K, Philip JH. Defining segments and phases of a time capnogram. Anesthesia and Analgesia 2000;(4):973-7

2.     Kim JT, Kim HJ, Ahn W, et al.. Head rotation, flexion, and extension alter endotracheal tube position in adults and children. Can J Anaesth.2009;56(10):751–756.

3.     Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency intubation. Intensive Care Med. 2002;28:701–4.

4.     Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of outof-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med. 2005;45:497–503.

5.     Krauss B. Capnography as a rapid assessment and triage tool for chemical terrorism. Pediatr Emerg Care, 2005; 21:493-497.

6.     Krauss B. Advances in the Use of Capnography for Nonintubated Patients. Israeli Journal of Emergency Medicine. 2008;8:3–15.

7.     Krauss B, Heightman AJ.  15-second triage tool. The use of capnography for the rapid assessment & triage of critically injured patients & victims of chemical terrorism.  JEMS. 2006 Jun;31(6):60-2, 64-6, 68.

8.     Levine RL, Wayne MA, Miller CC.  End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.  N Engl J Med. 1997 Jul 31;337(5):301-6.

9.     Kolar M, Krizmaric M, Klemen P, Grmec S.  Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study.  Crit Care. 2008;12(5):R115. doi: 10.1186/cc7009. Epub 2008 Sep 11.

10.   Hazinski MF, Nolan JP, Aicken R, et al. Part 1: executive summary: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2015;132(16)(suppl 1).

11.  Neumar RW, Shuster M, Callaway CW, et al. Part 1: executive summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132(18)(suppl 2).

12.  Sutton RM, French B, Meaney PA, Topjian AA, Parshuram CS, Edelson DP, Schexnayder S, Abella BS, Merchant RM, Bembea M, Berg RA, Nadkarni VM. Physiologic monitoring of CPR quality during adult cardiac arrest: A propensity-matched cohort study. Resuscitation. 2016 Sep;106:76-82. doi: 10.1016/j.resuscitation.2016.06.018. Epub 2016 Jun 24.

13.  Hartmann SM, Farris RW, Di Gennaro JL, Roberts JS. Systematic Review and Meta-Analysis of End-Tidal Carbon Dioxide Values Associated With Return of Spontaneous Circulation During Cardiopulmonary Resuscitation.  J Intensive Care Med. 2015 Oct;30(7):426-35. doi: 10.1177/0885066614530839. Epub 2014 Apr 22.

14.  Bou Chebl RMadden BBelsky J, Harmouche E, Yessayan L.  Diagnostic value of end tidal capnography in patients with hyperglycemia in the emergency department. BMC Emerg Med. 2016 Jan 29;16:7. doi: 10.1186/s12873-016-0072-7.

15.  Soleimanpour H, Taghizadieh A, Niafar M, Rahmani F, Golzari SE, Esfanjani RM. Predictive value of capnography for suspected diabetic ketoacidosis in the emergency department. West J Emerg Med. 2013;14(6):590–4.

16.  Fearon DM, Steele DW. End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002;9(12):1373–8.

17.  Guerra, W. F., Mayfield, T. R., Meyers, M. S., Clouatre, A. E., & Riccio, J. C. (2013). Early detection and treatment of patients with severe sepsis by prehospital personnel. The Journal of emergency medicine, 44(6), 1116-1125.)

18.  Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. American Journal of Emergency Medicine. 2013 Jan; 31(1):64-71.

19.  Hunter CL, Silvestri S, Ralls R, Stone A, Walker A, Papa L. A prehospital screening tool utilizing end-tidal carbon dioxide predicts sepsis and severe sepsis.  American Journal of Emergency Medicine.  2016 May; 34(5):813-819.

20.  Yamanaka MK, Sue DY. Comparison of arterial-end-tidal Pco2 difference and dead space/tidal volume ratio in respiratory failure. Chest. 1987;92:832-835.

21.  Hardman JG, Aitkenhead AR. Estimating alveolar dead space from the arterial to end-tidal CO2 gradient: a modeling analysis. Anesth Analg. 2003;97:1846-1851.

Additional articles of Interest:

EMS One: 5 Things to Know About Capnography in Cardiac Arrest

Yes or No? Prehospital Endotracheal Intubation For Patients With Traumatic Brain Injury

by Kevin Baumgartner, MD

EMS MEd Editor: Maia Dorsett (@maiadorsett)

Case:  EMS is dispatched to the scene of a Motor Vehicle Accident. They arrive to find a 45 year old male who was riding his bicycle when he was hit by a car traveling at approximately 35 mph.  Eyewitnesses state that the man was thrown from his bicycle and hit his head on the pavement.  On their initial assessment, paramedics find a poorly responsive middle-aged male who will not open eyes spontaneously, makes no verbal response but withdraws to painful stimuli.  He has obvious head trauma with a large hematoma and laceration overlying his parietal scalp.  The patient has rapid and shallow spontaneous respirations and the paramedics need to decide how to best manage his airway during their twenty minute transport to the local trauma center.

Clinical Question:  Do patients with severe traumatic brain injury benefit from prehospital intubation?

Literature Review:

Airway management is a cornerstone of both basic and advanced life support. Paramedics and other EMS providers frequently encounter patients who can no longer protect their own airways (traumatic brain injury, major polytrauma, intoxication and overdose) or who are experiencing impending respiratory failure (exacerbations of congestive heart failure and obstructive lung disease). In-hospital management for these patients typically includes endotracheal intubation (ETI), which provides definitive control of the airway, reduces aspiration risk, and allows for mechanical ventilatory support. Do any of these patients benefit from pre-hospital ETI? Should EMS providers intubate in the field, or should they use airway adjuncts such as bag-valve mask ventilation, supraglottic airway devices, or non-invasive positive pressure ventilation to temporize their patients during rapid transport to the hospital?

As one might expect, the data on this issue are mixed and generally poor in quality. Given the ethical and logistical difficulties involved in designing true randomized controlled trials of field vs. in-hospital ETI, most research has been retrospective and observational.   As Pepe and colleagues point out in their 2015 review, patients who are intubated in the field are almost by definition the sickest patients encountered by EMS providers; as such, any naïve univariate analysis will almost certainly find that prehospital ETI is associated with poor outcomes [1].

Pepe and colleagues also note that success of prehospital ETI (and thus overall patient outcomes) is strongly influenced by the type, intensity, and duration of training that is provided for EMS personnel, as well as the structure of the individual EMS service being studied. This intuitive conclusion was reinforced by a 2015 meta-analysis by Bossers and colleagues, which demonstrated that prehospital ETI by EMS providers with “limited proficiency” was associated with increased mortality (OR 2.33, 95% CI 1.61-3.38), while prehospital ETI by EMS providers with “extended proficiency” was not associated with increased mortality [2].  Given the relative rarity of pre-hospital ETI (“critical procedures” including ETI, cardioversion, and defibrillation were performed during only 2.4% of EMS calls in 2011) and the difficulty of allowing a large pool of EMS providers sufficient access to clinical situations requiring ETI, it can be very challenging to allow EMS personnel to acquire the “extended” skills required for routinely successful ETI [1,3].

Pre-hospital ETI has been studied in specific clinical contexts. Severe traumatic brain injury (TBI) frequently robs patients of the ability to protect their own airway from aspiration and oral secretions.   Furthermore, every effort must be taken to ensure adequate oxygenation as hypoxia in itself can lead to secondary brain injury and worsen patient outcomes. Unfortunately, the literature is ambivalent on the value of pre-hospital ETI in this population; an abundance of studies suggest that pre-hospital ETI does not improve outcomes, and some suggest that it may actually worsen outcomes. One retrospective cohort study, for example, showed that timing of ETI (pre-hospital vs. in ED) had no effect on mortality in TBI patients [4]. As mentioned above, one large meta-analysis showed no influence of pre-hospital ETI on mortality when ETI was performed by experienced providers [2].  A Californian retrospective case-control study showed that patients with severe TBI managed with pre-hospital ETI had higher mortality and worse admission pO2 than patients who underwent only BLS airway interventions [5]. A cohort-matched retrospective study involving over twenty-seven thousand patients demonstrated that pre-hospital ETI was independently associated with higher in-hospital mortality (OR 1.399, 95% CI 1.205-1.624) [6].   In the OPALS study comparing survival before and after the introduction of Advanced Life support, patients with severe TBI has a lower survival rate during the advanced life-support phase (50.9% vs. 60.0%; P = 0.02) [7].  Indeed, a systematic review of 13 studies on prehospital intubation for TBI published in 2008 found the unadjusted ORs for an effect of pre-hospital intubation on in-hospital mortality varied widely, ranging from 0.17 (95% CI: 0.10–0.31) to 2.43 (95% CI: 1.78–3.33) [8].

While the majority of studies on prehospital intubation for TBI are retrospective or observational, a prospective, randomized control trial of prehospital intubation vs transport and intubation in ED for patients with severe TBI was completed in Australia [9].   The trial included 312 patients with a GCS < 9, evidence of head trauma, age ≥15 years and intact airway reflexes.  Patients randomized to undergo prehospital intubation underwent RSI with fentanyl/versed/succinylcholine and subsequent sedation/paralysis with a single dose of pancuronium (0.1 mg/kg), and an intravenous infusion of morphine and midazolam at 5 to 10 mg/h each after confirmation of successful endotracheal tube placement. The primary outcome was neurologic outcome at 6 months post-injury.  Using the extended Glasgow Outcome Scale (eGOS) as this measureable outcome, the study found that the median eGOS for patients who underwent prehospital intubation was 5 (moderate disability), while those who underwent hospital intubation had a median eGOS of 3 (severe disability).  This difference was not significant (p = 0. 28).  There was a significant difference in "good neurologic outcome" (defined as eGOS 5-8) between the two groups (51% prehospital intubation vs. 39% hospital intubation, p = 0.046), but 13 patients were lost to follow-up, the majority of which were in the hospital intubation group.  While this study suggests that there may be a benefit of prehospital intubation for patients with severe brain injury, there are important differences between the study and average prehospital practice.  First, intubation success rate was 97%.  Reports of success rates for prehospital intubation in North America are generally lower, ranging from 83 to 97% [10,11,12].   Second, they had full RSI (sedative and paralytic) as well as post-intubation sedation that would inhibit disadvantageous consequences such as coughing in a severely brain-injured patient. 

Table 3 from: Bernard, S. A., Nguyen, V., Cameron, P., Masci, K., Fitzgerald, M., Cooper, D. J., ... &amp; Patrick, I. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial.  Annals of surgery , 2010; 252(6), 959-965

Table 3 from: Bernard, S. A., Nguyen, V., Cameron, P., Masci, K., Fitzgerald, M., Cooper, D. J., ... & Patrick, I. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial. Annals of surgery, 2010; 252(6), 959-965

Given the available data, it is reasonable to conclude that pre-hospital ETI in patients with TBI does not improve relevant patient-centered outcomes in most prehospital settings. It is unclear why this is true—possible explanations include delay of transport to definitive care (multiple studies demonstrated increased scene times in patients undergoing ETI), greater willingness on the part of EMS personnel to intubate patients who are overall “sicker,” hypoxia during intubation attempts, hyperventilation leading to decreased cerebral perfusion or simply the high success rate of non-invasive ventilation and oxygenation strategies in this patient population [4,7,13].  At least when it comes to ground transport, where invasive airways are less necessary and overall frequency of intubation as a procedure low, BVM or supraglottic devices may be the preferred method of airway management for patients with severe TBI.

References

1. Pepe et al. Prehospital endotracheal intubation: elemental or detrimental? Crit Care. 2015; 19(1): 121

2. Bossers et al. Experience in Prehospital Endotracheal Intubation Significantly Influences Mortality of Patients with Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis. PLoS One. 2015; 10(10): e0141034.

3. Carlson et al. Procedures Performed by Emergency Medical Services in the United States. Prehosp Emerg Care. 2016;20(1):15-21.

4. Lansom et al. The Effect of Prehospital Intubation on Treatment Times in Patients With Suspected Traumatic Brain Injury. Air Med J. 2016 Sep-Oct;35(5):295-300

5. Karamanos et al. Is prehospital endotracheal intubation associated with improved outcomes in isolated severe head injury? A matched cohort analysis. Prehosp Disaster Med. 2014 Feb;29(1):32-6

6. Haltmeier et al. Prehospital intubation for isolated severe blunt traumatic brain injury: worse outcomes and higher mortality. Eur J Trauma Emerg Surg. 2016 Aug 27

7.Stiell IG, Nesbitt LP, Pickett W; OPALS Major Trauma Study Group. Impact of advanced life-support on survival and morbidity. CMAJ. 2008;178:1141– 1152.

8. Von Elm, E., Schoettker, P., Henzi, I., Osterwalder, J., & Walder, B. Pre-hospital tracheal intubation in patients with traumatic brain injury: systematic review of current evidence. British journal of anaesthesia, 2009; 103(3), 371-386.

9. Bernard, S. A., Nguyen, V., Cameron, P., Masci, K., Fitzgerald, M., Cooper, D. J., ... & Patrick, I. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial. Annals of surgery, 2010; 252(6), 959-965.

10. Bernard S, Smith K, Foster S, Hogan P, Patrick I. The use of rapid sequence intubation by ambulance paramedics for patients with severe head injury.  Emerg. Med. 2002; 14: 406–11.

11.Davis DP, Hoyt DB, Ochs M et al. The effect of paramedic rapid sequence intubation on outcome in patients with severe trau- matic brain injury. J. Trauma 2003; 54: 444–53.

12. Wayne MA, Friedland E. Prehospital use of succinylcholine: a 20 year review. Prehosp. Emerg. Care 1999; 3: 107–9.

13.Bernard, S. A. Paramedic intubation of patients with severe head injury: a review of current Australian practice and recommendations for change. Emergency Medicine Australasia,  2006; 18(3), 221-228.

Can Negativity be a Good thing? The Impedance Threshold Device in CPR.

by Zachary Hafez MD & Melissa Kroll MD

expert reviewed by Hawnwan Philip Moy MD (@pecpodcast)

It's a slow Saturday morning and you as the medical director are riding out enjoying the unusually warm 60 degree weather...in February no less!  To celebrate, you decide to visit your favorite coffee shop and get the world's best latte.  Just as you pull in, dispatch suddenly pages out a 58-year-old male in cardiac arrest.  It looks like your coffee is going to have to wait...but don't worry, you'll be receiving your daily dose of adrenaline soon. 

When you arrive 5 minutes later, the first responders and paramedics are already hard at work pit crewing away.  On an initial survey, you notice an odd appearing plastic device with flashing lights.  Having read about them before, you ask your first responder where the Impedance Threshold Device (ITD) came from?  Apparently, one of your Emergency Medical Response Agencies (EMRAs) is trialing ITDs.  "We got a pulse!" exclaims one of your medics.  As everyone breaths a sigh of relief, your fire first responder wipes her brow and asks, "So doc...what do you think of the ITD?"   Before answering, you quickly try to buy some time by helping your crews prepare for transport and scramble to recount the evidence behind ITDs and cardiac arrest...

Background

In 1960 the American Heart Association (AHA) introduced cardiopulmonary resuscitation (CPR) to physicians and thereby becoming the premier educator in CPR training.  Despite multiple advances in ACLS over the last 50 years, only modest improvement in survival rates have been achieved.  In 2011, EMS responded to over 326,000 out-of-hospital cardiac arrests in the United States with a survival to hospital discharge of only 10.6% [1].

The reason for the lack of improvements in survival is multifactorial. Standard CPR is inherently less effective than a beating heart providing less than 25% of normal blood flow to the heart and brain [2]. Furthermore, the resuscitation is often limited by inadequate CPR, namely incomplete chest compression and chest recoil [3, 4, 5].  One of the more recent developments to augment the effect of CPR is the impedance threshold device (ITD).

Physiology of CPR and the Role of the ITD

The goal of CPR is to circulate blood from the heart to the body during chest compression and allow return of blood back to the heart during chest recoil.  There are two predominantly accepted theories that explain how this may occur [6].  The first is the “cardiac pump theory” which is based on the principle that the heart is compressed between the sternum and vertebral column leading to mechanical ejection of the blood from the heart [7].  The second is the “thoracic pump theory” which is based on the principle that the thoracic cavity is a confined space whereby compression of the chest wall leads to an increase in intrathoracic pressure that causes ejection of blood from the heart into the systemic circulation and expiration of air from the lungs [8].  Decompression of the chest wall (i.e. natural chest recoil) leads to a decrease in intrathoracic pressure, resulting in venous return of blood.  However, the hemodynamic gradient of the vacuum is attenuated by passive inspiration of air that occurs with chest recoil.

The ITD is designed to limit this passive inspiration of air during CPR.  It is a disposable, plastic, cylindrical shaped device containing a silicon diaphragm which works as a one-way valve that can be attached to an endotracheal tube, laryngeal mask airway, or bag valve mask in line with the airway circuit.  During chest compression, intrathoracic pressure becomes higher than atmospheric pressure opening the unidirectional valve and air is freely expired from the lung.  During chest recoil, the intrathoracic pressure falls below atmospheric pressure leading to valve closure.  A closed valve prevents air in the airway circuit from re-entering the lungs preserving a negatively pressured intrathoracic cavity.

Creating a negatively pressured intrathoracic cavity, potentially leads to two primary circulatory benefits. First, the vacuum within the chest enhances venous return to the right side of the heart, which leads to increases in preload, systolic blood pressure, circulation, and ultimately priming the heart for the next compression.  Second, use of the ITD reduces intracranial pressures more rapidly and to a greater degree during the decompression phase of CPR by maintaining lower intrathoracic pressures. This provides less resistance to cerebral perfusion during the next compression5. This leads to improved perfusion of the brain.

Literature Review

In 1995, Lurie demonstrated that the use of ITDs with CPR improved coronary perfusion pressures and a decreased in the number of defibrillation during resuscitation of swine models [9].  Even though the study only included 15 animals, it prompted discussion and future studies on the applicability of ITDs in cardiac arrest resuscitations   Later, Mader et al performed a blinded, randomized controlled study with swine models.  This study demonstrated that ITDs improved both coronary perfusion pressure and ventilation as measured by PaCO2, PaO2, and arterial pressures of the chest during standard CPR [10].  However, not all studies showed benefits associated with the use of an ITD.   A study performed by Menegazzi et. al, unfortunately discovered that by adding ITDs to their standard CPR, there was a reduced survival rate of ventricular tachycardia in 36 randomized pigs (33% survival in the pigs that were revived with an ITD compared to 78% in pigs who were revived with standard CPR practices) [11].

Complicating the issue further was the inclusion of active CPR (compression-decompression) compared to standard CPR in subsequent ITD studies.  Active CPR was first researched after a man successfully performed high-quality CPR with a plunger at home during a cardiac arrest.  It is believed that during active CPR, forced recoiling of the chest wall increases the negative pressure in the intrathoracic cavity and, in effect, improving venous blood return.  Thus, adding an ITD to active CPR would further potentiate a negative intrathoracic pressure and increase blood return.  The combination of Active CPR with ITDs was first studied by Shih et. al. by using ITDs in conjunction with a novel adhesive glove device to provide active CPR on swine models.  While the adhesive glove CPR improved flow with active compression-decompression, this study concluded that the addition of an ITD to the adhesive glove CPR had no statistical difference in perfusion compared to the adhesive glove CPR alone [12].  

Despite Shih’s findings, Plaisance continued Shih’s thought process by studying ITD use with active CPR in human resuscitations.   In 2000, Plaisance et al completed a prospective, randomized, blinded trial to compare active CPR to active CPR with the use of ITD [13].  Their use of the sham ITD allowed for blinding of the subjects and became the basis for most future blinded studies.  The primary objective was to elucidate the effect of the ITD on end tidal CO2, diastolic blood pressure, coronary perfusion pressure, and return of spontaneous circulation (ROSC).   Their results not only showed that the usage of an ITD with active CPR improved end tidal CO2 and mean peak arterial pressures, but also 70% higher mean coronary perfusion when compared to the control group.  They further demonstrated a decreased time to ROSC in the patients with the ITD.  Although the utilization of ITDs with active CPR appear to have a benefit based on this study, only 21 patients were included decreasing the strength of this study.   A second study was performed by Plaisance in 2004, but this time the objective looked at 24-hour survival in 400 patients [14].   This study was also a randomized controlled double-blinded prospective trial comparing active CPR with ITD to active CPR alone.   They found a statistically significant increase number of patients surviving to 24 hours when ITD was used (64% in the ITD group compared to 44% when active CPR is used alone; OR 1.67 [1.07-2.6]) compared to the control.

The early successes of the Plaisance trials were echoed by the prospective controlled trial performed by Wolcke et al in 2003.  Wolcke et al performed a prospective controlled trial comparing standard CPR to active CPR with ITD [15].   Their primary end point was 1-hour survival and 24-hour survival. They noted that nearly twice as many witnessed arrest patients survived for 1 hour and 24 hours when active CPR with ITD was used as compared to standard CPR alone (OR 2.4 [1.28-4.62]).  However, a major critique of this study is that the authors compared standard CPR against two different variables, active CPR and ITD use, leading to serious confounding variables.  This limitation is echoed in future studies.  Other critiques include the size of the study (only 200 patients) and the lack of blinding.  

These previous studies were the backbone for the 2005 AHA guidelines recommending the use of ITD in resuscitations, despite the fact no long-term survival benefit had been demonstrated [16].   In an attempt to address this perceived deficiency, a systematic review and meta-analysis was performed by Cabrini et al in 2008.  This analysis looked at 5 studies including 833 patients and found improved ROSC (46% for ITD compared to 36% control, relative risk 1.45 [1.16-1.80]) and early survival (32% in those with ITD use compared to 22% without, RR 2.35[1.30-4.24]) [17].  They did not find a benefit in survival at the longest available follow-up or in favorable neurologic outcome when looking at all survivors.

In an effort to find a difference between long-term survival and overall neurological outcome, a multi-center, randomized-controlled, blinded, prospective study was completed by Aufderheide et al.   Over 1,600 patients from 7 different locations and 46 EMS agencies in the United States were selected with the exception of patients believed to have an arrest from non-cardiac causes [18].   They compared standard CPR to active CPR with ITD and found improvement in survival to hospital discharge with favorable neurological function when active CPR with ITD was used (6% in standard CPR compared to 9% in the active CPR with ITD [OR1.58; 1.07-2.36]).  Additionally, a 1-year survival was improved when active CPR with ITD was used compared to standard CPR alone (9% vs 6%; p=0.03).  A follow up study looking at all patients, from both cardiac and non-cardiac causes, found that while standard CPR and active CPR with ITD had similar rates of ROSC, the active CPR with ITD had a 38% increase survival to discharge with favorable neurological outcome (OR 1.42 [CI 1.04-1.95]) and a 39% relative increase in survival to 1 year.  These studies were widely criticized for using the ITD in active CPR and comparing the results to standard CPR alone.  The benefit of survival could not be attributed to the ITD alone, as active CPR may have been part (or all) of the benefit.  Hmmm...

In response to criticisms, Aufderheide et al. performed the largest randomized, double blinded, prospective study comparing standard CPR with standard CPR with ITD with the objective of assessing survival to hospital discharge with a favorable neurological outcome (modified Rankin score of 3 or less), known as the ROC PRIMED trial [19].  The study included 10 sites across the US and Canada involving 8,718 patients.  Surprisingly, this study showed no difference in survival to hospital discharge with favorable neurological outcome (6.0% in the standard CPR with sham ITD compared to 5.8% in the standard CPR with active ITD).   To further support the findings in the NIH PRIMED trial a subsequent systematic review and meta-analysis was performed that showed no survival benefit [20].  The authors noted significant heterogeneity between studies and that the ROC PRIMED study was by far the largest, significantly weighing results.  However, a sub-analysis looking at the use of ITD in active CPR found potential benefit.  The authors noted an increased likelihood of ROSC (odds ratio=1.19 [1.00-1.40], p=0.045), favorable neurologic outcome (odds ratio=1.60 [1.14-2.25]), and long-term survival (odds ratio=1.52 [1.11-2.08]) in those patients resuscitated with an ITD.  These findings are reflected in the newest AHA guidelines in which it states that “[t]he routine set of ITD as an adjunct during conventional CPR is not recommended. The combination of ITD with active compression decompression CPR may be a reasonable alternative to conventional CPR in settings with available equipment and properly trained personnel [Class III recommendation].” [21]

Despite the newest AHA recommendations, the discussion on the potential benefit of the ITD is far from over.  Yannopoulos et al re-evaluated the data collected in the ROC PRIMED trial to evaluate the quality of CPR performed during the study [22].  They found that of the 8,719 patients in the study, only 1,675 had quality CPR recorded.  Of those who received acceptable CPR, ITD use with standard CPR increased survival to hospital discharge with modified Rankin score equal or less than 3 (7.2% compared to 4.1%; p=0.007).  However, when the quality of CPR was not acceptable, the group receiving standard CPR with the ITD had a worse survival to hospital discharge with good neurological outcome (3.4% compared to 5.8%; p=0.007).

The complex interplay between multiple factors was again supported by the most recent systematic review and meta-analysis performed by Wang et al [23].  This meta-analysis looked at 15 studies to evaluate if either active CPR or ITD showed benefit over standard CPR. They compared active to standard CPR, standard CPR to standard CPR with ITD, and standard CPR to active CPR with ITD.  They found no benefit for ITD or active CPR.  However, in a regression analysis they found the results of their analysis may have been mitigated by the confounding variables of witnessed arrest and response time. When those two factors were adjusted, they found improved ROSC with ITD and active CPR.  The meta-analysis again noted heterogeneity between studies, but stated that the biggest effect on survival was actually witnessed arrest and response times.

Take Home Points

Although initial studies demonstrated great potential for the ITD, the current, more powered studies do not absolutely support the use of the ITD with standard CPR.  The limited benefit of the ITD may be confounded by other factors affecting CPR, such as the depth and rate of chest compressions.  Future studies may show a benefit for the ITD in quality CPR.  There is a potential benefit for the use of the ITD in active CPR, but this benefit is questionable.  It is also difficult to state that any survival benefit is from the ITD and not the active CPR.  What can be said is that early, good chest compressions and CPR does in fact show benefit.  Once an EMS system masters these crucial initial steps, then perhaps devices like the ITD and processes like active CPR can provide a meaningful outcome for your patients.  

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References

1) Mozzaffarian D, Benjamin E, Go A. Heart Disease and Stroke Statistics-2015 Update. Circulation. 2015; 206-209.

2) Andreka P, Frenneaux M. Haemodynamics of cardiac arrest and resuscitation. Curr Opin Crit Care. 2006; 12:198-203.

3) Yannopolous D, Aufderheide T, Abella B, et al. Quality of CPR: An important effect modifier in cardiac arrest clinical outcomes and intervention effectiveness trials. Resuscitation. 2015; 94:106-113,

4) Aufderheide TP, Alexander C, Lick C, et al.  From laboratory science to six emergency medical services systems: New understanding of the physiology of cardiopulmonary resuscitation increases survival rates after cardiac arrest.  Brit Care Med October 2008;36(11)[Suppl.]S397-S404.

5) Schleien S, Berkowitz I, Trastman R, Rogers M. Controversial Issues in Cardiopulmonary Resuscitation. Anesthesiology. 1989; 71:133-149.

6) Jude W. Kouwenhoven W, Ing, Knickerbocker G. Cardiac Arrest. 1961; 178(11): 85-92.

7) Rudikoff M. Maughan L, Effron M, Freund P, Weisfeldt M. Mechanisms of Blood Flow During Cardiopulmonary Resuscitation. Circulation. 1980; 61(2):345-352. doi: 10.1161/01.CIR.61.2.345.

8) Lurie K, Coffeen P, Shultz J, McKnite S, Detloff B, Mulligan K. Improving Active Compression-Decompression Cardiopulmonary Resuscitation with an Inspiratory Impedance Valve. 1995;91:1629-1632. doi:10.1161/01.CIR.91.6.1629

9) Mader T, Kellogg A, Smith J, Decoteau R, et.al. A blinded, randomized controlled evaluation of an impedance threshold device during cardiopulmonary resuscitation in swine. Resuscitation 2008; 77:387-394.

10) Menegazzi JJ, Salcido DD, Menegazzi MT, et al. Effects of an impedance threshold device on hemodynamics and restoration of spontaneous circulation in prolonged porcine ventricular fibrillation. Prehosp Emerg Care. 2007; 11(2):179-85.

11) Shih A, Udassi S, Porvasnik S, et al. Use of Impedance threshold device in conjunction with our novel adhesive gloe device for ACD-CPR does not result in additional chest decompression. Resuscitation. 2013; 84:1433-1438.

12) Plaisance P, Lurie K, Payen D. Inspiratory Impedance During Active Compression-Decompression Cardiopulmonary Resuscitation: A Randomized Evaluation in Patients in Cardiac Arrest. Circulation. 2000; 101;989-994.

13) Plaisance P, Lurie K, Vicaut E et al. Evaluation of an impedance threshold device in patients receiving active compression-decompression cardiopulmonary resuscitation for out of hospital cardiac arrest. Resuscitation. 2004; 61:265-271.

14) Wolcke B, Mauer D, Schoefmann M et al. Comparison of Standard Cardiopulmonary Resuscitation Versus the Combination of Active Compression-Decompression Cardiopulmonary Resuscitation and an Inspiratory Impedance Threshold Device for Out-of-Hospital Cardiac Arrest. Circulation. 2003; 108;2201-2205.

15) AHA guidelines 2005

16) Cabrini L, Beccaria P, Landoni G et al. Impact of impedance threshold devices on cardiopulmonary resuscitation: A systematic review and meta-analysis of randomized controlled studies. Crit Care Med. 2008; 35(5);1625-1632. DOI: 10.1097/CCM.0b013e318170ba80.

17) Aufderheide T, Frascone R, Wayne M, et al. Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitatin with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomized trial. Lancet. 2011; 377:301-311. DOI:10.1016/S01406736(10)62103-4.

18) Aufderheide T, Nichol G, Rea T et al. A Trial of an Impedance Threshold Device in Out-of-Hospital Cardiac Arrest. N Engl J Med 2011; 365:798-806.

19) Biondi G, Abbate A, Landoni G, Zangrillo A, Vincent J, D’Ascenzo F, Frati G. An updated systematic review and meta-analysis on impedance threshold devices in patients undergoing cardiopulmonary resuscitation. Heart, Lung and Vessels. 2014; 6(2): 105-113.

20) AHA 2015 guidelines

21) Yannopolous D, Aufderheide T, Abella B, et al. Quality of CPR: An important effect modifier in cardiac arrest clinical outcomes and intervention effectiveness trials. Resuscitation. 2015; 94:106-113.

22) Wang C, Tsai M, Chang W, et al. Active Compression-Decompression Resuscitation and Impedance Threshold Device for Out-of-Hospital Cardiac Arrest: A Systematic Review and Metaanalysis of Randomized Controlled Trials. Crit Care Med. 2015; 43(4):889-896. DOI: 10.1097/CCM.0000000000000820.

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The New 12-Lead: Prehospital Point of Care Ultrasound

by Brandon Bleess, MD

EMS MEd Editor: Maia Dorsett, MD PhD (@maiadorsett)

Case Scenario #1

image.001.jpeg

EMS is dispatched to scene of a witnessed cardiac arrest.  A 54 yo male was at a family gathering when he suddenly clutched his chest prior to collapsing and becoming unresponsive. First responders arrived within 4 minutes of initial call to find a bystander attempting CPR. On ALS arrival, first responders are performing compressions, have applied a monitor and shocked once for ventricular fibrillation.  Cardio Cerebral Resuscitation (CCR) is continued as patient deteriorates into asystole.  He has continuous CPR performed with a supraglottic airway placed as well as epinephrine given every 3-5 minutes and resuscitation is continued for 20 minutes.  The paramedic performs a cardiac Point of Care Ultrasound (POCUS) and finds the following:

Cardiac Standstill on Point-of-Care Cardiac Ultrasound

Case Scenario #2

EMS is dispatched to a vehicle motor vehicle collision (MVC).  Upon arrival EMS finds significant intrusion into the driver’s side of a vehicle that has been T-Boned by another vehicle.  The fire department is finishing extrication of the patient.  He is responsive to verbal stimuli and follows commands.  He has a heart rate of 122 and blood pressure of 120/56. Given the noise level on scene, the paramedic is unable to auscultate lung sounds in any fields.  The patient complains of abdominal pain and a seat belt sign is noted.  Local protocols state to transport to the closest facility, however the astute paramedic knows that the patient could be better served at a trauma center if surgery is needed.  Noting his vital signs and exam, he knows that intraperitoneal hemorrhage, tension pneumothorax, or pericardial effusion could be the cause of his presentation.  The paramedic performs a eFAST exam and finds the following:

Free Fluid in the Right Upper Quadrant on FAST exam

Normal Lung Slide

POCUS has improved the clinical practice of emergency medicine, begging the question of whether it should be incorporated into prehospital care.   Is POCUS practical for prehospital use?  How may it be used for triage and/or clinical management in the prehospital setting? 

Literature Review:

The use of ultrasound to improve clinical decision-making and management has ventured out of hospitals and into the prehospital realm.  In some clinical scenarios, including cardiac arrest and trauma triage, decreasing “time to ultrasound” may accelerate clinical decisions or lead to more appropriate utilization of healthcare resources. 

POCUS in Prehospital Management of Cardiac Arrest

Recent changes in management of Out-of-Hospital Cardiac Arrest (OHCA) from “load and go” to the “stay and play” method of cardiocerebral resuscitation (CCR) have shifted the burden of termination of resuscitation onto prehospital providers.  Multiple studies have addressed whether Point-of-Care Cardiac ultrasound would be useful in prehospital management of OHCA [1].

For example, a prospective study of 88 patients in cardiac arrest (PEA or asystole) conducted in Germany published in 2010 evaluated the prognostic value of cardiac ultrasound in OHCA.  Among patients with cardiac activity, 34% of patients survived to hospital admission compared to only 6% of those without cardiac activity on initial ultrasound [2].  They did not report survival to hospital discharge or neurologically-intact survival.

Another small prehospital study published in 2012 enrolled 42 patients in cardiac arrest with any rhythm [3].  Among 32 patients with no cardiac activity on initial field echocardiogram, only one survived to hospital admission.   In contrast, 4 of the 10 patients with cardiac activity survived to hospital admission. Only one of forty-two patients survived to hospital discharge (and did so with full neurology recovery).   He had cardiac activity on his prehospital ultrasound.

While these results were interesting, both studies were underpowered to detect the key outcome of neurologically-intact survival without cardiac activity on ultrasound due to the overall low incidence of survival from OHCA.

However, an adequately-powered multi-center Emergency Department study of 993 pre-hospital and ED patients with cardiac arrest in PEA or asystole was recently published [4].  Lack of cardiac activity portended an extremely poor likelihood of survival to hospital discharge (0.6%, neurologic status not reported).  In addition, POCUS was able to identify causes (Pulmonary embolism, cardiac tamponade) of cardiac arrest not amenable to traditional ACLS interventions. 

Given high utilization of resources with prolonged resuscitation and the potential to identify reversible causes of cardiac arrest, these results suggest that cardiac ultrasound may be beneficial in prehospital management of OHCA.

The FAST Exam and Trauma Triage

In emergency department patients with torso trauma, performing a FAST exam decreases time to operative care and the number of CT examinations of the torso [5].  FAST and eFAST (FAST + lung ultrasound) have since become key clinical decision making tools in the triage and management of trauma patients in the ED.  Extrapolating this to the field, could early identification of free fluid on abdominal exam better delineate which patients require one trauma center versus another?  Could lung ultrasound be used to help identify who needs needle decompression versus who does not, thus avoiding unnecessary intervention?

The prehospital FAST exam may allow for more appropriate transport destination decisions by providing valuable information to be obtained[6,7,8].  One prospective, multicenter study carried out in Germany study sought to compare the accuracy of physical exam and prehospital FAST exam to detect hemoperitoneum and to determine whether it changed clinical management [9].  They enrolled 230 patients with blunt trauma.  Among 202 patients who were fully scanned and were not lost to follow-up, 28 patients were found to have hemoperitoneum by ED ultrasound or CT imaging.  26 of these were identified prehospital, leading the authors to conclude that prehospital FAST has a sensitivity of 93 % (95 % CI 76 – 99 %) and specificity of 99 % (95% CI 97 -100 %).   However, as the study excluded patients lost to follow-up or in whom ultrasound was too technically difficult, the sensitivity of prehospital FAST for accurate detection of hemoperitoneum could be falsely inflated.   The study was interesting in that the there were several examples where prehospital detection of abdominal free fluid changed patient management, including minimizing prehospital interventions and alerting the receiving hospital to reduce time to surgical intervention.  As this was not a randomized trial, it was unclear whether this actually changed to the time to surgical intervention, but based on results of ED-based studies it is likely to have done so.

Several systematic reviews have examined the current evidence regarding the potential usefulness of prehospital ultrasound to change diagnosis or treatment of trauma patients  [10,11].  Their overwhelming conclusion?  The evidence is promising, although the quality of evidence very low and more studies are needed.

Practical for prehospital use?

Development of handheld, battery-powered, low-weight US machines has created the possibility of bringing US to the prehospital setting.  In addition, field ultrasound images can be transmitted en route to the emergency department (ED) similar to 12 lead EKGs [12,13,14].

A 2014 survey of medical directors using the NAEMSP mailing list demonstrated that 4.1% of EMS systems were already using ultrasound and that an additional 21.7% of systems were considering the implementation of pre-hospital ultrasound [15].  The vast majority cited equipment costs (89.4%), as well as training costs (73.7%), and challenges related to the training process (53.5%) as the major points of concern of why they the medical directors thought that it could not be implemented in their system. 

As a corollary to this, it is not surprising to see that medical directors would be willing to implement ultrasound into their system if there was decreased cost (69.7%), practice guidelines that included prehospital ultrasound (66.1%), a

nd studies demonstrating improvement in patient morbidity (73%) and mortality (71.8%).

Prehospital POCUS use has been more thoroughly investigated in Europe than in the United States [16,17].  This is somewhat of a confounding issue given that many EMS services and Europe use physicians in the field compared to the paramedic model in the United States.  So, is training paramedics to accurately perform prehospital POCUS feasible?  The current evidence suggests that it is.

Ultrasound education centers on two related but distinct skills:  Image acquisition and Image Interpretation. 

A 2015 study examined the ability of US EMS Providers’ (EMT, Paramedics, and Students) to interpret ultrasound images and identify pericardial effusion, pneumothorax, and cardiac standstill [18].  They were given a pre-test followed by an hour didactic session covering scanning techniques, normal anatomy, and image interpretation of both normal and pathologic videos.  After the didactic they were given an immediate post-test as well as a post-test one week later.

The study found that following a short educational intervention, paramedics could more accurately and confidently identify key ultrasound findings that would affect clinical management.  While this study only looked at image recognition and not image acquisition, it showed that the US EMS providers are able to identify pathologic conditions on ultrasound. 

Several studies have examined educational programs to train paramedics to both acquire and interpret prehospital ultrasound images.

A 2010 study looked at US paramedics and their ability to perform and interpret FAST exams and abdominal aortic (AA) exams [19].  Paramedics from two EMS agencies received a 6 hour training program with ongoing refresher education.  All ultrasound exams were then reviewed by a blinded physician overreader (PO).  A total of 104 patients were evaluated (84 FAST and 20 AA) using ultrasound, of which 76 FAST exams were adequate for evaluation and all 20 AA exams were adequate.  Of that, 6 FAST exams were deemed positive by the paramedics and the PO.  All 20 of the AA exams were deemed negative by the paramedics and the PO.  With these, there was a 100% proportion of agreement between the paramedics and the PO.  The study also looked at the amount of time that it would take paramedics to perform the exams as this could be a possible downside prior to transport.  The mean time for image acquisition for the FAST exam was 156 seconds (2.6 minutes) with the median being 138 seconds (range of 76-357 seconds).

Figure 3,&nbsp; PAUSE study (Ref 20)

Figure 3,  PAUSE study (Ref 20)

A 2013 study looking at the viability of a Prehospital Assessment with Ultrasound for Emergencies (PAUSE) Protocol enrolled 20 firefighter/paramedics that did not have prior ultrasound training.  They underwent a 2 hour didactic session on the use of ultrasound on the lungs and heart to look for pneumothorax, pericardial effusion, and cardiac activity [20]. 

As noted in Figure 3 from the PAUSE study, 18 of the 20 subjects scored an 80% or higher and the mean score was 9.1 overall.

There was one image of cardiac standstill that 6 of the 20 paramedics answered incorrectly.  The authors note that the believed this to be due to the perceived cardiac movements as a result of the ultrasound probe being moved across the patient’s chest.

When evaluating image acquisition, 100% of the images for the evaluation of pneumothorax were noted to be satisfactory.  The Cardiac Ultrasound Structural Assessment Scale (CUSAS) was used to assess for adequate cardiac views for diagnosis [21].   The authors noted that for the purposes of determining cardiac standstill, being able to visualize any myocardium (CUSAS Score 3) should be adequate.  If this is true, there is a 100% success rate in the study.  They also believed that a significant pericardial effusion causing tamponade would likely be seen with CUSAS score of ≥4, as these images offer at least a partial view of the pericardium. Given these assumptions, in this study, 95% of the participants (19/20) were able to quickly acquire images that would likely be useful in assessing for both cardiac activity and a pericardial effusion.  In terms of time, views of the lung were acquired in less than 5 seconds. The views of the heart were acquired in less than 10 seconds for 16 paramedics. One paramedic took approximately 90 seconds, and the other three ranged between 10 and 25 seconds.

Take Home

In the hands of physicians and paramedics, POCUS is a promising technology to direct clinical care and utilization of prehospital resources.  However, the use of prehospital ultrasound must improve patient outcomes for it to become a reality and the standard of care.

 

Credits

Videos courtesy of Washington University in St. Louis Division of Emergency Medicine, Section of Emergency Ultrasound.

References

1.    Kellum MJ, Kennedy KW, Barney R, et al. (2008) Cardiocerebral resuscitation improves neurologically intact survival of patients with out-of-hospital cardiac arrest. Ann Emerg Med;52:244–52.
2.    Breitkreutz, R., Price, S., Steiger, H. V., Seeger, F. H., Ilper, H., Ackermann, H., Walcher, F. (2010). Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: A prospective trial. Resuscitation, 81(11), 1527-1533.
3.    Aichinger, G., Zechner, P. M., Prause, G., Sacherer, F., Wildner, G., Anderson, C. L., Fox, J. C. (2012). Cardiac movement identified on prehospital echocardiography predicts outcome in cardiac arrest patients. Prehospital Emergency Care Prehosp Emerg Care, 16(2), 251-255.
4.    Gaspari, R., Weekes, A., Adhikari, S., Noble, V. E., Nomura, J. T., Theodoro, D., ... & Caffery, T. (2016). Emergency department point-of-care ultrasound in out-of-hospital and in-ED cardiac arrest. Resuscitation, 109, 33-39.
5.    Melniker, L. A., Leibner, E., McKenney, M. G., Lopez, P., Briggs, W. M., & Mancuso, C. A. (2006). Randomized controlled clinical trial of point-of-care, limited ultrasonography for trauma in the emergency department: the first sonography outcomes assessment program trial. Annals of emergency medicine, 48(3), 227-235.
6.    Chaudery, M., Clark, J., Wilson, M. H., Bew, D., Yang, G., & Darzi, A. (2015). Traumatic intra-abdominal hemorrhage control. Journal of Trauma and Acute Care Surgery, 78(1), 153-163.
7.    O'Dochartaigh, D., & Douma, M. (2015). Prehospital ultrasound of the abdomen and thorax changes trauma patient management: A systematic review. Injury, 46(11), 2093-2102.
8.    Ruesseler, M., Kirschning, T., Breitkreutz, R., Marzi, I., & Walcher, F. (2009). Prehospital and emergency department ultrasound in blunt abdominal trauma. Eur J Trauma Emerg Surg European Journal of Trauma and Emergency Surgery, 35(4), 341-346.
9.    Walcher F, Weinlich M, Conrad G, et al. Prehospital ultrasound imaging improves management of abdominal trauma. Br J Surg. 2006; 93:238–42.
10.    Jørgensen, H., Jensen, C. H., & Dirks, J. (2010). Does prehospital ultrasound improve treatment of the trauma patient? A systematic review. European Journal of Emergency Medicine, 17(5), 249-253.
11.    O’Dochartaigh, D., & Douma, M. (2015). Prehospital ultrasound of the abdomen and thorax changes trauma patient management: A systematic review. Injury, 46(11), 2093-2102.
12.    Sibert, K., Ricci, M. A., Caputo, M., Callas, P. W., Rogers, F. B., Charash, W., . . . Kocmoud, C. (2008). The feasibility of using ultrasound and video laryngoscopy in a mobile telemedicine consult. Telemedicine and E-Health, 14(3), 266-272.
13.    Strode, C. A. (2003). Satellite and mobile wireless transmission of focused assessment with sonography in trauma. Academic Emergency Medicine, 10(12), 1411-1414.
14.    Takeuchi, R., Harada, H., Masuda, K., Ota, G., Yokoi, M., Teramura, N., & Saito, T. (2008). Field testing of a remote controlled robotic tele-echo system in an ambulance using broadband mobile communication technology. J Med Syst Journal of Medical Systems, 32(3), 235-242.
15.    Taylor, J., McLaughlin, K., McRae, A., Lang, E., & Anton, A. (2014). Use of prehospital ultrasound in North America: a survey of emergency medical services medical directors. BMC Emergency Medicine, 14, 6
16.    Walcher F, Petrovic T, Heegaard W, et al.(2008) Prehospital ultrasound: perspectives from four countries. In: MAJ, MateerJ, BlaivasM, eds. Emergency Ultrasound. New York, NY: McGraw Hill.
17.    Nelson BP, Chason K. Use of ultrasound by emergency medical services: a review(2008). Int J Emerg Med. 1:253–9.
18.    Bhat SR, Johnson DA, Pierog JE, Zaia BE, Williams SR, Gharahbaghian L. (2015) Prehospital Evaluation of Effusion, Pneumothorax, and Standstill (PEEPS): Point-of-care Ultrasound in Emergency Medical Services. Western Journal of Emergency Medicine. 16(4):503-509.
19.    Heegaard, W., Hildebrandt, D., Spear, D., Chason, K., Nelson, B. and Ho, J. (2010), Prehospital Ultrasound by Paramedics: Results of Field Trial. Academic Emergency Medicine, 17: 624–630.
20.    Chin E, Chan C, Mortazavi R. (2013) A pilot study examining the viability of a Prehospital Assessment with UltraSound for Emergencies (PAUSE) protocol. J Emerg.44:142–149.
21.    Backlund, B., Bonnett, C., Faragher, J., Haukoos, J., and Kendall, J.  (2010) Pilot study to determine the feasibility of training Army National Guard medics to perform focused cardiac ultrasonography. Prehosp Emerg Care. 14: 118–123.

It Takes a Village...: Pediatric Out of Hospital Cardiac Arrest

by Melissa Puffenbarger MD

Expert review/editor Joelle Donofrio DO (@PEMEMS) & Hawnwan Moy MD (@Pecpodcast)

It’s eerily quiet in the Pediatric Emergency Department (ED) and everyone implicitly hopes that the peace will linger for the last hour of your overnight shift.  However, as an experienced Pediatric Emergency Medicine (PEM)/Emergency Medical Services (EMS) physician, you know that's probably not going to happen.  

Within minutes, your staff receives an emergent call from EMS. “We’re inbound with a 6-month-old male in cardiac arrest, compressions in progress, not intubated but being bagged, IO placed, 1 round of epi given, last rhythm check 2 minutes ago was PEA, and ETA 2 minutes.”  You can visibly see the anxiety build in the ED as everyone starts to shakes off their fatigue to get ready for this patient.

On arrival, EMS rushes the tiny patient into the resuscitation room.  As compressions are handed over to the Peds ED staff, the visibly shaken paramedic slowly drifts to the corner of the room looking on in concern.  As the resuscitation continues, you have a brief thought...with all the emphasis on adult prehospital cardiac arrest, what evidence do we have to provide the best care for pediatric out of hospital cardiac arrest (p-OHCA) patient?  

Literature Review:

When you hear about OHCA, the conversation will inevitably mention topics like pit crew CPR, the Cardiac Arrest Registry for Enhanced Survival (CARES) database, and the Resuscitation Outcomes Consortium (ROC). Yet, p-OHCA is often absent in these conversations, not because there is a lack of passion (there are a LOT of eager pediatric EM/EMS researchers out there), but because there are a lot of unanswered clinical questions concerning this topic.  Why is that?  First off, the number of p-OHCA is low. The incidence of p-OHCA is around 8 per 100,000 person-years with a dismal 6% survival to hospital discharge [7].  Additionally, only 13% of EMS runs are for pediatric patients [1].  As a result, not only do our EMS providers receive minimal pediatric clinical experience, but the low incidence makes p-OHCA research more difficult.

Nonetheless, to start to improve outcomes, we have to know where the baseline lies.  In a recent observational study utilizing data from the ROC, Fink et al. attempted to define how p-OHCA survival rates have changed in a 5-year time span from July 1, 2007, to June 30, 2012, by studying 1738 children with OHCA.  Unfortunately, the study showed that mortality rates and neurologic outcomes for pediatric out-of-hospital cardiac arrest have not improved [2]. Annual survival rates for p-OHCA were 6.7-10.2%, compared to a reported increase in survival rate of in-hospital cardiac arrest at 14-43% [2].  This large difference in survival between in-hospital and out-of-hospital arrests is likely related to multiple factors. These factors include time to compressions for an unwitnessed arrest, quality of bystander CPR, and a low frequency of initial shockable rhythms in pediatric patients.  

Although these findings are not a huge surprise, the real interesting data arises when this manuscript compares survival to discharge of the different regions of the ROC study.  For a brief refresher, the ROC is a collaboration of 10 regional sites in the United States and Canada.  Thus, when the authors compared regions to each other, ROSC rates of p-OHCA ranged from 2.5% to 34.7%.  Additionally, survival to discharge rates ranged from 2.6% to 14.7%.  We need to determine why ROSC and survival to discharge varied so widely across regions in order to replicate best practices in p-OHCA.  Fink et al. found that “...the regions with the greatest increases in survival over time exhibited increases in EMS-witnessed OHCA, increased the frequency of bystander CPR, and increased EMS-defibrillation compared to regions that did NOT see increases in survival over time [2].”    

What might be the first step in improving our p-OHCA ROSC and survival to discharge?  One place would be increasing provider knowledge and comfort when taking care of pediatric patients.   When EMS providers were asked to self-identify educational priorities, Paramedics, EMT-Basics, and first responders prioritized pediatric airway management, anxiety when working with children, and general pediatric skills as primary areas for targeted education [3]. Specifically, these providers identified a need for training regarding IV and IO access, when and how to perform an advanced airway, recognizing normal neonatal vital signs, and prevention of hypothermia [3]. Intuitively, targeting education to these areas and providing a foundation for continuously updating EMS skills and pediatric protocols can help bridge these knowledge gaps and perhaps help improve p-OHCA outcomes.  

The scant amount of literature available on p-OHCA supports the self-identified educational needs of our EMS providers. One study assessed pediatric airway management from a large database that included EMS encounters in 40 states and identified that EMS airway management should be a target for continuing skill development [4]. This study showed that endotracheal intubation (ETI) was the most commonly used advanced airway technique among EMS encounters.  There was a significantly lower success rate for out-of-hospital ETI vs. in-hospital (81.1% success rate for out-of-hospital in this series vs. reported 97-99% success rate among PEM physicians), and alarmingly low use of CO2-based placement confirmation [4]. The higher in-hospital success rate likely reflects access to adjunctive airway equipment as well as very different levels of experience with the pediatric airway. One series reported that paramedic students received only 6-10 intubation attempts in the OR during training, and most of these were adults [5]. Pediatric patients in full arrest are unique in that they most commonly have a primary respiratory issue, and focusing on providing adequate ventilation and oxygenation is the key to their resuscitation. While improving the EMS provider’s advanced airway skills may help patients in more extreme situations, the biggest impact will likely be seen in striving for perfection with basic airway management: positioning to open the airway, providing a good seal during BVM, and ventilating at an appropriate rate and volume.  Currently, there is no good data supporting prehospital pediatric intubation.    

In addition to skills in pediatric airway management, EMS CPR quality has also been shown to require improvement. A large prospective observational study demonstrated that prehospital CPR only met AHA guidelines during p-OHCA resuscitations 16% of the time and less than 25% of events met both rate and CPR fraction target [6]. While we know that many, many factors affect p-OHCA survival, this study identifies that consistently performing high-quality CPR is critical. The goals of high-quality CPR are the same for both pediatric and adult patients with a focus on providing adequate depth and rate of compressions, minimizing interruptions to compressions, and providing effective oxygenation and ventilation. Processes that may help maintain high-quality CPR in the field include asking EMS partners to coach, praise and correct each other as needed when performing CPR, periodic skill sessions, and staying up to date on any AHA guideline changes.

Remaining up-to-date on the most recent practice guidelines as well as maintaining proficiency of certain skills should be approached as a team effort. EMS physicians should provide scheduled educational sessions that meet the expressed needs of EMS providers and periodically review how to care for special patient populations such as the arresting child.  EMS providers should continue to improve pre-hospital care in their communities by evaluating themselves and each other, and remain involved in community outreach projects focused on prevention of injuries and improved bystander CPR.  As an example, a bill in California was passed that mandates high schools with a health requirement to graduate to require CPR training [8].  To take this one step further, as part of the San Diego EMS County cardiac arrest task force’s agenda, fire and EMS  are even teaching middle schoolers the art of bystander CPR.  It's actions like these that can really help our sick pediatric patients and EMS providers.  Finally, a culture of open dialogue with direct and timely feedback between ED personnel and EMS providers after transporting a critically ill patient will create an environment where all parties involved help improve the pre-hospital care of the pediatric patient.   

Take Home Points:

Although a rare event, in the case of pediatric out of hospital cardiac arrest, factors that have been shown to increase ROSC and survival to discharge include EMS-witnessed OHCA, increased frequency of bystander CPR, and increased EMS-defibrillation.  Additionally solid CPR mechanics, BASIC airway management, solid CPR education of the youth in our community and consistent, great pediatric education of our EMS providers allows us to provide the best care for the children in our communities.  As the old proverb goes, “It takes a village to raise a child.”  So too does it take a village- from our EMS providers, our community, our pediatric EMS researchers, to our medical directors- to save a child.

 

References

1. Shan, MN. et al. The epidemiology of emergency medical services use by children: an analysis of the National Hospital Ambulatory Medical Care Survey. Prehosp Emerg Care. 2008 Jul;12(3):269-76

2. Fink, E.L., Prince, D.K., et al. Unchanged pediatric out-of-hospital cardiac arrest incidence and survival rates with regional variation in North America. Resuscitation. 2016;107:121-128

3. Hansen, M., Meckler, G., et al. Children’s safety initiative: A national assessment of pediatric educational needs among emergency medical services providers. Prehosp Emerg Care. 2015; 19(2):287-291

4. Hansen, M., Lambert, W., et al.Out-of-hospital pediatric airway management in the United States. Resuscitation. 2016;90:104-110

5. Johnson, B.D., Seitz S.R., et al. Limited opportunities for paramedic student endotracheal intubation training in the operating room. Acad Emerg Med. 2006;13:1051-5

6. Sutton, R., Case, E., et al. A quantitative analysis of out-of-hospital pediatric and adolescent resuscitation quality – A report from the ROC epistry-cardiac arrest. Resuscitation. 2015;93:150-157

7. Atkins DL, Everson-Stewart S, Sears GK, et al.  Epidemiology and outcomes from out-of-hospital cardiac arrest in children: the Resuscitation Outcomes Consortium Epistry-Cardiac Arrest.  Circulation 2009;119:1282-91.  

8.  "Text." Bill Text - AB-1719 Pupil Instruction: Cardiopulmonary Resuscitation. Web. 10 Jan. 2017.

Images from:

1. http://www.ukprogressive.co.uk/wp-content/uploads/2016/12/hospital-emergency-room-1.jpg

2. http://www.christianitytoday.com/images/46719.png

3. http://cosmouk.cdnds.net/15/31/1600x800/landscape-1438173668-cute-success-kid.jpg

4. http://www.thedebutanteball.com/wp-content/uploads/2015/11/117dfdafbd688ea2f7745cb21b742895.1000x998x1.jpg

 

Time to Stop Beating a Dead Horse: Termination of Resuscitation in the Field

by Al Lulla, MD (@al_lulla) and Bridgette Svancarek, MD

Expert/Peer Reviewed by J. Brent Myers, MD, MPH    (@bmyersmd)

You arrive on scene to a cardiac arrest.  Your patient is a 64 yo male found pulseless by his wife when she returned from walking the family dog.  The patient’s initial rhythm was a narrow complex PEA.  Twenty-five minutes and 12 cycles of CPR later the rhythm remains unchanged.  The man’s wife is distraught and tearful.  Your clinical experience tells you that the likelihood of a good outcome is poor.

Termination of resuscitation (TOR) is commonplace in the ED and ICU setting, but there is a role for TOR in the pre-hospital setting as well. When is it appropriate to do so?  What are the risks and benefits of such this decision?

Literature Review

Nontraumatic out of hospital cardiopulmonary arrest (OHCA) is considered to be a catastrophic event that is associated with a poor prognosis. According to a report published by the American Heart Association, it is estimated that there is an annual incidence of 326,000 OHCAs occurring in the United States [1]. Several studies have reported that for the majority of patients, only those who regain pulses in the field may end up surviving to hospital discharge. For patients who do not regain pulses, outcomes are generally poor. Bonnin, et al. reported a 0.6% survival rate in patients who did not achieve return of spontaneous circulation (ROSC) within 25 minutes of paramedic arrival [2]. Another study performed in Japan demonstrated that death was 25.8 times more likely in patients without prehospital ROSC [3]. Despite these dismal statistics, in attempt to maximize chance for survival, patients who have suffered an OHCA are often continuously resuscitated by EMS and transported to the ED.

In 2011, the National Association of EMS Physicians (NAEMSP) released a position statement regarding termination of resuscitation in patients with non-traumatic cardiopulmonary arrest. In the statement, the NAEMSP affirmed the following: 

… As there are patients who will not be successfully resuscitated, an evidence-based methodology to determine those patients with out-of-hospital non traumatic cardiopulmonary arrest that will not result in a favorable outcome would contribute to the public health by conserving valuable health care resources and decreasing the number of emergency vehicles in transit with warning lights and sirens.

In addition to the poor outcomes associated with OHCA, the NAEMSP position statement touches upon several points that favor TOR versus transporting patients [4]:

·      Lights and sirens can be dangerous: According to the National Highway Traffic Safety Administration (NHTSA) Fatality Analysis System, approximately 59.6% of ambulance crashes occur during emergency use. Another study identified 45.9 ambulance crashes per 100,000 patients with lights and sirens versus 27.0 ambulance crashes per 100,000 patients without lights and sirens [5].

·      High quality CPR: Guidelines put forth by the American Heart Association highlight the importance of high quality CPR. There is some evidence to suggest that on scene chest compressions are higher quality in comparison to compressions done en route. Russi, et al. evaluated quality of chest compressions on scene vs transport in 140 patients. The study reported significantly lower quality compressions (i.e. decreased depth) during transport versus on scene. [6]

·      Financial cost and resource depletion: The cost of an unsuccessful resuscitation is significant, especially given scarce EMS resources. In addition, there is a cost to the general public when an EMS crew is out of service transporting a patient. For EMS physicians and providers in the field, it’s important to ask: is continuing resuscitation in the best interest of the patient? 

The points highlighted by the NAEMSP position paper as well as pre-hospital research which confirms poor outcomes for OHCA have served as an impetus for the implementation of TOR criteria in EMS systems. While multiple different sets of criteria have been studied and subsequently validated, by far the most widely accepted and researched were the criteria put forth by the Ontario Prehospital Advanced Life Support (OPALS) group.

From their registry of cardiac arrest patients, the OPALS investigators derived two sets of TOR rules, one for basic life support (BLS) providers and one for advanced life support (ALS) providers. These rules were retrospectively developed based on the goal of identifying all non-survivors. The BLS rule included three criteria of which all need to be fulfilled in order to terminate the resuscitation: unwitnessed by EMS, no AED or shock delivered, and no ROSC. The ALS criteria included the BLS rules and two additional criteria: the arrest had to be unwitnessed by a bystander, and no bystander CPR was performed.

The data from the OPALS cardiac arrest registry showed that patients who fulfill all of the TOR criteria do not have good outcomes. For the BLS TOR protocol, Verbeek et al reported the rule to be 100% sensitive in identifying survivors and had a negative predictive value of 100% in identifying non-survivors in patients with OHCA [7]. These findings were validated in subsequent studies. Sasson, et al. demonstrated in a retrospective cohort study that in 2592 patients who suffered from OHCA and met BLS TOR criteria, only 0.2% survived to hospital discharge (98.7% specificity, CI 97.0-99.6). In the 1192 patients who met ALS TOR criteria, 0 survived to hospital discharge (100% specificity, CI 99.1-100). In essence both rules have close to 100% positive predictive value for predicting death in patients with OHCA [8].

Morrison, et al. had similar findings in their study, which just looked at BLS termination criteria regardless if there were BLS or ALS providers on scene. They found that in 776 patients who fulfilled BLS TOR criteria, only 4 patients (0.5%) survived, with a positive predictive value of 99.5% for predicting death. Of the 4 survivors, 3 were characterized as having good cerebral performance, with 1 patient having severe neurological disability. The study showed that implementation of the BLS TOR criteria would theoretically reduce rate of transport by 62.6%!  How to reconcile this benefit with three neurologically-intact survivors who met BLS TOR criteria was not explicitly addressed. [9]

No matter which way you look at it, the research on pre-hospital TOR is clear: OHCA patients who fulfill BLS or ALS TOR criteria most often do not survive to hospital discharge. Studies consistently show a survival of less than 0.5% if BLS TOR criteria are followed and 0% if ALS criteria are followed. Studies also show transportation rates of 40-60% if BLS criteria are followed and around 80% if ALS criteria are followed.  In spite of this, research suggests that there are barriers to the implementation of TOR criteria by EMS providers. The Termination of Resuscitation Implementation Trial (TORIT) was a multi-center prospective trial that evaluated the implementation of TOR rules in patients with OHCA. The investigators showed that in 953 patients who were BLS TOR eligible, EMS providers correctly applied the rule in 755 patients (79%) and did not apply the rule in 198 patients (21%). All of the 198 patients in whom the rule was not applied (i.e. they were transported to the hospital despite meeting BLS TOR criteria) did not survive. For these patients, providers were surveyed regarding their decision to transport. Family distress was the most commonly cited reason for continuing resuscitation and transporting patients [10]. 

Is there a magic number?

Studies have shown that pre-hospital ROSC is the most important predictor of survival for patients with OHCA. An important question often arises: how long should EMS providers work these patients in the field? The prospective 1993 study by Bonnin, et al. showed that in 1471 patients with OHCA, only 370 patients achieved ROSC on scene. Of these 370 patients, all patients achieved ROSC within 25 minutes of paramedic arrival. Newer research coming out of Wake County EMS has shown that working patients longer may be of benefit. In 2905 adult OHCA patients that were examined retrospectively, 363 survived (12.5%). Of the survivors, 300 patients (83%) were neurologically intact. The investigators found that duration of prehospital resuscitation was less than 40 minutes in 90% of neurologically intact survivors [11]. Other studies have shown neurologically intact survival with duration of resuscitation times ranging between 35 to 60 minutes. This broad range may likely be attributed to variation in EMS practice and available resources (i.e. therapeutic hypothermia) as it pertains to agency specific protocols for OHCA.

And what about traumatic cardiopulmonary arrest?

Prehospital TOR may also play a significant role in patients suffering from traumatic arrest as well. While there are sets of robust decision rules validated for TOR and nontraumatic cardiopulmonary arrest, the research on TOR in traumatic arrest patients is scarce.

In 2012, the NAEMSP in conjunction with the American College of Surgeons Committee on Trauma (ACSCOT) released a joint position statement addressing this issue. Based on a review of the literature, the NAEMSP-ACSCOT paper estimated that survival rates for traumatic cardiopulmonary arrest is approximately 2%. This position paper differentiates between withholding resuscitation in cardiopulmonary arrest and TOR.

The guidelines recommend withholding resuscitation in the following patients with traumatic arrest [12]:

·      Whom death is the predictable outcome

·      Injuries incompatible with life (i.e. decapitation, hemicorporectomy)

·      Blunt or penetrating trauma with evidence of prolonged cardiac arrest (i.e. rigor mortis)

·      Blunt trauma patients who are apneic, pulseless, without organized EKG activity

·      Penetrating trauma patients who are apneic without signs of life (i.e. no spontaneous movement, EKG activity, pupillary response)

 

The paper makes the following comments regarding TOR in traumatic arrest:

·      The primary focus should be evacuation to an appropriate facility for definitive care

·      EMS systems should implement protocols that allow for TOR in cases of traumatic arrest

·      TOR should be considered in patients without signs of life or without ROSC

·      Protocols should be in place that require for a specific interval of CPR (for example, up to 15 minutes prior to termination)

·      TOR protocols should be accompanied by procedures to ensure appropriate management of the deceased patient and support services for family members

·      Physician oversight is a mandatory component of TOR protocols

·      TOR protocols should include locally specific clinical, environmental or population based situations for which the protocol may not be applicable

·      Further research is required to determine optimal duration of CPR before TOR

A criticism of the NAEMSP-ACSCOT guidelines is their degree of detail and likely inability to be implemented in the field. A recent paper published in 2016 from Taiwan looked at a simplified decision rule for TOR in patients with traumatic cardiopulmonary arrest modified from the NAEMSP-ACSCOT guidelines. The simplified decision rule included two criteria: 1) blunt trauma injury AND 2) presence of asystole. The study found that this TOR rule could accurately predict 100% of non-survivors and had the potential to decrease ambulance transports for traumatic cardiopulmonary arrest between 16.4-29.0% [13].

Take home points

·      The majority of patients with nontraumatic OHCA who do not achieve ROSC in the field have a very poor prognosis

·      Identifying patients with OHCA who will most likely have an unfavorable outcome and not benefit from transport with lights and sirens is important with regards to EMS safety and utilization. 

·      The BLS and ALS TOR criteria derived from the OPALS cardiac arrest registry have been validated and are good predictors for which patients can be pronounced dead in the field

·      TOR may have an important role in patients suffering from traumatic arrest, however further research is still needed

·      There is still no widely accepted guidelines in terms of duration of prehospital resuscitation for OHCA, however several studies have shown successful outcomes ranging from 25 to 60 minutes

·      There are still barriers to implementation of TOR criteria which may explain underutilization by EMS agencies.  As family distress is the most commonly cited region for falling out of protocol, additional training of EMS personnel in communication skills, as well as public education will be important to successful implementation.

EMS MEd Editors: Maia Dorsett (@maiadorsett) & Hawnwan P. Moy (@PECpodcast)

References:

1.                Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics--2015 update: a report from the American Heart Association. Circulation. 2015;131(4):e29-322.

2.                Bonnin MJ, Pepe PE, Kimball KT, Clark PS. Distinct criteria for termination of resuscitation in the out-of-hospital setting. JAMA. 1993;270(12):1457-62.

3.                Goto Y, Maeda T, Goto YN. Termination-of-resuscitation rule for emergency department physicians treating out-of-hospital cardiac arrest patients: an observational cohort study. Crit Care. 2013;17(5):R235.

4.               Millin MG, Khandker SR, Malki A. Termination of resuscitation of nontraumatic cardiopulmonary arrest: resource document for the National Association of EMS Physicians position statement. Prehosp Emerg Care. 2011;15(4):547-54.

5.               Saunders CE, Heye CJ. Ambulance collisions in an urban environment. Prehosp Disaster Med. 1994;9(2):118-24.

6.     Russi CS, Myers LA, Kolb LJ, Lohse CM, Hess EP, White RD. A Comparison of Chest Compression Quality Delivered During On-Scene and Ground Transport Cardiopulmonary Resuscitation. West J Emerg Med. 2016;17(5):634-9.

7.                Verbeek PR, Vermeulen MJ, Ali FH, Messenger DW, Summers J, Morrison LJ. Derivation of a termination-of-resuscitation guideline for emergency medical technicians using automated external defibrillators. Acad Emerg Med. 2002;9(7):671-8.

8.                Sasson C, Hegg AJ, Macy M, et al. Prehospital termination of resuscitation in cases of refractory out-of-hospital cardiac arrest. JAMA. 2008;300(12):1432-8.

9.                Morrison LJ, Visentin LM, Kiss A, et al. Validation of a rule for termination of resuscitation in out-of-hospital cardiac arrest. N Engl J Med. 2006;355(5):478-87.

10.            Morrison LJ, Eby D, Veigas PV, et al. Implementation trial of the basic life support termination of resuscitation rule: reducing the transport of futile out-of-hospital cardiac arrests. Resuscitation. 2014;85(4):486-91.

11.          Bachman MW, Williams JG, Myers JB, et al. Duration of prehospital resuscitation for adult out-of-hospital cardiac arrest: Neurologically intact survival approaches overall survival despite extended efforts. Prehosp Emerg Care. 2014;18(1):134–135.

12.          Hopson LR, Hirsh E, Delgado J, et al. Guidelines for withholding or termination of resuscitation in prehospital traumatic cardiopulmonary arrest: a joint position paper from the National Association of EMS Physicians Standards and Clinical Practice Committee and the American College of Surgeons Committee on Trauma. Prehosp Emerg Care. 2003;7(1):141-6.

13.          Chiang WC, Huang YS, Hsu SH, et al. Performance of a simplified termination of resuscitation rule for adult traumatic cardiopulmonary arrest in the prehospital setting. Emerg Med J. 2016;

Prehospital Ketamine: The sweet ain't as sweet without the sour

By: Hawnwan Philip Moy MD @pecpodcast

Expert Reviewed by: Minh Le Cong MD @ketaminh

Case Scenario

It’s an unusually warm Halloween night and you, the medical director, are riding along with the EMS supervisor when you hear Medic 2 urgently request assistance on scene with a “bizarre behavior” patient.  Your supervisor gives you a side long glance and says, “...And we were having such a good night!”  He quickly puts his truck in gear and you both speed off to the scene.

On arrival...you find a large, athletic male patient in his 30s, who is only wearing purple, tattered pants, painted green, screaming, “Hulk Smash!!!” as he proceeds to...well...SMASH EVERYTHING!!!

 

You get a quick report from your exasperated paramedic: “This is a 30 year old male with no past medical history (we think) who took A LOT of...SOMETHING.  We (2 fireman, 2 policeman, and his partner) pinned him down and tried to de-escalate him verbally...but he’s still Hulking out!  What do we do?" 

As the patient turns to you (UH OH!) and you ask yourself...is it time to use our Ketamine protocol?  You remember reading that Ketamine can help sedate these patients...but is Ketamine safe to use in the prehospital environment?  What are its pros and cons?!?!?

Fortunately, with your adrenaline-filled, razor sharp mind is firing on all cylinders... time slows down and you quickly recall the your most up to date research on Ketamine.

Background

Excited Delirium (ExDS) is a syndrome described by the American College of Emergency Physicians (ACEP) as those patients with altered mental status who demonstrate severe agitation with combative and/or assaultive behavior.  Also known as Agitated Delirium, Excited Derlium, or Sudden Death in Custody Syndrome, ExDS is characterized by the following [1, 2]:

  • Hyper-aggressive or Bizarre behavior

  • Lack of Sensitivity to Pain

  • Hyperthermia

  • Diaphoresis

  • Attraction to light or shiny objects

The scariest thing about ExDS is not just the harm it can do to our prehospital providers, but the harm it could cause to the patient himself.  These patients can die with mortality rates of up to 10% with causes that are relatively unknown (click here to see ExDS from the beginning to the death of the patient) [1, 2].  Many prehospital providers are called to utilize a variety of medications (see below) to try to sedate the patient before harm to providers or harm to the patient himself can occur [3]. 

3. Vilke, G. M., Bozeman, W. P., Dawes, D. M., DeMers, G., &amp; Wilson, M. P. (2012). Excited delirium syndrome (ExDS): treatment options and considerations.&nbsp;  Journal of forensic and legal medicine  ,&nbsp;  19  (3), 117-121.

3. Vilke, G. M., Bozeman, W. P., Dawes, D. M., DeMers, G., & Wilson, M. P. (2012). Excited delirium syndrome (ExDS): treatment options and considerations. Journal of forensic and legal medicine19(3), 117-121.

At present, the most popular medications for chemical restraint are Benzodiazepines with Antipsychotics.  Unfortunately, Benzodiazepines have a relatively long onset (18 minutes) as do antipsychotics like Haldol (17 min)[4-7].  These prolonged times place prehospital providers at a higher risk of physical harm.

To attempt to ameliorate this inefficiency, researchers have decided to visit our old friend Ketamine as a potential treatment option.

Literature Review

Ketamine

the good, the bad, and the ugly

In 2014, Scheppke et al. retrospectively studied 52 agitated patients who were given 4mg/kg IM of Ketamine8.  The average time to sedation was 2 minutes (yeah!).

However, 3/52 patients had significant respiratory depression with 2 of those 3 patients requiring intubation in the Emergency Department (ED).  Should we be concerned?  Maybe.  On one hand, intubating is a high risk procedure and should make every medical director a little squeamish.  However,  those three respiratory depressed patients also received IV Midazolam to prevent an emergence reaction.  As a result Scheppke et al. concluded that “Ketamine may be safely and effectively used by trained paramedics following a specific protocol.” A major limitation to this study is that the authors did not evaluate outcomes of these patients in the ED.  However, so far so good for Ketamine in that 1) providers can provide it safetly and 2) it works pretty darn fast.

Earlier this year (2016), Cole et al. performed a prospective study in their urban/suburban midwest community that services approximately 1,000,000 citizens while transporting 70,000 patients a year [9].  To minimize bias from seasonal changes, this service provided 10 mg of Haldol intramuscularly (IM) for severely agitated patients (defined as an altered mental status score of 2 or 3) for the first 3 months of the year.  Subsequently,  the authors changed the sedation medication to Ketamine 5mg/kg IM for the next 6 months.  Afterwards, in the final three months of the year, they switched the sedative medications back to Haldol.  So what did they observe?  A total of 146 patients were treated with a median time for sedation of 5 minutes compared to Haldol’s 17 minutes to sedation.  It appears that time to sedation using Ketamine was much faster in making the scene safe for our providers...but at what cost?!?!

 It turns out that the Ketamine cohort had more side effects with more patients vomiting, more patients suffering laryngospasm (5% compared to 0.3%), and more patients being intubated (an intubation rate of 39% in the Ketamine cohort compared to 4% in the Haldol cohort).  

Now, before we jump to any drastic conclusions about airway compromise, let’s take a little deeper dive into these intubated patients of this study.  First, there was no association with the dosage of Ketamine and intubation rates.  Next, the reasons for intubating these patients were documented as “Not Protecting Airway NOS.”  Cole et al hypothesized that perhaps receiving physicians may be uncomfortable receiving patients in this dissociated state or may have, “misapplied the axiom ‘intubation for a GCS of 8.’”  Certainly, those of us who are Emergency Physicians (EP),  have had drunk patients arrive in the ED with a Glasgow Coma Scale (GCS) less than 8 and let them sleep it off without even a nasal cannula.  Perhaps, when Ketamine is involved, EPs can also take this into account.  However, is it because the EP wasn’t used to dealing with patients in the K-hole or was it truly an airway issue where the EP had to secure a compromised airway?  Honestly, we can’t say for sure, but it is something to think upon when considering this manuscript for Ketamine in your system.

Finally, Olives et al. recently published their findings on the use of Ketamine (5mg/kg IM) for severely agitated patients in the prehospital environment [10].  In this 2 year retrospective study, they studied a total of 135 patients who displayed “...active physical violence to himself/herself or others and usual chemical or physical restraints may not be appropriate or safely used.”  Prehospital providers reported an initial improvement in agitation in 91.8% of ketamine treated agitated patients.  Awesome news! 

So it appears that Ketamine is safe for our providers and easy to provide.  But...wait for it...endotracheal intubation was performed on 85 patients (63%) in which 4 patients (2.96%) were intubated by prehospital providers.  Of note, laryngospasm, hypersalivation, and pulmonary edema were not listed as any complications and there was no difference (p=0.68) in the dosage of ketamine for those intubated (5.25 mg/kg IM) and those not intubated (5.14 mg/kg IM).  :(

Again, before jumping to any conclusions, let’s look at Olives et al’s analysis of those intubated patients.  Among the four patients in whom prehospital intubation was undertaken, one experienced post ketamine vomiting and jaw clenching resulting in intubation and another suffered severe hypoxemia.  Fair enough.  The other two patients were combative, altered on scene, and required both physical and chemical restraints.  After sedation both patients went into cardiac arrest and died.  The medical examiner determined that cause of death was Citalopram and Amphetamine toxicity for one patient and seizure disorder, sub therapeutic dose of valproic acid, hypertension and history of substance abuse for the other patient.  Essentially, Ketamine nor hypoxia was not deemed to be the cause of the patient’s death.  However...did Ketamine exacerbate the situation or help?  Again hard to say.  Now for the other 81 patients intubated in the ED.  Olives et al. found that intubation had a higher association if they were male and presented to the ED overnight.  More interestingly, among the 31 staffed EPs at that facility, two providers accounted for 50.9% (28/55) of overnight encounters, but 65.9% (27/41) of overnight intubations.  The same two providers comprised just 7.5% (6/80) of daytime encounters, but 11.4% (5/44) of all daytime intubations.  So could this be physician practice, resource availability associated with time of day, or staffing that justified intubation?  Again, it is hard to say, but certainly something to consider when looking at these numbers.  Of note, arterial PH of those intubated versus those not intubated were similar (7.33 v. 7.32), lactate was slightly higher in the non intubated group (5.6 v. 7.05), and ethanol levels were similar as well (0.18 g/dL v. 0.19 g/dL).  At least physiologically, intubated versus nonintubated groups appeared to be very similar, suggesting that intubation was more of a clinical decision.  Again this is hard to tell as this is sometimes difficult to articulate in medical charts.   

Bottom Line:

Overall, ExDS is dangerous for both our patients and our providers in the field.  Ketamine is one shield that we can use to help sedate our patients and keep our providers safe.

It has a great treatment profile, especially for prehospital care in that it sedates quickly, can be administered in a safe manner, and has a relatively short duration of action.  However, the sweet ain’t as sweet without the sour. There are those side effects that you have to watch out for...mainly airway issues that are up for debate, but should be considered.  That being said, there is always a risk-benefit assessment in everything we do in medicine. In a prehospital environment, the benefits of Ketamine administration for quick and safe sedation in a truly chaotic, dangerous environment does appear to outweigh the risk to your providers.  More importantly, Ketamine's quick sedation profile protects your patients from themselves and the harms of physical restraint. Thus, if you decide to use Ketamine in your system, ensure that you have adequate safeguards within your protocols to monitor airways (i.e. ETCO2 & paramedic training) as well as assuage receiving facility's discomfort by informing them that Ketamine may be provided in the prehospital environment, careful monitoring of these patients is important, and GCS <8 may not always indicate intubation (i.e. we do not intubate every inebriated patient in the ED).  

Bonus:

For your entertainment, here is a video of when I had to be procedurally sedated with Ketamine and Propfol.  I suffered a nasty open left subtalar ankle dislocation (there are pics, ask me about them via email or at the NAEMSP Conference and I'll show them to you!).  I have no recollection of this at all...but man...what a video! We swear there no editing was done :)!  Enjoy and Happy Holidays!

Screen Shot 2016-12-11 at 2.30.34 PM.png

References:

1. Vilke, G. M., DeBard, M. L., Chan, T. C., Ho, J. D., Dawes, D. M., Hall, C., ... & Bozeman, W. P. (2012). Excited delirium syndrome (ExDS): defining based on a review of the literature. The Journal of emergency medicine, 43(5), 897-905.

2. Vilke, G. M., Payne-James, J., & Karch, S. B. (2012). Excited delirium syndrome (ExDS): redefining an old diagnosis. Journal of forensic and legal medicine, 19(1), 7-11.

3. Vilke, G. M., Bozeman, W. P., Dawes, D. M., DeMers, G., & Wilson, M. P. (2012). Excited delirium syndrome (ExDS): treatment options and considerations. Journal of forensic and legal medicine, 19(3), 117-121.

4.  Nobay F, Simon BC, Levitt MA, Dresden GM.  A prospective, double-blind, randomized trial of midazolam versus haloperidol versus lorazepam in the chemical restraint of violent and severely agitated patients.  Acad Emerg Med.  2004; 11(7):744-749.

5. Spain D, Crilly J, Whyte I, Jenner L, Carr V, Baker A.  Safety and effectiveness of high-dose midazolam for severe behavioral disturbance in an emergency department with suspected psychostimulant-affected patients.  Emerg Med Australas.  2008; 20(2):112-120.

6. Isbister GK, Calver LA, Page CB, Stokes B, Bryant JL, Downes MA.  Randomized controlled trial of intramuscular droperidol versus midazolam for violence and acute behavioral disturbance: the DORM study.  Ann Emerg Med.   2010;56(4):392-401.c1.

7. Takeuchi A, Ahern TI, Henderson SO.  Excited Delirium.  West J Emerg Med.  2011;12(1):77-83.

8.  Scheppke, K. A., Braghiroli, J., Shalaby, M., & Chait, R. (2014). Prehospital use of IM ketamine for sedation of violent and agitated patients. Western Journal of Emergency Medicine, 15(7), 736.

9. Cole, J. B., Moore, J. C., Nystrom, P. C. et al. (2016). A Prospective study of ketamine versus haloperidol for severe prehospital agitation.  Clinical Toxicology, 54(7), 556-562.

10.  Olives, T. D., Nystrom, P. C., Cole, J. B., Dodd, K. W., Ho, J. D. (2016).  Intubation of Profoundly Agitated Patients Treated with Prehospital Ketamine. Prehospital and Disaster Medicine, 31(6), 1-10.  

 

Transporting Stroke Patients in the Era of Endovascular therapy

by Richard T. Benson II, MD, Joseph Grover, MD, Jane Brice, MD, MPH

Clinical Scenario:

EMS is dispatched to a possible stroke patient whose last seen normal time was 1.5 hours prior to dispatch.  The patient lives 15 minutes from a primary stroke center and 45 minutes from a comprehensive stroke center.  The patient has complete hemiparesis on the right, aphasia, with facial droop.  Which facility should the patient be transported to via EMS?

Literature Review:

Stroke is the fifth leading cause of death in the United States and is a major cause of adult disability [1].  About 800,000 people in the United States have a stroke each year; and on average, one American dies from a stroke every 4 minutes [1,2]. Most strokes (85%) are ischemic, meaning an artery that supplies oxygen-rich blood to the brain becomes blocked. There are also hemorrhagic strokes (15%) where an artery in the brain leaks out blood or completely ruptures. An acute stroke represents a neurologic emergency that requires time-dependent treatments to mitigate the insult. Over the past 20 years, EMS has played a vital role in the triage and management of stroke.  In 1995 an article published in the New England Journal of Medicine (NEJM) revolutionized the care of stroke patients when it demonstrated the benefit of tissue plasminogen activator (tPA) in the treatment of acute ischemic stroke [3].  Nationally, this led to the creation of Primary stroke centers – facilities capable of administering systemic tPA. Because of this, many EMS systems created specific destination plans, with the goal of getting possible stroke patients to a Primary stroke center as fast as possible. In addition, stroke scales were developed to aid providers in the early recognition of stroke. Ultimately, providers were able to appropriately triage possible stroke patients, transporting them to capable facilities, and provide pre-notification to those facilities or “Code strokes.” This decreased in-hospital delays and led to quicker dispositions and treatments. Ekundayo et al demonstrated that EMS play a major role in stroke management, transporting the majority of stroke patients (63.7%), as well as, those stroke patients with the higher stroke severity scores [4].  In 2015, almost 20 years after the FDA approved tPA for the management of stroke, the NEJM published five studies which demonstrated the superiority of endovascular treatment for Large Vessel Occlusion (LVO) strokes over the standard treatment of tPA alone. 5-9 It should be noted, that approximately 70% of the patients in the mentioned trials received intravenous (IV) tPA, in addition to endovascular treatment. This led to the creation of Comprehensive stroke centers – facilities capable to administering IV tPA and administering intra-arterial thrombolysis. These studies provide compelling evidence to support transporting LVO stroke patients to a comprehensive stroke center over primary stroke center, if available.  With EMS transporting the majority of stroke patients and those patients with the highest stroke severity scores, this fundamental change in the management of stroke patients with LVOs should have a significant impact on how EMS systems triage and transport stroke patients. 

The greatest difficulty for current EMS systems is differentiating LVO stroke patients from the standard stroke patient in the hopes of getting them to the most appropriate stroke center.  Many EMS systems utilize either the Cincinnati Prehospital Stroke Scale (CPSS) or the Los Angeles Prehospital Stroke Scale (LAPSS) for their stroke recognition.  Multiple studies have been done looking at these scales with the results showing varying sensitivities with relatively low specificities [10-11].  None of these current scales differentiate a LVO from a stroke and therefore could not aid providers in making a decision to bypass a primary stroke center for a comprehensive stroke center.  To address this need newer scales have been developed to aid providers in this regard.  The simplest scale utilizes severe hemiparesis as their sole criteria, and found 26.7% had an LVO that was treated with thrombectomy [12]. Other scales have been developed including the Cincinnati Prehospital Stroke Severity Scale (CPSSS), RACE scale, and the FAST-ED scale which show promising results in differentiating LVO from a standard stroke [13,14,15].  The associated time delays of transferring a patient from one facility to the other would likely prevent patients from receiving endovascular therapy and therefore every effort must be made to accurately triage these patients to the most appropriate facility first [16].

Take Home Points:

Over the past 20 years, the early recognition and treatment of strokes have come a long way, with the help of stroke scales and tPA administration. EMS has always been a key component in effective and timely management of these patients. Emerging evidence demonstrates the superiority of combined systemic IV tPA with endovascular treatment in patients with LVO over systemic tPA alone, challenging EMS systems to develop sensitive screening tools for LVO and updated destination plans.

References

1. Kochanek KD, Xu JQ, Murphy SL, Arias E. Mortality in the United States, 2013. NCHS Data Brief, No. 178. Hyattsville, MD: National Center for Health Statistics, Centers for Disease Control and Prevention, US Dept. of Health and Human Services; 2014.

2. Mozzafarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Circulation. 2015:e29–322.

3. Tissue plasminogen activator for acute ischemic stroke. the national institute of neurological disorders and stroke rt-PA stroke study group. N Engl J Med. 1995;333(24):1581-1587.

4. Ekundayo OJ, Saver JL, Fonarow GC, et al. Patterns of emergency medical services use and its association with timely stroke treatment: Findings from get with the guidelines-stroke. Circ Cardiovasc Qual Outcomes. 2013;6(3):262-269

5. Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372(1):11-20.

6. Campbell BC, Mitchell PJ, Kleinig TJ, et al. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015;372(11):1009-1018.

7. Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med. 2015;372(11):1019-1030.

8. Jovin TG, Chamorro A, Cobo E, et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med. 2015;372(24):2296-2306.

9. Saver JL, Goyal M, Bonafe A, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med. 2015;372(24):2285-2295.

10. Asimos AW, Ward S, Brice JH, Rosamond WD, Goldstein LB, Studnek J. Out-of-hospital stroke screen accuracy in a state with an emergency medical services protocol for routing patients to acute stroke centers. Ann Emerg Med. 2014;64(5):509-515.

11. Oostema JA, Konen J, Chassee T, Nasiri M, Reeves MJ. Clinical predictors of accurate prehospital stroke recognition. Stroke. 2015;46(6):1513-1517.

12. Gupta R, Manuel M, Owada K, et al. Severe hemiparesis as a prehospital tool to triage stroke severity: A pilot study to assess diagnostic accuracy and treatment times. J Neurointerv Surg. 2015.

13. Katz BS, McMullan JT, Sucharew H, Adeoye O, Broderick JP. Design and validation of a prehospital scale to predict stroke severity: Cincinnati prehospital stroke severity scale. Stroke. 2015;46(6):1508-1512.

14. Perez de la Ossa N, Carrera D, Gorchs M, et al. Design and validation of a prehospital stroke scale to predict large arterial occlusion: The rapid arterial occlusion evaluation scale. Stroke. 2014;45(1):87-91.

15. Prabhakaran S, Ward E, John S, et al. Transfer delay is a major factor limiting the use of intra-arterial treatment in acute ischemic stroke. Stroke. 2011;42(6):1626-1630.

16. Lima FO, Silva GS, Furie KL, et al. Field Assessment Stroke Triage for Emergency Destination: A Simple and Accurate Prehospital Scale to Detect Large Vessel Occlusion Strokes. Stroke. 2016 Jun 30

 

EMS MEd Editor: Maia Dorsett

Good Care Starts Early: Pre-Hospital Lung Protective Ventilation

Daniel Kolinsky MD, Nicholas M Mohr, MD MS & Brian M Fuller, MD, MSCI

Case Scenario

‘Not again,’ you think to yourself as you listen to the dispatch report. “Call for inter-hospital transport. The patient is a 58 year-old male with a recent diagnosis of pneumonia, in the ED with acute respiratory failure, and is now intubated. Needs transport to the ICU.” This presentation is all too familiar. You remember transporting a similar patient two hours ago. How could you forget? He was hypoxic in the 80’s from his pneumonia.

On arrival to the ED, you get report from the nurses. During sign out you notice that the patient’s ventilator settings are different, specifically the tidal volume is substantially higher than the previous patient’s. You remember that lung-protective ventilation improves outcome in patients with ARDS. You wonder if the same lung-protective strategy should be used in patients at risk for ARDS?

 

Clinical Question

Does the early use of lung-protective ventilation reduce the incidence of ARDS?

Literature Review

Pre-hospital care of the critically ill and injured patient often requires airway management and subsequent mechanical ventilation. Modern transport ventilators can support critically ill patients across the spectrum of illness severity, and also provide more reliable tidal volume and respiratory rates than manual bag-valve positive pressure ventilation. [1] Furthermore, they also free up the advanced care medic to perform other necessary patient care activities. [2]

Although portable mechanical ventilators have advanced critical care transport capabilities, they are not without risk. Ventilator associated lung injury (VALI) is a general term that refers to how a ventilator can propagate injury in already damaged lungs, or initiate injury in at-risk lungs. [3] Lung-protective ventilation aims to mitigate VALI by reducing the mechanical power applied to the lungs. [4] In patients with established ARDS, lung-protective ventilation with low tidal volume and effective PEEP is standard of care. [5-6] There is also a growing body of evidence from critically ill patients in the ICU and operating room demonstrating that low tidal volume ventilation [6-8 mL/kg predicted ideal body weight (PBW)] is associated with improved outcomes in mechanically ventilated patients without ARDS. [7-12] Although the data are not definitive, the current body of evidence suggests that using lung-protective ventilation strategies can mitigate VALI and prevent progression to ARDS.

Pre-hospital transport and the emergency department (ED) are the common entry points into the hospital for critically ill patients, yet only recently has research been devoted to mechanical ventilation in these arenas. Low tidal volume ventilation initiated in the ED is more likely to be continued in the ICU. [13-14] Additionally, it has been demonstrated that the mechanical ventilation strategy started in the pre-hospital setting is often continued in the ED and in the ICU.15 Together, these studies demonstrate that “ventilator inertia” is real and reinforce the importance of initiating lung protective ventilator strategies from the outset. Unfortunately, compliance with lung protective ventilation strategies in the pre-hospital setting (13%) and ED (range 27.1%-55.7%) leaves much room for improvement. [13-15]

As more studies show that earlier diagnoses with commensurate time-sensitive interventions for the critically ill improves outcomes, pre-hospital personnel will be expected to implement these new standards into practice. [16] Among these interventions, ventilator management is paramount as mechanical ventilation is one of the most common indications for intensive care. [17-18] Providers transporting these patients in the post-intubation period must think about the potential for VALI, as ARDS develops early in the course of critical illness. [12]

Setting the Ventilator

In order to determine the appropriate tidal volume for lung protective ventilation, one needs to know the patient’s gender and height in order to calculate the PBW. PBW can then be derived from a table for low tidal volume ventilation.

Other ventilator parameters to monitor when using lung protective ventilation are positive end-expiratory pressure (PEEP) and the plateau pressure. PEEP can be used to keep diseased alveoli open and limit physiologic shunting thus reducing hypoxemia. Setting the PEEP to 5 cm H2O and titrating PEEP and fraction of inspired oxygen (FiO2) combinations using a PEEP table is a simple way to maintain alveolar recruitment and limit derecruitment injury (i.e. atelectrauma). Targeting oxygen saturations of 88% or greater can limit the dangers of hyperoxia as well.[19] Additionally, maintaining plateau pressures less than 30 cm H2O helps to limit alveolar stretch.

Take Home Points

Acknowledgement that the pre-hospital period is part of the continuum of critical care has led to a focus on implementing best care practices early. In the intubated patient, this includes ventilator management and institution of lung-protective ventilation. Currently, there is a growing body of evidence for using lung-protective ventilation to reduce VALI and to prevent to ARDS. Several large studies testing prophylactic lung protective ventilation are underway. [20-21] Their results will provide further insight into the use of early lung-protective ventilation to improve outcomes.

References

1.     Gervais HW, Eberle B, Konietzke D, Hennes HJ, Dick W, “Comparison of blood gases of ventilated patients during transport”. Critical Care Medicine 1987;15:761-763.

2.     Weiss, Steven J., et al. "Automatic Transport Ventilator Versus Bag Valve In The EMS Setting: A Prospective, Randomized Trial." Southern Medical Journal 98.10 (2005): 970-976.

3.     Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med. 2013 Nov 28;369(22):2126-36.

4.     Gattinoni L, Tonetti T, Cressoni M, Cadringher P, Herrmann P, Moerer O, Protti A, Gotti M, Chiurazzi C, Carlesso E, Chiumello D, Quintel M. Ventilator-related causes of lung injury: the mechanical power. Intensive Care Med. 2016 Oct;42(10):1567-75.

5.     The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000, 342:1301-1308.

6.     Putensen C, Theuerkauf N, Zinserling J, Wrigge H, Pelosi P. Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury. Ann Intern Med. 2009;151:566–76.

7.     Determann RM, Royakkers A, Wolthuis EK, Vlaar AP, Choi G, Paulus F, et al. Ventilation with lower tidal volumes as compared with conventional tidal volumes for patients without acute lung injury: a preventive randomized controlled trial. Crit Care 2010;14:R1.

8.     Mascia L, Pasero D, Slutsky AS, Arguis MJ, Berardino M, Grasso S, Munari M, Boifava S, Cornara G, Della Corte F, Vivaldi N, Malacarne P, Del Gaudio P, Livigni S, Zavala E, Filippini C, Martin EL, Donadio PP, Mastromauro I, Ranieri VM. Effect of a lung protective strategy for organ donors on eligibility and availability of lungs for transplantation: a randomized controlled trial. JAMA. 2010 Dec 15;304(23):2620-7.

9.     Futier E, Constantin JM, Paugam-Burtz C, Pascal J, Eurin M, Neuschwander A, et al. A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. N Engl J Med 2013;369:428–37.

10. Serpa Neto A, Cardoso SO, Manetta JA, et al. Association between use of lung- protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory dis- tress syndrome: a meta-analysis. JAMA. 2012;308(16):1651-1659.

11. Serpa Neto A, Simonis FD, Barbas CS,et al. Association between tidal volume size, duration of ventilation, and sedation needs in patients without acute respi- ratory distress syndrome: an individual patient data meta-analysis. Intensive Care Med. 2014;40(7):950-970.

12. Fuller BM, Mohr NM, Drewry AM, Carpenter CR. Lower tidal volume at initiation of mechanical ventilation may reduce progression to acute respiratory distress syndrome: a systematic review. Crit Care. 2013;17(1):R11.

13. Fuller BM, Mohr NM, Miller CN, Deitchman AR, Levine BJ, Castagno N, Hassebroek EC, Dhedhi A, Scott-Wittenborn N, Grace E, Lehew C, Kollef MH. Mechanical Ventilation and ARDS in the ED: A Multicenter, Observational, Prospective, Cross-sectional Study. Chest. 2015 Aug;148(2):365-74.

14. Fuller BM, Mohr NM, Dettmer M, Kennedy S, Cullison K, Bavolek R, Rathert N, McCammon C. Mechanical ventilation and acute lung injury in emergency department patients with severe sepsis and septic shock: an observational study. Acad Emerg Med. 2013 Jul;20(7):659-69.

15. Stoltze AJ, Wong TS, Harland KK, Ahmed A, Fuller BM, Mohr NM. Prehospital tidal volume influences hospital tidal volume: A cohort study.J Crit Care. 2015 Jun;30(3):495-501.

16. Seymour CW, Rea TD, Kahn JM, Walkey AJ, Yealy DM, Angus DC. Severe sepsis in pre-hospital emergency care: analysis of incidence, care, and outcome. Am J Respir Crit Care Med 2012;186:1264–71.

17. Esteban A, Anzueto A, Frutos F, et al; Mechanical Ventilation International Study Group. Characteristics and outcomes in adult patients receiving mechanical ventilation: a 28-day interna- tional study. JAMA. 2002;287(3):345-355.

18. Needham DM, Bronskill SE, Calinawan JR, Sibbald WJ, Pronovost PJ, Laupacis A. Projected incidence of mechanical ventilation in Ontario to 2026: preparing for the aging baby boomers. Crit Care Med. 2005;33(3):574-579.

19. Girardis M, Busani S, Damiani E, Donati A, Rinaldi L, Marudi A, Morelli A, Antonelli M, Singer M. Effect of Conservative vs Conventional Oxygen Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA. 2016 Oct 5.

20. Fuller BM, Ferguson I, Mohr NM, Stephens RJ, Briscoe CC, Kolomiets AA, Hotchkiss RS, Kollef MH. Lung-protective ventilation initiated in the emergency department (LOV-ED): a study protocol for a quasi-experimental, before-after trial aimed at reducing pulmonary complications. BMJ Open. 2016 Apr 11;6(4):e010991.

21. Simonis FD, Binnekade JM, Braber A, Gelissen HP, Heidt J, Horn J, Innemee G, de Jonge E, Juffermans NP, Spronk PE, Steuten LM, Tuinman PR, Vriends M, de Vreede G, de Wilde RB, Serpa Neto A, Gama de Abreu M, Pelosi P, Schultz MJ. PReVENT--protective ventilation in patients without ARDS at start of ventilation: study protocol for a randomized controlled trial. Trials. 2015 May 24;16:226.