EMTALA and Patient Transfers

Expert Commentary

While EMTALA was first enacted to address issues with “patient dumping”, it has had broad influence on how patients are treated, dispositioned, and transferred in emergency department and hospital settings. In addition, EMTALA law has taken on almost mythic proportions among healthcare workers and administrators, likely due to high-profile cases, the fear of potential violation of the law and subsequent penalties, the potential for it to bolster civil malpractice claims, misunderstanding of it by healthcare personnel, and variability in interpretation by regulatory bodies.

Emergency physicians are often called upon to make decisions as the default expert in EMTALA for patients presenting for emergency care or in fielding hospital transfer calls. Unfortunately, on-call specialty physicians involved in the acceptance of transfers, and even hospital transfer centers, may not have a good understanding of the statue. As such, emergency physicians who are not versed in EMTALA can put both the hospital and themselves at risk.

The infographic by Dr. Tandlich gives an excellent summary of EMTALA. In addition, it is imperative that hospitals and emergency departments establish clear processes and appropriate documentation for EMTALA-related situations. More specifically, important concepts to consider include:

When conducting a medical screening exam (MSE), approach it as a process with consistent implementation for all patients and understand this often includes more than just a physical exam
When accepting transfers from outside hospitals, do not solely rely on on-call physicians to make the decisions
When transferring patients to outside hospitals, make clear the reasoning, the patient status, and the risks and benefits

It behooves emergency physicians, emergency department staff, and transfer centers to understand the basic concepts around EMTALA. Overall, the best advice is to do that which is in the best interest of the patient, as this will usually lead to the right decision.

Michael Schmidt, MD

Chief of Staff

Department of Emergency Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Tandlich, M. Feiger, D. (2022, Oct 31). EMTALA. [NUEM Blog. Expert Commentary by Schmidt, M]. Retrieved from http://www.nuemblog.com/blog/emtala-transfers

Health Insurance Basics

**Written by:** Evelyn Huang, MD (NUEM ‘24) **Edited by:** Vytas Karalius, MD, MPH (NUEM ‘22)
**Expert Commentary by**: Cedric Dark, MD, MPH

Health Insurance: The Basics Every Doctor Should Know

A Brief History of Insurance in the U.S.

In 1929, teachers in Dallas contracted with Baylor University Hospital to have monthly payments in exchange for up to 21 days of inpatient care a year. By 1937, there were 26 similar plans that all combined to form the Blue Cross network. In the 1930s, physicians also formed a network of insurance plans known as Blue Shield [1].
During World War II, wage controls prevented employers from raising salaries. As a result, they started to offer health insurance. The IRS added that employers and employees did not have to include these costs in their taxable income [1].
In 1944, President Franklin Roosevelt called for an “Economic Bill of Rights” that included the right to medical care that was never passed. President Truman proposed national health insurance for all Americans that was unpopular due to anti-communist sentiment [1, 2].
In 1965, Medicare and Medicaid were created. In 1972, Medicare was extended for people under 65 who had long-term disabilities and/or end-stage renal disease [2].
In 2010, the Patient Protection and Affordable Care Act (ACA) was passed [2].

Medicare Basics

As of 2019, Medicare covers approximately 61.4 million people [4]. Medicare is federally-run and has four parts:

Part A: inpatient services, nursing care, home health
Part B: outpatient services, ED visits
Part C: “Medicare Advantage,” enrolling in Medicare benefits through private insurers
Part D: prescription medications

Medicaid Basics

As of 2019, Medicaid covers approximately 75.8 million people and includes low-income adults, pregnant, and children [4]. Medicaid is unique from Medicare in that it is state-run with set federal regulations. The Affordable Care Act expanded eligibility to households with income up to 138% of the federal poverty level [2]. To date, 39 states including DC have adopted this expansion and 12 states have not, as seen in the map below [5].

Medicaid also includes the Children’s Health Insurance Program (CHIP) for children living in households that are under 200% of the federal poverty level and is state-run [2]. As of 2019, CHIP covers approximately 7.2 million children [4].

Patients that come to the emergency room are also able to apply for emergency Medicaid if they are currently uninsured. The details of this vary from state to state.

The Affordable Care Act

Signed into law 2010, the Patient Protection and Affordable Care Act had three main goals: expanding healthcare coverage, decreasing health care costs, and improving health care delivery.

Expanding healthcare coverage
- Medicaid expansion
- Individual mandate (discussed in “Private Insurance Basics”)
- Requirements for employers to offer health insurance plans
- Dependent coverage for children up to age 26
- Removed insurance exclusions for patients with pre-existing conditions
Decreasing health care costs
- Tax credits for small business employers that purchase health insurance for employees
- Creation of health insurance exchanges
- Insurance market rules, such as limiting deductibles and prohibiting lifetime limits of coverage
- Discounts for prescription drugs for patients covered by Medicare
Improving health care delivery
- National quality improvement strategies
- Required health plans to cover preventative services
- Bonus payments for primary care physicians
- Grants for wellness programs
- Required chain restaurants to disclose nutritional content

For more information on the ACA, visit this website.

Private Insurance Basics

The ACA enacted an individual mandate, which required Americans to have health insurance or face a tax fee. However, the individual mandate penalty was repealed starting in 2019. Private insurance can be purchased individually, through an exchange/marketplace (third-party markets created by the ACA) or is provided by employers [2].

The ACA also set up 10 essential health services that must be covered with insurance plans. This includes hospitalizations, ambulatory services, lab tests, prescriptions, and emergency services [7].

There are different types of private health insurances, and it is important to have a basic knowledge of this when caring for your patients [9]:

HMO (Health Maintenance Organization): you choose a primary care physician (PCP) that is in-network, you will need a PCP referral for any specialists, no out-of-network care is covered
PPO (Preferred Provider Organization): you can choose in-network providers (typically lower cost) or out-of-network providers, no referral needed for specialists
EPO (Exclusive Provider Organization): does not cover out-of-network providers, but do not need a referral for specialists
POS (Point of Service): you have a PCP that is in-network and that must give you a referral to see a specialist, but you can also access out-of-network options for a higher cost
Catastrophic plan: only available for people under 30 or with a hardship exemption (affordability exemption), low premium and high deductible, theoretically only used for serious illness

Insurance plans on the marketplace also have different metal tiers to their plans. As you go up in tiers, the insurance company pays more when you get healthcare, with a higher associated monthly premium. If someone utilizes a lot of health care, a higher tier choice is better [8].

Bronze: lowest premium, higher cost that you must pay when obtaining care, high deductible
Silver: moderate premium, moderate cost when obtaining care
Gold: high premium, low cost when obtaining care, low deductible
Platinum: highest premium, lowest cost when obtaining care, low deductible

Insurance Definitions You Should Know

Premium: monthly payment to insurance company regardless of whether you use the insurance
Deductible: how much you pay for health services before insurance starts to pay
- Plans with lower premiums typically have higher deductibles
- Usually, you will still need to pay copays and coinsurance if you reach your deductible until you meet your out-of-pocket maximum
Out-of-pocket maximum: after this level, insurance will pay for 100%
- Includes deductible, copay, and coinsurance
- The ACA established that policies must include an out-of-pocket maximum
  - For 2020: $8,150 for an individual and $16,300 for a family [9]
Copay(ment): fixed payment for specific service or medication
- E.g. You pay $20 every time you see your PCP
Coinsurance: Percentage of cost that you pay before the out-of-pocket maximum
- E.g. You pay 20% every time you see your PCP

Part of medical care is knowing that there is an associated cost with every test and treatment that we use. Medical insurance is essential to this, and it is important to know the basic ideas and language surrounding insurance, so that we can better serve our patients.

References

1. Moseley III GB. The U.S. Health Care Non-System, 1908-2008. AMA Journal of Ethics. 2008;10(5):324-331.

2. Schlicher N, Haddock A. Emergency Medicine Advocacy Handbook. 5th ed. Irving: Emergency Medicine Residents’ Association; 2019:1-8.

3. What's Medicare?. Medicare.gov. https://www.medicare.gov/what-medicare-covers/your-medicare-coverage-choices/whats-medicare. Accessed August 18, 2020.

4. CMS Fast Facts. Cms.gov. https://www.cms.gov/Research-Statistics-Data-and-Systems/Statistics-Trends-and-Reports/CMS-Fast-Facts. Published 2020. Accessed August 18, 2020.

5. Status of State Medicaid Expansion Decisions: Interactive Map. KFF. https://www.kff.org/medicaid/issue-brief/status-of-state-medicaid-expansion-decisions-interactive-map/. Published 2020. Accessed August 18, 2020.

6. Summary of the Affordable Care Act. KFF. https://www.kff.org/health-reform/fact-sheet/summary-of-the-affordable-care-act/. Published 2013. Accessed November 10, 2020.

7. Norris L. Obamacare's essential health benefits. healthinsurance.org. https://www.healthinsurance.org/obamacare/essential-health-benefits/. Published 2020. Accessed August 18, 2020.

8. The 'metal' categories: Bronze, Silver, Gold & Platinum. HealthCare.gov. https://www.healthcare.gov/choose-a-plan/plans-categories/. Published 2020. Accessed September 8, 2020.

9. Lalley C. Health insurance basics: The 101 guide to health insurance. Policygenius.com. https://www.policygenius.com/health-insurance/learn/health-insurance-basics-and-guide/. Published 2020. Accessed August 18, 2020.

10. Out-of-pocket maximum/limit. HealthCare.gov. https://www.healthcare.gov/glossary/out-of-pocket-maximum-limit/. Published 2020. Accessed August 18, 2020.

Expert Commentary

Every year, I instruct our medical students and residents on the “Anatomy & Physiology of the United States Health Care System” using a historical journey from the first Blue Cross plan in Dallas crafted for schoolteachers until the modern era of the Affordable Care Act. Along the way, we have added in a piecemeal fashion to our nation’s health care system such that seniors and low-income Americans have coverage carved out for them. Everyone else is reliant upon employer insurance for coverage or must purchase for themselves. Because of our country’s surprisingly involvement in financing health care for its citizens – over 36 percent is paid by the federal government – some commentators have declared the U.S. is an “insurance company with an army.”

While national health expenditures and financing our system are big picture items everyone in the health care sector should understand, we must also understand the small details that are most relevant to patients, such as common terminology regarding their insurance types and the payments they are required to pay at the point of service.

Cedric Dark, MD, MPH

Assistant Professor

Department of Emergency Medicine

Baylor College of Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Huang, E. Karalius, V. (2022, Oct 10). Health Insurance Basics. [NUEM Blog. Expert Commentary by Dark, C]. Retrieved from http://www.nuemblog.com/blog/health-insurance-basics

Debriefing in the ED

**Written by:** Diana Halloran (NUEM ‘24) & Andrew Long (NUEM ‘25) **Edited by:** Nick Wleklinski (NUEM ‘22)
**Expert Commentary by**: John Bailitz, MD

Introduction

The Emergency Department is a challenging work environment for a variety of reasons. It is not surprising that unpredictable work hours mixed with frequent interactions with patients undergoing physical and emotional trauma can cause spillover into the personal lives of ED staff. However, in the recent years there has been an increasing body of literature that highlights the challenges that we face as ED personnel.

The American Heart Association even recommends a “hot” debrief for every cardiac arrest attended by a healthcare professional. We know debriefing has concrete and tangible advantages. Previous studies have shown that debriefing immediately after an event can improve individual and team performance by 20-25%, issues can be identified for interventions, and mental health and emotional trauma can be addressed. It is well-documented that ED physicians have historically high rates of burnout compared to other specialties as well as a high incidence of post-traumatic stress disorder (PTSD) compared to the general population. PTSD is 2 times more prevalent in physicians (14.8%), with EM resident physicians falling in the range from 11.9%-21.5%.

As a field, we are now starting to design and implement interventions to preserve our own mental wellbeing. In fact, debriefing has been shown to be one method for managing PTSD. One article described an initiative that implemented an immediate (also known as “hot”) debrief protocol immediately following all cardiac arrests during which 90% of participants felt they benefited psychologically, and 100% felt it improved their clinical practice. In this post, we will give a brief overview of a landmark study in the ED debrief literature, which advocates for a “hot” debrief model in resuscitation cases using the STOP5 model.

Study Analysis

This study published in 2019 designed, tested, and developed the STOP5 model to facilitate safer patient care, team development, and quality improvement within the Emergency Department. The STOP5 model, the first widespread debriefing tool, was designed as a “hot debrief”: “an interactive and structured team dialogue that takes place either immediately or very shortly after a clinical case”. Any team member of the resuscitation may lead the hot debrief.

Figure 1: The STOP5 Model Debriefing Framework (proposed by CA Walker et al 2020)

After an initial check-in the team moves to a group discussion and follows the STOP framework above: Summarize the case, Things that went well, Opportunities to improve, and Points to action and responsibilities. Inclusion criteria for these hot debriefing cases were major traumas, deaths in resuscitation, and any cases upon request by any staff member. No potential resuscitation cases were formally excluded.

After 18 months the ER staff was re-surveyed to ascertain STOP5 rating scores, the number of staff involved in the debriefs, any possible benefits or barriers to team performance, and if staff believed there should be more or less hot debriefing in the ER. In this 18-month review all STOP5 debriefs were rated “good” to “excellent”, suggesting the debriefing was highly valued. 98% of respondents believed that there should continue to be more hot debriefs in the emergency department. In a 12-month review there were 10 process and equipment changes (“hard outcomes”) as a direct result of the STOP5 hot debriefs and 14 additional opportunities for improvement. The hot debrief allowed for concrete actions to be taken about these issues and for a dedicated plan of action for correction. These hard outcomes identified issues such as those listed below which allowed for concrete solutions for all the identified problems.

Shortage of resuscitation room equipment
Drug stocking issues
Drug preparation/infusion regime for vital but rarely used medications difficult for staff to find
Faulty equipment (doors, machines)

Reported barriers to enacting hot debriefs include time constraints, workload, low staff confidence in leading the debrief, or absence of team members (consultants who might have left the department, change of shift). For these reasons hot debriefing is still not standard practice. However, a hot debrief such as STOP5, with a concrete checklist, is an inexpensive and quick way to enhance team performance, improve patient care, and assist with emotional trauma and mental check-ins for the team. Debriefing is a valuable and important aspect of our medical career. We hope to bring more of a focus to debriefing within our institution by beginning to enact the STOP5 based hot debriefing after clinical events.

Expert Commentary

Whether working in a community or academic Emergency Department, recurrent extraordinary cases threaten the well-being of the clinical team during that shift and after. Although resources often exist for individual employee assistance after a difficult shift has ended, few interventions have been described to help the team regroup and recover during that particular shift. Furthermore, department level morbidity and mortality conferences or hospital level quality assurance reviews focus more on the technical case details and less on team wellness.

With the primary purpose of quickly restoring team performance and wellness, hot debriefs at NUEM provide the opportunity for our ED teams to have a structured yet brief meeting immediately after an extraordinary case. Using STOP5, team leaders have a step-by-step plan to quickly yet effectively help every clinician on the team properly mentally frame the case, share gratitude, and then identify and assign opportunities for immediate improvement. Building on life support courses and residency training, specific education on the STOP5 framework quickly prepares senior clinicians to lead hot debriefs. Utilizing change management principles to identify and address logistical barriers helps to create a culture that supports immediate debriefing. Successful strategies in our NUEM ED include protocols to pause new inflow and cover existing patient demands, designating meeting spaces, adding positive program reminders to clinical areas and recurring meetings, and tracking and celebrating program success.

References

1. Get With The Guidelines - Resuscitation Clinical Tools. (2021, August 16). Www.Heart.Org. https://www.heart.org/en/professional/quality-improvement/get-with-the-guidelines/get-with-the-guidelines-resuscitation/get-with-the-guidelines-resuscitation-clinical-tools

2. Gilmartin, S., Martin, L., Kenny, S., Callanan, I., & Salter, N. (2020). Promoting hot debriefing in an emergency department. BMJ Open Quality, 9(3), e000913. https://doi.org/10.1136/bmjoq-2020-000913

3. Tannenbaum, S. I., & Cerasoli, C. P. (2012). Do Team and Individual Debriefs Enhance Performance? A Meta-Analysis. Human Factors: The Journal of the Human Factors and Ergonomics Society, 55(1), 231–245. https://doi.org/10.1177/0018720812448394

4. Vanyo, L., Sorge, R., Chen, A., & Lakoff, D. (2017). Posttraumatic Stress Disorder in Emergency Medicine Residents. Annals of Emergency Medicine, 70(6), 898–903. https://doi.org/10.1016/j.annemergmed.2017.07.010

5. Walker, C. A., McGregor, L., Taylor, C., & Robinson, S. (2020). STOP5: a hot debrief model for resuscitation cases in the emergency department. Clinical and Experimental Emergency Medicine, 7(4), 259–266. https://doi.org/10.15441/ceem.19.086

John Bailitz, MD

Vice Chair for Academics, Department of Emergency Medicine

Professor of Emergency Medicine, Feinberg School of Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Halloran, D. Long, A. Wleklinski, N. (2022, Sept 12). Debriefing in the ED. [NUEM Blog. Expert Commentary by Bailitz, J]. Retrieved from http://www.nuemblog.com/blog/debriefing-ED

Proper Preparation for Mass Casualty Incidents

**Written by:** August Grace, MD (NUEM ‘24) **Edited by:** Andrew Rogers, MD, MBA (NUEM ‘22)
**Expert Commentary by**: Andra Farcas, MD (NUEM ‘21)

Introduction

In the setting of trauma, most hospitals are adept at treating and managing patients with a variety of injuries. However, the ability of a hospital to handle a mass casualty incident (MCI) requires a completely different approach and, most importantly, adequate triage and pre-planning. An MCI is defined as “an event that overwhelms the local healthcare system, where the number of casualties vastly exceeds the local resources and capabilities in a short period of time [7].” MCI events can include anything from hurricanes, earthquakes, and other natural disasters to terrorism or other man-made situations that include the use of explosive or biological weapons, mass shootings, or dysfunction in modes of transportation (car, plane, train crash) [3]. Although this is just a short list of the possibilities, each hospital must prioritize its response preparedness to match the likelihood of events that it could receive. For example, as a major urban center, Chicago is more likely to encounter events such as mass shootings, biological terrorism, or explosive injuries. Mobile, Alabama, on the other hand, must have adequate preparation for hurricanes and floods [4]. This post will discuss a brief overview of hospital planning and operational setup with key elements of a disaster response from events that cause high numbers of blunt trauma, penetrating trauma, burns or crush injuries that may be seen following explosive events, mass shootings, or large scale motor vehicle collisions, to name a few.

Casualty Planning & Staffing Considerations

Arguably the most important step in an MCI is the planning that occurs before a single patient is even seen. In most events, hospitals have communication with EMS personnel that are on scene allowing them to have some sort of estimation of the scale of the event and type of disaster encountered. If the mechanism and scale are appropriate, a properly planned disaster response should be initiated and set in motion a sequence of coordinated events.

In creating a disaster response plan, the first step is the designation of the Disaster Medical Officer (DMO). This person should be the most senior ED attending physician and he/she oversees available hospital medical personnel and resources [1]. This person will have no role in patient care and instead will be in charge of all ED operations, delegating tasks, and problem solving issues that arise in the future.

The first task of the DMO is to get help and get it now. Approximately half of all casualties will arrive at the hospital within a one hour window, with 50-80% arriving within 90 minutes. Time begins after the first patient arrives at the hospital [8]. Therefore, getting the appropriate staff to the hospital as quickly as possible is vital to saving lives. How much staff is needed? This can be gauged by the type of disaster encountered and with assistance from EMS personnel at the scene. A five-car motor vehicle collision (MVC) will not require as much additional staff as a collapsed high rise building. The DMO will delegate the task of calling available staff to maximize the number of staff present in the ED and hospital. Contacting surgeons, scrub techs, anesthesiologists, and nurses to get as many ORs operational is invaluable to saving lives.

Continuous staffing adjustments can be monitored and made by using the casualty predictor tool (Figure 2). When in doubt, it is better to have more staff available than needed. To reiterate, the most important part of any disaster situation is to GET HELP.

Triage/ED Setup

Once the process is underway for increasing the level of resources available, the next step is hospital setup and triage. The most important part of this step is creating enough space to allow for the massive influx of patients and maintaining proper flow throughout the ED. It is well known that most hospitals in large population centers already operate at or near full capacity [4]. This makes it even more challenging when presented with an acute influx of patients in a short period of time. There is not much that can be done in the acute setting about patients that are already admitted; however, the ED can be restructured to account for the increased surge. Patients currently in the ED with a condition deemed to be stable (will likely not require an acute intervention in the next 24 hours) can be moved to a different area (green triage area, discussed below). The patients who have a more acute condition can be triaged and recategorized using the same criteria as the incoming casualties.

One current method of triaging patients is the tagging method. In this system, patients are tagged with a red, yellow, or green identification that categorizes patients based on acuity. Other things listed on tags can be a patient’s name, bar code, MRN or other tracking criteria. These patients are then able to be treated based on the level of care needed. In theory, this is a good way for patients to be tracked and accounted for. However, some experts believe that when there is a large volume of patients, this can slow the triage process and extend the amount of time it takes the patient to receive care that may be lifesaving. Another limitation is that it does not allow for a dynamic system, it provides a false sense of security, and can cause confusion. For example, a patient may have a green tag when initially triaged but could decompensate to a yellow or red tag [6]. Thus, there should be an appropriate system for re-evaluation if resources allow.

One system that could be used instead is a tag zone. In this system, the ED could be set up into different zones that would correlate with the tag color and acuity of the condition. Who should triage? The second most senior ED attending physician. The zone system could be set up as follows:

Red zone: Patients that need immediate medical or surgical attention. This includes patients presenting with an acute airway, circulatory or neurologic problem, multi-system involvement, or penetrating injuries to the head, neck, or chest. These patients are likely to need the vast majority of resources and staff.

Orange zone: Not originally categorized in the tag system. These patients are expected to decompensate within the hour but did not need immediate resuscitation [2].

Yellow zone: Patients that are relatively stable that will likely not decompensate within the hour. Extremity injuries or conditions that have time to be worked up.

Green zone: Patients with minor injuries that are unlikely to decompensate. “Walking wounded.” Will not require vast amounts of resources or staffing to be cared for.

The different zones allow for a dynamic system. Patients in each zone will be cared for by a team of physicians and nurses with the majority of staffing located in Red and Orange zones. Patients can be moved “up” a zone (from yellow to orange) if their condition deteriorates or could be moved “down” a zone (from yellow to green) if they are able to be stabilized [1, 2, 3]. The “black tag” patients were not categorized into a zone as they were patients who were either already dead, or not likely to survive given the current staffing and resources available. Figure 3 shows a brief triaging algorithm (without the orange designation). This is one possible system to triage patients and get them to an appropriate level of care rapidly. The hospital system is now ready for the rapid influx of critical patients.

Implementation

All patients should enter through a single triage area. Multiple points of entry can cause confusion and overwhelm each area by not knowing the number of patients entering from each point [4]. As the number of patients in each zone starts to fill up, adequate communication about the space and number of resources available should be communicated to the DMO and charge nurse. Once patients are able to be stabilized in each zone, the goal is to get them to the OR for immediate surgery if needed, or to move them down a zone (yellow to green) in order to make space for additional critically injured patients.

Who are the first patients to arrive? The “dual wave phenomenon” explains how patients usually present to the hospital following MCIs. The first wave of casualties are described as the “walking wounded” or those who are able to self-ambulate and usually only require minor care. These patients begin to arrive within 15-30 minutes of the incident depending on the distance from the scene to the hospital. It is important that these patients do not take up too many hospital resources or staff as they are likely well enough to survive with minimal therapeutic interventions. These patients can easily overwhelm the system and prevent proper care to more critical patients. The second wave includes the patients that arrive via EMS or other assistance from bystanders as they are not well enough to transport themselves. These are the patients who will require a vast majority of hospital staffing, resources, and time in order to prevent deaths [3, 4].

Summary

The first step to preparing for an MCI is having a plan in place.
GET HELP. If you only have time to do one thing it should be this. It does not matter how many resources you have or how much space is available if you do not have enough staff to use them.
Have a triage plan. Create zones of various acuity with the majority of staff occupying the higher acuity areas. Patients can always be moved to a higher zone if they need more care or a lower zone if they have been stabilized.
Get patients to the proper provider. If the patient needs surgery, get them to the OR. This also creates space for new patients to be seen.
Have one single area of entry. This allows the system to maintain consistency and flow.

References

Emergency Safety Officer Management Plan For Mass Casualty. Kings County Hospital Center, www.downstate.edu/emergency_medicine/pdf/KCHCSection03.pdf.
Menes, Kevin. “How One Las Vegas ED Saved Hundreds of Lives After the Worst Mass Shooting in U.S. History: Emergency Physicians Monthly.” EPM, 5 Apr. 2020, epmonthly.com/article/not-heroes-wear-capes-one-las-vegas-ed-saved-hundreds-lives-worst-mass-shooting-u-s-history/.
Hospital Medical Surge Planning for Mass Casualty Incidents. Florida Department of Health, www.urmc.rochester.edu/MediaLibraries/URMCMedia/flrtc/documents/WNY-Hospital-Medical-Surge-Planning-For-Mass-Casualty-Incidents.pdf.
Institute of Medicine. 2007. Hospital-Based Emergency Care: At the Breaking Point. Washington, DC: The National Academies Press. https://doi.org/10.17226/11621
“SALT Mass Casualty Triage Algorithm - CHEMM.” U.S. National Library of Medicine, National Institutes of Health, chemm.nlm.nih.gov/salttriage.htm.
“Report: Mass Casualty Trauma Triage Paradigms and Pitfalls .” Journal of Emergency Medical Services , Office of the United States Assistant Secretary for Preparedness and Disaster Response.
DeNolf, Renee L. “EMS Mass Casualty Management.” StatPearls [Internet]., U.S. National Library of Medicine, 15 Oct. 2020, www.ncbi.nlm.nih.gov/books/NBK482373/.
“Mass Casualty Predictor .” Homeland Security Digital Library , Centers for Disease Control and Prevention .

Expert Commentary

This is a great review of MCI management in the Emergency Department by Drs. Grace and Rogers. Although the past few years of the COVID-19 pandemic have felt like we’ve been working in a perpetual MCI, these are important principles to review on a regular basis, as they are not something we necessarily practice every day in the emergency department.

The authors do a good job of emphasizing the importance of preparing for an MCI ahead of time. Another important aspect of preparation is decontamination. An ED disaster response plan should incorporate how to effectively put patients (both walk-ins and EMS arrivals) through decontamination if the disaster at hand requires it. The authors emphasize the importance of having patients enter through a single triage area, and the decontamination station should be similarly set up nearby allowing for one-directional flow of patients through the decontamination process. This is not only vital to patient treatment but also to ensuring staff safety. Additionally, it is necessary to ensure that the ED has sufficient and adequate level Personal Protective Equipment and that the appropriate staff are trained on donning/doffing procedures.

In addition to gathering the staffing resources, there should also be an emphasis on gathering disaster-specific supplies: alerting the blood bank if it is a traumatic MCI, amassing antidotes if it is toxicological in nature, compiling medical equipment (such as ventilators) as applicable, etc. Additionally, alerting other EDs in the system as to the impending influx of patients as well as reaching out to disaster-specific specialty centers (ie, hyperbarics facility for a structure fire for carbon monoxide treatment) can also help take pressure off and allocate more resources.

Finally, the importance of a hotwash or after-action review cannot be emphasized enough. This is a process by which participants can have an open and honest professional discussion about what went well and what can be improved in the future. It centers around four main questions (What was supposed to happen? What did happen? What caused the difference? What can we learn from this?) and is vital for building an ED’s capacity for conducting an adequate emergency response to an MCI.

References

Blackwell, T.H., DeAtley, C., Yee, A. (2021). Medical support for hazardous materials response. Cone, D.C. (ed). Emergency Medical Services Clinical Practice and Systems Oversight; Volume 2: Medical Oversight of EMS. (3rd edition, p339-351). UK: John Wiley and Sons, Ltd.
Greenberg, T., Adini, B., Eden, F., Chen, T., Ankri, T., Aharonson-Daniel, L. An after-action review tool for EDs: learning from mass casualty incidents. Am J Emerg Med. May 2013;31(5):798-802. Doi 10.1016/j.ajem.2013.01.025. Epub 2013 Mar 6. PMID: 23481154.
Metz, T. How to Facilitate an After-Action Review (AAR or Hot Wash): Agenda and Tips. MG Rush Facilitation Training & Meeting Design. https://mgrush.com/blog/after-action-review/.
Salem-Schatz, S., Ordin, D., Mittman, B. Guide to the after action review. Center for Evidence-Based Management. Oct 2010. https://www.cebma.org/wp-content/uploads/Guide-to-the-after_action_review.pdf.

Andra Farcas, MD

Emergency Medicine & EMS Physician

CU Department of Emergency Medicine

University of Colorado School of Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Grace, A. Rogers, A. (2021, Apr 26). Proper Preparation for Mass Casualty Incidents. [NUEM Blog. Expert Commentary by Farcas, A]. Retrieved from http://www.nuemblog.com/blog/mass-casualty-incident-preparation

Nephrolithiasis: Ultrasonography versus Computed Tomography

**Written by:** Kishan Ughreja , MD (NUEM ‘23) **Edited by:** Ade Akhentuamhen, MD (NUEM ‘21)
**Expert Commentary by**: Tim Loftus, MD, MBA

Journal Club: Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis

A 70-year-old man with BPH s/p TURP, hypertension, hyperlipidemia and stroke presents to the ED with acute onset of intermittent sharp left flank pain radiating into the groin that awoke him from sleep. He endorses nausea without vomiting and denies fever. He also endorses slightly decreased urination with “dribbling.” His urinalysis shows >100 RBC and no signs of infection. Nephrolithiasis is likely high on your differential diagnosis. How do you proceed?

What is your initial imaging test of choice, ultrasound (US) or non-contrast CT, and why?

Would you be satisfied with only US and no follow-up CT?

Would you be confident in a point-of-care-ultrasound evaluation or a formal ultrasound?

Do outcomes for patients with suspected nephrolithiasis differ based on the initial imaging?

Should your medical decision-making change if the patient has a history of nephrolithiasis?

What would you do if the same patient presented again with persistent pain from a previously diagnosed stone?

Pain from suspected nephrolithiasis is a very common complaint in the ED and the incidence of the disease continues to increase. The estimated incidence over the past two decades is up to 340 visits per 100,000 individuals.1 Low-dose non-contrast abdominal CT has become the gold standard for diagnosis as it has become readily available in emergency departments nationwide, with some studies touting sensitivity and specificity of 97% and 95%, respectively.2 However, low dose CT still exposes the patient to radiation and may increase their risk of cancer, as many nephrolithiasis patients often undergo repeat imaging because of recurring pain or urological intervention. Additionally, CT scans prolong average ED lengths of stay. However, with ultrasonography becoming more prevalent in EDs, it may be possible that initial imaging may avoid this radiation risk and still have similar outcomes for patients. Let’s analyze this NEJM article comparing US to CT for the assessment of nephrolithiasis.

Study design: a multicenter, pragmatic, randomized comparative effectiveness trial

Population

N = 2759
ages 18- 76 yo
reported flank or abdominal pain that the treating physician wished to order imaging to establish or rule out a primary diagnosis of nephrolithiasis
not considered at high risk for serious alternative diagnoses e.g. cholecystitis, appendicitis, aortic aneurysm, or bowel disorders
no pregnant patients
no men >129 kg, no women >113 kg
no history of single kidney, renal transplantation, undergoing dialysis

Patient selection

Intervention protocol

patients randomized to 3 groups each using a different initial imaging modality (POCUS vs. Radiology US vs. CT)
patients contacted at 3, 7, 30, 90, and 180 days after randomization to assess study outcomes

Outcome measures

Primary Outcomes

high-risk diagnoses with complications that could be related to missed or delayed diagnoses — within 30 days of ED visit, including:
AAA w/rupture, PNA w/sepsis, appendicitis w/rupture, diverticulitis w/abscess or sepsis, bowel ischemia or perforation, renal infarction, renal stone w/abscess, pyelonephritis w/urosepsis or bacteremia, ovarian torsion w/necrosis, aortic dissection w/ischemia
cumulative radiation exposure from all imaging within 6 months after randomization
total cost (not reported in this study, ongoing analysis)

Secondary Outcomes

serious adverse events (FDA definition)
serious adverse events related to study participation
delayed diagnosis, like acute cholecystitis, appendicitis, bowel obstruction
return ED visits
hospitalizations after being discharged from ED
self-reported pain scores
diagnostic accuracy for nephrolithiasis
by comparing ED diagnosis at discharge to reference standard of confirmed stone by patient’s observation of passage or report of surgical removal

Results

no significant differences among groups in terms of pain scores, medical history, physical exam findings, and ED physician’s assessment of the likelihood of other diagnoses (Table 2)
POCUS and US groups had significantly lower cumulative radiation exposure over 6 months than the CT group (difference attributed to initial ED visit’s imaging choice)
11 patients (0.4%) had high risk diagnoses with complications during first 30 days after randomization, with no significant difference among the 3 groups
no difference when stratified by patients with a history of nephrolithiasis
no significant difference among groups in the number of patients with serious adverse events; total of 466 SAE in 316 patients (91.4% were hospitalizations during f/u period; 26.4% involved surgical treatment of complications of nephrolithiasis)
5 reported deaths (occurred between 38 and 174 days after randomization) — none thought to be related to study participation
the proportion of patients with a confirmed stone diagnosis within 6 months was similar in all 3 groups (POCUS 34.5% vs. US 31.2% vs. 32.7% CT)
diagnostic accuracy based on result of initial imaging modality
- POCUS sensitivity 54% [48 - 60]; specificity 71% [67 - 75]
- US sensitivity 57% [51 - 64]; specificity 73% [69 - 77]
- CT sensitivity 88% [84 - 92]; specificity 58% [55 - 62]

Interpretation

The US group was exposed to less radiation than the CT group and had no significant differences in the incidence of high-risk diagnoses with complications, total serious adverse events, or related serious adverse events.
There also were no significant differences in pain scores, hospitalizations, ED readmissions among the groups.
Many patients in the ultrasound groups did get additional imaging, but this was not the majority.
Patients with a history of nephrolithiasis were less likely to undergo additional imaging with CT if they already had an ultrasound first (31% vs 36%). They did not have poorer outcomes than patients without a history of nephrolithiasis.
Patients only undergoing POCUS and no other testing had a significantly shorter ED stay (1.3 hours)
It is safe to pursue ultrasound as the initial imaging of choice for suspected nephrolithiasis (with additional imaging ordered as necessary at clinical discretion), though it should not necessarily be the only testing performed.

Strengths

large size, diversity in ED settings, randomized design, assessment of clinically important outcomes, a high follow-up rate

Weaknesses

no blinding of investigators, physicians, or patients as this was a pragmatic trial design
independent review was used to characterize serious adverse events related to study participation
strict reference standard for stone diagnosis which was unbiased, but prone to error based on the patient’s memory of self-reporting of stone passage

Internal/external validity

Given the aforementioned strengths of this study and its pragmatic design, these findings appear both internally and externally valid and may be applied to daily clinical practice

Take-Home Points

What is your initial imaging test of choice, ultrasound (US) or non-contrast CT, and why?

Ultrasound is a good choice for initial imaging as most patients do not end up requiring additional imaging during their visit. This leads to reduced cumulative radiation exposure.

Would you be satisfied with only US and no follow-up CT?

In this study, 40.7% of those in the POCUS group and 27% in the formal ultrasound group underwent subsequent CT. Follow up CT should depend on the patient and ultrasound operator. Keep in mind that this study excluded patients with kidney disease, pregnant patients, and obese patients. They also excluded patients who were high risk for other pelvic and abdominal diseases. Lastly the POCUS operators were ED physicians with training “recommended by ACEP.”

Would you be confident in a point-of-care-ultrasound evaluation compared to a formal ultrasound?

Yes. Sensitivity and specificity between these groups were similar.

Do outcomes for patients with suspected nephrolithiasis differ based on the initial imaging?

No. There was no significant difference in subsequent adverse events, pain, return visits or hospitalizations, or delayed diagnoses of other serious conditions.

Should your medical decision-making change if the patient has a history of nephrolithiasis?

In this study, patients with a history of nephrolithiasis were less likely to undergo additional imaging with CT if they already had an ultrasound first. They did not have poorer outcomes than patients without a history of nephrolithiasis. This suggests that it is safe to avoid ordering a CT in patients with recurrent stones.

What would you do if the same patient presented again with persistent pain from a previously diagnosed stone?

The majority of patients with adverse outcomes were due to infectious causes. Consider alternative diagnoses such as pyelonephritis. Additionally, although rare, renal infarct can present with acute flank pain and is diagnosed with a contrast CT.

References

Fwu, C. W., Eggers, P. W., Kimmel, P. L., Kusek, J. W., & Kirkali, Z. (2013). Emergency department visits, use of imaging, and drugs for urolithiasis have increased in the United States. Kidney international, 83(3), 479-486.
Coursey, C. A., Casalino, D. D., Remer, E. M., Arellano, R. S., Bishoff, J. T., Dighe, M., ... & Leyendecker, J. R. (2012). ACR Appropriateness Criteria® acute onset flank pain–suspicion of stone disease. Ultrasound quarterly, 28(3), 227-233.
Smith-Bindman, R., Aubin, C., Bailitz, J., Bengiamin, R. N., Camargo Jr, C. A., Corbo, J., ... & Kang, T. L. (2014). Ultrasonography versus computed tomography for suspected nephrolithiasis. New England Journal of Medicine, 371(12), 1100-1110.

Expert Commentary

Thank you very much to Dr.’s Ughreja and Akhetuamhen for an excellent blog post on a very relevant clinical topic. This is a great summary of the landmark randomized trial published in NEJM in 2014 assessing CT vs two types of US for patients with suspected renal colic in the ED setting. It is worth mentioning that this study was a multicenter study based in the US with representation from ED, Radiology, and Urology. The above study was well summarized and bears repeating that, in this multicenter randomized study assessing CT vs POCUS vs radiology performed US in patients with suspected renal colic in the ED setting, initial US reduced radiation exposure without adversely affecting patient-centered outcomes. It is worth mentioning several additional considerations and placing emphasis on others elucidated from this journal club review.

First, a subsequent systematic review (1) incorporating multispecialty (ED, Radiology, Urology) expert panel consensus recommendations has reiterated that in younger patients without a high suspicion for alternative diagnoses or complicating features of nephroureterolithiasis (such as fever, pyelonephritis, solitary kidney, dialysis, etc), US should be the initial diagnostic imaging modality of choice, if any. It's a great paper, worth reading (and appreciating who the authors are), and worth recalling for bedside teaching to junior learners in the ED.

Additionally, this paper brings to mind my second point, and something that is worth shouting from the hilltops -- a kidney stone is a clinical diagnosis! Now, of course, this is exclusive of those patients with high-risk or complicating features (e.g. pediatrics, pregnancy, solitary kidney, fever, unstable/critically ill, unrelenting pain, atypical features, etc). You don’t need any imaging to tell you the diagnosis in the vast majority of patients. US or CT are helpful in confirming the diagnosis when there is uncertainty or non-trivial pretest probability of alternative diagnoses, excluding alternative diagnoses, and identifying exact stone location and size, which can be used to help counsel patients at the bedside regarding the anticipated clinical course and next steps in management.

Third, for those with proper training, and with some exceptions (see the systematic review paper for case vignettes that highlight these), POCUS is non-inferior to radiology-performed US. And, it's not a “formal” US. I can’t remember the last time I attended a black-tie ultrasonography session, but that's just me.

Fourth, it's worth mentioning that although CT use can lead to the identification of incidental findings more commonly than US, identification of these incidental findings still happens rather often with POCUS (a common example is a renal cyst). Please ensure that you document and discuss with the patient accordingly.

Finally, a burden on us as EM clinicians is training in and awareness of clinical practice guidelines and recommendations from specialties outside of EM. As it relates to the diagnostic evaluation of suspected renal colic in the ED setting, the Choosing Wisely recommendations endorsed by the AUA are worth perusing as are the European/EUA guidelines, both of which suggest US as the initial diagnostic imaging modality of choice, for pediatric (CW) and non-high-risk patients without complicating features (EUA).

The bottom line is that CT is helpful for older patients or those in whom you are less sure about the diagnosis of renal colic. For younger or low-risk patients, suspected renal colic is a clinical diagnosis and often needs no imaging, but ultrasound would be an evidence-based first step. Thanks again toDr.’s Ughreja and Akhetuamhen.

References

1) Moore et al. Imaging in suspected renal colic: a systematic review of the literature and multispecialty consensus. J Urol 2019. 202(3):475-483.

Tim Loftus, MD, MBA

Assistant Professor of Emergency Medicine

Fellowship Director of the Clinical Operations and Administration Fellowship Program, Northwestern Department of Emergency Medicine

Medical Director of Emergency Services Northwestern Lake Forest Hospital and Grayslake Emergency Center

How To Cite This Post:

[Peer-Reviewed, Web Publication] Ughreja, K. Akhentuamhen, A. (2022, May 16). Journal Club: Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis. [NUEM Blog. Expert Commentary by Loftus, T]. Retrieved from http://www.nuemblog.com/blog/nephrolithiasis-ultrasonography-versus-computed-tomography.

Neuroleptic Malignant Syndrome

Expert Commentary

This is an awesome, focused review of neuroleptic malignant syndrome (NMS). NMS is hard to diagnose because it's rare. There is no gold standard with respect to its definition, and it requires a medication history (which we typically don't do very well in the emergency department). A tricky cause of NMS is the removal of a dopamine agonist. For this reason, carbidopa/levodopa should never be discontinued during hospital admission - or ED boarding. [1]

Supportive care is more important than antidotal therapy during NMS management. The most acute cause of death from NMS is hyperthermia, which is induced both by D2 receptor antagonism leading to rigidity and impaired thermoregulation from the striatum and hypothalamus. Any life-threatening hyperthermia should be treated immediately with an ice bath.[2] Rigidity will lead to rhabdomyolysis with subsequent hyperkalemia and myoglobin-induced renal failure. Therefore, fluid resuscitation and maintenance are important. Profound immobility can precipitate DVT, so anticoagulation may be necessary.

In terms of pharmacotherapy, benzodiazepines are universally used. Dantrolene inhibits calcium-mediated muscle contraction to reduce muscle rigidity. However, it doesn't address the underlying central D2 antagonism, and its efficacy has only been shown in case reports. Bromocriptine acts more centrally as a dopamine agonist but should be used cautiously in patients with psychiatric diseases as it may exacerbate psychosis. Overall, benzodiazepine use and supportive care should get you through most cases of NMS, though additional therapies may be necessary in severe cases.

References

1. Institute for Safe Medication Practices. Delayed Administration and Contraindicated Drugs Place Hospitalized Parkinson’s Disease Patients at Risk. 12 March 2015. Accessed February 11, 2022.

2. Juurlink JN. Antipsychotics. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank's Toxicologic Emergencies, 11e. Page 1037-1039. McGraw Hill; 2019. Accessed February 11, 2022.

Zachary Schmitz, MD

Toxicology Fellow

Ronald O. Perelman Department of Emergency Medicine

NYU Langone Health

How To Cite This Post:

[Peer-Reviewed, Web Publication] Leibowitz, M. Wleklinski, N. (2022, May 9). Neuroleptic Malignant Syndrome. [NUEM Blog. Expert Commentary by Schmitz, Z]. Retrieved from http://www.nuemblog.com/blog/neuroleptic-malignant-syndrome.

Beyond the Burns: Toxic House Fire Gases

Expert Commentary

Congratulations to Drs. Payne and Wessling on an excellent post.

Management of toxic gas exposure from a house fire is essential knowledge for all emergency physicians. The two major toxic gases of interest are carbon monoxide and hydrogen cyanide; it is important to note that fires in other environments, such as factories or industrial sites, may result in alternative exposures based on the nature of the fire and materials present. The post goes into detail on the pathophysiology, signs, symptoms, and diagnosis of both carbon monoxide and cyanide poisonings, so this commentary will focus on the clinical approach.

I recommend the following simplified process to streamline diagnosis and treatment decision making:

1. Start high flow oxygen (15L NRB) immediately (or, if intubated, give 100% FiO2)

High flow oxygen reduces the half life of carbon monoxide from ~5 hours to ~90 minutes. Oxygen can be discontinued once carboxyhemoglobin normalizes (<2%)

2. Obtain a carboxyhemoglobin level, lactic acid level, and a venous blood gas (arterial is unnecessary unless oxygenation is also a concern) as soon as possible

Unfortunately, there is some disagreement as to what constitutes a “toxic” carboxyhemoglobin level. Weaver, et al. established 25% as an inflection point for the development of severe sequelae, which is now a commonly used (though not universally agreed upon) threshold value. Also, when evaluating a carboxyhemoglobin level, it is essential to consider the time period prior to the level being drawn to avoid false reassurance. For example, a level drawn after 90 minutes of high flow oxygen will be reduced by roughly 50% and interpreted accordingly. Further, do not rely on external co-oximeters alone to rule out carbon monoxide poisoning given limited sensitivity at the moment (though the technology will likely improve over time).

3. Treat with hydroxocobalamin empirically if symptomatic and/or if lactic acid elevated

Hydroxocobalamin is a low risk intervention with significant potential therapeutic benefit, so it should be given early if there is any clinical concern. The other major cyanide antidote, sodium thiosulfate, should only be used if hydroxocobalamin is not available as it has no efficacy advantage and an undesirable side effect profile. It is essential to avoid using nitrites, as inducing methemoglobinemia in the setting of coincidental carbon monoxide poisoning can dramatically worsen tissue hypoxia.

An elevated lactic acid is a surrogate for cyanide poisoning, specifically a level of 8-10 mmol/L or greater is sensitive and should prompt intervention. More modest lactic acid elevations are less likely to be related to cyanide poisoning and should not prompt intervention, especially in an asymptomatic patient, unless the level is persistently elevated despite adequate resuscitation. Cyanide levels, while diagnostic, are of no acute clinical utility since they are rarely available in a timely manner.

4. Consider hyperbaric oxygen therapy (HBOT) if readily available

HBOT for the treatment of carbon monoxide poisoning is controversial. While HBOT reduces the half life of carbon monoxide to roughly 20-30 minutes, HBOT is not used for this purpose alone. In fact, HBOT is primarily used to reduce associated cognitive, behavioral, and neurologic changes (collectively known as delayed neuropsychiatric sequelae). There is lower quality evidence for reduced myocardial infarction and mortality risk as well.

However, several factors limit HBOT use. Primarily, it is not universally available at most institutions, incurring the risk and cost of transport to a distant site. The benefit is thought to be highest when the treatment is performed early (ideally within six hours of exposure), which adds to the logistical burden. Additionally, many chambers are not operated on nights and weekends, and of those available at off hours, many are unable to accommodate intubated patients. Recognizing the controversial nature of HBOT, the 2016 ACEP position statement noted that HBOT or high flow, normobaric oxygen can be used to treat carbon monoxide poisoning; though it likely carries clinical benefit in certain situations, at this time HBOT is not the standard of care for severe carbon monoxide poisoning. Rather, it should be offered if it can be readily and reasonably arranged.

Keeping this in mind, the following are generally accepted indications for HBOT in the setting of carbon monoxide poisoning

Loss of consciousness associated with exposure
Altered mental status
Focal neurologic changes
Evidence of end organ ischemia (pH ≤ 7.1, EKG changes, elevated troponin, angina)
Pregnancy (with some resources citing a level ≥20%)
Carboxyhemoglobin level ≥25%

Importantly, these are not hard and fast rules and there is no firm guideline mandating when HBOT should or should not be used. As a result, it is prudent to involve a medical toxicologist early in the process.

In summary, a few key take home points:

Carbon monoxide and cyanide are strongly associated with house fires – assume exposure to both until proven otherwise
It is reasonable to treat any undifferentiated, symptomatic patient with high flow oxygen and hydroxocobalamin empirically; asymptomatic patients can wait safely for blood work on high flow oxygen alone
The decision making regarding use of HBOT, in particular, is complex – early consultation with a medical toxicologist is strongly encouraged

Justin Seltzer, MD

Toxicology Fellow

Department of Emergency Medicine

University of California, San Diego

How To Cite This Post:

[Peer-Reviewed, Web Publication] Payne, A. Wessling, E. (2022, May 2). Toxic House Fire Gases. [NUEM Blog. Expert Commentary by Seltzer, J]. Retrieved from http://www.nuemblog.com/blog/toxic-house-fire-gases

Traumatic Arthrotomy

**Written by:** Parisa Kermani, MD (NUEM ‘23) **Edited by:** Alex Herndon, MD (NUEM ‘21)
**Expert Commentary by**: Matt Levine, MD

Case: A 25-year-old male comes into the ER after a saw accident at work. The patient was using a circular saw to cut wood when it slipped and the saw touched up against his knee. The patient has a 10cm linear vertical laceration over the anterior surface of his left knee (Figure 1). Bleeding is controlled. Patient ambulatory. Reporting 10/10 pain over the laceration.

What are the next best steps for evaluation and treatment of his injury?

Background

Traumatic arthrotomy is defined as a soft tissue injury over a joint that penetrates the joint space. Violation of the joint capsule exposes the sterile intra-articular space to the environment which can result in a deep infection and sepsis. The morbidity associated with septic arthritis is high, so it is important that providers have a high index of suspicion when evaluating wounds over joint surfaces.

The knee joint is the most common joint to be affected, followed by the ankle. Penetrating injuries have a higher rate of capsule violation so a history of knives or bullets should raise suspicion, though MVCs, falls, motorcycle accidents can also result in a deep injury. The capsule has little protection lateral to the patella (Figure 2 & 3), so even if the laceration does not appear deep there is potential that it penetrates the joint space.

Evaluation

Exploration: The first step of evaluation is local wound exploration. It is useful to anesthetize the wound at this point, as this will make the patient more comfortable and allow for a better exam. Irrigate the wound with sterile saline. It is extremely important to visualize the base of the wound. Using a hemostat or q-tip to probe the tissue at the base can be helpful as to not miss any tunneling segments. Keep a close eye out for bubbles, synovial fluid (appears straw colored and oily) or visible bone/tendon as all of these indicate joint involvement. It is important to note that the absence of these findings does not rule out a traumatic arthrotomy.

X-ray: Many times, next step will be to get an X-ray to look for associated fractures. Though this is not the most sensitive test for evaluating for joint space violation, if you see intra-articular air, this signifies joint involvement and no further imaging is required before calling the orthopedic surgeons. Many times, the X-ray will be normal and further testing will need to be completed. Of note, an x-ray is not required if there is no concern about injury to the bone as it is unlikely going to give a definitive answer on traumatic arthrotomy in less obvious cases.
CT Scan: As far as imaging goes, CT scan is the imaging modality of choice for traumatic arthrotomy. Though not currently the gold standard for ruling out joint violation, CT scan has become more accepted as an alternative to saline load testing the joint. Although limited, a 2013 study by Konda et al, where direct arthroscopic visualization or septic arthritis at follow-up were used as the gold standard for diagnosis, found imaging by CT scan to be 100% sensitive and specific for diagnosing traumatic knee arthrotomy. When viewing a CT scan to evaluate for traumatic arthrotomy, the presence of gas in the joint, known as pneumarthrosis, indicates intra-articular extension (Figure 4).

Figure 4: Traumatic arthrotomy on CT scan
Source: Konda et al, 2013

Saline Load Test (SLT): Though not strongly backed by the literature, SLT is a standard tool used to assess for traumatic arthrotomy. SLT is done by performing an arthrocentesis of the affected joint away from laceration, once confirmed in the correct space, sterile saline is injected into the joint and the laceration site is observed for extravasation. The provider should also passively range the joint while injecting to ensure greater sensitivity. Table 1 below summarizes how much sterile saline should be injected to obtain 95% sensitivity for traumatic arthrotomy. Adding methylene blue to the saline has not been proven to increase sensitivity and generally no longer recommended. The sensitivity will be highly variable based on provider experience with the procedure and patient tolerance. It is important to remember that this procedure can be exquisitely painful and special attention should be paid towards the patient’s comfort.

Table 1: Amount of saline for 95% sensitivity SLT

Because strong, conclusive literature is lacking, the choice between CT versus SLT to rule out traumatic arthrotomy will depend on many different factors including provider procedural comfort, local practice patterns, available resources and patient input.

Treatment

Once a diagnosis of traumatic arthrotomy is confirmed through an above modality, orthopedics should be emergently consulted. Tetanus prophylaxis should be updated and the patient should be started on an IV antibiotic that covers both strep and staph. A 1st generation cephalosporin is usually sufficient. Other antibiotics should be considered if injury is from a human/animal bite, happened underwater, or if there is concern for fecal/other contamination. Definitive treatment is joint wash out in the Operating Room.

If the above modalities do not show evidence of arthrotomy the patient’s laceration may be repaired in usual fashion. The patient should be given strict return precautions and have close follow-up for wound/joint reevaluation and suture removal.

Sources

Browning BB, Ventimiglia AV, Dixit A, Illical E, Urban WP, Jauregui JJ. Does the saline load test still have a role in the orthopaedic world? a systematic review of the literature. Acta orthopaedica et traumatologica turcica. 2016;50(6):597-600. doi:10.1016/j.aott.2016.01.004

Gittings D, Dattilo J, Fryhofer G, Martin A, Hast M, Mehta S. The saline load test is effective at diagnosing traumatic arthrotomies of the shoulder. Journal of surgical orthopaedic advances. 2019;28(4):268-271.

Gittings DJ, Fryhofer GW, Hast MW, Steinberg DR, Levin LS, Gray BL. The saline load test is effective at diagnosing traumatic arthrotomies of the wrist. Techniques in hand & upper extremity surgery. 2019;23(2):59-61. doi:10.1097

Jonathan Michael Strong. Saline Load or CT: What’s the Best Test for Traumatic Arthrotomy. Acepnow magazine. 2020; https://www.acepnow.com/article/saline-load-or-ct-whats-the-best-test-for-traumatic-arthrotomy

Konda SR, Howard D, Davidovitch RI, Egol KA. The saline load test of the knee redefined: a test to detect traumatic arthrotomies and rule out periarticular wounds not requiring surgical intervention. Journal of orthopaedic trauma. 2013;27(9):491-497. doi:10.1097/BOT.0b013e31828211f3

Konda SR, Davidovitch RI, Egol KA. Computed tomography scan to detect traumatic arthrotomies and identify periarticular wounds not requiring surgical intervention: an improvement over the saline load test. Journal of orthopaedic trauma. 2013;27(9):498-504. doi:10.1097/BOT.0b013e31828219bc

Metzger P, Carney J, Kuhn K, Booher K, Mazurek M. Sensitivity of the saline load test with and without methylene blue dye in the diagnosis of artificial traumatic knee arthrotomies. Journal of orthopaedic trauma. 2012;26(6):347-349. doi:10.1097/BOT.0b013e3182255167

Nord RM, Quach T, Walsh M, Pereira D, Tejwani NC. Detection of traumatic arthrotomy of the knee using the saline solution load test. The journal of bone and joint surgery american volume. 2009;91(1):66-70. doi:10.2106/JBJS.G.01682

Timothy D. Roberts. Traumatic arthrotomy with pneumarthrosis on plain radiograph of the knee. Western journal of emergency medicine. 2016;17(2):184-185. doi:10.5811/westjem.2015.12.29317

Expert Commentary

What a great review of traumatic arthrotomy! You now have a concise reference that teaches you everything you would probably ever need to know about this tricky diagnosis! These injuries are so uncommon that the first hurdle to overcome is actually considering the diagnosis. If you don’t consider it, then you hopefully just get lucky by a diagnostic x-ray that was ordered for other reasons!

Physical exam and exploration is indeed important but has limitations and does not rule out the diagnosis if the suspicion is high enough. The tract may be small, jagged, or there may be soft tissue destruction that limits your visualization. Be sure to inspect the wound while passively ranging the joint in question since it is often unclear the precise position of the joint (fully flexed, fully extended, or somewhere in between) when the wound occurred. This may bring the wound tract into your field of view. Ideally your exploration should be in a bloodless, painless field and documented as such.

While x-rays lack sensitivity, they are a worthwhile starting point since they are less expensive, noninvasive, readily available, and you can stop if they are positive. X-rays may also better define the extent and trajectory of the wound tract which my either heighten your suspicion or provide reassurance that the trajectory was away from the joint.

If the diagnosis is still in question, I prefer CT in most scenarios. It provides additional information about any associated fractures. CT is painless. Intra-articular air is very easy to see on CT. The downside is increased cost. Saline load testing seems to have more room for error. The joint must be properly entered. Enough fluid must be injected to fill the joint enough to cause visible extravasation. And the diagnosis can still be missed if it is forgotten to range the joint during the SLT. It is also quite painful. Consider all the patients you see who present with a painful joint effusion that has gradually accumulated. In the SLT you are giving the patient a sudden acute joint effusion. Ouch! So just be thoughtful about the route you choose to go.

Matthew Levine, MD

Associate Professor

Department of Emergency Medicine

Northwestern Memorial Hospital

How To Cite This Post:

[Peer-Reviewed, Web Publication] Kermani, P. Herndon, A. (2022, Apr 25). Traumatic Arthrotomy. [NUEM Blog. Expert Commentary by Levine, M]. Retrieved from http://www.nuemblog.com/blog/traumatic-arthrotomy

Toxic Alcohols

**Written by:** Rafael Lima, MD (NUEM ‘23) **Edited by:** Laurie Aluce, MD (NUEM ‘21)
**Expert Commentary by**: Zachary Schmitz (NUEM ‘21)

Methanol Toxicity

Methanol itself is not toxic to the body. Methanol’s metabolite, formic acid, causes toxicity at serum levels greater than 20mg/dl [1].

Clinical Findings of Methanol Poisoning

CNS sedation
Seizures
Rapid, Deep Breathing
Hypotension
Ocular findings:
- Blindness
- Afferent pupillary defect
- Optic disk hyperemia
- Mydriasis

Ethylene Glycol Toxicity

Similarly, the toxic metabolites of ethylene glycol cause end-organ damage at levels greater than 20mg/dl. The most notable toxic metabolites are glycolic acid and oxalic acid.” [1] .

Clinical Findings of Ethylene Glycol Poisoning

CNS sedation
Seizures
Cranial nerve palsies
Rapid, deep breathing
Hypotension
Hypocalcemia (can result in tetany)
Renal findings:
- Oliguria
- Acute renal failure
- Flank pain
- Hematuria
- Oxalate crystals in the urine under fluorescence

Isopropyl Alcohol Toxicity

Found in hand sanitizers and disinfectants, isopropyl alcohol is a less common source of alcohol poisoning. The parent molecule does exhibit toxic effects here, unlike methanol and ethylene glycol. If untreated, the lethal dose is between 4-8 g/kg [2].

Alcohol dehydrogenase metabolizes isopropyl alcohol into acetone. Because acetone is a ketone, and ketones are not oxidized into carboxylic acids, isopropyl alcohol poisoning does not result in anion gap metabolic acidosis.

Clinical Findings of Isopropyl Alcohol Poisoning

CNS sedation
Disconjugate gaze
Fruity breath odor
Hypotension
Hematemesis
Pulmonary edema

Plasma Osmolal Gap

One of the most reliable laboratory markers of toxic alcohol poisoning is a large osmolal gap. The osmolal gap is defined as the difference between the measured serum osmolality and the calculated, or expected, plasma osmalality:

OSMOLAR GAP = Measured plasma osmolality – calculated/expected plasma osmolality

The common equation for calculating the expected plasma osmolality is listed below [3]. Of note, there are other formulas with slight variations. Using an online calculator can be helpful.

Expected Serum Osmolality=2[Na]+BUN/2.8+Glucose/18

A gap < 10 is considered normal. Any elevation above 10 should raise the clinician’s suspicion of toxic alcohol ingestion.

Note: this tool is not helpful in late presentations as the metabolized forms of the different alcohols do not contribute to the osmolal gap. The calculated gap will be falsely low in late-stage poisoning.

Treatment of Toxic Alcohol Ingestions

Consult your medical toxicologist or poison control center if toxic alcohol ingestion is suspected.

The national poison control center hotline telephone number is 1(800)-222-1222.

Fomepizole

Fomepizole should be used only for methanol and ethylene glycol ingestions. It is not indicated for isopropyl alcohol intoxications [4]. It is an inhibitor of alcohol dehydrogenase (ADH). Evidence shows that it is a superior antidote to ethanol [5].

Loading dose 15 mg/kg IV
Then 10 mg/kg every 12 hours

Continue until blood pH is normal and serum alcohol concentration is less than 20 mg/dL in the presence of retinal or renal injury.

Ethanol

Ethanol works as a competitive inhibitor of ADH, having a higher affinity for the enzyme compared to the other alcohols. Ethanol was used historically before the effects of fomepizole were studied. Fomepizole is now the preferred treatment because the administration of ethanol is more difficult, ethanol causes sedation, and titration of the therapy is challenging in co-ingestions [6]. If ethanol must be used, the preferred route is IV and the studied therapeutic target level is 100 mg/dL [7].

Supplemental Therapy

Methanol poisoning patients should also receive folic acid (50mg IV every 6 hours) [7].

Ethylene glycol poisoning patients should also receive thiamine (100mg IV) and pyridoxine (50mg IV) [8].

Hemodialysis

Consult your nephrologist early if you are considering hemodialysis. Renal replacement therapy should be considered in the following situations [9]:

Anion gap metabolic acidosis with known toxic alcohol ingestion
End-organ damage
- Renal failure
- Vision changes
Unexplained anion gap metabolic acidosis with elevated osmolal gap in suspected toxic alcohol ingestion

References

1. Liesivuori, J. and H. Savolainen, Methanol and formic acid toxicity: biochemical mechanisms. Pharmacol Toxicol, 1991. 69(3): p. 157-63.

2. Slaughter, R.J., et al., Isopropanol poisoning. Clin Toxicol (Phila), 2014. 52(5): p. 470-8.

3. Bhagat, C.I., et al., Calculated vs measured plasma osmolalities revisited. Clin Chem, 1984. 30(10): p. 1703-5.

4. Su, M., R.S. Hoffman, and L.S. Nelson, Error in an emergency medicine textbook: isopropyl alcohol toxicity. Acad Emerg Med, 2002. 9(2): p. 175.

5. McMartin, K., D. Jacobsen, and K.E. Hovda, Antidotes for poisoning by alcohols that form toxic metabolites. Br J Clin Pharmacol, 2016. 81(3): p. 505-15.

6. Zakharov, S., et al., Fomepizole versus ethanol in the treatment of acute methanol poisoning: Comparison of clinical effectiveness in a mass poisoning outbreak. Clin Toxicol (Phila), 2015. 53(8): p. 797-806.

7. Barceloux, D.G., et al., American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol, 2002. 40(4): p. 415-46.

8. Ghosh, A. and R. Boyd, Leucovorin (calcium folinate) in "antifreeze" poisoning. Emerg Med J, 2003. 20(5): p. 466.

9. Moreau, C.L., et al., Glycolate kinetics and hemodialysis clearance in ethylene glycol poisoning. META Study Group. J Toxicol Clin Toxicol, 1998. 36(7): p. 659-66.

Expert Commentary

Thank you for this great review of a difficult subject! The combination of a lack of quick, confirmatory testing with delayed onset of symptoms makes toxic alcohol poisoning an incredibly difficult diagnosis to make. Additionally, even small ingestion can lead to major complications. For example, if a typical four-year-old (19kg) child drank windshield washer fluid that contained 50% methanol (a fairly standard formulation), it would take only 5.7 mL to potentially produce a methanol serum concentration of 25 mg/dL. Given the average 4-year-old’s mouthful is 8.9 mL, you can run into trouble quickly.[1]

We frequently see misuse or misunderstanding of osmol and anion gaps in diagnosing toxic alcohol ingestion when history is unclear. First, although a normal osmol gap is generally less than 10, baseline osmol gaps range from -10 to +14.[2] Therefore, a gap of 16 may represent a true gap of +2 in one person and +26 in another. Second, ethanol must be included in the osmol gap equation. An ethanol concentration of 200 mg/dL would increase your osmol gap by 43.5. Third, given metabolism over time, all values included in an anion gap calculation need to be drawn off of the same blood sample.

These considerations make finding the diagnosis even more complicated, but there are a few things that can help you out. First, an osmol gap > 50 is highly concerning for toxic alcohol. Second, an ethanol concentration > 100 mg/dL is sufficient to block ADH, meaning that few toxic metabolites from methanol or ethylene glycol could be made.[3] This means that an anion gap present with an ethanol > 100 mg/dL is not from toxic alcohol (unless the patient drank the ethanol after the toxic alcohol, which is very rare). Third, sequential values over time can be helpful. Metabolism of toxic alcohols should lead to a decreased osmol gap and increased anion gap over time. Proper use of the osmol and anion gap can help identify patients at high risk for morbidity and mortality while decreasing unnecessary administration of fomepizole, which typically costs thousands of dollars.

References

Ratnapalan S, Potylitsina Y, Tan LH, Roifman M, Koren G. Measuring a toddler's mouthful: toxicologic considerations. Journal of Pediatrics. 2003 Jun;142(6):729-30. doi: 10.1067/mpd.2003.216
Hoffman RS, Smilkstein MJ, Howland MA, Goldfrank LR. Osmol gaps revisited: normal values and limitations. J Toxicol Clin Toxicol. 1993;31(1):81-93. doi: 10.3109/15563659309000375.
Jacobsen D, McMartin KE. Methanol and ethylene glycol poisonings: mechanism of toxicity, clinical course, diagnosis and treatment. Med Toxicol. 1986;1:309-334.

Zachary Schmitz, MD

Toxicology Fellow

Ronald O. Perelman Department of Emergency Medicine

NYU Langone Health

How To Cite This Post:

[Peer-Reviewed, Web Publication] Lima, R. Aluce, L. (2022, Jan 24). Toxic Alcohols. [NUEM Blog. Expert Commentary by Schmitz, Z]. Retrieved from http://www.nuemblog.com/blog/toxic-alcohols

Marine Envenomations

Expert Commentary

An excellent post by Drs. Tandlich and Renshaw. Marine envenomations are common problems around the world. Like with land-based envenomations, the venomous organisms of note vary with geography; jellyfish encountered in Australia are different from those encountered in Florida, for example. As a result, we will focus on major envenomations in the United States.

The invertebrates account for a large but ultimately unknown number of envenomations. Cnidaria includes jellyfish, hydrozoa, anemones, and fire coral. A majority of stings from this group result in painful dermatitis; tentacles create a “whip-like” pattern on the skin, whereas fire coral creates localized skin wheals. The sea nettle and Portuguese man-of-war are of greatest interest, given their potential to cause severe systemic symptoms. Box jellyfish are rare in US coastal waters but produce a life-threatening toxicity.

Initial treatment is somewhat controversial. Many resources advocate for the use of seawater for the initial decontamination, given concern for vinegar triggering nematocyst release in some species common to US waters. However, further research is needed to determine which is best. At this time, seawater is recommended for empiric decontamination in the US unless a box jellyfish is strongly suspected, in which case vinegar is appropriate (a very rare circumstance). Systemically ill box jellyfish envenomations should be treated with pain and blood pressure control. The antivenom is not readily available in the US and is unlikely to be beneficial in the time course it would take to obtain it.

Echinodermata, which includes sea urchins, have mild venom on their spines that can cause local tissue irritation and pain. There are reports of severe envenomations with systemic symptoms, but this is ultimately quite rare. These injuries respond well to hot water immersion. Imaging and local wound exploration for retained spines are recommended. Soaking the wound in vinegar may help dissolve superficial spines.

Of the vertebrates, stingrays and spiny fish are of primary concern.

Stingrays stings are common and can cause serious penetrating trauma but envenomation mainly produces localized pain and swelling. The venom is heat-labile, so significant pain relief can be achieved with hot water immersion. Stingrays stings have the potential for both retained stinger and wound infections; evaluation for retained stinger with radiographs and local wound exploration is recommended along with prophylactic antibiotics.

Spinyfish, in particular stonefish, lionfish, and scorpionfish, have venom located in their spines. Stonefish have the most potent venom of any known fish. Lionfish are not native to the US but have become an invasive species. Human contact with these fish occurs both in the wild and in aquariums. These fish also have heat-labile venom susceptible to hot water immersion. However, systemically ill stonefish envenomations should receive the antivenom as this envenomation can be life-threatening; the antivenom will likely work against other spiny fish too, however, these other envenomations are usually much less severe and rarely require more than hot water immersion and supportive care.

So key learning points:

Most marine envenomations involve heat-labile venom. Hot water immersion is likely to help reduce local symptoms.
Systemic illness is rare but some marine envenomations can produce life-threatening toxicity. Be very wary of a systemically ill envenomation and try to figure out the source due to the limited availability of antivenoms.
Prophylactic antibiotics are recommended for stingray stings as they tend to get infected but otherwise are generally not necessary in most populations. Good wound care, evaluation for retained foreign bodies, and tetanus prophylaxis are the mainstays.
For further information, see this review article

Justin Seltzer, MD

UCSD Health Toxicology Fellow

Emergency Physician, UCSD Health

How To Cite This Post:

[Peer-Reviewed, Web Publication] Tandlich, M. Renshaw, C. (2022, Mar 7). Marine Envenomations. [NUEM Blog. Expert Commentary by Seltzer, J]. Retrieved from http://www.nuemblog.com/blog/marine-envenomations

Crashing Patient on a Ventilator

Expert Commentary

Thank you for this succinct summary of an incredibly important topic. We as emergency physicians spend a lot of time thinking about peri-intubation physiology but the challenges do not end once the plastic is through the cords. The frequency with which our ventilated patients stay with us in the ED has been increasing for years and will likely continue to do so1. This means that managing both acute decompensation and refractory hypoxemia needs to be in our wheelhouse.

The crashing patient on the ventilator can be truly frightening and your post effectively outlines a classic cognitive forcing strategy for managing these emergencies. A truism in resuscitation is to always rule out the easily correctable causes immediately. In this case, it means removing the complexity of the ventilator and making things as idiot-proof as possible. Once you’ve ruled out the life threats like pneumothorax, tube displacement, and vent malfunction, you can try to bring their sats up by bagging. Just make sure that you have an appropriately adjusted PEEP valve attached to your BVM for your ARDS patients; the patient who was just requiring a PEEP of 15 isn’t going to improve with you bagging away with a PEEP of 5.

Once you’ve gotten the sats up and the patient back on the vent, your ventilator display can provide you with further data as to why your patient decompensated. Does the flow waveform fail to reach zero suggesting breath stacking and a need for a prolonged expiratory time? Is the measured respiratory rate much higher than your set rate with multiple breaths in a row indicating double-triggering? The measured tidal volume might fall short of your set tidal volume. This points towards a circuit leak, cuff leak, or broncho-pleural fistula. Maybe you’re seeing the pressure wave dip below zero mid-inspiration and the patient is telling you that they are in need of faster flow, a bigger breath, or deeper sedation. In these situations, your respiratory therapist is going to be your best friend in managing this patient-ventilator interactions2.

As your post alludes to, sometimes patients remain hypoxemic despite our usual efforts and refractory hypoxemia can be an intimidating beast when you’ve got a busy ED burning down around you. If your cursory efforts to maintain vent synchrony by playing with the ventilator dials have failed, there’s no shame in deepening sedation which will work to decrease oxygen consumption and prevent derecruitment. Once sedated, work with your RT to find appropriate PEEP and tidal volumes to meet your goals.

Most patients can be managed with usual lung-protective ventilation but some patients will require more support and you’ve correctly identified several salvage therapies. My general approach is to pursue prone positioning in any patient with a P:F ratio approaching 150 despite optimal vent settings as it has the only strong mortality benefit of the therapies outlined above. Proning in the ED is resource intensive and is probably better pursued as a department-wide protocol rather than you and your charge nurse trying to figure it out in the middle of the night3.

As you’ve pointed out, the neuromuscular blockade has more limited evidence and is not required for prone ventilation. Upstairs, we accomplish this with continuous infusions but in the ED you may be more comfortable using intermittent boluses of intubation dose rocuronium. Just make sure your patient is unarousable. I reach for this if I’m unable to achieve ventilator synchrony with sedation alone as it allows for very low tidal volumes and inverse ratio ventilation. I see inhaled pulmonary vasodilators in a similar light: there’s no data on patient-oriented outcomes but they can make your numbers look prettier while you wait for more definitive interventions such as transfer.

This finally brings me to VV ECMO for refractory hypoxemia. It’s worth considering that while there is some evidence for a mortality benefit for ECMO in ARDS, the evidence base is mixed. The CESAR trial did show a mortality benefit in patients transferred to an ECMO center but only 76% of patients actually received ECMO upon transfer4. The larger and more recent EOLIA trial failed to demonstrate this improvement in mortality5. The conclusion I take from this is that treatment at a high volume center matters and that a boarding patient with refractory hypoxemia warrants an early consideration for transfer to a tertiary center if high-quality ARDS care can’t be accomplished upstairs at your shop.

References

Mohr NM, Wessman BT, Bassin B, et al. Boarding of Critically Ill Patients in the Emergency Department. Crit Care Med. 2020;48(8):1180-1187. doi:10.1097/CCM.0000000000004385
Sottile PD, Albers D, Smith BJ, Moss MM. Ventilator dyssynchrony – Detection, pathophysiology, and clinical relevance: A Narrative review. Ann Thorac Med. 2020;15(4):190. doi:10.4103/atm.ATM_63_20
McGurk K, Riveros T, Johnson N, Dyer S. A primer on proning in the emergency department. J Am Coll Emerg Physicians Open. 2020;1(6):1703-1708. doi:10.1002/emp2.12175
Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet Lond Engl. 2009;374(9698):1351-1363. doi:10.1016/S0140-6736(09)61069-2
Combes A, Hajage D, Capellier G, et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. N Engl J Med. Published online May 23, 2018. doi:10.1056/NEJMoa1800385

Matt McCauley, MD

How To Cite This Post:

[Peer-Reviewed, Web Publication] King, P. Akehtuamhen, A. (2022, Feb 28). Crashing Ventilator Patient. [NUEM Blog. Expert Commentary by McCauley, M]. Retrieved from http://www.nuemblog.com/blog/crashing -vent-patient.

End of Life Care in the ED

**Written by:** Savannah Vogel, MD (NUEM ‘24) **Edited by:** Logan Wedel, MD (NUEM ‘22)
**Expert Commentary by**: Matt Pirotte, MD

References

“Discussing Goals of Care.” UpToDate, www.uptodate.com/contents/discussing-goals-of-care

Ganta, Niharika, et al. “SUPER: A New Framework for Goals of Care Conversation.” SGIM Forum, vol. 40, no. 3, 2017.

“Transitions/Goals of Care.” VitalTalk, 9 May 2019, www.vitaltalk.org/guides/transitionsgoals-of-care

Expert Commentary

This is a nice review of the steps of what can be a very difficult conversation from Drs. Vogel and Wedel; I encourage emergency providers (especially residents) to run towards these situations aggressively and not expect other doctors to begin these challenging discussions.

While their piece is chock full of great tips, let me throw out a few of my own that might help you on your next shift.

“I am worried” is a great phrase to open the conversation. These are confusing topics for families and loved ones, our medical jargon is usually not fully suppressed and generally makes things even worse. While a family member can misunderstand a diagnosis or a prognosis, no one can misunderstand another person’s worry. “I am worried that your husband might not survive this illness” is very clear.
Be the first step. Remember that you might be the first step in what might be a series of conversations. When you are admitted to a patient who you think is in big trouble, have a frank honest conversation with the family but do not force them to make decisions. Then your conversation becomes part of your handoff to the inpatient team. The care of the patient will benefit from open communication upfront that minimizes false hope. Emergency doctors know intuitively what trajectory patients are on, a chronically ill elderly patient presenting with shock requiring pressors have an extremely high mortality risk and we should be clear with families about that.
Reassure and validate at every opportunity. Jim Adams gave me a great pearl when I was training at Northwestern which was that when you see worried first-time parents at 3am in the ED with a benign newborn issue you compliment, reassure, and validate. “This kid looks great, you guys are doing a great job.” Same thing with families. Simple statements like “it’s obvious that you care about them” and “I know you are trying to make the right decision and you’re asking great questions” will go a long way towards helping families process this information.
Humanize the body filled with tubes and lines. A few minutes to ask about the patient at the beginning of a tough conversation go a long way. What did they do for a living? What were their hobbies? Families usually end up smiling a little bit here, reminiscing, and telling you some really cool stuff. Sometimes you find yourself laughing with a family that came in the door sobbing. I find these few minutes spent getting to know your patient also helps to steer discussions towards what the patient would have wanted.
Anticipatory guidance is not just for well-child checks! After tough goals of care conversations especially those that end in decisions to move towards palliative care goals I always do 2 things. First I tell the decision-maker that they are making a good and loving decision, that it is the decision I would make for a member of my family, and to not let anyone tell them otherwise. Second, I insist that the family especially the decision-maker drink a bottle of water and eat a sandwich. We’ve all seen an end-of-life situation generate a second patient with dehydration mediated syncopal episode at the bedside, let’s try to prevent that.

I am forever grateful to my PD at NUEM Mike Gisondi for sparking my interest in this topic, it has been an unbelievable gift to me in my clinical practice. As I frequently say in the ED, you cannot avoid difficult goals of care conversations and then complain about the lack of beds in the hospital.

Matt Pirotte, MD

Program Director & Associate Professor of Emergency Medicine

Vanderbilt University Medical Center

How To Cite This Post:

[Peer-Reviewed, Web Publication] Vogel, S. Wedel, L. (2022, Feb 21). End of Life Care in the ED. [NUEM Blog. Expert Commentary by Pirotte, M]. Retrieved from http://www.nuemblog.com/blog/end-of-life-care

Review of the ATHOS 3 trial

**Written by:** Saabir Kaskar, MD (NUEM ‘23) **Edited by:** Amanda Randolph, MD (NUEM ‘20)
**Expert Commentary by**: Matt McCauley, MD (NUEM’ 21)

Review of the ATHOS 3 Trial: Angiotensin II for the Treatment of Vasodilatory Shock

Angiotensin, first isolated in the late 1930s, in recent years has become the new innovative vasopressor used in intensive care units, a change driven largely by the results of the ATHOS-3 trial. The ATHOS-3 trial in 2017 explored the efficacy of angiotensin II as a vasopressor for severe vasodilatory shock. Severe shock is defined as persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65mmHg and serum lactate <2 despite adequate volume resuscitation. Two classes of vasopressors have been used in the past for hypotension. They are catecholamines and vasopressin-like peptides. The human body, however, employs a third class which is angiotensin. Angiotensin II is an octapeptide hormone and a potent vasopressor that is an integral component of the renin-angiotensin-aldosterone system. It works by activating the ANGII type 1 receptor which subsequently activates a G coupled protein pathway and phospholipase C, thereby inducing vasoconstriction.

The ATHOS-3 trial compared the efficacy and safety of angiotensin II versus placebo in catecholamine-resistant hypotension, which is defined as an inadequate response to standard doses of vasopressors. The study was designed as a phase III multicenter randomized placebo control trial taking place across 75 intensive care units in the United States from 2015 to 2017. The three main inclusion criteria were catecholamine-resistant hypotension (defined as >0.2ug/kg/min of norepinephrine or equivalent for 6-48 hours to maintain a MAP 55-70 mmHg), adequate volume resuscitation (25mL/kg of crystalloid), and features of vasodilatory shock (mixed venous O2 >70% and CVP >8mmHg or cardiac index >2.3 L/min/m2).

Patients in vasodilatory shock that met the criteria of catecholamine-resistant hypotension were randomized to treatment with angiotensin II or placebo. Angiotensin II was initiated at an infusion rate of 20ng/kg/min and adjusted during the first three hours to increase MAP to at least 75mmHg. The primary outcome of the study was the response in MAP three hours after the start of angiotensin II infusion. A response was deemed as a MAP increase of 10mmHg from baseline or a MAP over 75mmHg without an increase in baseline vasopressor infusions. During the first three hours, the angiotensin II group had a significantly greater increase in MAP than placebo (12.5mmHg vs 2.9 mmHg). Angiotensin II also allowed for rapid increases in MAP which permitted decreases in doses of baseline catecholamine vasopressor. Additionally, improvement in the cardiovascular SOFA score was significantly greater in the angiotensin II group than in the placebo group. However, the overall SOFA score did not differ between groups. Rates of adverse events such as tachyarrhythmias, distal ischemia, ventricular tachycardia, and atrial fibrillation were similar in the angiotensin II and placebo groups. Overall serious adverse events that included infectious, cardiac, respiratory, gastrointestinal, or neurologic events were reported in 60.7% of patients who received angiotensin II and 67.1% of patients who received placebo.

The strengths and limitations of the ATHOS 3 trial are critical to how its author’s conclusions should be interpreted. The strengths of the study include that it was a randomized double-blind control trial examining a new class of vasopressor for refractory vasodilatory shock. Refractory shock is a common condition with high mortality, and so the investigation of an additional treatment modality can be of great clinical impact. However, one limitation of the study was that it was underpowered to demonstrate a mortality difference. It showed improvement in blood pressure which is a clinically important parameter but not a patient-oriented outcome. Interestingly, when vasopressin was studied in 2008, it similarly did not show a mortality benefit when added to norepinephrine infusion in septic shock2. It did, however, show a decrease in norepinephrine dosing which parallels the findings of the ATHOS 3 trial.

An additional point of contention with the ATHOS 3 trial is that the manuscript does not report an increase in thrombotic risk. It has been shown that angiotensin II increases thrombin formation and impairs thrombolysis3. The FDA even reports angiotensin II has a risk for thrombosis as there was a higher incidence (13% vs 5%) of arterial and venous thrombotic events in the angiotensin II vs placebo group in the ATHOS 3 trial itself. For this reason, the FDA recommends concurrent VTE prophylaxis with the use of angiotensin II. Further data regarding the thrombotic risk of angiotensin II would be helpful to determine which patient populations the vasopressor should be avoided in.

Overall, the author’s conclusion in the ATHOS 3 trial is that angiotensin II increased blood pressure in patients with a vasodilatory shock that did not respond to high doses of conventional vasopressors. It has been shown to raise mean arterial pressure over 75 mm Hg or by an increase of 10 mm Hg within three hours. The ATHOS 3 trial, however, did not demonstrate a mortality benefit when using angiotensin II. Further studies are needed to elucidate whether Angiotensin II truly improves patient outcomes in vasodilatory shock.

Expert Commentary

Thank you for this great summary of the ATHOS 3 trial. While this trial paved the way for the clinical use of angiotensin II as a vasopressor, you’ve raised some salient points as to why we should approach this emerging intervention with skepticism. The biggest shortcoming in my mind is the primary outcome of the study; it’s not particularly impressive that a vasopressor resulted in higher blood pressures compared to a placebo. Mortality benefit is an extremely elusive goal in critical care research1 but that doesn’t discount the fact that ATHOS 3 wasn’t designed to demonstrate an improvement in any patient-oriented outcome. ICU length of stay, hospital length of stay, ventilator-dependent days, or rate of renal replacement therapy: these are all things that matter to our patients and to our health systems and they are more fruitful targets when we investigate interventions.

There’s been some study of angiotensin II in the years since it has landed in our hospital formularies and there has not been robust data supporting its use. Some of the most recent data come from a multi-center retrospective study that includes patients from Northwestern. This review of 270 patients receiving angiotensin II demonstrated that 67% of patients were able to maintain a MAP of 65 with stable or reduced vasopressor doses. Univariate analysis showed that these patients that responded did have a statistically significant mortality benefit over the patients deemed nonresponders (41% vs 25%)2. If we are going to find a benefit of this drug, further study predicting which patients will be responders is necessary but this study did note that patients already receiving vasopressin and those with lower lactates (6.5 vs 9.5) were more likely to respond. Outside of septic shock, there is interest in the use of angiotensin II in refractory vasoplegia associated with post-cardiac surgery3 and anti-hypertensive overdose4. These are, of course, only hypothesis-generating.

But what does that mean to us clinically in the ED and ICU? This data shows us that angiotensin II can make the blood pressure better but I would never let it distract you from the things we know matter in sepsis resuscitation. Source control timely antibiotics, rational fluid resuscitation, and ruling out other causes of vasopressor refractory shock to include anaphylaxis, hemorrhage, adrenal insufficiency, LVOT obstruction, and any other cause of cardiogenic shock need to be ruled out and addressed. In my personal practice, I make sure to optimize these and start vasopressin shortly after the initiation of norepinephrine. In a patient already on vaso that has stopped responding to escalating doses of norepinephrine, I reach for my ultrasound probe and reassure myself that there isn’t significant sepsis-related myocardial dysfunction because those patients may benefit from a trial of an inotrope like epinephrine. In those with a good cardiac squeeze, I think it’s appropriate to discuss with your intensivist and clinical pharmacist the utility of adding angiotensin II as part of a kitchen-sink approach. Until we have more data about the benefits of this extremely expensive intervention, I wouldn’t lose sleep if you’re unable to secure it for your patient.

References

Chawla LS et al. Intravenous Angiotensin II for the Treatment of High-Output Shock (ATHOS Trial): A Pilot Study. Crit Care 2014; 18(5): 534. PMID: 25286986
Russell JA et al. Vasopressin Versus Norepinephrine Infusion in Patients with Septic Shock. NEJM 2008; 358(9): 877 – 87. PMID: 18305265
Celi A et al. Angiotensin II, Tissue Factor and the Thrombotic Paradox of Hypertension. Expert Review of Cardiovascular Therapy 2010; 8(12): 1723-9 PMID: 21108554
Santacruz CA, Pereira AJ, Celis E, Vincent JL. Which Multicenter Randomized Controlled Trials in Critical Care Medicine Have Shown Reduced Mortality? A Systematic Review. Crit Care Med. 2019;47(12):1680-1691. doi:10.1097/CCM.0000000000004000
Wieruszewski PM, Wittwer ED, Kashani KB, et al. Angiotensin II Infusion for Shock: A Multicenter Study of Postmarketing Use. Chest. 2021;159(2):596-605. doi:10.1016/j.chest.2020.08.2074
Papazisi O, Palmen M, Danser AHJ. The Use of Angiotensin II for the Treatment of Post-cardiopulmonary Bypass Vasoplegia. Cardiovasc Drugs Ther. Published online October 21, 2020. doi:10.1007/s10557-020-07098-3
Carpenter JE, Murray BP, Saghafi R, et al. Successful Treatment of Antihypertensive Overdose Using Intravenous Angiotensin II. J Emerg Med. 2019;57(3):339-344. doi:10.1016/j.jemermed.2019.05.027

Matt McCauley, MD

How To Cite This Post:

[Peer-Reviewed, Web Publication] Kaskar, S. Randolph, A. (2022, Feb 14). Review of ATHOS 3 trial. [NUEM Blog. Expert Commentary by McCauley, M]. Retrieved from http://www.nuemblog.com/blog/review-athos3-trial.

Nursemaid's Elbow

Expert Commentary

This is an excellent summary of the diagnosis and management of radial head subluxation (nursemaid’s elbow) in children. Clinically, as pointed out, these patients are usually toddlers and will come in after an injury to the arm. Usually, the clinical history will involve the child’s arm having been pulled on while the elbow was extended leading to sudden onset of pain and reduced mobility of the arm. The patient will most often be holding the elbow in flexion and be resistant to having it manipulated. In general, I have a low threshold to obtain radiographs on these patients. If the story and exam is classic for a radial head subluxation, imaging is technically not indicated, and reduction can be attempted. However, more often than not, the history can be vague, and the mechanism of injury may be unclear. In this situation, it is better to rule out a fracture first than to attempt a reduction without imaging. Attempted reduction could worsen or lead to displacement of a supracondylar humerus fracture if that is present. Keep in mind that it is not uncommon for the subluxation to reduce spontaneously during the process of obtaining x-rays.

There are two preferred techniques for reduction of a radial head subluxation. The method I start with is to support the patient's elbow and forearm and gently supinate the forearm while flexing the elbow and applying gentle pressure over the radial head. A “pop” sensation will often be felt as the radial head reduces. The other technique that can be used is to hyper-pronate the forearm while maintaining the elbow in a flexed position. Both of these techniques have a high success rate. Typically, the child will start using the arm again, but it may not be immediate. I will typically reassess the patient about 10-15 minutes post-reduction to ensure they are using their arm normally again. If the child is using their arm and able to extend and flex at the elbow without pain, they can be discharged, and no splinting is necessary. If no radiographs were obtained prior to reduction and the patient is not back to baseline post-reduction, x-rays should be obtained to rule out a fracture. Keep a broad differential, especially if the patient is not responding as you would expect or has other vital sign or exam abnormalities.

Jacob Stelter, MD, CAQ-SM

Division of Emergency Medicine | NorthShore University HealthSystem

NorthShore Orthopaedic Institute | Primary Care Sports Medicine

Clinical Assistant Professor | University of Chicago Pritzker School of Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Castillo, R. Luo, F. (2022, Feb 7). Nursemaid’s Elbow. [NUEM Blog. Expert Commentary by Stelter, J]. Retrieved from http://www.nuemblog.com/blog/nursemaids-elbow.

Vasopressor Nonresponse

**Written by:** Elizabeth Stulpin, MD (NUEM ‘23) **Edited by:** Aaron Wibberly, MD (NUEM ‘22)
**Expert Commentary by**: Joshua Zimmerman, MD (NUEM ‘17)

Non-Response to Vasopressors

Shock is defined as a state of cellular and tissue hypoxia resulting in end organ dysfunction. This state may arise due to impaired oxygen delivery to tissues, impaired oxygen utilization by the tissues themselves, increased oxygen consumption, or a combination of these mechanisms. Due to its extremely high morbidity and mortality as well as high healthcare costs, the prompt recognition, diagnosis and resuscitation of shock is key. And for most forms, EM physicians are not typically shocked by shock. They have a toolbox of strategies, mainly fluids and vasopressors, to stabilize these critically ill patients.

However, what happens when the trusted treatment paradigm fails? There is a subset of patients who, despite aggressive conventional resuscitation, have an inadequate hemodynamic response and develop refractory shock. This is seen in approximately 7 percent of patients, with short-term mortality ranging from 50 to 80 percent. Due to this significantly lower incidence and increased mortality, alternate causes for refractory shock must be considered when vasopressors do not have the desired effect.

Acidosis

Acidosis in shock states can present from multiple different sources, including sepsis, hypoxemia, ingestions, hyperlactatemia from hypoperfusion, amongst others. With increasing acidosis, calcium influx is reduced, contractility is inhibited and the binding affinity of pressors is reduced, all of which lead to excess vasodilation and refractory hypotension. While bicarbonate is sometimes given in an effort to increase cellular pH, it is controversial for any pH >7.0. At those levels, bicarbonate administration has not been shown to improve cardiac output, MAP or pressor response. While a bicarbonate drip and hyperventilation can temporize an acidosis, emergent HD or CRRT is a definitive treatment if the cause cannot be quickly reversed.

Adrenal Insufficiency

Cortisol has a myriad of functions in the body, not limited to its synergistic effects with catecholamines to help cause vasoconstriction. Thus, when the adrenal glands are chronically suppressed and then experience an acute stressor, hypotension can ensue. The most common cause of chronic suppression is long-term steroid use, and a stressor can include surgery, infection, hypovolemia, pregnancy, medications, or reduced steroid use. Clues that suggest adrenal insufficiency include nausea/vomiting, cutaneous hyperpigmentation, and multiple electrolyte abnormalities (hyponatremia, hyperkalemia, hypoglycemia). Previously healthy individuals, in the setting of critical illness, can also infrequently decompensate into a state of relative adrenal insufficiency. To reverse these effects as well as refractory hypotension, hydrocortisone is the preferred agent due to both its glucocorticoid and mineralocorticoid properties. A loading dose of 100mg IV should be given, followed by 50mg every 6 hours thereafter.

Alternate Shock

Not all shock is declared equal. For example, a patient in cardiogenic shock will likely worsen with the administration of fluids and the wrong vasopressors. Similarly, obstructive shock as seen in massive PEs, tension pneumothoraces or cardiac tamponade will not improve without addressing the cause.

Anaphylaxis

Anaphylaxis may present as hypotension alone. Thus, it may easily be confused with a different form of shock and treated with vasopressors such as norepinephrine and vasopressin, which are not first line for anaphylaxis. Along with using epinephrine as the pressor of choice and other conventional therapies for anaphylaxis, there are alternate medications available for persistent refractory hypotension. One of these is methylene blue. While typically reserved for treatment of methemoglobinemia, the cellular mechanism of methylene blue can decrease vasodilation. Data suggest that this effect can be seen with a one-time dose of 1-2mg/kg.

Hemorrhage

Often a common cause of refractory shock in the post op setting, bleeding can be obscure in its early stages before a hemoglobin drop is appreciated or before the patient develops abdominal distension and flank dullness (retroperitoneal bleed). If concerned, empiric uncrossed unmatched blood can be transfused.

Hypocalcemia

Calcium homeostasis is necessary for the proper maintenance of myocardial contractility and vascular tone. Hypocalcemia can be hinted at through history or by hints such as a prolonged QTc on an ECG. Those at higher risk of hypocalcemia (vitamin D deficiency, ESRD, hyperparathyroidism, burns, multiple blood transfusions, etc.) may have greater severity of shock with increased mortality. In repleting calcium, co-administration of phosphorous and magnesium may allow for reversal of the patient’s shock state.

Hypothyroidism

Decompensated hypothyroidism can have profound effects, including bradycardia, impaired myocardial contractility, and decreased peripheral vasoconstriction. However, even subclinical hypothyroidism with an elevated TSH but normal T4 increases risk of poor outcomes due to effects on cardiac function. While the diagnosis of hypothyroidism can be delayed by lab results, clues to the diagnosis include thyroidectomy scar, non-pitting edema of the extremities, macroglossia, altered mental status, hypoglycemia and hypothermia. Initial hypotension may not respond to vasopressors, but shock should improve once thyroid hormone is given. Stress dose steroids (hydrocortisone 100mg IV) should also be given due to the association between adrenal insufficiency and hypothyroidism, and giving thyroid hormone without steroids can precipitate adrenal crisis.

Ingestions

When in doubt, look at the medication list! Both beta blocker and calcium channel blocker toxicity can cause profound myocardial depression, bradycardia and hypotension due to their inhibition of calcium signaling. Refractory hypotension can be overcome with the use of direct cardiac pacing, calcium, glucagon, or high dose insulin. And if all else fails, ECMO can overcome medication toxicity until it can be fully metabolized or cleared.

When conventional resuscitation for shock with fluids, vasopressors and/or inotropes fails, it is time for a cognitive pause. By running through this list of alternate causes of refractory shock, other methods of resuscitation can be added to improve patient outcomes and stabilize the patient.

Sources:

1) Amrein K, Martucci G, and Hahner S. Understanding adrenal crisis. Intensive Care Medicine. 2018; 44(5): 652-655.

2) Boyd J, Walley K. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Curr Opin Crit Care. 2008;14:379-83.

3) Farkas J. Decompensated Hypothyroidism. The Internet Book of Critical Care. 2016. Accessed https://emcrit.org/ibcc/myxedema/

4) Ho H, Chapital A, and Yu M. Hypothyroidism and Adrenal Insufficiency in Sepsis and Hemorrhagic Shock. Arch Surgery. 2004; 139(11):1199-1203.

5) Kerns W. Management of B-Adrenergic Blocker and Calcium Channel Antagonist Toxicity. Emergency Medicine Clinics of North America. 2007; 25: 309-331.

6) Levy B, Collin S, Sennoun N, et. al. Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside. Intensive Care Medicine. 2010; 36: 2019-2029.

7) Manji F, Wierstra B, and Posadas J. Severe Undifferentiated Vasoplegic Shock Refractory to Vasoactive Agents Treated with Methylene Blue. Case Reports in Critical Care. 2017.

8) Minisola, S et al. Serum Calcium Values and Refractory Vasodilatory Shock. Chest. 2019; 155(1): 242.

9) Nandhabalan P, Ioannou N, Meadows C and Wyncoll D. Refractory septic shock: our pragmatic approach. Critical Care. 2018; 22(1):215.

10) Smith L, and Branson B. Refractory Hypotension – Diagnosis and Management in Surgical Patients. California Medicine. 1961; 95(3): 150-155

11) Velissaris D, Karamouzos V, Ktemopoulos N, Pierrakos C, and Karanikolas M. The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate. Critical Care Research and Practice. 2015.

12) Wang H, Jones A, and Donnelly J. Revised National Estimates of Emergency Department Visits for Sepsis in the United States. Critical Care Medicine. 2017; 45(9): 1443-1449.

Expert Commentary

Dr. Stulpin's review of a very critical topic is well articulated and concise. I would like to particularly emphasize her final points before delving into the details. As she pointed out, patients failing to respond to typical resuscitative efforts represent quite a quagmire to the ED physician. It is easy to arrive at premature closure and presume all shock to be sepsis simply needing more fluids or vasopressors. However, there is significant risk in this practice, and I would thus advocate very strongly for a “pause” and thorough reassessment of the patient’s presentation and condition. Much akin to a pre-procedural time out, this should be deliberate and uninterrupted to prevent diagnostic momentum from building and arriving at a premature closure on the etiology of the patient’s condition.

This review covers much of the differential and pathophysiology that is germane to a discussion of refractory shock. Rather than review this in detail, I would like to discuss a practical approach to application of this knowledge at the bedside. So, as we approach the patient who is refractory to standard resuscitation, one’s first task is to confirm the patient is receiving the desire therapy and that this is truly shock refractory to intervention. Check all access points for infiltration –the single most reversible cause for refractory hypotension is that the patient is not receiving fluids/vasopressors, etc. due to inadequate access. Check dosing and confirm with nursing that infusions have been running appropriately. If access is the issue, I would advocate placing a more reliable form such as central access or, in the very unstable, IO access early in the reassessment. While I am an advocate for US guided access in stable patients and feel that this is often a great tool, this is a scenario I would advocate against US guided peripheral access. This form of access is often time consuming, and more importantly, signs of infiltration are less evident in deeper IV sites which is a serious concern if you are running peripheral vasopressors.

Presuming your access is adequate, the next task is to reassess perfusion in its entirety. While not mandatory, this is a point where I would consider placing an arterial line for optimally reliable BP monitoring. One must perform a complete re-examination as well. If not already completed, a rectal exam for the occult GI bleeding. One should additionally particular attention on reassessment to skin and perfusion. Check capillary refill, skin temperature and coloration as a matter of habit for cases of refractory shock. Cool extremities are not typically associated with distributive shock and should make you consider shock states with high SVR such as cardiogenic or acute blood loss. In addition, a repeat skin exam may reveal new rashes – I look specifically for the presence of petechiae, purpura or urticaria. Urticaria should prompt consideration of anaphylaxis. If the patient has received any antibiotics yet this is an important consideration given antibiotics are one of the most common medication precipitants of anaphylaxis and this may be the source of their worsening shock state.

After completing your thorough exam, I strongly advocate for a sonographic assessment as well. This is where the RUSH exam, or at least a modified version, fits well into patient assessment and can offer a great deal of information. I pay particularly close attention to the cardiac and abdominal windows. This can aid in the rapid diagnosis of an obstructive shock state such as cardiac tamponade, or acute RV failure in the setting of massive PE. Free intra-abdominal fluid should be considered hemorrhage until proven otherwise in the shock patient. One reminder is that when assessing for occult bleeding, the FAST exam views are an excellent tool but not sufficiently sensitive for definitive rule out. In particular, the FAST exam lacks sensitivity for retroperitoneal bleeding and therefore if there remains high clinical concern, CT imaging should also be considered.

Once a thorough re-examination is completed, reconsider the patient’s medications as another source. Patients are on a myriad of antihypertensives and other agents that can lower blood pressure. Many of the pathways that metabolize or eliminate these drugs are compromised in a state of hypoperfusion and can lead to a synergistic worsening of hypotension. One example of this is the case of BRASH Syndrome. In addition to antihypertensives, a review of the patient’s medication list should include a particular search for steroids or other adrenal replacements such as fludrocortisone. An extremely important cause of refractory hypotension to consider is that of adrenal insufficiency. As Dr. Stulpin reviewed in her discussion above, this can come in both primary and secondary forms. The latter is far more common and induced by exogenous steroid use. A wise ICU attending once taught that no patient should die without stress dose steroids. While perhaps a bit morbid, the take home point here was that adrenal insufficiency can present in any patient, not just those with underlying disorders of glucocorticoid production. Pay particular attention to patients with autoimmune disorders or others on chronic steroid therapy as these are the populations that are particularly at risk. Patients presenting with unexplained hypoglycemia in the setting of sepsis or shock of any kind should also be strongly considered to receive stress dose steroids. Do not wait for a cortisol level to treat this condition. Consider, as well, checking TSH and free T3/T4 as patients with adrenal insufficiency can simultaneously harbor other endocrinopathies.

To summarize, refractory hypotension or failure to respond to traditional interventions is relatively uncommon but critical to identify in shock patients. Often these patients have a primary diagnosis of septic shock but can suffer from concurrent shock related to one or more of the differential considerations we have reviewed above. A thoughtful reassessment, both of the patient’s physical exam findings, US and other diagnostics, medication list and history of present illness will offer clues that may uncover an additional etiology critical to treat and to ensure the best outcome possible.

Joshua D. Zimmerman, MD

Health System Clinician

Feinberg School of Medicine

Northwestern Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Stulpin, E. Wibberly, A. (2022, Jan 24). Vasopressor Nonresponse. [NUEM Blog. Expert Commentary by Zimmerman, J]. Retrieved from http://www.nuemblog.com/blog/vasopressor-nonresponse

Hyponatremia

Expert Commentary

Thanks for a great review on hyponatremia by Drs. O’Brien & Kaltman. I’ve recruited the expert insight from one of my favorite colleagues and fellow Northwestern University Feinberg School of Medicine graduate Joshua Waitzman, MD PhD, Instructor of Nephrology at Beth Israel Deaconess Medical Center in Boston, MA.

I’ll highlight a few points from an emergency medicine point of view with Dr. Waitzman’s additional commentary from the nephrology perspective.

I’d argue the primary question you need to answer in the ED for hyponatremia patients is whether or not hypertonic saline is indicated. For those well-appearing neurologically intact hyponatremia patients w/ sodium levels > 120, further work-up & analysis of the underlying etiology can be deferred to the inpatient side. It’s always appreciated to send the hyponatremia labs (eg urine lytes, osms, TSH, etc) for the admitting team, however differentiating SIADH from cerebral salt-wasting should not be at the top of your priority list. Especially as the etiology of hyponatremia is commonly multifold.
- Dr. Waitzman: additionally, a key reminder is to STOP AND THINK before giving isotonic fluids (0.9% NS, LR, bicarb gtt, etc). For most patients with moderate-to-severe hyponatremia, giving a liter of normal saline is normally the wrong answer.
  - If your patient has SIADH, heart failure, or cirrhosis (common causes of hyponatremia), additional IV fluids will end up worsening the hyponatremia.
  - If your patient is volume depleted, isotonic fluids will fix the volume problem and shut off ADH, leading to rapid increases in urine output and rises in sodium. The worst thing we can do to patients with bad hyponatremia is overcorrect them too quickly.
If you are considering hypertonic saline, make sure to get your nephrologist on board early. Nephrology is the primary team that will be following your patient from arrival in the ED through discharge so if you’re debating whether the patient requires 3% NaCl, please consult your nephrology team ASAP. Though w/ that said, if your patient is seizing due to hyponatremia, push the hypertonic then get nephrology on board afterwards.
- Dr. Waitzman: 100%. If you’re debating on hypertonic saline, call nephrology at any time. However, for the sake of your friendly overworked nephrology fellow, please wait until the AM before calling about patients who appear well and have sodium > 125. When consulting nephrology for hyponatremia, please have a urine sodium, potassium, and creatinine at the ready.
Hypertonic saline is not only indicated for seizures, coma, suspected cerebral herniation or focal neurological deficits as noted above. Keep in mind the indication for 3% also extends to altered mental status and can present w/ simple confusion or even “just acting off” from baseline. Do keep in mind the acuteness of the neurologic status is also imperative to determining the need of hypertonic. More acute symptoms = higher likelihood of needing 3%. It’s essential to get background information from family/friends if the patient is unable to provide any additional history regarding their own baseline level of functioning.
- Dr. Waitzman: In my mind, using hypertonic saline should be based on three things.
  - First, how bad is the sodium level? It’s normally not worth it for most patients above 120.
  - Second, how acute is the hyponatremia? Hypertonic can be risky for those with chronic hyponatremia but curative for those with hyperacute hyponatremia like marathon runners.
  - Third, how severe are the symptoms? Seizures attributed to hyponatremia need treatment ASAP.
- Because I’m a nephrologist, I approach the use of hypertonic saline like an equation, combining the acuteness of the hyponatremia with the severity of symptoms. For example, the more recent the sodium drop w/ more severe symptoms = more comfortable w/ hypertonic. The more chronic the hyponatremia and the less severe symptoms = hypertonic may have more risk than benefit.
Of note, you do NOT need a central line for hypertonic saline administration. Though this is dictated by your own hospital protocols, hypertonic saline has been shown to be safe when pushed in small doses through a large-bore peripheral (proximally placed) IV [1,2]. Though if your administration says differently, do not waste time putting in a triple lumen catheter if hypertonic is truly indicated in your hyponatremia patient. Drill an IO and push the 100-150cc 3% NaCl as soon as possible.
- Dr. Waitzman: PREACH.
Do remember that pseudo-hyponatremia is a thing. Most commonly seen in our ED patients w/ hyperglycemia, other solutes which can lead to pseudo-hyponatremia are mannitol, glycol, or maltose (all three most commonly encountered on the inpatient side or post-outpatient urologic procedures). If you appreciate an elevated glucose on your chemistry panel, you can use the following equation

Corrected Na = Measured Na + [(1.6 * (glucose-100)/100)] [3]

or this helpful link via MDCalc (https://www.mdcalc.com/sodium-correction-hyperglycemia) to determine the appropriate corrected sodium.

Dr. Waitzman: If you hate math, consider a blood gas sodium. There is no pseudohyponatremia on a blood gas sodium and it results faster than your normal chemistry panel sodium level.

MDMA/ecstasy use is an uncommon cause of hyponatremia that should not be forgotten [4]. Keep that in mind in your presumed “intoxicated” young party-goers, especially those where these drugs are prevalent (eg raves, music-festivals, etc). MDMA leads to hyponatremia by activation of arginine vasopressin which increases kidney free water absorption [5].
Vaptans have not been established as standard of care for hyponatremia in emergency medicine. If these are to be utilized in an ED patient, it is essential that there is a nephrologist on board who is actively involved in the patient’s management.
- Dr. Waitzman: wholeheartedly agree. Vaptans don’t have a place in the acute settings (like the ED) and have a huge risk of over-correcting the sodium. If you need to acutely correct hyponatremia, hypertonic is the answer, not vaptans.
With boarding being a nation-wide issue, one final piece of commentary from both the emergency medicine & nephrology perspective: if you’re sending your patient to the ICU for hyponatremia, it’s because they require q2hr sodium levels. Please continue those q2hr sodium levels while they remain under your care in the ED while waiting for an ICU bed. Blood gas sodiums are a great way to trend sodium levels as they’re accurate & result quickly (and avoid the potential for pseudohyponatremia as described above).

I’d like to extend an incredibly huge thank you & sincere gratitude to Dr. Waitzman for his assistance & expertise on this expert commentary. We’re all exceptionally lucky to work with such fantastic nephrology colleagues and are eternally appreciative for all their help, insight, and expertise.

References:

Alenazi AO, Alhalimi ZM, Almatar MH, Alhajji TA. Safety of Peripheral Administration of 3% Hypertonic Saline in Critically Ill Patients: A Literature Review. Crit Care Nurse. 2021 Feb 1;41(1):25-30. doi: 10.4037/ccn2021400. PMID: 33560431.
Mesghali E, Fitter S, Bahjri K, Moussavi K. Safety of Peripheral Line Administration of 3% Hypertonic Saline and Mannitol in the Emergency Department. J Emerg Med. 2019 Apr;56(4):431-436. doi: 10.1016/j.jemermed.2018.12.046. Epub 2019 Feb 8. PMID: 30745195.
Katz MA. Hyperglycemia-induced hyponatremia--calculation of expected serum sodium depression. N Engl J Med. 1973 Oct 18;289(16):843-4. doi: 10.1056/NEJM197310182891607. PMID: 4763428.
Petrino R, Marino R. Fluids and Electrolytes. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; Accessed July 21, 2021.
Campbell GA, Rosner MH. The agony of ecstasy: MDMA (3,4-methylenedioxymethamphetamine) and the kidney. Clin J Am Soc Nephrol. 2008 Nov;3(6):1852-60. doi: 10.2215/CJN.02080508. Epub 2008 Aug 6. PMID: 18684895.

Sarah Dhake, MD

Division of Emergency Medicine, NorthShore University HealthSystem

Clinical Assistant Professor, University of Chicago - Pritzker School of Medicine

Twitter: @ssandersEM

sdhake@northshore.org

Joshua Waitzman, MD PhD

Instructor in Medicine, Harvard Medical School
Division of Nephrology, Department of Medicine
Beth Israel Deaconess Medical Center

Twitter: @Jwaitz
jswaitzm@bidmc.harvard.edu

How To Cite This Post:

[Peer-Reviewed, Web Publication] O’Brien, J. Kaltman, D. (2022, Jan 10). Hyponatremia. [NUEM Blog. Expert Commentary by Dhake, S and Waitzman, J]. Retrieved from http://www.nuemblog.com/blog/hyponatremia

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Posted on January 10, 2022 by NUEM Blog and filed under Endocrine and tagged hyponatremia endocrine hypertonic Marathon mdma.

Running Injuries

Written by: Eric Power, MD (NUEM ‘24) Edited by: Justin Seltzer, MD (NUEM '21) Expert review by: Terese Whipple, MD (NUEM '20)

With over 40 million runners in the United States alone and an ever-increasing interest in fitness among the general population, the frequency of running injuries presented to urgent care and emergency departments will only grow with time. This is especially true due to the high rate of injury among runners, with a published annual incidence rate ranging from 19% to 79%; with even conservative estimates, that is nearly 8 million running injuries annually.

There are several risk factors for running injuries with which the emergency physician should be familiar. Running injuries are generally the sequela of repetitive stress. Acute injuries represent a small minority of cases and are usually not serious. The strongest risk factors include older age, high mileage running, beginners or suddenly restarting running, those making a rapid increase in speed and/or distance, low bone density, and those with a history of previous injuries.

This article will focus primarily on several “low acuity” running injuries along with their initial evaluation and management. A vast majority of running injuries are not serious, however, the evaluation of the injured runner still demands detailed musculoskeletal examination and thoughtful consideration of more dangerous potential causes of the symptoms. Proper clinical diagnosis and recommendations can certainly speed recovery and return to activity.

Iliotibial (IT) band syndrome

Major population: Young, active with a recent change in running mileage and/or runs on hilly terrain

Presentation: Lateral knee pain, especially with activity, with or without lateral thigh and hip pain

Diagnosis: Tenderness along lateral thigh extending into the lateral knee, swelling at the distal aspect may be present, Ober’s test for IT band tightness (not diagnostic)

EM differential: meniscus injury, stress fracture, lateral ligamentous injury

Initial treatment: No running until pain resolves then gradual return at painless speeds, distances, home exercise program to stretch IT band

Follow-up: Routine primary care, consider PT referral

Patellofemoral pain syndrome

Major population: Young, usually female, participating in sports with high volume running and/or jumping

Presentation: Anterior, aching knee pain worse with knee flexion (e.g. climbing stairs)

Diagnosis: Anterior patella tenderness; pain with patellar grind test, deep knee flexion

EM differential: meniscus injury, stress fracture, ligamentous injury

Initial treatment: home exercise program or formal physical therapy to strengthen quadriceps, core, and hip abductors. consider a patella stabilizing knee brace

Follow-up: Routine primary care, consider PT referral

Medial Tibial Stress Syndrome (“Shin Splints”)

Major population: Any patient with a recently initiated intense exercise regimen

Presentation: Anteromedial tibial pain provoked by activity and improved with rest

Diagnosis: Reproduction of pain with palpation of a diffuse area of the posteromedial border of the tibia

EM differential: stress fracture, DVT, exertional compartment syndrome

Initial treatment: Rest, icing (~20 minutes per hour) until the pain has resolved, then a gradual return to activity at painless speeds, distances

Follow-up: Routine primary care, consider PT, sports medicine referral due to high failure rate of conservative management

Achilles Tendinopathy

Major population: Usually middle-aged with recently initiated exercise or increased intensity/frequency

Presentation: Chronic, gradually worsening posterior heel and foot pain, often worst in the morning, with an impaired plantarflexion and explosive movements of the ankle

Diagnosis: Tendon palpation reproduces the pain, diminished range of motion and strength, calf muscle atrophy (late finding)

EM differential: calcaneal stress fracture, DVT, Achilles tendon rupture

Initial treatment: Reduce the intensity of activity to walking only until pain resolves, home exercise program to stretch and eccentrically load the Achilles tendon

Follow-up: Sports medicine and PT referrals due to benefit of rehabilitation and availability of multiple specialized therapies; some cases are treated surgically

Plantar Fasciitis

Major population: High volume or newly initiated/increased running or sports, slightly more common in women

Presentation: Classically plantar midfoot to heel pain worse with the “first step” in the morning

Diagnosis: Pain reproduced with palpation of the medial tubercle of the calcaneus and proximal plantar fascia, positive windlass test

EM differential: Foot stress fracture

Initial treatment: Avoid triggering activities, home exercise program to stretch and deeply massage the plantar fascia

Follow-up: Referral to PT and a foot and ankle specialist (orthopedic surgeon or podiatrist) as chronic symptoms are common

Key points

A majority of running injuries are not serious or acute but can be function limiting if not properly diagnosed and managed
It is important to rule out major relevant differential diagnoses such as stress fractures, DVT, and ligament/tendon injuries prior to discharge
Universal management is with rest, as needed NSAIDs, a gradual return to activity when the pain has resolved, and routine primary care follow up; primary care sports medicine or orthopedic surgery should be reserved for severe symptoms or failure of conservative management
Alongside home exercises and stretches, consider PT referral routinely

References

Li HY, Hua YH. Achilles Tendinopathy: Current Concepts about the Basic Science and Clinical Treatments. Biomed Res Int. 2016;2016:6492597.
McClure CJ, Oh R. Medial Tibial Stress Syndrome. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538479/
Petersen W, Ellermann A, Gösele-Koppenburg A, et al. Patellofemoral pain syndrome. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2264-2274.
Petraglia F, Ramazzina I, Costantino C. Plantar fasciitis in athletes: diagnostic and treatment strategies. A systematic review. Muscles Ligaments Tendons J. 2017;7(1):107-118. Published 2017 May 10.
Strauss EJ, Kim S, Calce JG, Park D. Iliotibial Band Syndrome: Evaluation and Management. American Academy of Orthopaedic Surgeon. 2011;19(12):728-736.
van der Worp MP, ten Haaf DS, van Cingel R, de Wijer A, Nijhuis-van der Sanden MW, Staal JB. Injuries in runners; a systematic review on risk factors and sex differences. PLoS One. 2015;10(2):e0114937. Published 2015 Feb 23.

Expert Commentary

Thank you to Drs. Power and Seltzer for their concise and relevant review of common overuse injuries seen in runners. Although most of these injuries would not be considered emergent, correct diagnosis and referral of these patients is important to keep them active and decrease their likelihood of suffering the heart attacks, strokes, and chronic pain we see daily. This post did an excellent job of walking through several common injuries however, there is one more that I would like Emergency Physicians to consider in their differential for runners with extremity pain: Stress Fracture.

A stress fracture is break down in bone that occurs when abnormal stress is applied to healthy bone or normal stress is applied to unhealthy bone (osteopenia/porosis)
Female athletes are at particular risk if they are not fueling well enough, sometimes manifesting in menstrual dysfunction and decreased bone density
Commonly occurs in healthy runners when an athlete is increasing their training volume or intensity, or other new stress is applied such as a new running surface
Complain of insidious onset pain that worsens with running and other pounding activity. Pain is often better with rest early on.
If the bone is palpable from the surface, it will have point tenderness over the area. Pain will be reproduced with the hop test and the fulcrum test.
X-rays may be normal early on, later in the course, they may show periosteal reaction or fracture line. MRI can be obtained on an outpatient basis if needed.
Most stress injuries can be managed by decreased weight bearing through alterations in training, however, sometimes offloading with a walking boot or crutches may be necessary depending on severity and location.
High-risk stress injuries that warrant prompt sports medicine or orthopedics referral: femoral neck (superior aspect), patella, anterior tibia, medial malleolus, talus, tarsal navicular, the proximal fifth metatarsal, tarsal sesamoids.
- If strong suspicion of a high-risk stress injury or diagnosis is confirmed in the ED, these patients should be given crutches and made non-weight bearing until follow-up.

Hopefully, this post will help you build a differential for overuse injuries you may encounter in the ED, and provide proper follow-up in order to keep our patients healthy, active, and engaged in the activities they enjoy.

Terese Whipple, MD

Assistant Professor

Department of Emergency Medicine

University of Iowa Hospitals and Clinics

How To Cite This Post:

[Peer-Reviewed, Web Publication] Power, E. Seltzer, J. (2022, Jan 3). Running Injuries. [NUEM Blog. Expert Commentary by Whipple, T]. Retrieved from http://www.nuemblog.com/blog/runninginjuries

Top Blogs of 2021

Congratulations to all of the authors with the most popular posts of 2021!

1. Pill in the Pocket (23,646 views)

The runaway favorite of this year was Dr. David Feiger’s (NUEM ’22) and Dr. Jon Andereck’s (NUEM ’19) post reviewed by Dr. Kaustubha Patel of Northwestern's Bluhm Cardiovascular Institute about the “pill-in-the-pocket” approach to treating atrial fibrillation.

Take-Home Point: In select patients, the “pill-in-the-pocket” approach is a safe and effective way to treat infrequent but symptomatic paroxysmal atrial fibrillation that reduces ED visits and improves patients’ quality of life.

2. Peripheral Vasopressors: Do I need that central line? (8,683 views)

In the second most popular blog of the year, Dr. Saabir Kaskar (NUEM '23) and Dr. Abiye Ibiebele (NUEM '21), with commentary by Northwestern pulmonologist/intensivist, Dr. Marc Sala, summarize the current literature on the peripheral infusion of vasopressors, which is becoming more and more commonplace as the evidence evolves to support earlier initiation of pressors and more judicious use of crystalloid for many forms of shock.

Take-Home Point: While the evidence at this time is limited, clinicians should feel comfortable administering peripheral vasopressors as a bridge to central infusion for a limited time. Peripheral vasopressors have a lower risk of complications than previously thought and allow clinicians to minimize delays in administering vasoactive medications that may have a mortality benefit.

3. Pericardiocentesis (2,553 views)

Rounding out the top three is Dr. David Feiger's (NUEM '22) and Dr. Abiye Ibiebele's (NUEM '21) post on emergent pericardiocentesis, a potentially life-saving procedure in a patient with hemodynamically significant cardiac tamponade, with expert commentary by Northwestern interventional cardiologist, Dr. Dan Schimmel.

Take-Home Point: Bedside pericardiocentesis is a rare but important procedure that can be performed emergently using ultrasound or landmark guidance. While a subxiphoid approach is commonly performed, an apical or parasternal approach may be considered to minimize potential complications. Consider exchanging the needle for a drain once the pericardium is accessed to bridge to definitive therapy.

4. Hanging Injury (959 views)

Dr. Vytas Karalius (NUEM '22), Dr. Nery Porras (NUEM '21), and expert commentator Dr. Kevin Emmerich describe the mechanisms of injury and management of patients presenting with hanging injuries, an unfortunate but all-too-common method of self-harm worldwide.

Take-Home Point: Hanging injuries can have wide-ranging immediate and delayed complications on multiple organ systems and clinicians should evaluate for cervical spine and cerebrovascular injury and anticipate a difficult airway due to evolving airway edema. Clinicians should have a high index of suspicion for polytrauma or toxic ingestion. Even with an initial negative workup, all patients should be admitted for observation (with a low threshold to transfer to a trauma center) and ultimately a psychiatry consult.

5. Paronychia (623 views)

In one of two procedural infographics to make the top ten this year, Dr. Richmond Castillo (NUEM '23), Dr. Andra Farcas (NUEM '21), and Dr. Matthew Kippenhan provide a visual guide to diagnosing and treating a common "fast-track" complaint.

Take-Home Point: Paronychia is a common infection of the nail fold that often requires an incision and drainage procedure if a purulent fluid collection is present. Be wary of several other "can't miss" visual diagnoses on the differential, such as herpetic whitlow, felon, and proximal onychomycosis.

6. Antiemetics/Gastroparesis (572 views)

With expert commentary by NUEM faculty Dr. Howard Kim, Dr. Nery Porras (NUEM '21) and Dr. Terese Whipple (NUEM '20) provide an overview of the role of antipsychotics in the treatment of gastroparesis and other cyclic vomiting syndromes. These conditions can be difficult to treat, frustrating for both patients and providers, and refractory to traditional antiemetic therapies.

Take-Home Point: Antipsychotic medications such as haloperidol and droperidol are effective therapies for nausea, vomiting, and abdominal pain associated with gastroparesis. Despite previous black box warnings on droperidol causing it to fall out of favor, it is safe and well-tolerated at the doses typically used in an emergency department setting.

7. Basic Capnography Interpretation (560 views)

Dr. Shawn Luo (NUEM '22) and Dr. Matthew McCauley (NUEM '21) review the basics of interpreting continuous waveform capnography, a versatile tool with multiple uses in both the emergency department and critical care settings. Dr. Seth Trueger, NUEM faculty, provides expert commentary.

Take-Home Point: Continuous waveform capnography (otherwise known as end-tidal CO2) is a valuable tool that can inform real-time management decisions in both intubated and non-intubated patients. Recognizing several common patterns can guide providers during several use-cases such as confirming endotracheal tube placement, cardiac arrest, and procedural sedation.

8. Knee Dislocation (436 views)

Knee dislocations are a rare but highly morbid condition for which Dr. Andrew Rogers (NUEM '22) and Dr. Amanda Randolph (NUEM '21) provide a streamlined approach to diagnosing and treating. NUEM's own emergency orthopedic guru, Dr. Matthew Levine, provides expert commentary.

Take-Home Point: Knee dislocations are time-sensitive injuries that require rapid diagnosis and treatment because of the high rate of vascular complications. Emergent closed reduction is key, with a thorough neurovascular exam before and after. All patients require ABIs (with CT angiography if the ABI is abnormal) and admission for neurovascular checks. Speak with your consultants early.

9. TPA in Frostbite (422 views)

For those who practice in colder climates, Dr. Patrick King's (NUEM '23) and Dr. Nery Porras's (NUEM '21) review of the current literature on the role of tPA in frostbite is timely as we enter into the winter season. Expert commentary is provided by Dr. Anne Lambert Wagner, medical director of the Burn and Frostbite Center at the University of Colorado Health.

Take-Home Points: While literature continues to evolve, current evidence supports the use of tPA in select patients with severe frostbite injuries in multiple digits, multiple limbs, or proximal limb segments presenting within 24 hours of injury. Combined with active rewarming strategies, tPA use results in significantly improved outcomes.

10. Felon (381 views)

Rounding out the top 10 for 2021 is the second procedural infographic, which is closely related to our Paronychia post. The expert review of Dr. Matthew Levine, Dr. Daniel Levine (NUEM '23), and Dr. Will LaPlant (NUEM '20) illustrate the diagnosis and management of felons in the emergency department.
Take-Home Point: Understanding finger anatomy is key to understanding felons, which present as tense, throbbing, purulent infections of the distal finger pad. Incision and drainage is the mainstay of therapy for felons, with a course of oral antibiotics and mandatory hand surgery follow-up to avoid complications such as flexor tenosynovitis or osteomyelitis of the distal phalanx.

Posted on December 27, 2021 by NUEM Blog and filed under top 10 2021 and tagged Top 10.

Hip Pain in Pediatrics

Written by: Tommy Ng, MD (NUEM ‘24) Edited by: Patricia Bigach, MD (NUEM ‘22) Expert review by: Terese Whipple, MD '20

So your kid won’t walk

One of the most common complaints in a pediatric Emergency Department is a child refusing or inability to ambulate. For normal development, a child is typically able to stand at 9 months, walk at 12 months, and run at 18 months. There is a certain degree of variability for these age constraints however any acute decrease in mobility should prompt an evaluation. A limp is defined as any abnormality in gait caused by pain, weakness, or deformity [1]. There are a plethora of conditions that can manifest with an antalgic gait or refusal to bear weight and it may be difficult to distinguish between etiologies given a child’s age.

History and physical

Age is an important factor as certain conditions are more likely depending on the patient’s age

Acuity should be determined as the chronicity of limp as certain etiologies are more acute while others are indolent. Additionally, certain infectious etiologies are more likely to present acutely or chronically.

Fever may suggest an infectious or rheumatologic cause

Trauma can help distinguish soft tissue vs orthopedic injuries

Past medical history is important to be focused on recent illnesses, antibiotic use, history of sickle cell disease, or hormonal diseases.

Physical examination should always include an attempt to ambulate the child unless there is an obvious contraindication noted immediately (eg open fracture). If the child refuses to bear weight, the child should be made non-weight bearing until serious pathology which can be worsened by walking is ruled out. Strength and range of motion of both lower extremities should also be examined [2].

Differential: the bad, the worse, and the ugly

Infectious

Transient Synovitis - Relatively common with a lifetime risk of 3%. Affects ages 3-8, males to females 2:1 [3]. Typically well appearing with normal labs, however, this is a diagnosis of exclusion and a septic joint should be ruled out. Management includes NSAID use and return to activity as tolerated [4].
Septic Arthritis - A “do not miss” diagnosis, commonly ages 3-6 with a slight male predominance [5]. Typically presenting with fevers and abnormal labs. The Kocher Criteria (originally developed in 1999 and validated in 2004) can be helpful in determining the likelihood of septic arthritis [6]. Management includes imaging studies, typical ultrasound to assess for a joint effusion, then a diagnostic arthrocentesis & antibiotics. The antibiotic regimen should be tailored to the child’s age and other predisposing factors to certain pathogens.

Osteomyelitis - Occurs in 1:5000-7700 kids in increased prevalence with MRSA communities; 2:1 male to female predominance with half of all cases occurring in ages less than 5 [7]. Commonly hematogenous spread from bacteremia; clinical suspicion should prompt radiologic evaluation. X-rays may be likely to be normal/inconclusive early in the disease course and MRI may be often indicated. Labs can be helpful but are not specific; a systematic review of >12,000 patients showed that elevated WBC was only present in 36% of patients [7]. ESR and CRP are non-specific but have a sensitivity of 95% [7]. Antibiotic therapy guidelines are similar to the management of septic arthritis. Surgical intervention may be indicated if there is a lack of improvement after 48-72 hours [8].

Osteomyelitis of the distal tibia (orthobullets.com)

Orthopedic

Legg-Calve-Perthes / Avascular Necrosis of the Hip - Age range 3-12 with a peak at 5-7, male to female ratio 3:1, can be bilateral in 10-20% of patients [9]. Radiographs should be obtained with high clinical suspicion but are often normal early in the course. An MRI would show fragmentation of the femoral head. The patient should be made non-weight bearing and be referred to a specialist. Children under 8 typically have a better prognosis however long-term management is poorly defined as there has been no long-term study [10].

Avascular necrosis of bilateral hip (orthobullets.com)

Slipped Capital Femoral Epiphysis - Typically obese child, median age 12, bilateral in 20-40% of cases [11]. Presentation is classically chronic hip pain with antalgic gait however may present with knee pain. Physical exam classically shows external rotation and abduction of the hip during hip flexion. Management is orthopedic consultation for operative stabilization [12].

References

Smith E, Anderson M, Foster H. The child with a limp: a symptom and not a diagnosis. Archives of disease in childhood - Education & practice edition. 2012;97(5):185-193. doi:10.1136/archdischild-2011-301245.
Naranje S, Kelly DM, Sawyer JR. A Systematic Approach to the Evaluation of a Limping Child. Am Fam Physician. 2015 Nov 15;92(10):908-16. PMID: 26554284.
Landin LA, Danielsson LG, Wattsgård C. Transient synovitis of the hip. Its incidence, epidemiology and relation to Perthes' disease. J Bone Joint Surg Br. 1987;69(2):238-242.
Kermond S, Fink M, Graham K, Carlin JB, Barnett P. A randomized clinical trial: should the child with transient synovitis of the hip be treated with nonsteroidal anti-inflammatory drugs?. Ann Emerg Med. 2002;40(3):294-299. doi:10.1067/mem.2002.126171
Bennett OM, Namnyak SS. Acute septic arthritis of the hip joint in infancy and childhood. Clin Orthop Relat Res. 1992;(281):123-132.
Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-1670. doi:10.2106/00004623-199912000-00002
Dartnell J, Ramachandran M, Katchburian M. Haematogenous acute and subacute paediatric osteomyelitis: a systematic review of the literature. J Bone Joint Surg Br. 2012;94(5):584-595. doi:10.1302/0301-620X.94B5.28523
Kaplan SL. Osteomyelitis in children. Infect Dis Clin North Am. 2005;19(4):787-vii. doi:10.1016/j.idc.2005.07.006
Johansson T, Lindblad M, Bladh M, Josefsson A, Sydsjö G. Incidence of Perthes' disease in children born between 1973 and 1993. Acta Orthop. 2017;88(1):96-100. doi:10.1080/17453674.2016.1227055
Canavese F, Dimeglio A. Perthes' disease: prognosis in children under six years of age. J Bone Joint Surg Br. 2008 Jul;90(7):940-5. doi: 10.1302/0301-620X.90B7.20691. PMID: 18591607.
Herngren B, Stenmarker M, Vavruch L, Hagglund G. Slipped capital femoral epiphysis: a population-based study. BMC Musculoskelet Disord. 2017;18(1):304. Published 2017 Jul 18. doi:10.1186/s12891-017-1665-3
Reynolds RA. Diagnosis and treatment of slipped capital femoral epiphysis. Curr Opin Pediatr. 1999;11(1):80-83. doi:10.1097/00008480-199902000-00016

Expert Commentary

Thank you to Drs. Ng and Bigach for compiling a concise approach to a common chief complaint encountered by Emergency Physicians across the county: a child with a new limp or the refusal to bear weight.

The first step to this often-challenging problem is to try to localize the pain, and in non-verbal kiddos, this can be the most difficult task. As highlighted above, if the child is able, observe their ambulation and establish laterality of the limp and when it occurs during the gait cycle. Most of the disease processes we as Emergency Physicians are concerned about will cause an antalgic gait or a shortened stance phase. Shortening the stance phase decreases the amount of time that the child is bearing weight on the painful limb in an effort to decrease their pain. Sometimes this is so effective that their parents will observe a limp, but the child will not complain of any pain. A thorough exam of the back and lower extremities including inspection, palpation, and range of motion of all joints is also imperative for trying to localize the cause of their symptoms.

Let your exam and history guide lab evaluation and imaging, however, a good place to start is usually basic labs and inflammatory markers and a plain film of the affected joint. In some cases, you won’t be able to localize pain or exam findings at all, and a broad workup including plain film imaging of the entire extremity may be necessary.

A few additional pearls:

Always consider non-accidental trauma in children with new limp or refusal to bear weight.
Systemic symptoms such as fever should raise your suspicion for infectious etiology such as osteomyelitis or septic arthritis.
Classically children with transient synovitis will have had a recent viral illness, but this is not always the case.
Always examine the hips and consider hip plain films in children complaining of knee or thigh pain, but with a benign knee exam. They could be hiding an SCFE or Leg-Calve-Perthes disease.
Don’t forget to examine the SI joint, as it too can become infected or inflamed.
History of night pain should raise your antenna for malignancy like osteosarcoma, Ewing’s sarcoma, or leukemia.
Consider Lyme arthritis in your differential for joint pain and swelling in endemic areas.
Ultrasound can be useful when evaluating for septic arthritis and transient synovitis and can be performed at the bedside. However, both septic arthritis and transient synovitis can cause effusion, and therefore it is not useful in differentiating between the two. (That’s where the Kocher Criteria should be used to risk-stratify and determine if joint aspiration and fluid analysis are warranted)

Ultrasound evaluation of a pediatric hip joint demonstrating effusion courtesy of Dr. Maulik S Patel (https://radiopaedia.org)

Finally, make sure that the parents understand the diagnosis, expected course, and follow-up plan. If the child continues to refuse to bear weight, their symptoms worsen or do not improve, or they develop new concerning symptoms such as new fever or new urinary retention, they should return to the Emergency Department or their pediatrician for re-evaluation. More than once I’ve had patients who seemed for all the world to have transient synovitis eventually be diagnosed with spinal cord tumor, chronic recurrent multifocal osteomyelitis, etc.

Terese Whipple, MD

Assistant Professor

Department of Emergency Medicine

University of Iowa Hospitals and Clinics

How To Cite This Post:

[Peer-Reviewed, Web Publication] Ng, T. Bigach, P. (2021, Dec 20). Hip Pain in Pediatrics. [NUEM Blog. Expert Commentary by Whipple, T]. Retrieved from http://www.nuemblog.com/blog/hippainpediatrics

Resuscitative Hysterotomy

**Written by:** Aldo Gonzalez, MD (NUEM ‘23) **Edited by:** Justine Ko, MD (NUEM ‘21)
**Expert Commentary by**: Paul Trinquero, MD (NUEM '19) & Pietro Bortoletto, MD

Introduction

Resuscitative hysterotomy (RH) is the new term for what was previously called perimortem cesarean delivery (PMCD). The new nomenclature is being adopted to highlight the importance of the procedure to a successful resuscitation during maternal cardiopulmonary arrest (MCPA). It is defined as the procedure of delivering a fetus from a gravid mother through an incision in the abdomen during or after MCPA. The goal of the procedure is to improve the survival of the mother and the neonate.

Physiology

There are physiologic changes that occur during pregnancy which reduce the probability of return of spontaneous circulation (ROSC) during cardiac arrest. Physiologic anemia of pregnancy reduces the oxygen carrying capacity of blood and results in decreased delivery of oxygen during resuscitation. The large gravid uterus elevates the diaphragm and reduces the lung’s functional reserve capacity (FRC), which when combined with increased oxygen demand from the fetus results in decreased oxygen reserves and resultant risk for rapid oxygen desaturations. The size of a gravid uterus at 20 weeks results in aortocaval compression which reduces the amount of venous return from the inferior vena cava and reduces cardiac output during resuscitation. The theory behind resuscitative hysterotomy is to increase the probability of ROSC by reducing the impact of aortocaval compression.

Supporting Evidence

A 2012 systematic review primarily investigated the neonatal and maternal survival rates after perimortem cesarean delivery and secondarily attempted to evaluate maternal and fetal neurological outcome and the ability to perform the procedure within the recommended time frame.

Inclusion Criteria

original articles, case series, case reports and letters to the editor, and reports from databases
had minimum of least five clinical details of the case (e.g. patient age, gravidity, parity, obstetric history, medical history, presenting rhythm, or location of arrest)
AND
the care administered (chest compression, ventilation, monitoring, drug administration)
AND
maternal return of spontaneous circulation or survival to hospital discharge or fetal neonatal outcome

Exclusion Criteria

Post-delivery arrests
Studies without enough data to understand the details of the arrests
Studies with unclear maternal and fetal outcomes

Population

Pregnant woman that
- (1) had a cardiac arrest or a non-perfusing rhythm
- (2) received chest compression and/or advanced life support medications and/or defibrillation
Average maternal age: 30.5±6.5 years (median 32, range 17–44, IQR, 26.5–35.5, n = 80)
Gravidity: 2.5±1.5 (median 2, range 1–7, IQR 1–4, n = 59)
Parity: 1.1±1.3 (median 1, range 0–6, IQR 0–2, n = 57)
Singleton Pregnancies: 90.4% (n = 85)
Average gestational age at arrest: 33±7 weeks (median 35, range 10–42, IQR 31–39, n = 85)

Results

for cases undergoing PMCD, earlier time from arrest to delivery was associated with increased survival (p < 0.001, 95%CI 6.9–18.2)
- surviving mothers: 27/57; 10.0±7.2 min (median 9, range 1–37)
- non-surviving mother: 30/57; 22.6±13.3 min (median 20, range 4–60)]
for neonates delivered by PMCD/RH earlier time from arrest to delivery was associated with increased survival (p = 0.016)
- surviving neonates: 14±11 min (median = 10, range = 1–47)
- non-survivor neonates: 22±13 min (median = 20, range = 4–60)
Only 4 cases met the timeframe of less than minutes

Take-Aways: Performing a PMCD/RH in the 4-5 minutes time frame is difficult. However, PMCD/RH beyond the proposed time is still beneficial and earlier time to delivery from arrest is associated with better outcomes

Guideline Recommendations

Perform basic life support (BLS) in the same way as non-pregnant patients

Place patient in supine position
- Left lateral decubitus (left lateral tilt) positioning is no longer recommended during compressions because of reduced efficacy of chest compressions
No modification of Chest compressions
- Rate: 100-120 per minute
- Depth: at least 2 inches (5 cm)
- Allow for full chest recoil between compressions
- Avoid interruptions as much as possible
No modification of Ventilation
- Use bag-ventilation
- Compression to breath ratio: 30:2 before advanced airway

Perform advanced cardiac life support (ACLS) as in non-pregnant women

No modification of Ventilation
- Once breath every 6 seconds (10 BPM) with advanced airway
No modification of medications
- Use 1 mg Epinephrine of epinephrine every 3-5 minutes
No modification to defibrillation
- Use adhesive pads on patient
- Place in anterolateral position
  - Lateral pad should be placed under breast tissue
- Defibrillate for Ventricular fibrillation or Ventricular tachycardia
- Use usual Voltages
  - Biphasic: 120-200 Joules
- Resume compressions after shock is delivered

Special considerations during resuscitation

Obtain access above the diaphragm to minimize the effect of aortocaval compression on the administration of drugs
Perform left uterine deviation during resuscitation to reduce aortocaval compression
If a gravid patient suffers a cardiac arrest mobilize resources to prepare for the need for resuscitative hysterotomy and the resuscitation of the fetus early

Palpate the size of the gravid uterus
- If above the height of the umbilicus then patient is most likely greater than 20 weeks gravid and a candidate for RH
Strongly consider performing RH (PMCD) if the patient does not achieve ROSC by the 4-minute mark and qualified staff to perform the procedure are present
Aim to have the procedure done by the 5-minute mark
Consider performing RH (PMCD) sooner if maternal prognosis is poor or prolonged period of pulselessness
RH should be performed at the site of the resuscitation
Do not delay procedure to prepare abdomen
- May pour iodine solution over abdomen prior to incision
Do not delay procedure for surgical equipment if scalpel is available
Continue performing LUD while performing RH

Figure 1: One-handed left uterine deviation technique

Figure 2: Two-handed left uterine deviation technique

Steps for Resuscitative Hysterectomy

Pre-procedure

Gather supplies to perform RH
- Personal Protective Equipment
  - Gloves
  - Face mask
  - Apron/gown
- Resuscitative Hysterotomy Equipment
  - Scalpel(the minimum equipment to perform procedure)
  - Blunted Scissors
  - Clamps/Hemostats
  - Gauze
  - Suction
  - Large absorbable sutures
  - Needle Holder
  - Antiseptic Solution
- Neonatal resuscitation equipment
  - Dry Linens
  - Neonatal Bag Valve Mask
  - Neonatal Airway supplies
  - Suction
  - Umbilical venous access equipment
  - Neonatal resuscitation drugs
  - Baby Warmer
  - Plastic Bag
Form teams to perform Resuscitative Hysterotomy
- Resuscitative Team
- Resuscitative Hysterotomy Team
- Neonatal Resuscitation Team

Procedure

Maintain patient in supine position and continue compressions
Continue Left Uterine Deviation until the start of incision
Quickly prepare the skin with antiseptic solution (do not delay for skin prep)
Perform midline vertical Incision with scalpel on the abdomen from pubic symphysis to umbilicus and cut through skin and subcutaneous tissue until fascia is reached
Use fingers to bluntly dissect the rectus muscle fascia access the peritoneum (can use scalpel or blunt scissors)
Locate the uterus and differentiate it from the bladder (bladder yellow and enveloped in fatty tissue)
Make a vertical incision from the lower uterus to the fundus with scalpel (can use blunt scissors)
If the placenta is encountered while entering the uterus, cut through it
Use a cupped hand to locate the fetal part closest to pelvis
Elevate the located fetal part and pass through uterine incision while applying transabdominal pressure with other hand
Use traction and transabdominal pressure to deliver the rest of the baby
Clamp the cord at two spots and cut in between both clamps
Hand the baby to the neonatal team
Deliver placenta with gentle traction

Post-procedure

Continue performing compressions
Consider stopping if ROSC not achieved after several rounds and depending on the cause of PMCA
Give medications to promote uterine contraction
Analgesia and sedation may be required if patient achieves ROSC
Bleeding will be worse if ROSC achieved and may require pharmacologic and nonpharmacologic interventions
Closure will depend on whether the patient achieves ROSC and may necessitate careful closure to prevent further bleeding. Best performed by an obstetrician. If an obstetrician is unavailable, pack the uterus with gauze and clamps actively bleeding vessels to reduce bleeding.
Administer prophylactic antibiotics

References

Einav, S., et al. (2012). "Maternal cardiac arrest and perimortem caesarean delivery: evidence or expert-based?" Resuscitation 83(10): 1191-1200.
Jeejeebhoy, F. M., et al. (2015). "Cardiac Arrest in Pregnancy: A Scientific Statement From the American Heart Association." Circulation 132(18): 1747-1773.
Kikuchi, J. and S. Deering (2018). "Cardiac arrest in pregnancy." Semin Perinatol 42(1): 33-38.
Parry, R., et al. (2016). "Perimortem caesarean section." Emerg Med J 33(3): 224-229.
Rose, C. H., et al. (2015). "Challenging the 4- to 5-minute rule: from perimortem cesarean to resuscitative hysterotomy." Am J Obstet Gynecol 213(5): 653-656, 653 e651.
Soskin, P. N. and J. Yu (2019). "Resuscitation of the Pregnant Patient." Emerg Med Clin North Am 37(2): 351-363.
Walls, R. M., et al. (2018). Rosen's emergency medicine: concepts and clinical practice. Philadelphia, PA, Elsevier.

Expert Commentary

This is an excellent review of an extremely rare, but potentially life-saving procedure. It may seem daunting to perform (and it should), but the evidence would say that a resuscitative hysterotomy (RH), especially if performed promptly, drastically improves survival during the catastrophic scenario of maternal cardiac arrest. This is even more important because these patients are young (and often relatively healthy) and could potentially have decades of meaningful quality of life if they can survive the arrest. That being said, this procedure is so rare that most of us not only have never performed it, but often have never even seen it. Not only that, but unlike other rare lifesaving procedures (such as cricothyroidotomy or resuscitative thoracotomy), RH is extremely difficult to practice in cadaver labs due to the unavailability of pregnant cadavers. So, we are left with the next best thing: familiarizing ourselves with the anatomy, physiology, and simplified technique of the procedure and mentally rehearsing it so that when the time comes, we can be ready.

For these rare procedures, in addition to the excellent and thorough review above, it is also helpful to simplify and rehearse the fundamental steps. I’m not an obstetrician and certainly not an expert on this procedure, but I’ve mentally prepared myself for what I would do in the event that I am faced with this grave situation and categorized it into the following simplified five step plan. Also, prior to writing this commentary I got a curbside consult from a friend from med school and actual obstetrician and gynecologic surgeon, Dr. Pietro Bortoletto.

First off, the indications-- basically, a pregnant woman estimated to be >20 weeks EGA who has suffered a cardiac arrest. Don’t worry about the 4 minutes, make the decision to perform a RH right away and start prepping. Delegate someone to call the appropriate resuscitation teams if available. Then start the procedure.

Step 1: Setup. You probably don’t have a c section kit in your trauma bay, so instead open the thoracotomy tray and you’ll have most of what you need. Go ahead and set aside the finochietto rib spreaders so that you don’t have a panic attack trying to remember how to put those together with other people watching. But everything else you’ll need will be in that tray (basically a scalpel, blunt scissors, and hemostats).

Step 2: Cut into the Abdomen. Splash prep the abdomen with betadine. Then make your long vertical incision from the uterine fundus to the pubic symphysis. Cut through the skin and subcutaneous tissue then bluntly separate the rectus and enter the peritoneum with scalpel or blunt scissors. Extend the peritoneal incision with blunt scissors.

Step 3: (carefully) Cut into the Uterus. First, locate the uterus. Then, take a deep breath and remember that there is a fetus inside the uterus. With that terrifying thought in mind, cut vertically into the uterus, insert your fingers, and extend the incision upwards with blunt scissors and a steady hand. If you encounter an anterior placenta, cut right through it.

Step 4: Delivery. Deliver the fetus either by cupping the head and elevating it through the incision or by grabbing a leg, wiggling out the shoulders, and then flexing the head. Hand over the neonate to whoever is taking the lead on the neonatal resuscitation (will need to be warmed, stimulated, and potentially aggressively resuscitated). Clamp and cut the cord, leaving a long enough umbilical stump for an easy umbilical line if needed. Then using gentle traction, attempt delivery of the placenta. If it isn’t coming easily, leave it alone so as not to stir up more bleeding.

Step 5: Extra credit. If you’ve made it this far as an emergency physician and there is still no obstetrician in sight, you can continue resuscitation, focusing on stopping the uterine bleeding. While you don’t need to close the fascia or skin, it can be helpful to close the uterine incision to prevent additional blood loss. You can do this with a whip stitch using 0-0 vicryl (or if that seems like showing off, you can just pack it with sterile gauze. If you’ve got it handy, give 10 IU oxytocin to stimulate uterine contraction and further slow bleeding. Feel free to order some antibiotics as well. Otherwise, continue maternal resuscitation following typical ACLS.

The big picture here is that this is a heroic, potentially life-saving procedure that most of us will never do. But we can all take a few minutes to read an excellent review like the blog post above, watch a video, and mentally walk ourselves through the simplified steps. That preparation will afford us some much-needed confidence if we are ever faced with this terrifying scenario.

Paul Trinquero, MD

Medical Director

Department of Emergency Medicine

US Air Force Hospital - Langley

Pietro Bortoletto, MD

Clinical Fellow

Reproductive Endocrinology & Infertility

Weill Cornell Medical College

How To Cite This Post:

[Peer-Reviewed, Web Publication] Gonzalez, A. Ko, J. (2021, Dec 13). Resuscitative Hysterotomy. [NUEM Blog. Expert Commentary by Trinquero, P and Bortoletto, P]. Retrieved from http://www.nuemblog.com/blog/resuscitative-hysterotomy.

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Expert Commentary

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Non-Response to Vasopressors

Acidosis