Specialty Sections From CHEST® Physician

Does this sound like your day?

You show up to work after a terrible night’s sleep. Your back is tense, and you do some kind of walking/stretching combo as you walk through the doors. Your focus fades during the mind-numbing routine of the morning shift sign out. As the day moves forward, you begin to feel resentful as you sign orders, see patients, and address your ICU team needs. You know that’s not right, that it’s not in line with who you want to be, but the irritation doesn’t go away.

Your lunchtime is filled with computer screens, notes, billing, and more billing. The previous feelings of irritation begin to boil into anger because more of your day is filled with bureaucratic demands and insurance reports rather than actually helping people. This isn’t what you signed up for. Years and years of training so you could be a paper pusher? The thought leads to rage ... or sometimes apathy on days you give in to the inevitable.

You finish your shift with admissions, procedures, code blues, and an overwhelming and exhausting night shift sign out. You feel like a hamster in a wheel. You’re going nowhere. What’s the point of all of this? You find yourself questioning why you went into medicine anyways ... yeah, that’s burnout.

I know what you’re thinking. You keep hearing about this, and it’s important to recognize, but then you hear the same old solutions: be more positive, find balance, do some yoga, take this resilience module, be mindful (what on earth does this mean anyways?), get some more sleep. Basically, it’s our problem. It’s our burden. If all of these were easy to understand and implement, don’t you think doctors and health-care providers would have done it already? I think you and I are a lot alike. These were my exact feelings. But stick with me on this one. I have a solution for you, albeit a little different. I’ll show you a more “positive” spin on the DIY.

I burned out early. After fellowship, I didn’t want to be a doctor anymore. I desperately sought to alter my career somehow. I looked into website development, something I had been good at in high school. I took a few refresher classes on my days off and started coding my own sites, but I had bills to pay. Big bills. Student loan bills. Luckily, my first job out of fellowship accepted many of my schedule demands, such as day shifts only, and after about a year, I recovered and remembered why I had loved medicine to begin with.
 

What is burnout?

Mind-body-soul exhaustion caused by excessive stress. Stress and burnout are closely related, but they’re more like distant cousins. Stress can be (and is) a normal part of our jobs. I bet you think you’re stressed, when you’re probably burned out. Critical care doctors have the highest rate of burnout among all physician subspecialties at >55%, and it is even higher in pediatric critical care. (Sessler C. https://www.mdedge.com/chestphysician/article/160951/society-news/turning-heat-icu-burnout). The main difference between stress and burnout is hope. With stress, you still feel like things can get better and you can get it all under control. Burnout feels hopeless.

What are the three core symptoms of burnout?

• Irritability and impatience with patients (depersonalization)

• Cynicism and difficulty concentrating (emotional exhaustion)

• What’s the point of all of this? Nothing I do matters or is appreciated (decreased self-efficacy)


We can talk about the symptoms of burnout all day, but what does that really look like? It looks like the day we described at the beginning. You know, the day that resonated with you and caused you to keep reading.
 

Why should we all be discussing this important topic?

Being burned out not only affects us on a soul level (achingly described above), but, more importantly, this can trickle down to our personal lives, family relationships, and how we care for our patients, with some studies showing that it affects our performance and, gulp, patient outcomes. That’s scary (Moss M et al. Crit Care Med. 2016;44[7]:1414).

Causes of burnout

There are many causes of burnout, and several studies have identified risk factors. A lack of control, conflicts with colleagues and leadership, and performing menial tasks can add to the irritation of a workday. This doesn’t even include the nature of our actual job as critical care doctors. We care for the sickest and are frequently involved in end-of-life care. Over time, the stress morphs into burnout. Female gender is also an independent risk factor for doctors (Pastores SM, et al. Crit Care Med. 2019;47[4]:550).

We’ve identified it. We’ve quantified it. But we’re not fixing it. In fact, there are only a few studies that have incorporated a needs assessment of doctors, paired with appropriate environmental intervention. A study done with primary care doctors in New York City clinics found that surveying a doctor’s “wish list” of interventions can help identify gaps in workflow, such as pairing one medical assistant with each attending (Linzer M, et al. J Gen Intern Med. 2015;30[8]:1105).

Without more data like this, we’re hamsters in a wheel. Luckily, organizations like CHEST have joined together with others to create the Critical Care Societies Collaborative and have an annual summit to discuss research strategies.
 

Solutions

Even millennials are sick of the mindful “chore” list. Yoga pants, yoga mats, crystals, chakras, meditation, and the list goes on and on. What millennials want are work-life integrations that are easy; workspaces that invite mindful behavior and daily rituals that excite and relax them. Co-working spaces like WeWork have designated self-care spaces.

Self-care is now essential, not an indulgence. I wasn’t sure how to create this space in my ICU, so I started small, with things I could carry with myself. The key is to find small rituals with big meanings. What could this look like for you? I began doing breathwork. Frankly, the idea came to me from my Apple® watch. It just started giving me these reminders one day, and I decided to take it seriously. I found that my mind and muscles eased after only 1 minute of breathing in and out slowly. This elevated my mood and was the refresher I needed in the afternoons. My body ached less after procedures.

I also got a little woo-woo (stay with me now) and began carrying around crystal stones. You don’t have to carry around crystals. Prayer books, religious symbols, your child’s toy car, anything can work if it has meaning for you, so when you see it or touch it during your day, you remember your big why. Why you’re serving people. Why you’re a doctor. I prefer the crystals over jewelry because it’s something unusual that I don’t expect to be sitting in my pocket. It’s always a nice gentle reminder of the love I have for my patients, my job, and humanity. When I put my hands in my pocket as I’m talking to yet another frustrated family member, my responses are more patient and calmer, which leads to a more productive conversation.

Lastly, I started what I call a new Pavlov home routine. When I’m done with work, I light a candle and write out three things I’m grateful for. Retrain your brain. Retrain your triggers. What’s your Pavlov’s bell going to be? Many of us come home hungry and stressed. Food then becomes linked to stress. This is not good. Link it with something else. Light a candle, count to 3, then blow it out. Use your kids to incorporate something fun. Use a toy with “super powers” to “beam” the bad feelings away. Taking a few extra minutes to shift gears has created a much happier home for me.

There are things that we can’t control. That’s called circumstances. We can’t control other people; we can’t control the hospital system; we can’t control our past. But the rest of everything we can control: our thoughts, feelings, and daily self-care rituals.

It reminds me of something my dad always said when I was a little girl. When crossing the street, you always look twice, oftentimes three. Why be so careful? It’s the pedestrian’s right of way after all. “Well..” he replied, “If a car hits you, nothing much happens to them, but your entire life will be destroyed, forever.”

Stop walking into traffic thinking everything will be ok. Take control of what you can.

Look, I get it. As health-care providers, we are an independent group. But just because you can do it alone, doesn’t mean you have to.

Choose one thing. Whether it be something I mentioned or something that came to your mind as you read this. Then, drop me a line at my personal email [email protected]. I will send you a reply to let you know I hear you and I’m in your corner.

Burnout happens.

But, so does joy, job satisfaction, and balance. Those things just take more effort.

Dr. Khan is Assistant Editor, Web and Multimedia, CHEST^® journal.

Does this sound like your day?

You show up to work after a terrible night’s sleep. Your back is tense, and you do some kind of walking/stretching combo as you walk through the doors. Your focus fades during the mind-numbing routine of the morning shift sign out. As the day moves forward, you begin to feel resentful as you sign orders, see patients, and address your ICU team needs. You know that’s not right, that it’s not in line with who you want to be, but the irritation doesn’t go away.

Your lunchtime is filled with computer screens, notes, billing, and more billing. The previous feelings of irritation begin to boil into anger because more of your day is filled with bureaucratic demands and insurance reports rather than actually helping people. This isn’t what you signed up for. Years and years of training so you could be a paper pusher? The thought leads to rage ... or sometimes apathy on days you give in to the inevitable.

You finish your shift with admissions, procedures, code blues, and an overwhelming and exhausting night shift sign out. You feel like a hamster in a wheel. You’re going nowhere. What’s the point of all of this? You find yourself questioning why you went into medicine anyways ... yeah, that’s burnout.

I know what you’re thinking. You keep hearing about this, and it’s important to recognize, but then you hear the same old solutions: be more positive, find balance, do some yoga, take this resilience module, be mindful (what on earth does this mean anyways?), get some more sleep. Basically, it’s our problem. It’s our burden. If all of these were easy to understand and implement, don’t you think doctors and health-care providers would have done it already? I think you and I are a lot alike. These were my exact feelings. But stick with me on this one. I have a solution for you, albeit a little different. I’ll show you a more “positive” spin on the DIY.

I burned out early. After fellowship, I didn’t want to be a doctor anymore. I desperately sought to alter my career somehow. I looked into website development, something I had been good at in high school. I took a few refresher classes on my days off and started coding my own sites, but I had bills to pay. Big bills. Student loan bills. Luckily, my first job out of fellowship accepted many of my schedule demands, such as day shifts only, and after about a year, I recovered and remembered why I had loved medicine to begin with.
 

What is burnout?

Mind-body-soul exhaustion caused by excessive stress. Stress and burnout are closely related, but they’re more like distant cousins. Stress can be (and is) a normal part of our jobs. I bet you think you’re stressed, when you’re probably burned out. Critical care doctors have the highest rate of burnout among all physician subspecialties at >55%, and it is even higher in pediatric critical care. (Sessler C. https://www.mdedge.com/chestphysician/article/160951/society-news/turning-heat-icu-burnout). The main difference between stress and burnout is hope. With stress, you still feel like things can get better and you can get it all under control. Burnout feels hopeless.

What are the three core symptoms of burnout?

• Irritability and impatience with patients (depersonalization)

• Cynicism and difficulty concentrating (emotional exhaustion)

• What’s the point of all of this? Nothing I do matters or is appreciated (decreased self-efficacy)


We can talk about the symptoms of burnout all day, but what does that really look like? It looks like the day we described at the beginning. You know, the day that resonated with you and caused you to keep reading.
 

Why should we all be discussing this important topic?

Being burned out not only affects us on a soul level (achingly described above), but, more importantly, this can trickle down to our personal lives, family relationships, and how we care for our patients, with some studies showing that it affects our performance and, gulp, patient outcomes. That’s scary (Moss M et al. Crit Care Med. 2016;44[7]:1414).

Causes of burnout

There are many causes of burnout, and several studies have identified risk factors. A lack of control, conflicts with colleagues and leadership, and performing menial tasks can add to the irritation of a workday. This doesn’t even include the nature of our actual job as critical care doctors. We care for the sickest and are frequently involved in end-of-life care. Over time, the stress morphs into burnout. Female gender is also an independent risk factor for doctors (Pastores SM, et al. Crit Care Med. 2019;47[4]:550).

We’ve identified it. We’ve quantified it. But we’re not fixing it. In fact, there are only a few studies that have incorporated a needs assessment of doctors, paired with appropriate environmental intervention. A study done with primary care doctors in New York City clinics found that surveying a doctor’s “wish list” of interventions can help identify gaps in workflow, such as pairing one medical assistant with each attending (Linzer M, et al. J Gen Intern Med. 2015;30[8]:1105).

Without more data like this, we’re hamsters in a wheel. Luckily, organizations like CHEST have joined together with others to create the Critical Care Societies Collaborative and have an annual summit to discuss research strategies.
 

Solutions

Even millennials are sick of the mindful “chore” list. Yoga pants, yoga mats, crystals, chakras, meditation, and the list goes on and on. What millennials want are work-life integrations that are easy; workspaces that invite mindful behavior and daily rituals that excite and relax them. Co-working spaces like WeWork have designated self-care spaces.

Self-care is now essential, not an indulgence. I wasn’t sure how to create this space in my ICU, so I started small, with things I could carry with myself. The key is to find small rituals with big meanings. What could this look like for you? I began doing breathwork. Frankly, the idea came to me from my Apple® watch. It just started giving me these reminders one day, and I decided to take it seriously. I found that my mind and muscles eased after only 1 minute of breathing in and out slowly. This elevated my mood and was the refresher I needed in the afternoons. My body ached less after procedures.

I also got a little woo-woo (stay with me now) and began carrying around crystal stones. You don’t have to carry around crystals. Prayer books, religious symbols, your child’s toy car, anything can work if it has meaning for you, so when you see it or touch it during your day, you remember your big why. Why you’re serving people. Why you’re a doctor. I prefer the crystals over jewelry because it’s something unusual that I don’t expect to be sitting in my pocket. It’s always a nice gentle reminder of the love I have for my patients, my job, and humanity. When I put my hands in my pocket as I’m talking to yet another frustrated family member, my responses are more patient and calmer, which leads to a more productive conversation.

Lastly, I started what I call a new Pavlov home routine. When I’m done with work, I light a candle and write out three things I’m grateful for. Retrain your brain. Retrain your triggers. What’s your Pavlov’s bell going to be? Many of us come home hungry and stressed. Food then becomes linked to stress. This is not good. Link it with something else. Light a candle, count to 3, then blow it out. Use your kids to incorporate something fun. Use a toy with “super powers” to “beam” the bad feelings away. Taking a few extra minutes to shift gears has created a much happier home for me.

There are things that we can’t control. That’s called circumstances. We can’t control other people; we can’t control the hospital system; we can’t control our past. But the rest of everything we can control: our thoughts, feelings, and daily self-care rituals.

It reminds me of something my dad always said when I was a little girl. When crossing the street, you always look twice, oftentimes three. Why be so careful? It’s the pedestrian’s right of way after all. “Well..” he replied, “If a car hits you, nothing much happens to them, but your entire life will be destroyed, forever.”

Stop walking into traffic thinking everything will be ok. Take control of what you can.

Look, I get it. As health-care providers, we are an independent group. But just because you can do it alone, doesn’t mean you have to.

Choose one thing. Whether it be something I mentioned or something that came to your mind as you read this. Then, drop me a line at my personal email [email protected]. I will send you a reply to let you know I hear you and I’m in your corner.

Burnout happens.

But, so does joy, job satisfaction, and balance. Those things just take more effort.

Dr. Khan is Assistant Editor, Web and Multimedia, CHEST^® journal.

Does this sound like your day?

You show up to work after a terrible night’s sleep. Your back is tense, and you do some kind of walking/stretching combo as you walk through the doors. Your focus fades during the mind-numbing routine of the morning shift sign out. As the day moves forward, you begin to feel resentful as you sign orders, see patients, and address your ICU team needs. You know that’s not right, that it’s not in line with who you want to be, but the irritation doesn’t go away.

Your lunchtime is filled with computer screens, notes, billing, and more billing. The previous feelings of irritation begin to boil into anger because more of your day is filled with bureaucratic demands and insurance reports rather than actually helping people. This isn’t what you signed up for. Years and years of training so you could be a paper pusher? The thought leads to rage ... or sometimes apathy on days you give in to the inevitable.

You finish your shift with admissions, procedures, code blues, and an overwhelming and exhausting night shift sign out. You feel like a hamster in a wheel. You’re going nowhere. What’s the point of all of this? You find yourself questioning why you went into medicine anyways ... yeah, that’s burnout.

I know what you’re thinking. You keep hearing about this, and it’s important to recognize, but then you hear the same old solutions: be more positive, find balance, do some yoga, take this resilience module, be mindful (what on earth does this mean anyways?), get some more sleep. Basically, it’s our problem. It’s our burden. If all of these were easy to understand and implement, don’t you think doctors and health-care providers would have done it already? I think you and I are a lot alike. These were my exact feelings. But stick with me on this one. I have a solution for you, albeit a little different. I’ll show you a more “positive” spin on the DIY.

I burned out early. After fellowship, I didn’t want to be a doctor anymore. I desperately sought to alter my career somehow. I looked into website development, something I had been good at in high school. I took a few refresher classes on my days off and started coding my own sites, but I had bills to pay. Big bills. Student loan bills. Luckily, my first job out of fellowship accepted many of my schedule demands, such as day shifts only, and after about a year, I recovered and remembered why I had loved medicine to begin with.
 

What is burnout?

Mind-body-soul exhaustion caused by excessive stress. Stress and burnout are closely related, but they’re more like distant cousins. Stress can be (and is) a normal part of our jobs. I bet you think you’re stressed, when you’re probably burned out. Critical care doctors have the highest rate of burnout among all physician subspecialties at >55%, and it is even higher in pediatric critical care. (Sessler C. https://www.mdedge.com/chestphysician/article/160951/society-news/turning-heat-icu-burnout). The main difference between stress and burnout is hope. With stress, you still feel like things can get better and you can get it all under control. Burnout feels hopeless.

What are the three core symptoms of burnout?

• Irritability and impatience with patients (depersonalization)

• Cynicism and difficulty concentrating (emotional exhaustion)

• What’s the point of all of this? Nothing I do matters or is appreciated (decreased self-efficacy)


We can talk about the symptoms of burnout all day, but what does that really look like? It looks like the day we described at the beginning. You know, the day that resonated with you and caused you to keep reading.
 

Why should we all be discussing this important topic?

Being burned out not only affects us on a soul level (achingly described above), but, more importantly, this can trickle down to our personal lives, family relationships, and how we care for our patients, with some studies showing that it affects our performance and, gulp, patient outcomes. That’s scary (Moss M et al. Crit Care Med. 2016;44[7]:1414).

Causes of burnout

There are many causes of burnout, and several studies have identified risk factors. A lack of control, conflicts with colleagues and leadership, and performing menial tasks can add to the irritation of a workday. This doesn’t even include the nature of our actual job as critical care doctors. We care for the sickest and are frequently involved in end-of-life care. Over time, the stress morphs into burnout. Female gender is also an independent risk factor for doctors (Pastores SM, et al. Crit Care Med. 2019;47[4]:550).

We’ve identified it. We’ve quantified it. But we’re not fixing it. In fact, there are only a few studies that have incorporated a needs assessment of doctors, paired with appropriate environmental intervention. A study done with primary care doctors in New York City clinics found that surveying a doctor’s “wish list” of interventions can help identify gaps in workflow, such as pairing one medical assistant with each attending (Linzer M, et al. J Gen Intern Med. 2015;30[8]:1105).

Without more data like this, we’re hamsters in a wheel. Luckily, organizations like CHEST have joined together with others to create the Critical Care Societies Collaborative and have an annual summit to discuss research strategies.
 

Solutions

Even millennials are sick of the mindful “chore” list. Yoga pants, yoga mats, crystals, chakras, meditation, and the list goes on and on. What millennials want are work-life integrations that are easy; workspaces that invite mindful behavior and daily rituals that excite and relax them. Co-working spaces like WeWork have designated self-care spaces.

Self-care is now essential, not an indulgence. I wasn’t sure how to create this space in my ICU, so I started small, with things I could carry with myself. The key is to find small rituals with big meanings. What could this look like for you? I began doing breathwork. Frankly, the idea came to me from my Apple® watch. It just started giving me these reminders one day, and I decided to take it seriously. I found that my mind and muscles eased after only 1 minute of breathing in and out slowly. This elevated my mood and was the refresher I needed in the afternoons. My body ached less after procedures.

I also got a little woo-woo (stay with me now) and began carrying around crystal stones. You don’t have to carry around crystals. Prayer books, religious symbols, your child’s toy car, anything can work if it has meaning for you, so when you see it or touch it during your day, you remember your big why. Why you’re serving people. Why you’re a doctor. I prefer the crystals over jewelry because it’s something unusual that I don’t expect to be sitting in my pocket. It’s always a nice gentle reminder of the love I have for my patients, my job, and humanity. When I put my hands in my pocket as I’m talking to yet another frustrated family member, my responses are more patient and calmer, which leads to a more productive conversation.

Lastly, I started what I call a new Pavlov home routine. When I’m done with work, I light a candle and write out three things I’m grateful for. Retrain your brain. Retrain your triggers. What’s your Pavlov’s bell going to be? Many of us come home hungry and stressed. Food then becomes linked to stress. This is not good. Link it with something else. Light a candle, count to 3, then blow it out. Use your kids to incorporate something fun. Use a toy with “super powers” to “beam” the bad feelings away. Taking a few extra minutes to shift gears has created a much happier home for me.

There are things that we can’t control. That’s called circumstances. We can’t control other people; we can’t control the hospital system; we can’t control our past. But the rest of everything we can control: our thoughts, feelings, and daily self-care rituals.

It reminds me of something my dad always said when I was a little girl. When crossing the street, you always look twice, oftentimes three. Why be so careful? It’s the pedestrian’s right of way after all. “Well..” he replied, “If a car hits you, nothing much happens to them, but your entire life will be destroyed, forever.”

Stop walking into traffic thinking everything will be ok. Take control of what you can.

Look, I get it. As health-care providers, we are an independent group. But just because you can do it alone, doesn’t mean you have to.

Choose one thing. Whether it be something I mentioned or something that came to your mind as you read this. Then, drop me a line at my personal email [email protected]. I will send you a reply to let you know I hear you and I’m in your corner.

Burnout happens.

But, so does joy, job satisfaction, and balance. Those things just take more effort.

Dr. Khan is Assistant Editor, Web and Multimedia, CHEST^® journal.

For most of us, social media is a daunting new reality that we are pressured to be part of but that we struggle to fit into our increasingly demanding schedules. My first social media foray as a physician was a Facebook fan page as a hobby rather than a professional presence. Years later, I have learned the incredible benefit that being on social media in other platforms brought to my profession.
 

What’s social media going to bring to my medical practice?
The days where physicians retreat to the safety of our offices to deliver our care, or to issue carefully structured opinions, or interactions with patients have made way for more direct interaction. Social media has, indeed, allowed us to share more personal glimpses of our daily struggle to save lives, behind-the-scenes snapshot of ethical struggles in decision making, our difficulties qualifying patients for therapies due to insurance complications, or real-time addressing medical news and combating misinformation. Moreover, when patients self-refer, or are referred to my practice, they look me up online before coming to my office. Online profiles are the new “first impression” of the bedside manner of a physician.

Other personal examples of social media benefits include being informed of new publications, since many journals now have an online presence; being able to interact in real-time with authors; learning from physicians in other countries how they handled issues, such as shortage of critical medications; or earning CME, such as the Twitter chats hosted by CHEST (eg, new biologic agents in difficult to treat asthma, or patient selection in triple therapy for COPD).

Why should I pay attention to social media presence?
The pace by which social media changed the landscape took the medical community by surprise. Patients, third-party websites, and online review agencies (official or not) adopted it well before physicians became comfortable with it. As such, when I decided to google myself online, I was shocked at the level of misinformation about me (as a pulmonologist, I didn’t know I had performed sigmoidoscopies, yet that’s what my patients learned before they met me). That was an important lesson: If I don’t control the narrative, someone else will. Consequently, I dedicated a few hours to establish an online presence in order to introduce myself accurately and to be accessible to my patients and colleagues online.

Who decides what’s ethical and what’s not?
As the lines blurred, our community struggled to define what was appropriate and what was not. Finally, we welcomed with relief the issuance of a Code of Ethics, regarding social media use by physicians, from several societies, including the American Medical Association (https://www.ama-assn.org/delivering-care/ethics/professionalism-use-social-media). The principles guiding physicians use of social media include respect for human dignity and rights, honesty and upholding the standards of professionalism, and the duty to safeguard patient confidences and privacy.

Which platform should I use? There are so many. 
While any content can be shared on any platform, social media sites have organically differentiated into being more amenable to one content vs the other. Some accounts tend to be more for professional use (ie, Twitter and LinkedIn), and other accounts for personal use (ie, Facebook, Instagram, Snapchat, and Pinterest). CHEST has selected Twitter to host its CME chats regarding preselected topics, post information about an upcoming lecture during the CHEST meeting, etc. New social media sites are now “physician only,” such as Sermo, Doximity, QuantiMD, and Doc2Doc. Many of these sites require doctors to submit their credentials to a site gatekeeper, recreating the intimacy of a “physicians’ lounge” in an online environment (J Med Internet Res. 2014:Feb 11;16[2]:e13). Lastly, Figure1 is a media sharing app between physicians allowing discussions of de-identified images or cases, recreating the “curbside” consult concept online.

I heard about hashtags. What are they?
Hashtags are simply clickable topic titles (#COPD #Sepsis # Education, etc.) that can be added to a post, in order to widen its reach. For instance, if I am interested in sepsis, I can click on the hashtag #Sepsis, and it would bring up all the posts on any Twitter account that added that hashtag. It’s a filter that takes me to that topic of interest. I can then click on the button “Like” on the message or the account itself where the post was found. The “Like” is similar to a bookmark for that account on my own Twitter. In the future, all the posts from that account would be available to me.

What are influencers or thought leaders?
Anyone who “liked” my account is now “following” me. The number of followers has become a measure of the popularity of anyone on social media. If it reaches a high level, then the person with the account is dubbed an “influencer.” Social media “influencers” are individuals whose opinion is followed by hundreds of thousands. Influencers may even be rewarded for harnessing their reach to make money off advertising. One can easily see how it is powerful for a physician to become an influencer or a “thought leader,” not to make money but to expand their reach on social media to spread the correct information about diets, drugs, e-cigarettes, and vaccinations, to name a few.

Can social media get me in trouble?
In 2012, a survey of the state medical boards published by JAMA (2012;307[11]:1141) revealed that approximately 30% of state medical boards reported complaints of “online violations of patient confidentiality.” More than 10% stated they had encountered a case of an “online depiction of intoxication.”

Another study a year earlier revealed that 13% of physicians reported they have discussed individual, though anonymized, cases with other physicians in public online forums (http://www.quantiamd.com/qqcp/DoctorsPatientSocialMedia.pdf).

Even if posted anonymously, or on a “personal” rather than professional social media site, various investigative methods may potentially be used to directly link information to a specific person or incident. The most current case law dictates that such information is “discoverable.” In fact, Facebook’s policy for the use of data informs users that, “we may access, preserve, and share your information in response to a legal request” both within and outside of U.S. jurisdiction”.

What kind of trouble could I be exposed to?
Poor quality of information, damage to our professional image, breaches of patient’s privacy, violation of patient-physician boundary, license revoking by state boards, and erroneous medical advice given in the absence of examining a patient, are all potential pitfalls for physicians in the careless use of social media.

• supplies offline contact information so that an appointment can be made, if desired; and

• identifies a source for emergency services if the inquirer cannot wait for an appointment.

In circumstances where a patient–physician relationship already exists, informed consent should be obtained, which should include a careful explanation regarding the risks of online communication, expected response times, and the handling of emergencies, then documented in the patient’s chart (PT. 2014 Jul;39[7]:491,520).

In Summary

Social media, much like any area of medicine one is interested in, can be daunting and exciting but fraught with potential difficulties. I liken its adoption in our daily practice to any other decision or interest, including being in a private or academic setting, adopting procedural medicine or sticking to diagnostic consultations, or participating in research. In the end, it’s an individual expression of our desire to practice medicine. However, verifying information already existing online about us is of paramount importance. If I don’t tell my story, someone else will, and they may not be as truthful.
 

Dr. Bencheqroun is Assistant Professor, University of California Riverside School of Medicine, Pulmonary/Critical Care Faculty Program Coordinator & Research Mentor - Internal Medicine Residency Program Desert Regional Medical Center, Palm Springs CA; and Immediate Past Chair of the CHEST Council of Networks.

For most of us, social media is a daunting new reality that we are pressured to be part of but that we struggle to fit into our increasingly demanding schedules. My first social media foray as a physician was a Facebook fan page as a hobby rather than a professional presence. Years later, I have learned the incredible benefit that being on social media in other platforms brought to my profession.
 

What’s social media going to bring to my medical practice?
The days where physicians retreat to the safety of our offices to deliver our care, or to issue carefully structured opinions, or interactions with patients have made way for more direct interaction. Social media has, indeed, allowed us to share more personal glimpses of our daily struggle to save lives, behind-the-scenes snapshot of ethical struggles in decision making, our difficulties qualifying patients for therapies due to insurance complications, or real-time addressing medical news and combating misinformation. Moreover, when patients self-refer, or are referred to my practice, they look me up online before coming to my office. Online profiles are the new “first impression” of the bedside manner of a physician.

Other personal examples of social media benefits include being informed of new publications, since many journals now have an online presence; being able to interact in real-time with authors; learning from physicians in other countries how they handled issues, such as shortage of critical medications; or earning CME, such as the Twitter chats hosted by CHEST (eg, new biologic agents in difficult to treat asthma, or patient selection in triple therapy for COPD).

Why should I pay attention to social media presence?
The pace by which social media changed the landscape took the medical community by surprise. Patients, third-party websites, and online review agencies (official or not) adopted it well before physicians became comfortable with it. As such, when I decided to google myself online, I was shocked at the level of misinformation about me (as a pulmonologist, I didn’t know I had performed sigmoidoscopies, yet that’s what my patients learned before they met me). That was an important lesson: If I don’t control the narrative, someone else will. Consequently, I dedicated a few hours to establish an online presence in order to introduce myself accurately and to be accessible to my patients and colleagues online.

Who decides what’s ethical and what’s not?
As the lines blurred, our community struggled to define what was appropriate and what was not. Finally, we welcomed with relief the issuance of a Code of Ethics, regarding social media use by physicians, from several societies, including the American Medical Association (https://www.ama-assn.org/delivering-care/ethics/professionalism-use-social-media). The principles guiding physicians use of social media include respect for human dignity and rights, honesty and upholding the standards of professionalism, and the duty to safeguard patient confidences and privacy.

Which platform should I use? There are so many. 
While any content can be shared on any platform, social media sites have organically differentiated into being more amenable to one content vs the other. Some accounts tend to be more for professional use (ie, Twitter and LinkedIn), and other accounts for personal use (ie, Facebook, Instagram, Snapchat, and Pinterest). CHEST has selected Twitter to host its CME chats regarding preselected topics, post information about an upcoming lecture during the CHEST meeting, etc. New social media sites are now “physician only,” such as Sermo, Doximity, QuantiMD, and Doc2Doc. Many of these sites require doctors to submit their credentials to a site gatekeeper, recreating the intimacy of a “physicians’ lounge” in an online environment (J Med Internet Res. 2014:Feb 11;16[2]:e13). Lastly, Figure1 is a media sharing app between physicians allowing discussions of de-identified images or cases, recreating the “curbside” consult concept online.

I heard about hashtags. What are they?
Hashtags are simply clickable topic titles (#COPD #Sepsis # Education, etc.) that can be added to a post, in order to widen its reach. For instance, if I am interested in sepsis, I can click on the hashtag #Sepsis, and it would bring up all the posts on any Twitter account that added that hashtag. It’s a filter that takes me to that topic of interest. I can then click on the button “Like” on the message or the account itself where the post was found. The “Like” is similar to a bookmark for that account on my own Twitter. In the future, all the posts from that account would be available to me.

What are influencers or thought leaders?
Anyone who “liked” my account is now “following” me. The number of followers has become a measure of the popularity of anyone on social media. If it reaches a high level, then the person with the account is dubbed an “influencer.” Social media “influencers” are individuals whose opinion is followed by hundreds of thousands. Influencers may even be rewarded for harnessing their reach to make money off advertising. One can easily see how it is powerful for a physician to become an influencer or a “thought leader,” not to make money but to expand their reach on social media to spread the correct information about diets, drugs, e-cigarettes, and vaccinations, to name a few.

Can social media get me in trouble?
In 2012, a survey of the state medical boards published by JAMA (2012;307[11]:1141) revealed that approximately 30% of state medical boards reported complaints of “online violations of patient confidentiality.” More than 10% stated they had encountered a case of an “online depiction of intoxication.”

Another study a year earlier revealed that 13% of physicians reported they have discussed individual, though anonymized, cases with other physicians in public online forums (http://www.quantiamd.com/qqcp/DoctorsPatientSocialMedia.pdf).

Even if posted anonymously, or on a “personal” rather than professional social media site, various investigative methods may potentially be used to directly link information to a specific person or incident. The most current case law dictates that such information is “discoverable.” In fact, Facebook’s policy for the use of data informs users that, “we may access, preserve, and share your information in response to a legal request” both within and outside of U.S. jurisdiction”.

What kind of trouble could I be exposed to?
Poor quality of information, damage to our professional image, breaches of patient’s privacy, violation of patient-physician boundary, license revoking by state boards, and erroneous medical advice given in the absence of examining a patient, are all potential pitfalls for physicians in the careless use of social media.

• supplies offline contact information so that an appointment can be made, if desired; and

• identifies a source for emergency services if the inquirer cannot wait for an appointment.

In circumstances where a patient–physician relationship already exists, informed consent should be obtained, which should include a careful explanation regarding the risks of online communication, expected response times, and the handling of emergencies, then documented in the patient’s chart (PT. 2014 Jul;39[7]:491,520).

In Summary

Social media, much like any area of medicine one is interested in, can be daunting and exciting but fraught with potential difficulties. I liken its adoption in our daily practice to any other decision or interest, including being in a private or academic setting, adopting procedural medicine or sticking to diagnostic consultations, or participating in research. In the end, it’s an individual expression of our desire to practice medicine. However, verifying information already existing online about us is of paramount importance. If I don’t tell my story, someone else will, and they may not be as truthful.
 

Dr. Bencheqroun is Assistant Professor, University of California Riverside School of Medicine, Pulmonary/Critical Care Faculty Program Coordinator & Research Mentor - Internal Medicine Residency Program Desert Regional Medical Center, Palm Springs CA; and Immediate Past Chair of the CHEST Council of Networks.

For most of us, social media is a daunting new reality that we are pressured to be part of but that we struggle to fit into our increasingly demanding schedules. My first social media foray as a physician was a Facebook fan page as a hobby rather than a professional presence. Years later, I have learned the incredible benefit that being on social media in other platforms brought to my profession.
 

What’s social media going to bring to my medical practice?
The days where physicians retreat to the safety of our offices to deliver our care, or to issue carefully structured opinions, or interactions with patients have made way for more direct interaction. Social media has, indeed, allowed us to share more personal glimpses of our daily struggle to save lives, behind-the-scenes snapshot of ethical struggles in decision making, our difficulties qualifying patients for therapies due to insurance complications, or real-time addressing medical news and combating misinformation. Moreover, when patients self-refer, or are referred to my practice, they look me up online before coming to my office. Online profiles are the new “first impression” of the bedside manner of a physician.

Other personal examples of social media benefits include being informed of new publications, since many journals now have an online presence; being able to interact in real-time with authors; learning from physicians in other countries how they handled issues, such as shortage of critical medications; or earning CME, such as the Twitter chats hosted by CHEST (eg, new biologic agents in difficult to treat asthma, or patient selection in triple therapy for COPD).

Why should I pay attention to social media presence?
The pace by which social media changed the landscape took the medical community by surprise. Patients, third-party websites, and online review agencies (official or not) adopted it well before physicians became comfortable with it. As such, when I decided to google myself online, I was shocked at the level of misinformation about me (as a pulmonologist, I didn’t know I had performed sigmoidoscopies, yet that’s what my patients learned before they met me). That was an important lesson: If I don’t control the narrative, someone else will. Consequently, I dedicated a few hours to establish an online presence in order to introduce myself accurately and to be accessible to my patients and colleagues online.

Who decides what’s ethical and what’s not?
As the lines blurred, our community struggled to define what was appropriate and what was not. Finally, we welcomed with relief the issuance of a Code of Ethics, regarding social media use by physicians, from several societies, including the American Medical Association (https://www.ama-assn.org/delivering-care/ethics/professionalism-use-social-media). The principles guiding physicians use of social media include respect for human dignity and rights, honesty and upholding the standards of professionalism, and the duty to safeguard patient confidences and privacy.

Which platform should I use? There are so many. 
While any content can be shared on any platform, social media sites have organically differentiated into being more amenable to one content vs the other. Some accounts tend to be more for professional use (ie, Twitter and LinkedIn), and other accounts for personal use (ie, Facebook, Instagram, Snapchat, and Pinterest). CHEST has selected Twitter to host its CME chats regarding preselected topics, post information about an upcoming lecture during the CHEST meeting, etc. New social media sites are now “physician only,” such as Sermo, Doximity, QuantiMD, and Doc2Doc. Many of these sites require doctors to submit their credentials to a site gatekeeper, recreating the intimacy of a “physicians’ lounge” in an online environment (J Med Internet Res. 2014:Feb 11;16[2]:e13). Lastly, Figure1 is a media sharing app between physicians allowing discussions of de-identified images or cases, recreating the “curbside” consult concept online.

I heard about hashtags. What are they?
Hashtags are simply clickable topic titles (#COPD #Sepsis # Education, etc.) that can be added to a post, in order to widen its reach. For instance, if I am interested in sepsis, I can click on the hashtag #Sepsis, and it would bring up all the posts on any Twitter account that added that hashtag. It’s a filter that takes me to that topic of interest. I can then click on the button “Like” on the message or the account itself where the post was found. The “Like” is similar to a bookmark for that account on my own Twitter. In the future, all the posts from that account would be available to me.

What are influencers or thought leaders?
Anyone who “liked” my account is now “following” me. The number of followers has become a measure of the popularity of anyone on social media. If it reaches a high level, then the person with the account is dubbed an “influencer.” Social media “influencers” are individuals whose opinion is followed by hundreds of thousands. Influencers may even be rewarded for harnessing their reach to make money off advertising. One can easily see how it is powerful for a physician to become an influencer or a “thought leader,” not to make money but to expand their reach on social media to spread the correct information about diets, drugs, e-cigarettes, and vaccinations, to name a few.

Can social media get me in trouble?
In 2012, a survey of the state medical boards published by JAMA (2012;307[11]:1141) revealed that approximately 30% of state medical boards reported complaints of “online violations of patient confidentiality.” More than 10% stated they had encountered a case of an “online depiction of intoxication.”

Another study a year earlier revealed that 13% of physicians reported they have discussed individual, though anonymized, cases with other physicians in public online forums (http://www.quantiamd.com/qqcp/DoctorsPatientSocialMedia.pdf).

Even if posted anonymously, or on a “personal” rather than professional social media site, various investigative methods may potentially be used to directly link information to a specific person or incident. The most current case law dictates that such information is “discoverable.” In fact, Facebook’s policy for the use of data informs users that, “we may access, preserve, and share your information in response to a legal request” both within and outside of U.S. jurisdiction”.

What kind of trouble could I be exposed to?
Poor quality of information, damage to our professional image, breaches of patient’s privacy, violation of patient-physician boundary, license revoking by state boards, and erroneous medical advice given in the absence of examining a patient, are all potential pitfalls for physicians in the careless use of social media.

• supplies offline contact information so that an appointment can be made, if desired; and

• identifies a source for emergency services if the inquirer cannot wait for an appointment.

In circumstances where a patient–physician relationship already exists, informed consent should be obtained, which should include a careful explanation regarding the risks of online communication, expected response times, and the handling of emergencies, then documented in the patient’s chart (PT. 2014 Jul;39[7]:491,520).

In Summary

Social media, much like any area of medicine one is interested in, can be daunting and exciting but fraught with potential difficulties. I liken its adoption in our daily practice to any other decision or interest, including being in a private or academic setting, adopting procedural medicine or sticking to diagnostic consultations, or participating in research. In the end, it’s an individual expression of our desire to practice medicine. However, verifying information already existing online about us is of paramount importance. If I don’t tell my story, someone else will, and they may not be as truthful.
 

Dr. Bencheqroun is Assistant Professor, University of California Riverside School of Medicine, Pulmonary/Critical Care Faculty Program Coordinator & Research Mentor - Internal Medicine Residency Program Desert Regional Medical Center, Palm Springs CA; and Immediate Past Chair of the CHEST Council of Networks.

Since the landmark ARMA trial, use of low tidal volume ventilation (LTVV) at 6 mL/kg predicted body weight (PBW) has become our gold standard for ventilator management in acute respiratory distress syndrome (ARDS) (Brower RG, et al. N Engl J Med. 2000;342[18]:1301). While other studies have suggested that patients without ARDS may also benefit from lower volumes, the recently published Protective Ventilation in Patients Without ARDS (PReVENT) trial found no benefit to using LTVV in non-ARDS patients (Simonis FD, et al. JAMA. 2018;320[18]:1872). Does this mean we let physicians set volumes at will? Is tidal volume (VT) even clinically relevant anymore in the non-ARDS population?

Prior to the PReVENT trial, our practice of LTVV for patients without ARDS was informed primarily by observational data. In 2012, a meta-analysis comparing LTVV with “conventional” VT (10-12 mL/kg IBW) in non-ARDS patients found that those given LTVV had a lower incidence of acute lung injury and lower overall mortality (Neto AS, et al. JAMA. 2012 308[16]:1651). While these were promising findings, there was limited follow-up poststudy onset, and the majority of included studies were based on a surgical population. Additionally, the use of VT > 10 mL/kg PBW has become uncommon in routine clinical practice. How comparable are those previous studies to today’s clinical milieu? When comparing outcomes for ICU patients who were ventilated with low (≤7mL/kg PBW), intermediate (>7, but <10 mL/kg PBW), and high (≥10 mL/kg PBW) VT, a second meta-analysis found a 28% risk reduction in the development of ARDS or pneumonia with low vs high, but the similar difference was not seen when comparing low vs intermediate groups (Neto AS, et al. Crit Care Med. 2015;43[10]:2155). This research suggested that negative outcomes were driven by the excessive VT.

To investigate the importance of timing of LTVV in ARDS, Needham and colleagues performed a prospective cohort study in patients with ARDS, examining the effect of VT received over time on the outcome of ICU mortality (Needham DM, et al. Am J Respir Crit Care Med. 2015;191[2]:177). They found that every 1 mL/kg increase in VT setting was associated with a 23% increase in mortality and, indeed, increases in subsequent VT compared with baseline setting were associated with increasing mortality. One may, therefore, be concerned that if we miss the ARDS diagnosis, the default to higher VT at the time of intubation may harm our patients. With or without clinician recognition of ARDS, LUNG SAFE revealed that the average VT for the patients with confirmed ARDS was 7.6 (95% CI 7.5-7.7) mL/kg PBW. While this mean value is well within the range of lung protective ventilation (less than 8 mL/kg PBW), over one-third of patients were exposed to larger VT. A recently published study by Sjoding and colleagues showed that VT of >8 mL/kg PBW was used in 40% of the cohort, and continued exposure to 24 total hours of these high VT was associated with increased risk of mortality (OR 1.82 (95% CI, 1.20–2.78) (Sjoding MW, et al. Crit Care Med. 2019;47[1]:56). All three studies support early administration of lung protective ventilation, considering the high mortality associated with ARDS.

Before consolidating what we know about empiric use of LTVV, we also must highlight the important concerns about LTVV that were investigated in the PReVENT trial. Over-sedation to maintain low VT, increased delirium, ventilator asynchrony, and possibility of effort-induced lung injury are some of the potential risks associated with LTVV. While there were no differences in the use of sedatives or neuromuscular blocking agents between groups in the PReVENT trial, more delirium was seen in the LTVV group with a P = .06, which may be a signal deserving further exploration.

Therefore, now understanding both the upside and downside of LTVV, what’s our best approach? While we lack prospective clinical trial data showing benefit of LTVV in patients without ARDS, we do not have conclusive evidence to show its harm. Remembering that even intensivists can fail to recognize ARDS at its onset, default utilization of LTVV, or at least lung protective ventilation of <8 mL/kg PBW, may be the safest approach for all patients. To be clear, this approach would still allow for active physician decision-making to personalize the settings to the individual patient’s needs, including the use of higher VT if needed for patient comfort, effort, and sedation needs. Changing the default settings and implementing friendly reminders about how to manage the ventilator has already been shown to be helpful for the surgical population (O’Reilly-Shah VN, et al. BMJ Qual Saf. 2018;27[12]:1008).

We must also consider the process of health-care delivery and the implementation of best practices, after considering the facilitators and barriers to adoption of said practices. Many patients decompensate and require intubation prior to ICU arrival, with prolonged boarding in the ED or medical wards being a common occurrence for many hospitals. As such, we need to consider a ventilation strategy that allows for best practice implementation at a hospital-wide level, appealing to an interprofessional approach to ventilator management, employing physicians outside of critical care medicine, respiratory therapists, and nursing. The PReVENT trial had a nicely constructed protocol with clear instructions on ventilator adjustments with frequent plateau pressure measurements and patient assessments. In the real world setting, especially in a non-ICU setting, ventilator management is not as straightforward. Considering that plateau pressures were only checked in approximately 40% of the patients in LUNG SAFE cohort, active management and attention to driving pressure may be a stretch in many settings.

Until we get 100% sensitive in timely recognition (instantaneous, really) of ARDS pathology augmented by automated diagnostic tools embedded in the medical record and/or incorporate advanced technology in the ventilator management to avoid human error, employing simple defaults to guarantee a protective setting in case of later diagnosis of ARDS seems logical. We can even go further to separate the defaults into LTVV for hypoxemic respiratory failure and lung protective ventilation for everything else, with future development of more algorithms, protocols, and clinical decision support tools for ventilator management. For the time being, a simpler intervention of setting a safer default is a great universal start.

Dr. Mathews and Dr. Howell are with the Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine; Dr. Mathews is also with the Department of Emergency Medicine; Icahn School of Medicine at Mount Sinai, New York, NY.

Since the landmark ARMA trial, use of low tidal volume ventilation (LTVV) at 6 mL/kg predicted body weight (PBW) has become our gold standard for ventilator management in acute respiratory distress syndrome (ARDS) (Brower RG, et al. N Engl J Med. 2000;342[18]:1301). While other studies have suggested that patients without ARDS may also benefit from lower volumes, the recently published Protective Ventilation in Patients Without ARDS (PReVENT) trial found no benefit to using LTVV in non-ARDS patients (Simonis FD, et al. JAMA. 2018;320[18]:1872). Does this mean we let physicians set volumes at will? Is tidal volume (VT) even clinically relevant anymore in the non-ARDS population?

Prior to the PReVENT trial, our practice of LTVV for patients without ARDS was informed primarily by observational data. In 2012, a meta-analysis comparing LTVV with “conventional” VT (10-12 mL/kg IBW) in non-ARDS patients found that those given LTVV had a lower incidence of acute lung injury and lower overall mortality (Neto AS, et al. JAMA. 2012 308[16]:1651). While these were promising findings, there was limited follow-up poststudy onset, and the majority of included studies were based on a surgical population. Additionally, the use of VT > 10 mL/kg PBW has become uncommon in routine clinical practice. How comparable are those previous studies to today’s clinical milieu? When comparing outcomes for ICU patients who were ventilated with low (≤7mL/kg PBW), intermediate (>7, but <10 mL/kg PBW), and high (≥10 mL/kg PBW) VT, a second meta-analysis found a 28% risk reduction in the development of ARDS or pneumonia with low vs high, but the similar difference was not seen when comparing low vs intermediate groups (Neto AS, et al. Crit Care Med. 2015;43[10]:2155). This research suggested that negative outcomes were driven by the excessive VT.

To investigate the importance of timing of LTVV in ARDS, Needham and colleagues performed a prospective cohort study in patients with ARDS, examining the effect of VT received over time on the outcome of ICU mortality (Needham DM, et al. Am J Respir Crit Care Med. 2015;191[2]:177). They found that every 1 mL/kg increase in VT setting was associated with a 23% increase in mortality and, indeed, increases in subsequent VT compared with baseline setting were associated with increasing mortality. One may, therefore, be concerned that if we miss the ARDS diagnosis, the default to higher VT at the time of intubation may harm our patients. With or without clinician recognition of ARDS, LUNG SAFE revealed that the average VT for the patients with confirmed ARDS was 7.6 (95% CI 7.5-7.7) mL/kg PBW. While this mean value is well within the range of lung protective ventilation (less than 8 mL/kg PBW), over one-third of patients were exposed to larger VT. A recently published study by Sjoding and colleagues showed that VT of >8 mL/kg PBW was used in 40% of the cohort, and continued exposure to 24 total hours of these high VT was associated with increased risk of mortality (OR 1.82 (95% CI, 1.20–2.78) (Sjoding MW, et al. Crit Care Med. 2019;47[1]:56). All three studies support early administration of lung protective ventilation, considering the high mortality associated with ARDS.

Before consolidating what we know about empiric use of LTVV, we also must highlight the important concerns about LTVV that were investigated in the PReVENT trial. Over-sedation to maintain low VT, increased delirium, ventilator asynchrony, and possibility of effort-induced lung injury are some of the potential risks associated with LTVV. While there were no differences in the use of sedatives or neuromuscular blocking agents between groups in the PReVENT trial, more delirium was seen in the LTVV group with a P = .06, which may be a signal deserving further exploration.

Therefore, now understanding both the upside and downside of LTVV, what’s our best approach? While we lack prospective clinical trial data showing benefit of LTVV in patients without ARDS, we do not have conclusive evidence to show its harm. Remembering that even intensivists can fail to recognize ARDS at its onset, default utilization of LTVV, or at least lung protective ventilation of <8 mL/kg PBW, may be the safest approach for all patients. To be clear, this approach would still allow for active physician decision-making to personalize the settings to the individual patient’s needs, including the use of higher VT if needed for patient comfort, effort, and sedation needs. Changing the default settings and implementing friendly reminders about how to manage the ventilator has already been shown to be helpful for the surgical population (O’Reilly-Shah VN, et al. BMJ Qual Saf. 2018;27[12]:1008).

We must also consider the process of health-care delivery and the implementation of best practices, after considering the facilitators and barriers to adoption of said practices. Many patients decompensate and require intubation prior to ICU arrival, with prolonged boarding in the ED or medical wards being a common occurrence for many hospitals. As such, we need to consider a ventilation strategy that allows for best practice implementation at a hospital-wide level, appealing to an interprofessional approach to ventilator management, employing physicians outside of critical care medicine, respiratory therapists, and nursing. The PReVENT trial had a nicely constructed protocol with clear instructions on ventilator adjustments with frequent plateau pressure measurements and patient assessments. In the real world setting, especially in a non-ICU setting, ventilator management is not as straightforward. Considering that plateau pressures were only checked in approximately 40% of the patients in LUNG SAFE cohort, active management and attention to driving pressure may be a stretch in many settings.

Until we get 100% sensitive in timely recognition (instantaneous, really) of ARDS pathology augmented by automated diagnostic tools embedded in the medical record and/or incorporate advanced technology in the ventilator management to avoid human error, employing simple defaults to guarantee a protective setting in case of later diagnosis of ARDS seems logical. We can even go further to separate the defaults into LTVV for hypoxemic respiratory failure and lung protective ventilation for everything else, with future development of more algorithms, protocols, and clinical decision support tools for ventilator management. For the time being, a simpler intervention of setting a safer default is a great universal start.

Dr. Mathews and Dr. Howell are with the Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine; Dr. Mathews is also with the Department of Emergency Medicine; Icahn School of Medicine at Mount Sinai, New York, NY.

Since the landmark ARMA trial, use of low tidal volume ventilation (LTVV) at 6 mL/kg predicted body weight (PBW) has become our gold standard for ventilator management in acute respiratory distress syndrome (ARDS) (Brower RG, et al. N Engl J Med. 2000;342[18]:1301). While other studies have suggested that patients without ARDS may also benefit from lower volumes, the recently published Protective Ventilation in Patients Without ARDS (PReVENT) trial found no benefit to using LTVV in non-ARDS patients (Simonis FD, et al. JAMA. 2018;320[18]:1872). Does this mean we let physicians set volumes at will? Is tidal volume (VT) even clinically relevant anymore in the non-ARDS population?

Prior to the PReVENT trial, our practice of LTVV for patients without ARDS was informed primarily by observational data. In 2012, a meta-analysis comparing LTVV with “conventional” VT (10-12 mL/kg IBW) in non-ARDS patients found that those given LTVV had a lower incidence of acute lung injury and lower overall mortality (Neto AS, et al. JAMA. 2012 308[16]:1651). While these were promising findings, there was limited follow-up poststudy onset, and the majority of included studies were based on a surgical population. Additionally, the use of VT > 10 mL/kg PBW has become uncommon in routine clinical practice. How comparable are those previous studies to today’s clinical milieu? When comparing outcomes for ICU patients who were ventilated with low (≤7mL/kg PBW), intermediate (>7, but <10 mL/kg PBW), and high (≥10 mL/kg PBW) VT, a second meta-analysis found a 28% risk reduction in the development of ARDS or pneumonia with low vs high, but the similar difference was not seen when comparing low vs intermediate groups (Neto AS, et al. Crit Care Med. 2015;43[10]:2155). This research suggested that negative outcomes were driven by the excessive VT.

To investigate the importance of timing of LTVV in ARDS, Needham and colleagues performed a prospective cohort study in patients with ARDS, examining the effect of VT received over time on the outcome of ICU mortality (Needham DM, et al. Am J Respir Crit Care Med. 2015;191[2]:177). They found that every 1 mL/kg increase in VT setting was associated with a 23% increase in mortality and, indeed, increases in subsequent VT compared with baseline setting were associated with increasing mortality. One may, therefore, be concerned that if we miss the ARDS diagnosis, the default to higher VT at the time of intubation may harm our patients. With or without clinician recognition of ARDS, LUNG SAFE revealed that the average VT for the patients with confirmed ARDS was 7.6 (95% CI 7.5-7.7) mL/kg PBW. While this mean value is well within the range of lung protective ventilation (less than 8 mL/kg PBW), over one-third of patients were exposed to larger VT. A recently published study by Sjoding and colleagues showed that VT of >8 mL/kg PBW was used in 40% of the cohort, and continued exposure to 24 total hours of these high VT was associated with increased risk of mortality (OR 1.82 (95% CI, 1.20–2.78) (Sjoding MW, et al. Crit Care Med. 2019;47[1]:56). All three studies support early administration of lung protective ventilation, considering the high mortality associated with ARDS.

Before consolidating what we know about empiric use of LTVV, we also must highlight the important concerns about LTVV that were investigated in the PReVENT trial. Over-sedation to maintain low VT, increased delirium, ventilator asynchrony, and possibility of effort-induced lung injury are some of the potential risks associated with LTVV. While there were no differences in the use of sedatives or neuromuscular blocking agents between groups in the PReVENT trial, more delirium was seen in the LTVV group with a P = .06, which may be a signal deserving further exploration.

Therefore, now understanding both the upside and downside of LTVV, what’s our best approach? While we lack prospective clinical trial data showing benefit of LTVV in patients without ARDS, we do not have conclusive evidence to show its harm. Remembering that even intensivists can fail to recognize ARDS at its onset, default utilization of LTVV, or at least lung protective ventilation of <8 mL/kg PBW, may be the safest approach for all patients. To be clear, this approach would still allow for active physician decision-making to personalize the settings to the individual patient’s needs, including the use of higher VT if needed for patient comfort, effort, and sedation needs. Changing the default settings and implementing friendly reminders about how to manage the ventilator has already been shown to be helpful for the surgical population (O’Reilly-Shah VN, et al. BMJ Qual Saf. 2018;27[12]:1008).

We must also consider the process of health-care delivery and the implementation of best practices, after considering the facilitators and barriers to adoption of said practices. Many patients decompensate and require intubation prior to ICU arrival, with prolonged boarding in the ED or medical wards being a common occurrence for many hospitals. As such, we need to consider a ventilation strategy that allows for best practice implementation at a hospital-wide level, appealing to an interprofessional approach to ventilator management, employing physicians outside of critical care medicine, respiratory therapists, and nursing. The PReVENT trial had a nicely constructed protocol with clear instructions on ventilator adjustments with frequent plateau pressure measurements and patient assessments. In the real world setting, especially in a non-ICU setting, ventilator management is not as straightforward. Considering that plateau pressures were only checked in approximately 40% of the patients in LUNG SAFE cohort, active management and attention to driving pressure may be a stretch in many settings.

Until we get 100% sensitive in timely recognition (instantaneous, really) of ARDS pathology augmented by automated diagnostic tools embedded in the medical record and/or incorporate advanced technology in the ventilator management to avoid human error, employing simple defaults to guarantee a protective setting in case of later diagnosis of ARDS seems logical. We can even go further to separate the defaults into LTVV for hypoxemic respiratory failure and lung protective ventilation for everything else, with future development of more algorithms, protocols, and clinical decision support tools for ventilator management. For the time being, a simpler intervention of setting a safer default is a great universal start.

Dr. Mathews and Dr. Howell are with the Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine; Dr. Mathews is also with the Department of Emergency Medicine; Icahn School of Medicine at Mount Sinai, New York, NY.

Michelle Cao, DO, FCCP

Dr. Michelle Cao is a Clinical Associate Professor in the Division of Sleep Medicine and Division of Neuromuscular Medicine, at the Stanford University School of Medicine. Her clinical expertise is in complex sleep-related respiratory disorders and home mechanical ventilation for chronic respiratory failure syndromes. She oversees the Noninvasive Ventilation Program for the Stanford Neuromuscular Medicine Center. Dr. Cao also holds the position of Vice-Chair for the Home-Based Mechanical Ventilation and Neuromuscular Disease NetWork with CHEST and is a member of the Scientific Presentations and Awards Committee.

Michelle Cao, DO, FCCP

Dr. Michelle Cao is a Clinical Associate Professor in the Division of Sleep Medicine and Division of Neuromuscular Medicine, at the Stanford University School of Medicine. Her clinical expertise is in complex sleep-related respiratory disorders and home mechanical ventilation for chronic respiratory failure syndromes. She oversees the Noninvasive Ventilation Program for the Stanford Neuromuscular Medicine Center. Dr. Cao also holds the position of Vice-Chair for the Home-Based Mechanical Ventilation and Neuromuscular Disease NetWork with CHEST and is a member of the Scientific Presentations and Awards Committee.

Michelle Cao, DO, FCCP

Dr. Michelle Cao is a Clinical Associate Professor in the Division of Sleep Medicine and Division of Neuromuscular Medicine, at the Stanford University School of Medicine. Her clinical expertise is in complex sleep-related respiratory disorders and home mechanical ventilation for chronic respiratory failure syndromes. She oversees the Noninvasive Ventilation Program for the Stanford Neuromuscular Medicine Center. Dr. Cao also holds the position of Vice-Chair for the Home-Based Mechanical Ventilation and Neuromuscular Disease NetWork with CHEST and is a member of the Scientific Presentations and Awards Committee.

Compared with obstructive sleep apnea (OSA), the prevalence of central sleep apnea (CSA) is low in the general population. However, in adults, CSA may be highly prevalent in certain conditions, most commonly among those with left ventricular systolic dysfunction, left ventricular diastolic dysfunction, atrial fibrillation, stroke, and opioid users (Javaheri S, et al. J Am Coll Cardiol. 2017; 69:841). CSA may also be found in patients with carotid artery stenosis, cervical neck injury, and renal dysfunction. CSA can occur when OSA is treated (treatment-emergent central sleep apnea, or TECA), notably, and most frequently, with continuous positive airway pressure (CPAP) devices. Though in many individuals, this frequently resolves with continued use of the device.

In addition, unlike OSA, adequate treatment of CSA has proven difficult. Specifically, the response to CPAP, oxygen, theophylline, acetazolamide, and adaptive-servo ventilation (ASV) is highly variable, with individuals who respond well, and individuals in whom therapy fails to fully suppress the disorder.

Our interest in phrenic nerve stimulation increased after it was shown that CPAP therapy failed to improve morbidity and mortality of CSA in patients with heart failure and reduced ejection fraction (HFrEF) (CANPAP trial, Bradley et al. N Engl J Med. 2005;353(19):2025). In fact, in this trial, treatment with CPAP was associated with significantly increased mortality during the first few months of therapy. We reason that a potential mechanism was positive airway pressure that had adverse cardiovascular effects (Javaheri S. J Clin Sleep Med. 2006;2:399). This is because positive airway pressure therapy decreases venous return to the right side of the heart and increases lung volume. This could increase pulmonary vascular resistance (right ventricular afterload), which is lung volume-dependent. Therefore, the subgroup of individuals with heart failure whose right ventricular function is preload-dependent and has pulmonary hypertension is at risk for premature mortality with any PAP device.

Interestingly, investigators of the SERVE-HF trial (Cowie MR, et al. N Engl J Med. 2015;373:1095) also hypothesized that one reason for excess mortality associated with ASV use might have been due to an ASV-associated excessive rise in intrathoracic pressure, similar to the hypothesis we proposed earlier for CPAP. We expanded on this hypothesis and reasoned that based on the algorithm of the device, in some patients, it could have generated excessive minute ventilation and pressure contributing to excess mortality, either at night or daytime (Javaheri S, et al. Chest. 2016;149:900). Other deficiencies of the algorithm of the ASV device could have contributed to excess mortality as well (Javaheri S, et al. Chest. 2014;146:514). These deficiencies of the ASV device used in the SERVE-HF trial have been significantly improved in the new generation of ASV devices.

Undoubtedly, therefore, mask therapy with positive airway pressures increases intrathoracic pressure and will adversely affect cardiovascular function in some patients with heart failure. Another issue for mask therapy is adherence to the device remains poor, as demonstrated both in the CANPAP and SERVE-HF trials, confirming the need for new approaches utilizing non-mask therapies both for CSA and OSA.

Given the limitations of mask-based therapies, over the last several years, we have performed studies exploring the use of oxygen, acetazolamide, theophylline, and, most recently, phrenic nerve stimulation (PNS). In general, these therapies are devoid of increasing intrathoracic pressure and are expected to be less reliant on patients’ adherence than PAP therapy. Long-term randomized clinical trials are needed, and, most recently, the NIH approved a phase 3 trial for a randomized placebo-controlled low flow oxygen therapy for treatment of CSA in HFrEF. This is a modified trial proposed by one of us more than 20 years ago!

Regarding PNS, CSA is characterized by intermittent phrenic nerve (and intercostal nerves) deactivation. It, therefore, makes sense to have an implanted stimulator for the phrenic nerve to prevent development of central apneas during sleep. This is not a new idea. In 1948, Sarnoff and colleagues demonstrated for the first time that artificial respiration could be effectively administered to the cat, dog, monkey, and rabbit in the absence of spontaneous respiration by electrical stimulation of one (or both) phrenic nerves (Sarnoff SJ, et al. Science. 1948;108:482). In later experiments, these investigators showed that unilateral phrenic nerve stimulation is also equally effective in man as that shown in animal models.

The phrenic nerves comes in contact with veins on both the right (brachiocephalic) and the left (pericardiophrenic vein) side of the mediastinum. Like a cardiac pacemaker, an electrophysiologist places the stimulator within the vein at the point of encounter with the phrenic nerve. Only unilateral stimulation is needed for the therapy. The device is typically placed on the right side of the chest as many patients may already have a cardiac implanted electronic device such as a pacemaker. Like the hypoglossal nerve stimulation, the FDA approved this device for the treatment of OSA. The system can be programmed using an external programmer in the office.

Phrenic nerve stimulation system is initially activated 1 month after the device is placed. It is programmed to be automatically activated at night when the patient is at rest. First, a time is set on the device for when the patient typically goes to bed and awakens. This allows the therapy to activate. The device contains a position sensor and accelerometer, which determine position and activity level. Once appropriate time, position, and activity are confirmed, the device activates automatically. Therapy comes on and can increase in level over several minutes. The device senses transthoracic impedance and can use this measurement to make changes in the therapy output and activity. If the patient gets up at night, the device automatically stops and restarts when the patient is back in a sleeping position. How quickly the therapy restarts and at what energy is programmable. The device may allow from 1 to 15 minutes for the patient to get back to sleep before beginning therapy. These programming changes allow for patient acceptance and comfort with the therapy even in very sensitive patients. Importantly, no patient activation is needed, so that therapy delivery is independent of patient’s adherence over time.

In the prospective, randomized pivotal trial (Costanzo et al. Lancet. 2016;388:974), 151 eligible patients with moderate-severe central sleep apnea were implanted and randomly assigned to the treatment (n=73) or control (n=78) groups. Participants in the active arm received PNS for 6 months. All polysomnograms were centrally and blindly scored. There were significant decreases in AHI (50 to 26/per hour of sleep), CAI (32 to 6), arousal index (46 to 25), and ODI (44 to 25). Two points should be emphasized: first, changes in AHI with PNS are similar to those in CANPAP trial, and there remained a significant number of hypopneas (some of these hypopneas are at least in part related to the speed of the titration when the subject sits up and the device automatically is deactivated, only to resume therapy in supine position); second, in contrast to the CANPAP trial, there was a significant reduction in arousals. Probably for this reason, subjective daytime sleepiness, as measured by the ESS, improved. In addition, PNS improved quality of life, in contrast to lack of effect of CPAP or ASV in this domain. Regarding side effects, 138 (91%) of 151 patients had no serious-related adverse events at 12 months. Seven (9%) cases of related-serious adverse events occurred in the control group and six (8%) cases were reported in the treatment group.—3.4% needed lead repositioning, a rate which is like that of cardiac implantable devices. Seven patients died (unrelated to implant, system, or therapy), four deaths (two in treatment group and two in control group) during the 6-month randomization period when neurostimulation was delivered to only the treatment and was off in the control group, and three deaths between 6 months and 12 months of follow-up when all patients received neurostimulation. Of 73 patients in the treatment group, 27 (37%) reported nonserious therapy-related discomfort that was resolved with simple system reprogramming in 26 (36%) patients but was unresolved in one (1%) patient.

Long-term studies have shown sustained effects of PNS on CSA with improvement in both sleep metrics and QOL, as measured by the Minnesota Living with Heart Failure Questionnaire (MLWHF) and patient global assessment (PGA). Furthermore, in the subgroup of patients with concomitant heart failure with LVEF ≤ 45%, PNS was associated with both improvements in LVEF and a trend toward lower hospitalization rates (Costanzo et al. Eur J Heart Fail. 2018; doi:10.1002/ejhf.1312).

Several issues must be emphasized. One advantage of PNS is complete adherence resulting in a major reduction in apnea burden across the whole night. Second, the mechanism of action prevents any potential adverse consequences related to increased intrathoracic pressure. However, the cost of this therapy is high, similar to that of hypoglossal nerve stimulation. Large scale, long-term studies related to mortality are not yet available, and continued research should help identify those patients most likely to benefit from this therapeutic approach.

Compared with obstructive sleep apnea (OSA), the prevalence of central sleep apnea (CSA) is low in the general population. However, in adults, CSA may be highly prevalent in certain conditions, most commonly among those with left ventricular systolic dysfunction, left ventricular diastolic dysfunction, atrial fibrillation, stroke, and opioid users (Javaheri S, et al. J Am Coll Cardiol. 2017; 69:841). CSA may also be found in patients with carotid artery stenosis, cervical neck injury, and renal dysfunction. CSA can occur when OSA is treated (treatment-emergent central sleep apnea, or TECA), notably, and most frequently, with continuous positive airway pressure (CPAP) devices. Though in many individuals, this frequently resolves with continued use of the device.

In addition, unlike OSA, adequate treatment of CSA has proven difficult. Specifically, the response to CPAP, oxygen, theophylline, acetazolamide, and adaptive-servo ventilation (ASV) is highly variable, with individuals who respond well, and individuals in whom therapy fails to fully suppress the disorder.

Our interest in phrenic nerve stimulation increased after it was shown that CPAP therapy failed to improve morbidity and mortality of CSA in patients with heart failure and reduced ejection fraction (HFrEF) (CANPAP trial, Bradley et al. N Engl J Med. 2005;353(19):2025). In fact, in this trial, treatment with CPAP was associated with significantly increased mortality during the first few months of therapy. We reason that a potential mechanism was positive airway pressure that had adverse cardiovascular effects (Javaheri S. J Clin Sleep Med. 2006;2:399). This is because positive airway pressure therapy decreases venous return to the right side of the heart and increases lung volume. This could increase pulmonary vascular resistance (right ventricular afterload), which is lung volume-dependent. Therefore, the subgroup of individuals with heart failure whose right ventricular function is preload-dependent and has pulmonary hypertension is at risk for premature mortality with any PAP device.

Interestingly, investigators of the SERVE-HF trial (Cowie MR, et al. N Engl J Med. 2015;373:1095) also hypothesized that one reason for excess mortality associated with ASV use might have been due to an ASV-associated excessive rise in intrathoracic pressure, similar to the hypothesis we proposed earlier for CPAP. We expanded on this hypothesis and reasoned that based on the algorithm of the device, in some patients, it could have generated excessive minute ventilation and pressure contributing to excess mortality, either at night or daytime (Javaheri S, et al. Chest. 2016;149:900). Other deficiencies of the algorithm of the ASV device could have contributed to excess mortality as well (Javaheri S, et al. Chest. 2014;146:514). These deficiencies of the ASV device used in the SERVE-HF trial have been significantly improved in the new generation of ASV devices.

Undoubtedly, therefore, mask therapy with positive airway pressures increases intrathoracic pressure and will adversely affect cardiovascular function in some patients with heart failure. Another issue for mask therapy is adherence to the device remains poor, as demonstrated both in the CANPAP and SERVE-HF trials, confirming the need for new approaches utilizing non-mask therapies both for CSA and OSA.

Given the limitations of mask-based therapies, over the last several years, we have performed studies exploring the use of oxygen, acetazolamide, theophylline, and, most recently, phrenic nerve stimulation (PNS). In general, these therapies are devoid of increasing intrathoracic pressure and are expected to be less reliant on patients’ adherence than PAP therapy. Long-term randomized clinical trials are needed, and, most recently, the NIH approved a phase 3 trial for a randomized placebo-controlled low flow oxygen therapy for treatment of CSA in HFrEF. This is a modified trial proposed by one of us more than 20 years ago!

Regarding PNS, CSA is characterized by intermittent phrenic nerve (and intercostal nerves) deactivation. It, therefore, makes sense to have an implanted stimulator for the phrenic nerve to prevent development of central apneas during sleep. This is not a new idea. In 1948, Sarnoff and colleagues demonstrated for the first time that artificial respiration could be effectively administered to the cat, dog, monkey, and rabbit in the absence of spontaneous respiration by electrical stimulation of one (or both) phrenic nerves (Sarnoff SJ, et al. Science. 1948;108:482). In later experiments, these investigators showed that unilateral phrenic nerve stimulation is also equally effective in man as that shown in animal models.

The phrenic nerves comes in contact with veins on both the right (brachiocephalic) and the left (pericardiophrenic vein) side of the mediastinum. Like a cardiac pacemaker, an electrophysiologist places the stimulator within the vein at the point of encounter with the phrenic nerve. Only unilateral stimulation is needed for the therapy. The device is typically placed on the right side of the chest as many patients may already have a cardiac implanted electronic device such as a pacemaker. Like the hypoglossal nerve stimulation, the FDA approved this device for the treatment of OSA. The system can be programmed using an external programmer in the office.

Phrenic nerve stimulation system is initially activated 1 month after the device is placed. It is programmed to be automatically activated at night when the patient is at rest. First, a time is set on the device for when the patient typically goes to bed and awakens. This allows the therapy to activate. The device contains a position sensor and accelerometer, which determine position and activity level. Once appropriate time, position, and activity are confirmed, the device activates automatically. Therapy comes on and can increase in level over several minutes. The device senses transthoracic impedance and can use this measurement to make changes in the therapy output and activity. If the patient gets up at night, the device automatically stops and restarts when the patient is back in a sleeping position. How quickly the therapy restarts and at what energy is programmable. The device may allow from 1 to 15 minutes for the patient to get back to sleep before beginning therapy. These programming changes allow for patient acceptance and comfort with the therapy even in very sensitive patients. Importantly, no patient activation is needed, so that therapy delivery is independent of patient’s adherence over time.

In the prospective, randomized pivotal trial (Costanzo et al. Lancet. 2016;388:974), 151 eligible patients with moderate-severe central sleep apnea were implanted and randomly assigned to the treatment (n=73) or control (n=78) groups. Participants in the active arm received PNS for 6 months. All polysomnograms were centrally and blindly scored. There were significant decreases in AHI (50 to 26/per hour of sleep), CAI (32 to 6), arousal index (46 to 25), and ODI (44 to 25). Two points should be emphasized: first, changes in AHI with PNS are similar to those in CANPAP trial, and there remained a significant number of hypopneas (some of these hypopneas are at least in part related to the speed of the titration when the subject sits up and the device automatically is deactivated, only to resume therapy in supine position); second, in contrast to the CANPAP trial, there was a significant reduction in arousals. Probably for this reason, subjective daytime sleepiness, as measured by the ESS, improved. In addition, PNS improved quality of life, in contrast to lack of effect of CPAP or ASV in this domain. Regarding side effects, 138 (91%) of 151 patients had no serious-related adverse events at 12 months. Seven (9%) cases of related-serious adverse events occurred in the control group and six (8%) cases were reported in the treatment group.—3.4% needed lead repositioning, a rate which is like that of cardiac implantable devices. Seven patients died (unrelated to implant, system, or therapy), four deaths (two in treatment group and two in control group) during the 6-month randomization period when neurostimulation was delivered to only the treatment and was off in the control group, and three deaths between 6 months and 12 months of follow-up when all patients received neurostimulation. Of 73 patients in the treatment group, 27 (37%) reported nonserious therapy-related discomfort that was resolved with simple system reprogramming in 26 (36%) patients but was unresolved in one (1%) patient.

Long-term studies have shown sustained effects of PNS on CSA with improvement in both sleep metrics and QOL, as measured by the Minnesota Living with Heart Failure Questionnaire (MLWHF) and patient global assessment (PGA). Furthermore, in the subgroup of patients with concomitant heart failure with LVEF ≤ 45%, PNS was associated with both improvements in LVEF and a trend toward lower hospitalization rates (Costanzo et al. Eur J Heart Fail. 2018; doi:10.1002/ejhf.1312).

Several issues must be emphasized. One advantage of PNS is complete adherence resulting in a major reduction in apnea burden across the whole night. Second, the mechanism of action prevents any potential adverse consequences related to increased intrathoracic pressure. However, the cost of this therapy is high, similar to that of hypoglossal nerve stimulation. Large scale, long-term studies related to mortality are not yet available, and continued research should help identify those patients most likely to benefit from this therapeutic approach.

Compared with obstructive sleep apnea (OSA), the prevalence of central sleep apnea (CSA) is low in the general population. However, in adults, CSA may be highly prevalent in certain conditions, most commonly among those with left ventricular systolic dysfunction, left ventricular diastolic dysfunction, atrial fibrillation, stroke, and opioid users (Javaheri S, et al. J Am Coll Cardiol. 2017; 69:841). CSA may also be found in patients with carotid artery stenosis, cervical neck injury, and renal dysfunction. CSA can occur when OSA is treated (treatment-emergent central sleep apnea, or TECA), notably, and most frequently, with continuous positive airway pressure (CPAP) devices. Though in many individuals, this frequently resolves with continued use of the device.

In addition, unlike OSA, adequate treatment of CSA has proven difficult. Specifically, the response to CPAP, oxygen, theophylline, acetazolamide, and adaptive-servo ventilation (ASV) is highly variable, with individuals who respond well, and individuals in whom therapy fails to fully suppress the disorder.

Our interest in phrenic nerve stimulation increased after it was shown that CPAP therapy failed to improve morbidity and mortality of CSA in patients with heart failure and reduced ejection fraction (HFrEF) (CANPAP trial, Bradley et al. N Engl J Med. 2005;353(19):2025). In fact, in this trial, treatment with CPAP was associated with significantly increased mortality during the first few months of therapy. We reason that a potential mechanism was positive airway pressure that had adverse cardiovascular effects (Javaheri S. J Clin Sleep Med. 2006;2:399). This is because positive airway pressure therapy decreases venous return to the right side of the heart and increases lung volume. This could increase pulmonary vascular resistance (right ventricular afterload), which is lung volume-dependent. Therefore, the subgroup of individuals with heart failure whose right ventricular function is preload-dependent and has pulmonary hypertension is at risk for premature mortality with any PAP device.

Interestingly, investigators of the SERVE-HF trial (Cowie MR, et al. N Engl J Med. 2015;373:1095) also hypothesized that one reason for excess mortality associated with ASV use might have been due to an ASV-associated excessive rise in intrathoracic pressure, similar to the hypothesis we proposed earlier for CPAP. We expanded on this hypothesis and reasoned that based on the algorithm of the device, in some patients, it could have generated excessive minute ventilation and pressure contributing to excess mortality, either at night or daytime (Javaheri S, et al. Chest. 2016;149:900). Other deficiencies of the algorithm of the ASV device could have contributed to excess mortality as well (Javaheri S, et al. Chest. 2014;146:514). These deficiencies of the ASV device used in the SERVE-HF trial have been significantly improved in the new generation of ASV devices.

Undoubtedly, therefore, mask therapy with positive airway pressures increases intrathoracic pressure and will adversely affect cardiovascular function in some patients with heart failure. Another issue for mask therapy is adherence to the device remains poor, as demonstrated both in the CANPAP and SERVE-HF trials, confirming the need for new approaches utilizing non-mask therapies both for CSA and OSA.

Given the limitations of mask-based therapies, over the last several years, we have performed studies exploring the use of oxygen, acetazolamide, theophylline, and, most recently, phrenic nerve stimulation (PNS). In general, these therapies are devoid of increasing intrathoracic pressure and are expected to be less reliant on patients’ adherence than PAP therapy. Long-term randomized clinical trials are needed, and, most recently, the NIH approved a phase 3 trial for a randomized placebo-controlled low flow oxygen therapy for treatment of CSA in HFrEF. This is a modified trial proposed by one of us more than 20 years ago!

Regarding PNS, CSA is characterized by intermittent phrenic nerve (and intercostal nerves) deactivation. It, therefore, makes sense to have an implanted stimulator for the phrenic nerve to prevent development of central apneas during sleep. This is not a new idea. In 1948, Sarnoff and colleagues demonstrated for the first time that artificial respiration could be effectively administered to the cat, dog, monkey, and rabbit in the absence of spontaneous respiration by electrical stimulation of one (or both) phrenic nerves (Sarnoff SJ, et al. Science. 1948;108:482). In later experiments, these investigators showed that unilateral phrenic nerve stimulation is also equally effective in man as that shown in animal models.

The phrenic nerves comes in contact with veins on both the right (brachiocephalic) and the left (pericardiophrenic vein) side of the mediastinum. Like a cardiac pacemaker, an electrophysiologist places the stimulator within the vein at the point of encounter with the phrenic nerve. Only unilateral stimulation is needed for the therapy. The device is typically placed on the right side of the chest as many patients may already have a cardiac implanted electronic device such as a pacemaker. Like the hypoglossal nerve stimulation, the FDA approved this device for the treatment of OSA. The system can be programmed using an external programmer in the office.

Phrenic nerve stimulation system is initially activated 1 month after the device is placed. It is programmed to be automatically activated at night when the patient is at rest. First, a time is set on the device for when the patient typically goes to bed and awakens. This allows the therapy to activate. The device contains a position sensor and accelerometer, which determine position and activity level. Once appropriate time, position, and activity are confirmed, the device activates automatically. Therapy comes on and can increase in level over several minutes. The device senses transthoracic impedance and can use this measurement to make changes in the therapy output and activity. If the patient gets up at night, the device automatically stops and restarts when the patient is back in a sleeping position. How quickly the therapy restarts and at what energy is programmable. The device may allow from 1 to 15 minutes for the patient to get back to sleep before beginning therapy. These programming changes allow for patient acceptance and comfort with the therapy even in very sensitive patients. Importantly, no patient activation is needed, so that therapy delivery is independent of patient’s adherence over time.

In the prospective, randomized pivotal trial (Costanzo et al. Lancet. 2016;388:974), 151 eligible patients with moderate-severe central sleep apnea were implanted and randomly assigned to the treatment (n=73) or control (n=78) groups. Participants in the active arm received PNS for 6 months. All polysomnograms were centrally and blindly scored. There were significant decreases in AHI (50 to 26/per hour of sleep), CAI (32 to 6), arousal index (46 to 25), and ODI (44 to 25). Two points should be emphasized: first, changes in AHI with PNS are similar to those in CANPAP trial, and there remained a significant number of hypopneas (some of these hypopneas are at least in part related to the speed of the titration when the subject sits up and the device automatically is deactivated, only to resume therapy in supine position); second, in contrast to the CANPAP trial, there was a significant reduction in arousals. Probably for this reason, subjective daytime sleepiness, as measured by the ESS, improved. In addition, PNS improved quality of life, in contrast to lack of effect of CPAP or ASV in this domain. Regarding side effects, 138 (91%) of 151 patients had no serious-related adverse events at 12 months. Seven (9%) cases of related-serious adverse events occurred in the control group and six (8%) cases were reported in the treatment group.—3.4% needed lead repositioning, a rate which is like that of cardiac implantable devices. Seven patients died (unrelated to implant, system, or therapy), four deaths (two in treatment group and two in control group) during the 6-month randomization period when neurostimulation was delivered to only the treatment and was off in the control group, and three deaths between 6 months and 12 months of follow-up when all patients received neurostimulation. Of 73 patients in the treatment group, 27 (37%) reported nonserious therapy-related discomfort that was resolved with simple system reprogramming in 26 (36%) patients but was unresolved in one (1%) patient.

Long-term studies have shown sustained effects of PNS on CSA with improvement in both sleep metrics and QOL, as measured by the Minnesota Living with Heart Failure Questionnaire (MLWHF) and patient global assessment (PGA). Furthermore, in the subgroup of patients with concomitant heart failure with LVEF ≤ 45%, PNS was associated with both improvements in LVEF and a trend toward lower hospitalization rates (Costanzo et al. Eur J Heart Fail. 2018; doi:10.1002/ejhf.1312).

Several issues must be emphasized. One advantage of PNS is complete adherence resulting in a major reduction in apnea burden across the whole night. Second, the mechanism of action prevents any potential adverse consequences related to increased intrathoracic pressure. However, the cost of this therapy is high, similar to that of hypoglossal nerve stimulation. Large scale, long-term studies related to mortality are not yet available, and continued research should help identify those patients most likely to benefit from this therapeutic approach.

More than 5 million patients are admitted to ICUs each year in the United States, and approximately 2% to 10% of these patients develop acute kidney injury requiring renal replacement therapy (AKI-RRT). AKI-RRT carries high morbidity and mortality (Hoste EA, et al. Intensive Care Med. 2015;41:1411) and is associated with renal and systemic complications, such as cardiovascular disease. RRT, frequently provided by nephrologists and/or intensivists, is a supportive therapy that can be life-saving when provided to the right patient at the right time. However, several questions related to the provision of RRT still remain, including the optimal timing of RRT initiation, the development of quality metrics for optimal RRT deliverables and monitoring, and the optimal strategy of RRT de-escalation and risk-stratification of renal recovery. Overall, there is paucity of randomized trials and standardized risk-stratification tools that can guide RRT in the ICU.

Current vexed questions of RRT deliverables in the ICU

There is ongoing research aiming to answer critical questions that can potentially improve current standards of RRT.

What is the optimal time of RRT initiation for critically ill patients with AKI?

Over the last 2 years, three randomized clinical trials have attempted to address this important question involving heterogeneous ICU populations and distinct research hypotheses and study designs. Two of these studies, AKIKI (Gaudry S, et al. N Engl J Med. 2016;375:122) and IDEAL-ICU (Barbar SD, et al. N Engl J Med. 2018;379:1431) yielded no significant difference in the primary outcome of 60-day and 90-day all-cause mortality between the early vs delayed RRT initiation strategies, respectively (Table 1). Further, AKIKI showed no difference in RRT dependence at 60 days and higher catheter-related infections and hypophosphatemia in the early initiation arm. It is important to note that IDEAL-ICU was stopped early for futility after the second planned interim analysis with only 56% of patients enrolled (main hypothesis was that early RRT initiation reduced 90-day all-cause mortality by 10%). In contrast, the ELAIN trial (Zarbock A, et al. JAMA. 2016;315:2190) showed a significant 90-day mortality reduction (39% vs 55%), reduced RRT need (9 days vs 25 days), and reduced length of stay (51 days vs 82 days) favoring early RRT initiation strategy. A larger study (STARRT-AKI) addressing this question with a more pragmatic approach (incorporating clinical judgment and equipoise among intensivists and nephrologists for patient eligibility) is underway. However, it is possible that STARRT-AKI will not provide a definitive answer for the inevitable search for implementing RRT initiation protocols in the ICU. Therefore, the scientific community may need to redirect the research focus to risk-stratification tools that can assist in the identification of patients who could benefit from early RRT initiation through an individualized approach rather than a standardized protocol.

How can RRT deliverables in the ICU be effectively and systematically monitored?

The provision of RRT to ICU patients with AKI requires an iterative adjustment of the RRT prescription and goals of therapy to accommodate changes in the clinical status with emphasis in hemodynamics, multiorgan failure, and fluid overload (Neyra JA. Clin Nephrol. 2018;90:1). The utilization of static and functional tests or point-of-care ultrasonography to assess hemodynamic variables can be useful. Furthermore, the implementation of customized and automated flowsheets in the electronic health record can facilitate remote monitoring. It is, therefore, essential that the multidisciplinary ICU team develops a process to monitor and ensure RRT deliverables. In this context, the standardization and monitoring of quality metrics (dose, modality, anticoagulation, filter life, downtime, etc) and the development of effective quality management systems are critically important. However, big multicenter data are direly needed to provide insight in this arena.

How can renal recovery be assessed and RRT effectively de-escalated?

The continuous examination of renal recovery in ICU patients with AKI-RRT is mostly based on urine output trend and, if feasible, interdialytic solute control. Sometimes, the transition from continuous RRT to intermittent modalities is necessary in the context of multiorgan recovery and de-escalation of care. However, clinical risk-prediction tools that identify patients who can potentially recover or already exhibit early signs of renal function recovery are needed. Current advances in clinical informatics can help to incorporate time-varying clinical parameters that may be informative for risk-prediction models. In addition, incorporating novel biomarkers of AKI repair and functional tests (eg, furosemide stress test, functional MRI) into these models may further inform these tools and aid the development of clinical decision support systems that enhance interventions to promote AKI recovery (Neyra JA, et al. Nephron. 2018;140: 99).

Is post-AKI outpatient care beneficial for ICU survivors who suffered from AKI-RRT?

Specialized AKI survivor clinics have been implemented in some centers. In general, this outpatient follow-up model includes survivors who suffered from AKI stage 2 or 3, some of them requiring RRT, and tailors individualized interventions for post-AKI complications (preventing recurrent AKI, attenuating incident or progressive CKD). However, the value of this outpatient model needs to be further evaluated with emphasis on clinical outcomes (eg, recurrent AKI, CKD, readmissions, or death) and elements that impact quality of life. This is an area of evolving research and a great opportunity for the nephrology and critical care communities to integrate and enhance post-ICU outpatient care and research collaboration.

Interdisciplinary communication among acute care team members

Two essential elements to provide effective RRT to ICU patients with AKI are: (1) the dynamics of the ICU team (intensivists, nephrologists, pharmacists, nurses, nutritionists, physical therapists, etc) to enhance the delivery of personalized therapy (RRT candidacy, timing of initiation, goals for solute control and fluid removal/regulation, renal recovery evaluation, RRT de-escalation, etc.) and (2) the frequent assessment and adjustment of RRT goals according to the clinical status of the patient. Therefore, effective RRT provision in the ICU requires the development of optimal channels of communication among all members of the acute care team and the systematic monitoring of the clinical status of the patient and RRT-specific goals and deliverables.

Perspective from a nurse and quality improvement officer for the provision of RRT in the ICU

The provision of continuous RRT (CRRT) to critically ill patients requires close communication between the bedside nurse and the rest of the ICU team. The physician typically prescribes CRRT and determines the specific goals of therapy. The pharmacist works closely with the nephrologist/intensivist and bedside nurse, especially in regards to customized CRRT solutions (when indicated) and medication dosing. Because CRRT can alter drug pharmacokinetics, the pharmacist closely and constantly monitors the patient’s clinical status, CRRT prescription, and all active medications. CRRT can also affect the nutritional and metabolic status of critically ill patients; therefore, the input of the nutritionist is necessary. The syndrome of ICU-acquired weakness is commonly encountered in ICU patients and is related to physical immobility. While ICU patients with AKI are already at risk for decreased mobility, the continuous connection to an immobile extracorporeal machine for the provision of CRRT may further contribute to immobilization and can also preclude the provision of optimal physical therapy. Therefore, the bedside nurse should assist the physical therapist for the timely and effective delivery of physical therapy according to the clinical status of the patient.

The clinical scenarios discussed above provide a small glimpse into the importance of developing an interdisciplinary ICU team caring for critically ill patients receiving CRRT. In the context of how integral the specific role of each team member is, it becomes clear that the bedside nurse’s role is not only to deliver hands-on patient care but also the orchestration of collaborative communication among all health-care providers for the effective provision of CRRT to critically ill patients in the ICU.

Dr. Neyra and Ms. Hauschild are with the Department of Internal Medicine; Division of Nephrology; Bone and Mineral Metabolism; University of Kentucky; Lexington, Kentucky.

More than 5 million patients are admitted to ICUs each year in the United States, and approximately 2% to 10% of these patients develop acute kidney injury requiring renal replacement therapy (AKI-RRT). AKI-RRT carries high morbidity and mortality (Hoste EA, et al. Intensive Care Med. 2015;41:1411) and is associated with renal and systemic complications, such as cardiovascular disease. RRT, frequently provided by nephrologists and/or intensivists, is a supportive therapy that can be life-saving when provided to the right patient at the right time. However, several questions related to the provision of RRT still remain, including the optimal timing of RRT initiation, the development of quality metrics for optimal RRT deliverables and monitoring, and the optimal strategy of RRT de-escalation and risk-stratification of renal recovery. Overall, there is paucity of randomized trials and standardized risk-stratification tools that can guide RRT in the ICU.

Current vexed questions of RRT deliverables in the ICU

There is ongoing research aiming to answer critical questions that can potentially improve current standards of RRT.

What is the optimal time of RRT initiation for critically ill patients with AKI?

Over the last 2 years, three randomized clinical trials have attempted to address this important question involving heterogeneous ICU populations and distinct research hypotheses and study designs. Two of these studies, AKIKI (Gaudry S, et al. N Engl J Med. 2016;375:122) and IDEAL-ICU (Barbar SD, et al. N Engl J Med. 2018;379:1431) yielded no significant difference in the primary outcome of 60-day and 90-day all-cause mortality between the early vs delayed RRT initiation strategies, respectively (Table 1). Further, AKIKI showed no difference in RRT dependence at 60 days and higher catheter-related infections and hypophosphatemia in the early initiation arm. It is important to note that IDEAL-ICU was stopped early for futility after the second planned interim analysis with only 56% of patients enrolled (main hypothesis was that early RRT initiation reduced 90-day all-cause mortality by 10%). In contrast, the ELAIN trial (Zarbock A, et al. JAMA. 2016;315:2190) showed a significant 90-day mortality reduction (39% vs 55%), reduced RRT need (9 days vs 25 days), and reduced length of stay (51 days vs 82 days) favoring early RRT initiation strategy. A larger study (STARRT-AKI) addressing this question with a more pragmatic approach (incorporating clinical judgment and equipoise among intensivists and nephrologists for patient eligibility) is underway. However, it is possible that STARRT-AKI will not provide a definitive answer for the inevitable search for implementing RRT initiation protocols in the ICU. Therefore, the scientific community may need to redirect the research focus to risk-stratification tools that can assist in the identification of patients who could benefit from early RRT initiation through an individualized approach rather than a standardized protocol.

How can RRT deliverables in the ICU be effectively and systematically monitored?

The provision of RRT to ICU patients with AKI requires an iterative adjustment of the RRT prescription and goals of therapy to accommodate changes in the clinical status with emphasis in hemodynamics, multiorgan failure, and fluid overload (Neyra JA. Clin Nephrol. 2018;90:1). The utilization of static and functional tests or point-of-care ultrasonography to assess hemodynamic variables can be useful. Furthermore, the implementation of customized and automated flowsheets in the electronic health record can facilitate remote monitoring. It is, therefore, essential that the multidisciplinary ICU team develops a process to monitor and ensure RRT deliverables. In this context, the standardization and monitoring of quality metrics (dose, modality, anticoagulation, filter life, downtime, etc) and the development of effective quality management systems are critically important. However, big multicenter data are direly needed to provide insight in this arena.

How can renal recovery be assessed and RRT effectively de-escalated?

The continuous examination of renal recovery in ICU patients with AKI-RRT is mostly based on urine output trend and, if feasible, interdialytic solute control. Sometimes, the transition from continuous RRT to intermittent modalities is necessary in the context of multiorgan recovery and de-escalation of care. However, clinical risk-prediction tools that identify patients who can potentially recover or already exhibit early signs of renal function recovery are needed. Current advances in clinical informatics can help to incorporate time-varying clinical parameters that may be informative for risk-prediction models. In addition, incorporating novel biomarkers of AKI repair and functional tests (eg, furosemide stress test, functional MRI) into these models may further inform these tools and aid the development of clinical decision support systems that enhance interventions to promote AKI recovery (Neyra JA, et al. Nephron. 2018;140: 99).

Is post-AKI outpatient care beneficial for ICU survivors who suffered from AKI-RRT?

Specialized AKI survivor clinics have been implemented in some centers. In general, this outpatient follow-up model includes survivors who suffered from AKI stage 2 or 3, some of them requiring RRT, and tailors individualized interventions for post-AKI complications (preventing recurrent AKI, attenuating incident or progressive CKD). However, the value of this outpatient model needs to be further evaluated with emphasis on clinical outcomes (eg, recurrent AKI, CKD, readmissions, or death) and elements that impact quality of life. This is an area of evolving research and a great opportunity for the nephrology and critical care communities to integrate and enhance post-ICU outpatient care and research collaboration.

Interdisciplinary communication among acute care team members

Two essential elements to provide effective RRT to ICU patients with AKI are: (1) the dynamics of the ICU team (intensivists, nephrologists, pharmacists, nurses, nutritionists, physical therapists, etc) to enhance the delivery of personalized therapy (RRT candidacy, timing of initiation, goals for solute control and fluid removal/regulation, renal recovery evaluation, RRT de-escalation, etc.) and (2) the frequent assessment and adjustment of RRT goals according to the clinical status of the patient. Therefore, effective RRT provision in the ICU requires the development of optimal channels of communication among all members of the acute care team and the systematic monitoring of the clinical status of the patient and RRT-specific goals and deliverables.

Perspective from a nurse and quality improvement officer for the provision of RRT in the ICU

The provision of continuous RRT (CRRT) to critically ill patients requires close communication between the bedside nurse and the rest of the ICU team. The physician typically prescribes CRRT and determines the specific goals of therapy. The pharmacist works closely with the nephrologist/intensivist and bedside nurse, especially in regards to customized CRRT solutions (when indicated) and medication dosing. Because CRRT can alter drug pharmacokinetics, the pharmacist closely and constantly monitors the patient’s clinical status, CRRT prescription, and all active medications. CRRT can also affect the nutritional and metabolic status of critically ill patients; therefore, the input of the nutritionist is necessary. The syndrome of ICU-acquired weakness is commonly encountered in ICU patients and is related to physical immobility. While ICU patients with AKI are already at risk for decreased mobility, the continuous connection to an immobile extracorporeal machine for the provision of CRRT may further contribute to immobilization and can also preclude the provision of optimal physical therapy. Therefore, the bedside nurse should assist the physical therapist for the timely and effective delivery of physical therapy according to the clinical status of the patient.

The clinical scenarios discussed above provide a small glimpse into the importance of developing an interdisciplinary ICU team caring for critically ill patients receiving CRRT. In the context of how integral the specific role of each team member is, it becomes clear that the bedside nurse’s role is not only to deliver hands-on patient care but also the orchestration of collaborative communication among all health-care providers for the effective provision of CRRT to critically ill patients in the ICU.

Dr. Neyra and Ms. Hauschild are with the Department of Internal Medicine; Division of Nephrology; Bone and Mineral Metabolism; University of Kentucky; Lexington, Kentucky.

More than 5 million patients are admitted to ICUs each year in the United States, and approximately 2% to 10% of these patients develop acute kidney injury requiring renal replacement therapy (AKI-RRT). AKI-RRT carries high morbidity and mortality (Hoste EA, et al. Intensive Care Med. 2015;41:1411) and is associated with renal and systemic complications, such as cardiovascular disease. RRT, frequently provided by nephrologists and/or intensivists, is a supportive therapy that can be life-saving when provided to the right patient at the right time. However, several questions related to the provision of RRT still remain, including the optimal timing of RRT initiation, the development of quality metrics for optimal RRT deliverables and monitoring, and the optimal strategy of RRT de-escalation and risk-stratification of renal recovery. Overall, there is paucity of randomized trials and standardized risk-stratification tools that can guide RRT in the ICU.

Current vexed questions of RRT deliverables in the ICU

There is ongoing research aiming to answer critical questions that can potentially improve current standards of RRT.

What is the optimal time of RRT initiation for critically ill patients with AKI?

Over the last 2 years, three randomized clinical trials have attempted to address this important question involving heterogeneous ICU populations and distinct research hypotheses and study designs. Two of these studies, AKIKI (Gaudry S, et al. N Engl J Med. 2016;375:122) and IDEAL-ICU (Barbar SD, et al. N Engl J Med. 2018;379:1431) yielded no significant difference in the primary outcome of 60-day and 90-day all-cause mortality between the early vs delayed RRT initiation strategies, respectively (Table 1). Further, AKIKI showed no difference in RRT dependence at 60 days and higher catheter-related infections and hypophosphatemia in the early initiation arm. It is important to note that IDEAL-ICU was stopped early for futility after the second planned interim analysis with only 56% of patients enrolled (main hypothesis was that early RRT initiation reduced 90-day all-cause mortality by 10%). In contrast, the ELAIN trial (Zarbock A, et al. JAMA. 2016;315:2190) showed a significant 90-day mortality reduction (39% vs 55%), reduced RRT need (9 days vs 25 days), and reduced length of stay (51 days vs 82 days) favoring early RRT initiation strategy. A larger study (STARRT-AKI) addressing this question with a more pragmatic approach (incorporating clinical judgment and equipoise among intensivists and nephrologists for patient eligibility) is underway. However, it is possible that STARRT-AKI will not provide a definitive answer for the inevitable search for implementing RRT initiation protocols in the ICU. Therefore, the scientific community may need to redirect the research focus to risk-stratification tools that can assist in the identification of patients who could benefit from early RRT initiation through an individualized approach rather than a standardized protocol.

How can RRT deliverables in the ICU be effectively and systematically monitored?

The provision of RRT to ICU patients with AKI requires an iterative adjustment of the RRT prescription and goals of therapy to accommodate changes in the clinical status with emphasis in hemodynamics, multiorgan failure, and fluid overload (Neyra JA. Clin Nephrol. 2018;90:1). The utilization of static and functional tests or point-of-care ultrasonography to assess hemodynamic variables can be useful. Furthermore, the implementation of customized and automated flowsheets in the electronic health record can facilitate remote monitoring. It is, therefore, essential that the multidisciplinary ICU team develops a process to monitor and ensure RRT deliverables. In this context, the standardization and monitoring of quality metrics (dose, modality, anticoagulation, filter life, downtime, etc) and the development of effective quality management systems are critically important. However, big multicenter data are direly needed to provide insight in this arena.

How can renal recovery be assessed and RRT effectively de-escalated?

The continuous examination of renal recovery in ICU patients with AKI-RRT is mostly based on urine output trend and, if feasible, interdialytic solute control. Sometimes, the transition from continuous RRT to intermittent modalities is necessary in the context of multiorgan recovery and de-escalation of care. However, clinical risk-prediction tools that identify patients who can potentially recover or already exhibit early signs of renal function recovery are needed. Current advances in clinical informatics can help to incorporate time-varying clinical parameters that may be informative for risk-prediction models. In addition, incorporating novel biomarkers of AKI repair and functional tests (eg, furosemide stress test, functional MRI) into these models may further inform these tools and aid the development of clinical decision support systems that enhance interventions to promote AKI recovery (Neyra JA, et al. Nephron. 2018;140: 99).

Is post-AKI outpatient care beneficial for ICU survivors who suffered from AKI-RRT?

Specialized AKI survivor clinics have been implemented in some centers. In general, this outpatient follow-up model includes survivors who suffered from AKI stage 2 or 3, some of them requiring RRT, and tailors individualized interventions for post-AKI complications (preventing recurrent AKI, attenuating incident or progressive CKD). However, the value of this outpatient model needs to be further evaluated with emphasis on clinical outcomes (eg, recurrent AKI, CKD, readmissions, or death) and elements that impact quality of life. This is an area of evolving research and a great opportunity for the nephrology and critical care communities to integrate and enhance post-ICU outpatient care and research collaboration.

Interdisciplinary communication among acute care team members

Two essential elements to provide effective RRT to ICU patients with AKI are: (1) the dynamics of the ICU team (intensivists, nephrologists, pharmacists, nurses, nutritionists, physical therapists, etc) to enhance the delivery of personalized therapy (RRT candidacy, timing of initiation, goals for solute control and fluid removal/regulation, renal recovery evaluation, RRT de-escalation, etc.) and (2) the frequent assessment and adjustment of RRT goals according to the clinical status of the patient. Therefore, effective RRT provision in the ICU requires the development of optimal channels of communication among all members of the acute care team and the systematic monitoring of the clinical status of the patient and RRT-specific goals and deliverables.

Perspective from a nurse and quality improvement officer for the provision of RRT in the ICU

The provision of continuous RRT (CRRT) to critically ill patients requires close communication between the bedside nurse and the rest of the ICU team. The physician typically prescribes CRRT and determines the specific goals of therapy. The pharmacist works closely with the nephrologist/intensivist and bedside nurse, especially in regards to customized CRRT solutions (when indicated) and medication dosing. Because CRRT can alter drug pharmacokinetics, the pharmacist closely and constantly monitors the patient’s clinical status, CRRT prescription, and all active medications. CRRT can also affect the nutritional and metabolic status of critically ill patients; therefore, the input of the nutritionist is necessary. The syndrome of ICU-acquired weakness is commonly encountered in ICU patients and is related to physical immobility. While ICU patients with AKI are already at risk for decreased mobility, the continuous connection to an immobile extracorporeal machine for the provision of CRRT may further contribute to immobilization and can also preclude the provision of optimal physical therapy. Therefore, the bedside nurse should assist the physical therapist for the timely and effective delivery of physical therapy according to the clinical status of the patient.

The clinical scenarios discussed above provide a small glimpse into the importance of developing an interdisciplinary ICU team caring for critically ill patients receiving CRRT. In the context of how integral the specific role of each team member is, it becomes clear that the bedside nurse’s role is not only to deliver hands-on patient care but also the orchestration of collaborative communication among all health-care providers for the effective provision of CRRT to critically ill patients in the ICU.

Dr. Neyra and Ms. Hauschild are with the Department of Internal Medicine; Division of Nephrology; Bone and Mineral Metabolism; University of Kentucky; Lexington, Kentucky.

Chronic thromboembolic pulmonary hypertension (CTEPH) is an elevation in pulmonary vascular resistance (PVR) resulting from chronic, “scarred-in” thromboembolic material partially occluding the pulmonary arteries. This vascular obstruction, over time, results in failure of the right ventricle and early mortality.

CTEPH was first characterized in an autopsy series from the Massachusetts General Hospital in 1931. On these postmortem examinations, it was noted that the affected patients had large pulmonary artery vascular obstruction, but also normal pulmonary parenchyma distal to this vascular obstruction and extensive bronchial collateral blood flow (Means J. Ann Intern Med. 1931;5:417). Although this observation set the groundwork for the theory that surgically removing the vascular obstruction to this preserved lung tissue could improve the condition of these patients, it would take until the mid-20th century until imaging and cardiac catheterization techniques allowed the recognition of the disease in real time.

CTEPH is thought to begin with an acute pulmonary embolus, but in approximately 3.4% of patients, rather than resolving over time, the thrombus will organize and incorporate into the pulmonary artery intimal layer (Simonneau G, et al. Eur Respir Rev. 2017;26:160112) A history of venous thromboembolism in a patient with persistent dyspnea should spur a screening evaluation for CTEPH; 75% of patients with CTEPH have a history of prior known acute pulmonary embolus and 56% of patients report a prior diagnosis of deep venous thrombosis. An acute pulmonary embolus will fibrinolyse early with the vast majority of the vascular obstruction resolving by the third month. Therefore, if the patient continues to report a significant exercise limitation after 3 months of therapeutic anticoagulation therapy, or has concerning physical exam signs, a workup should be pursued. The initial evaluation for CTEPH begins with a transthoracic echocardiogram (TTE) and ventilation/perfusion (V/Q) scintigraphy. A retrospective study comparing V/Q scan and multidetector CT scan revealed that V/Q scanning had a sensitivity and specificity of 97% and 95% for CTEPH, while CTPA had good specificity at 99% but only 51% sensitivity (Tunariu N, et al. J Nuc Med. 2007;48(5):680). If these are abnormal, then right-sided heart catheterization and invasive biplane digital subtraction pulmonary angiography are recommended. These studies confirm the diagnosis, grade its severity, and allow an evaluation for surgically accessible vs distal disease. Some CTEPH centers utilize additional imaging techniques, such as magnetic resonance angiography, optical resonance imaging, spectral CT scanning with iodine perfusion images, and intravascular ultrasound. These modalities and their place in the diagnostic algorithm are under investigation.

The goal of the initial evaluation process is to determine if the patient can undergo surgical pulmonary thromboendarterectomy (PTE), because in experienced hands, this procedure ensures the best long-term outcome for the patient. The first pulmonary thromboendarterectomy was performed at the University of California San Diego in 1970. Because the disease involves the intimal layer of the pulmonary artery, the surgery had to involve not just removal of the intravascular obstruction but also a pulmonary artery intimectomy. Surgical mortality rates were high in the initial experience. In 1984, a review of 85 worldwide cases reported an average mortality rate of 22%, and as high as 40% in some centers (Chitwood WR, Jr, et al. Clin Chest Med. 1984;5(3):507).

Dr. Bartolome is Associate Professor, Pulmonary and Critical Care Medicine; Director, CTEPH Program; and Associate Director, PH Program; UT Southwestern Medical Center, Dallas, Texas.

Chronic thromboembolic pulmonary hypertension (CTEPH) is an elevation in pulmonary vascular resistance (PVR) resulting from chronic, “scarred-in” thromboembolic material partially occluding the pulmonary arteries. This vascular obstruction, over time, results in failure of the right ventricle and early mortality.

CTEPH was first characterized in an autopsy series from the Massachusetts General Hospital in 1931. On these postmortem examinations, it was noted that the affected patients had large pulmonary artery vascular obstruction, but also normal pulmonary parenchyma distal to this vascular obstruction and extensive bronchial collateral blood flow (Means J. Ann Intern Med. 1931;5:417). Although this observation set the groundwork for the theory that surgically removing the vascular obstruction to this preserved lung tissue could improve the condition of these patients, it would take until the mid-20th century until imaging and cardiac catheterization techniques allowed the recognition of the disease in real time.

CTEPH is thought to begin with an acute pulmonary embolus, but in approximately 3.4% of patients, rather than resolving over time, the thrombus will organize and incorporate into the pulmonary artery intimal layer (Simonneau G, et al. Eur Respir Rev. 2017;26:160112) A history of venous thromboembolism in a patient with persistent dyspnea should spur a screening evaluation for CTEPH; 75% of patients with CTEPH have a history of prior known acute pulmonary embolus and 56% of patients report a prior diagnosis of deep venous thrombosis. An acute pulmonary embolus will fibrinolyse early with the vast majority of the vascular obstruction resolving by the third month. Therefore, if the patient continues to report a significant exercise limitation after 3 months of therapeutic anticoagulation therapy, or has concerning physical exam signs, a workup should be pursued. The initial evaluation for CTEPH begins with a transthoracic echocardiogram (TTE) and ventilation/perfusion (V/Q) scintigraphy. A retrospective study comparing V/Q scan and multidetector CT scan revealed that V/Q scanning had a sensitivity and specificity of 97% and 95% for CTEPH, while CTPA had good specificity at 99% but only 51% sensitivity (Tunariu N, et al. J Nuc Med. 2007;48(5):680). If these are abnormal, then right-sided heart catheterization and invasive biplane digital subtraction pulmonary angiography are recommended. These studies confirm the diagnosis, grade its severity, and allow an evaluation for surgically accessible vs distal disease. Some CTEPH centers utilize additional imaging techniques, such as magnetic resonance angiography, optical resonance imaging, spectral CT scanning with iodine perfusion images, and intravascular ultrasound. These modalities and their place in the diagnostic algorithm are under investigation.

The goal of the initial evaluation process is to determine if the patient can undergo surgical pulmonary thromboendarterectomy (PTE), because in experienced hands, this procedure ensures the best long-term outcome for the patient. The first pulmonary thromboendarterectomy was performed at the University of California San Diego in 1970. Because the disease involves the intimal layer of the pulmonary artery, the surgery had to involve not just removal of the intravascular obstruction but also a pulmonary artery intimectomy. Surgical mortality rates were high in the initial experience. In 1984, a review of 85 worldwide cases reported an average mortality rate of 22%, and as high as 40% in some centers (Chitwood WR, Jr, et al. Clin Chest Med. 1984;5(3):507).

Dr. Bartolome is Associate Professor, Pulmonary and Critical Care Medicine; Director, CTEPH Program; and Associate Director, PH Program; UT Southwestern Medical Center, Dallas, Texas.

Chronic thromboembolic pulmonary hypertension (CTEPH) is an elevation in pulmonary vascular resistance (PVR) resulting from chronic, “scarred-in” thromboembolic material partially occluding the pulmonary arteries. This vascular obstruction, over time, results in failure of the right ventricle and early mortality.

CTEPH was first characterized in an autopsy series from the Massachusetts General Hospital in 1931. On these postmortem examinations, it was noted that the affected patients had large pulmonary artery vascular obstruction, but also normal pulmonary parenchyma distal to this vascular obstruction and extensive bronchial collateral blood flow (Means J. Ann Intern Med. 1931;5:417). Although this observation set the groundwork for the theory that surgically removing the vascular obstruction to this preserved lung tissue could improve the condition of these patients, it would take until the mid-20th century until imaging and cardiac catheterization techniques allowed the recognition of the disease in real time.

CTEPH is thought to begin with an acute pulmonary embolus, but in approximately 3.4% of patients, rather than resolving over time, the thrombus will organize and incorporate into the pulmonary artery intimal layer (Simonneau G, et al. Eur Respir Rev. 2017;26:160112) A history of venous thromboembolism in a patient with persistent dyspnea should spur a screening evaluation for CTEPH; 75% of patients with CTEPH have a history of prior known acute pulmonary embolus and 56% of patients report a prior diagnosis of deep venous thrombosis. An acute pulmonary embolus will fibrinolyse early with the vast majority of the vascular obstruction resolving by the third month. Therefore, if the patient continues to report a significant exercise limitation after 3 months of therapeutic anticoagulation therapy, or has concerning physical exam signs, a workup should be pursued. The initial evaluation for CTEPH begins with a transthoracic echocardiogram (TTE) and ventilation/perfusion (V/Q) scintigraphy. A retrospective study comparing V/Q scan and multidetector CT scan revealed that V/Q scanning had a sensitivity and specificity of 97% and 95% for CTEPH, while CTPA had good specificity at 99% but only 51% sensitivity (Tunariu N, et al. J Nuc Med. 2007;48(5):680). If these are abnormal, then right-sided heart catheterization and invasive biplane digital subtraction pulmonary angiography are recommended. These studies confirm the diagnosis, grade its severity, and allow an evaluation for surgically accessible vs distal disease. Some CTEPH centers utilize additional imaging techniques, such as magnetic resonance angiography, optical resonance imaging, spectral CT scanning with iodine perfusion images, and intravascular ultrasound. These modalities and their place in the diagnostic algorithm are under investigation.

The goal of the initial evaluation process is to determine if the patient can undergo surgical pulmonary thromboendarterectomy (PTE), because in experienced hands, this procedure ensures the best long-term outcome for the patient. The first pulmonary thromboendarterectomy was performed at the University of California San Diego in 1970. Because the disease involves the intimal layer of the pulmonary artery, the surgery had to involve not just removal of the intravascular obstruction but also a pulmonary artery intimectomy. Surgical mortality rates were high in the initial experience. In 1984, a review of 85 worldwide cases reported an average mortality rate of 22%, and as high as 40% in some centers (Chitwood WR, Jr, et al. Clin Chest Med. 1984;5(3):507).

Dr. Bartolome is Associate Professor, Pulmonary and Critical Care Medicine; Director, CTEPH Program; and Associate Director, PH Program; UT Southwestern Medical Center, Dallas, Texas.

Now that we are in the midst of flu season, many discussions regarding the management of patients with influenza virus infections are ensuing. While prevention is always preferable, and we encourage everyone to get vaccinated, influenza remains a rapidly widespread infection. In the United States during last year’s flu season (2017-18), there was an estimated 49 million cases of influenza, 960,000 hospitalizations, and 79,000 deaths. Approximately 86% of all deaths were estimated to occur in those aged 65 and older (Centers for Disease Control and Prevention webpage on Burden of Influenza).

Despite our best efforts, there are inevitable times when some patients become ill enough to require hospitalization. Patients aged 65 and older make up the overwhelming majority of patients with influenza who eventually require hospitalization (Fig 1) (The Centers for Disease Control and Prevention FluView Database). Comorbidities also confer higher risk for more severe illness and potential hospitalization irrespective of age (Fig 2). In children with known medical conditions, asthma confers highest risk of hospitalization, as 27% of those with asthma were hospitalized after developing the flu. In adults, 52% of those with cardiovascular disease and 30% of adult patients with chronic lung disease who were confirmed to have influenza required hospitalization for treatment (Fig 2, The Centers for Disease Control and Prevention FluView Database).

The most severe cases of influenza can require ICU care and advanced management of respiratory failure as a result of the acute respiratory distress syndrome (ARDS). The lungs suffer significant injury due to the viral infection, and they lose their ability to effectively oxygenate the blood. Secondary bacterial infections can also occur as a complication, which compounds the injury. Given the fact that so many patients have significant comorbidities and are of advanced age, it is reasonable to expect that a fair proportion of those with influenza would develop respiratory failure as a consequence. For some of these patients, the hypoxemia that develops as a result of the lung injury can be exceptionally challenging to manage. In extreme cases, conventional ventilator management is insufficient, and the need for additional, advanced therapies arise.

Studies of VV ECMO in severe influenza

ECMO (extracorporeal membrane oxygenation) is a treatment that has been employed to help support patients with severe hypoxemic respiratory failure while their lungs recover from acute injury. Venovenous (VV) ECMO requires peripheral insertion of large cannulae into the venous system to take deoxygenated blood, deliver it through the membrane oxygenator and return the oxygenated blood back to the venous system. In simplest terms, the membrane of ECMO circuit serves as a substitute for the gas exchange function of the lungs and provides the oxygenation that the injured alveoli of the lung are unable to provide. The overall intent is to have the external ECMO circuit do all of the gas exchange work while the lungs heal.

Now that we are in the midst of flu season, many discussions regarding the management of patients with influenza virus infections are ensuing. While prevention is always preferable, and we encourage everyone to get vaccinated, influenza remains a rapidly widespread infection. In the United States during last year’s flu season (2017-18), there was an estimated 49 million cases of influenza, 960,000 hospitalizations, and 79,000 deaths. Approximately 86% of all deaths were estimated to occur in those aged 65 and older (Centers for Disease Control and Prevention webpage on Burden of Influenza).

Despite our best efforts, there are inevitable times when some patients become ill enough to require hospitalization. Patients aged 65 and older make up the overwhelming majority of patients with influenza who eventually require hospitalization (Fig 1) (The Centers for Disease Control and Prevention FluView Database). Comorbidities also confer higher risk for more severe illness and potential hospitalization irrespective of age (Fig 2). In children with known medical conditions, asthma confers highest risk of hospitalization, as 27% of those with asthma were hospitalized after developing the flu. In adults, 52% of those with cardiovascular disease and 30% of adult patients with chronic lung disease who were confirmed to have influenza required hospitalization for treatment (Fig 2, The Centers for Disease Control and Prevention FluView Database).

The most severe cases of influenza can require ICU care and advanced management of respiratory failure as a result of the acute respiratory distress syndrome (ARDS). The lungs suffer significant injury due to the viral infection, and they lose their ability to effectively oxygenate the blood. Secondary bacterial infections can also occur as a complication, which compounds the injury. Given the fact that so many patients have significant comorbidities and are of advanced age, it is reasonable to expect that a fair proportion of those with influenza would develop respiratory failure as a consequence. For some of these patients, the hypoxemia that develops as a result of the lung injury can be exceptionally challenging to manage. In extreme cases, conventional ventilator management is insufficient, and the need for additional, advanced therapies arise.

Studies of VV ECMO in severe influenza

ECMO (extracorporeal membrane oxygenation) is a treatment that has been employed to help support patients with severe hypoxemic respiratory failure while their lungs recover from acute injury. Venovenous (VV) ECMO requires peripheral insertion of large cannulae into the venous system to take deoxygenated blood, deliver it through the membrane oxygenator and return the oxygenated blood back to the venous system. In simplest terms, the membrane of ECMO circuit serves as a substitute for the gas exchange function of the lungs and provides the oxygenation that the injured alveoli of the lung are unable to provide. The overall intent is to have the external ECMO circuit do all of the gas exchange work while the lungs heal.

Now that we are in the midst of flu season, many discussions regarding the management of patients with influenza virus infections are ensuing. While prevention is always preferable, and we encourage everyone to get vaccinated, influenza remains a rapidly widespread infection. In the United States during last year’s flu season (2017-18), there was an estimated 49 million cases of influenza, 960,000 hospitalizations, and 79,000 deaths. Approximately 86% of all deaths were estimated to occur in those aged 65 and older (Centers for Disease Control and Prevention webpage on Burden of Influenza).

Despite our best efforts, there are inevitable times when some patients become ill enough to require hospitalization. Patients aged 65 and older make up the overwhelming majority of patients with influenza who eventually require hospitalization (Fig 1) (The Centers for Disease Control and Prevention FluView Database). Comorbidities also confer higher risk for more severe illness and potential hospitalization irrespective of age (Fig 2). In children with known medical conditions, asthma confers highest risk of hospitalization, as 27% of those with asthma were hospitalized after developing the flu. In adults, 52% of those with cardiovascular disease and 30% of adult patients with chronic lung disease who were confirmed to have influenza required hospitalization for treatment (Fig 2, The Centers for Disease Control and Prevention FluView Database).

The most severe cases of influenza can require ICU care and advanced management of respiratory failure as a result of the acute respiratory distress syndrome (ARDS). The lungs suffer significant injury due to the viral infection, and they lose their ability to effectively oxygenate the blood. Secondary bacterial infections can also occur as a complication, which compounds the injury. Given the fact that so many patients have significant comorbidities and are of advanced age, it is reasonable to expect that a fair proportion of those with influenza would develop respiratory failure as a consequence. For some of these patients, the hypoxemia that develops as a result of the lung injury can be exceptionally challenging to manage. In extreme cases, conventional ventilator management is insufficient, and the need for additional, advanced therapies arise.

Studies of VV ECMO in severe influenza

ECMO (extracorporeal membrane oxygenation) is a treatment that has been employed to help support patients with severe hypoxemic respiratory failure while their lungs recover from acute injury. Venovenous (VV) ECMO requires peripheral insertion of large cannulae into the venous system to take deoxygenated blood, deliver it through the membrane oxygenator and return the oxygenated blood back to the venous system. In simplest terms, the membrane of ECMO circuit serves as a substitute for the gas exchange function of the lungs and provides the oxygenation that the injured alveoli of the lung are unable to provide. The overall intent is to have the external ECMO circuit do all of the gas exchange work while the lungs heal.

In 2002, the European Society of Intensive Care Medicine, the Society of Critical Care Medicine, and the International Sepsis Forum formed the Surviving Sepsis Campaign (SSC) aiming to reduce sepsis-related mortality by 25% within 5 years, mimicking the progress made in the management of STEMI (http://www.survivingsepsis.org/About-SSC/Pages/History.aspx).

SSC bundles: a historic perspective

The first guidelines were published in 2004. Recognizing that guidelines may not influence bedside practice for many years, the SSC partnered with the Institute for Healthcare Improvement to apply performance improvement methodology to sepsis management, developing the “sepsis change bundles.” In addition to hospital resources for education, screening, and data collection, the 6-hour resuscitation and 24-hour management bundles were created. Subsequent data, collected as part of the initiative, demonstrated an association between bundle compliance and survival.

Comparing the 1-hour bundle to STEMI care

This year, the SSC published a 1-hour bundle to replace the 3- and 6-hour bundles (Levy MM et al. Crit Care Med. 2018;46[6]:997). Whereas previous bundles set time frames for completion of the elements, the 1-hour bundle focuses on the initiation of these components. The authors revisited the parallel between early management of sepsis and STEMI. The 1-hour bundle includes serum lactate, blood cultures prior to antibiotics, broad-spectrum antibiotics, a 30 mL/kg crystalloid bolus for patients with hypotension or lactate greater than or equal to 4 mmol/L, and vasopressors for persistent hypotension.

Elements of controversy after the publication of this bundle include:


1. One hour seems insufficient for complex clinical decision making and interventions for a syndrome with no specific diagnostic test: sepsis often mimics, or is mimicked by, other conditions.

2. Some bundle elements are not supported by high-quality evidence. No controlled studies exist regarding the appropriate volume of initial fluids or the impact of timing of antibiotics on outcomes.

3. The 1-hour time frame will encourage empiric delivery of fluids and antibiotics to patients who are not septic, potentially leading to harm.

4. While the 1-hour bundle is a quality improvement tool and not for public reporting, former bundles have been adopted as federally regulated measures.


Has the SSC gone too far? Are these concerns enough to abandon the 1-hour bundle? Or are the concerns regarding the 1-hour bundle an example of “perfect is the enemy of better”? To understand the potential for imperfect guidelines to drive tremendous patient-level improvements, one must consider the evolution of STEMI management.

Since the 1970s, the in-hospital mortality for STEMI has decreased from 25% to around 5%. The most significant factor in this achievement was the recognition that early reperfusion improves outcomes and that doing it consistently requires complex coordination. In 2004, a Door-to-Balloon (D2B) time of less than 90 minutes was included as a guideline recommendation (Antman EM, et al. Circulation. 2004;110[5]:588). CMS started collecting performance data on this metric, made that data public, and later tied the performance to hospital reimbursement.

Initially, the 90-minute goal was achieved in only 44% of cases. In 2006, the D2B initiative was launched, providing recommendations for public education, coordination of care, and emergent management of STEMI. Compliance with these recommendations required significant education and changes to STEMI care at multiple levels. Data were collected and submitted to inform the process. Six years later, compliance with the D2B goal had increased from 44% to 91%. The median D2B dropped from 96 to 64 minutes. Based on high compliance, CMS discontinued the use of this metric for reimbursement as the variation between high and low performers was minimal. Put simply, the entire country had gotten better at treating STEMI. The “time-zero” for STEMI was pushed back further, and D2B has been replaced with first-medical-contact (FMC) to device time. The recommendation is to achieve this as quickly as possible, and in less than 90 minutes (O’Gara P, et al. JACC. 2013;61[4]:485).

Consider the complexity of getting a patient from their home to a catheterization lab within 90 minutes, even in ideal circumstances. This short time frame encourages, by design, a low threshold to activate the system. We accept that some patients will receive an unnecessary catheterization or systemic fibrinolysis although the recommendation is based on level B evidence.

Compliance with the STEMI guidelines is more labor-intensive and complex than compliance with the 1-hour sepsis bundle. So, is STEMI a fair comparison to sepsis? Both syndromes are common, potentially deadly, and time-sensitive. Both require early recognition, but neither has a definitive diagnostic test. Instead, diagnosis requires an integration of multiple complex clinical factors. Both are backed by imperfect science that continues to evolve. Over-diagnosis of either will expose the patient to potentially harmful therapies.

The early management of STEMI is a valid comparison to the early management of sepsis. We must consider this comparison as we ponder the 1-hour sepsis bundle.

Is triage time the appropriate time-zero? In either condition, triage time is too early in some cases and too late in others. Unfortunately, there is no better alternative, and STEMI guidelines have evolved to start the clock before triage. Using a point such as “recognition of sepsis” would fail to capture delayed recognition.

Is it possible to diagnose and initiate treatment for sepsis in such a short time frame? Consider the treatment received by the usual care group of the PROCESS trial (The ProCESS Investigators. N Engl J Med. 2014;370:1683). Prior to meeting entry criteria, which occurred in less than 1 hour, patients in this group received an initial fluid bolus and had a lactate assessment. Prior to randomization, which occurred at around 90 minutes, this group completed 28 mL/kg of crystalloid fluid, and 76% received antibiotics. Thus, the usual-care group in this study nearly achieved the 1-hour bundle currently being contested.

Is it appropriate for a guideline to strongly recommend interventions not backed by level A evidence? The recommendation for FMC to catheterization within 90 minutes has not been studied in a controlled way. The precise dosing and timing of fibrinolysis is also not based on controlled data. Reperfusion devices and antiplatelet agents continue to be rigorously studied, sometimes with conflicting results.

Finally, should the 1-hour bundle be abandoned out of concern that it will be used as a national performance metric? First, there is currently no indication that the 1-hour bundle will be adopted as a performance metric. For the sake of argument, let’s assume the 1-hour bundle will be regulated and used to compare hospitals. Is there reason to think this bundle favors some hospitals over others and will lead to an unfair comparison? Is there significant inequity in the ability to draw blood cultures, send a lactate, start IV fluids, and initiate antibiotics?

Certainly, national compliance with such a metric would be very low at first. Therein lies the actual problem: a person who suffers a STEMI anywhere in the country is very likely to receive high-quality care. Currently, the same cannot be said about a patient with sepsis. Perhaps that should be the focus of our concern.


Dr. Uppal is Assistant Professor, NYU School of Medicine, Bellevue Hospital Center, New York, New York.
 

In 2002, the European Society of Intensive Care Medicine, the Society of Critical Care Medicine, and the International Sepsis Forum formed the Surviving Sepsis Campaign (SSC) aiming to reduce sepsis-related mortality by 25% within 5 years, mimicking the progress made in the management of STEMI (http://www.survivingsepsis.org/About-SSC/Pages/History.aspx).

SSC bundles: a historic perspective

The first guidelines were published in 2004. Recognizing that guidelines may not influence bedside practice for many years, the SSC partnered with the Institute for Healthcare Improvement to apply performance improvement methodology to sepsis management, developing the “sepsis change bundles.” In addition to hospital resources for education, screening, and data collection, the 6-hour resuscitation and 24-hour management bundles were created. Subsequent data, collected as part of the initiative, demonstrated an association between bundle compliance and survival.

Comparing the 1-hour bundle to STEMI care

This year, the SSC published a 1-hour bundle to replace the 3- and 6-hour bundles (Levy MM et al. Crit Care Med. 2018;46[6]:997). Whereas previous bundles set time frames for completion of the elements, the 1-hour bundle focuses on the initiation of these components. The authors revisited the parallel between early management of sepsis and STEMI. The 1-hour bundle includes serum lactate, blood cultures prior to antibiotics, broad-spectrum antibiotics, a 30 mL/kg crystalloid bolus for patients with hypotension or lactate greater than or equal to 4 mmol/L, and vasopressors for persistent hypotension.

Elements of controversy after the publication of this bundle include:


1. One hour seems insufficient for complex clinical decision making and interventions for a syndrome with no specific diagnostic test: sepsis often mimics, or is mimicked by, other conditions.

2. Some bundle elements are not supported by high-quality evidence. No controlled studies exist regarding the appropriate volume of initial fluids or the impact of timing of antibiotics on outcomes.

3. The 1-hour time frame will encourage empiric delivery of fluids and antibiotics to patients who are not septic, potentially leading to harm.

4. While the 1-hour bundle is a quality improvement tool and not for public reporting, former bundles have been adopted as federally regulated measures.


Has the SSC gone too far? Are these concerns enough to abandon the 1-hour bundle? Or are the concerns regarding the 1-hour bundle an example of “perfect is the enemy of better”? To understand the potential for imperfect guidelines to drive tremendous patient-level improvements, one must consider the evolution of STEMI management.

Since the 1970s, the in-hospital mortality for STEMI has decreased from 25% to around 5%. The most significant factor in this achievement was the recognition that early reperfusion improves outcomes and that doing it consistently requires complex coordination. In 2004, a Door-to-Balloon (D2B) time of less than 90 minutes was included as a guideline recommendation (Antman EM, et al. Circulation. 2004;110[5]:588). CMS started collecting performance data on this metric, made that data public, and later tied the performance to hospital reimbursement.

Initially, the 90-minute goal was achieved in only 44% of cases. In 2006, the D2B initiative was launched, providing recommendations for public education, coordination of care, and emergent management of STEMI. Compliance with these recommendations required significant education and changes to STEMI care at multiple levels. Data were collected and submitted to inform the process. Six years later, compliance with the D2B goal had increased from 44% to 91%. The median D2B dropped from 96 to 64 minutes. Based on high compliance, CMS discontinued the use of this metric for reimbursement as the variation between high and low performers was minimal. Put simply, the entire country had gotten better at treating STEMI. The “time-zero” for STEMI was pushed back further, and D2B has been replaced with first-medical-contact (FMC) to device time. The recommendation is to achieve this as quickly as possible, and in less than 90 minutes (O’Gara P, et al. JACC. 2013;61[4]:485).

Consider the complexity of getting a patient from their home to a catheterization lab within 90 minutes, even in ideal circumstances. This short time frame encourages, by design, a low threshold to activate the system. We accept that some patients will receive an unnecessary catheterization or systemic fibrinolysis although the recommendation is based on level B evidence.

Compliance with the STEMI guidelines is more labor-intensive and complex than compliance with the 1-hour sepsis bundle. So, is STEMI a fair comparison to sepsis? Both syndromes are common, potentially deadly, and time-sensitive. Both require early recognition, but neither has a definitive diagnostic test. Instead, diagnosis requires an integration of multiple complex clinical factors. Both are backed by imperfect science that continues to evolve. Over-diagnosis of either will expose the patient to potentially harmful therapies.

The early management of STEMI is a valid comparison to the early management of sepsis. We must consider this comparison as we ponder the 1-hour sepsis bundle.

Is triage time the appropriate time-zero? In either condition, triage time is too early in some cases and too late in others. Unfortunately, there is no better alternative, and STEMI guidelines have evolved to start the clock before triage. Using a point such as “recognition of sepsis” would fail to capture delayed recognition.

Is it possible to diagnose and initiate treatment for sepsis in such a short time frame? Consider the treatment received by the usual care group of the PROCESS trial (The ProCESS Investigators. N Engl J Med. 2014;370:1683). Prior to meeting entry criteria, which occurred in less than 1 hour, patients in this group received an initial fluid bolus and had a lactate assessment. Prior to randomization, which occurred at around 90 minutes, this group completed 28 mL/kg of crystalloid fluid, and 76% received antibiotics. Thus, the usual-care group in this study nearly achieved the 1-hour bundle currently being contested.

Is it appropriate for a guideline to strongly recommend interventions not backed by level A evidence? The recommendation for FMC to catheterization within 90 minutes has not been studied in a controlled way. The precise dosing and timing of fibrinolysis is also not based on controlled data. Reperfusion devices and antiplatelet agents continue to be rigorously studied, sometimes with conflicting results.

Finally, should the 1-hour bundle be abandoned out of concern that it will be used as a national performance metric? First, there is currently no indication that the 1-hour bundle will be adopted as a performance metric. For the sake of argument, let’s assume the 1-hour bundle will be regulated and used to compare hospitals. Is there reason to think this bundle favors some hospitals over others and will lead to an unfair comparison? Is there significant inequity in the ability to draw blood cultures, send a lactate, start IV fluids, and initiate antibiotics?

Certainly, national compliance with such a metric would be very low at first. Therein lies the actual problem: a person who suffers a STEMI anywhere in the country is very likely to receive high-quality care. Currently, the same cannot be said about a patient with sepsis. Perhaps that should be the focus of our concern.


Dr. Uppal is Assistant Professor, NYU School of Medicine, Bellevue Hospital Center, New York, New York.
 

In 2002, the European Society of Intensive Care Medicine, the Society of Critical Care Medicine, and the International Sepsis Forum formed the Surviving Sepsis Campaign (SSC) aiming to reduce sepsis-related mortality by 25% within 5 years, mimicking the progress made in the management of STEMI (http://www.survivingsepsis.org/About-SSC/Pages/History.aspx).

SSC bundles: a historic perspective

The first guidelines were published in 2004. Recognizing that guidelines may not influence bedside practice for many years, the SSC partnered with the Institute for Healthcare Improvement to apply performance improvement methodology to sepsis management, developing the “sepsis change bundles.” In addition to hospital resources for education, screening, and data collection, the 6-hour resuscitation and 24-hour management bundles were created. Subsequent data, collected as part of the initiative, demonstrated an association between bundle compliance and survival.

Comparing the 1-hour bundle to STEMI care

This year, the SSC published a 1-hour bundle to replace the 3- and 6-hour bundles (Levy MM et al. Crit Care Med. 2018;46[6]:997). Whereas previous bundles set time frames for completion of the elements, the 1-hour bundle focuses on the initiation of these components. The authors revisited the parallel between early management of sepsis and STEMI. The 1-hour bundle includes serum lactate, blood cultures prior to antibiotics, broad-spectrum antibiotics, a 30 mL/kg crystalloid bolus for patients with hypotension or lactate greater than or equal to 4 mmol/L, and vasopressors for persistent hypotension.

Elements of controversy after the publication of this bundle include:


1. One hour seems insufficient for complex clinical decision making and interventions for a syndrome with no specific diagnostic test: sepsis often mimics, or is mimicked by, other conditions.

2. Some bundle elements are not supported by high-quality evidence. No controlled studies exist regarding the appropriate volume of initial fluids or the impact of timing of antibiotics on outcomes.

3. The 1-hour time frame will encourage empiric delivery of fluids and antibiotics to patients who are not septic, potentially leading to harm.

4. While the 1-hour bundle is a quality improvement tool and not for public reporting, former bundles have been adopted as federally regulated measures.


Has the SSC gone too far? Are these concerns enough to abandon the 1-hour bundle? Or are the concerns regarding the 1-hour bundle an example of “perfect is the enemy of better”? To understand the potential for imperfect guidelines to drive tremendous patient-level improvements, one must consider the evolution of STEMI management.

Since the 1970s, the in-hospital mortality for STEMI has decreased from 25% to around 5%. The most significant factor in this achievement was the recognition that early reperfusion improves outcomes and that doing it consistently requires complex coordination. In 2004, a Door-to-Balloon (D2B) time of less than 90 minutes was included as a guideline recommendation (Antman EM, et al. Circulation. 2004;110[5]:588). CMS started collecting performance data on this metric, made that data public, and later tied the performance to hospital reimbursement.

Initially, the 90-minute goal was achieved in only 44% of cases. In 2006, the D2B initiative was launched, providing recommendations for public education, coordination of care, and emergent management of STEMI. Compliance with these recommendations required significant education and changes to STEMI care at multiple levels. Data were collected and submitted to inform the process. Six years later, compliance with the D2B goal had increased from 44% to 91%. The median D2B dropped from 96 to 64 minutes. Based on high compliance, CMS discontinued the use of this metric for reimbursement as the variation between high and low performers was minimal. Put simply, the entire country had gotten better at treating STEMI. The “time-zero” for STEMI was pushed back further, and D2B has been replaced with first-medical-contact (FMC) to device time. The recommendation is to achieve this as quickly as possible, and in less than 90 minutes (O’Gara P, et al. JACC. 2013;61[4]:485).

Consider the complexity of getting a patient from their home to a catheterization lab within 90 minutes, even in ideal circumstances. This short time frame encourages, by design, a low threshold to activate the system. We accept that some patients will receive an unnecessary catheterization or systemic fibrinolysis although the recommendation is based on level B evidence.

Compliance with the STEMI guidelines is more labor-intensive and complex than compliance with the 1-hour sepsis bundle. So, is STEMI a fair comparison to sepsis? Both syndromes are common, potentially deadly, and time-sensitive. Both require early recognition, but neither has a definitive diagnostic test. Instead, diagnosis requires an integration of multiple complex clinical factors. Both are backed by imperfect science that continues to evolve. Over-diagnosis of either will expose the patient to potentially harmful therapies.

The early management of STEMI is a valid comparison to the early management of sepsis. We must consider this comparison as we ponder the 1-hour sepsis bundle.

Is triage time the appropriate time-zero? In either condition, triage time is too early in some cases and too late in others. Unfortunately, there is no better alternative, and STEMI guidelines have evolved to start the clock before triage. Using a point such as “recognition of sepsis” would fail to capture delayed recognition.

Is it possible to diagnose and initiate treatment for sepsis in such a short time frame? Consider the treatment received by the usual care group of the PROCESS trial (The ProCESS Investigators. N Engl J Med. 2014;370:1683). Prior to meeting entry criteria, which occurred in less than 1 hour, patients in this group received an initial fluid bolus and had a lactate assessment. Prior to randomization, which occurred at around 90 minutes, this group completed 28 mL/kg of crystalloid fluid, and 76% received antibiotics. Thus, the usual-care group in this study nearly achieved the 1-hour bundle currently being contested.

Is it appropriate for a guideline to strongly recommend interventions not backed by level A evidence? The recommendation for FMC to catheterization within 90 minutes has not been studied in a controlled way. The precise dosing and timing of fibrinolysis is also not based on controlled data. Reperfusion devices and antiplatelet agents continue to be rigorously studied, sometimes with conflicting results.

Finally, should the 1-hour bundle be abandoned out of concern that it will be used as a national performance metric? First, there is currently no indication that the 1-hour bundle will be adopted as a performance metric. For the sake of argument, let’s assume the 1-hour bundle will be regulated and used to compare hospitals. Is there reason to think this bundle favors some hospitals over others and will lead to an unfair comparison? Is there significant inequity in the ability to draw blood cultures, send a lactate, start IV fluids, and initiate antibiotics?

Certainly, national compliance with such a metric would be very low at first. Therein lies the actual problem: a person who suffers a STEMI anywhere in the country is very likely to receive high-quality care. Currently, the same cannot be said about a patient with sepsis. Perhaps that should be the focus of our concern.


Dr. Uppal is Assistant Professor, NYU School of Medicine, Bellevue Hospital Center, New York, New York.
 

According to the Centers for Disease Control and Prevention, suicide is the 10th leading cause of mortality in the United States, with rates of suicide rising over the past 2 decades. In 2016, completed suicides accounted for approximately 45,000 deaths in the United States (Ivey-Stephenson AZ, et al. MMWR Surveill Summ. 2017;66[18]:1). While progress has been made to lower mortality rates of other leading causes of death, very little progress has been made on reducing the rates of suicide. The term “suicide,” as referred to in this article, encompasses suicidal ideation, suicidal behavior, and suicide death.

Researchers have been investigating potential risk factors and prevention strategies for suicide. The relationship between suicide and sleep disturbances, specifically insomnia and nightmares, has been well documented in the literature. Given that insomnia and nightmares are potentially modifiable risk factors, it continues to be an area of active exploration for suicide rate reduction. While there are many different types of sleep disorders, including excessive daytime sleepiness, parasomnias, obstructive sleep apnea, and restless legs syndrome, this article will focus on the relationship between insomnia and nightmares with suicide.
 

Insomnia

Insomnia disorder, according to the American Psychiatric Association’s DSM-5, is a dissatisfaction of sleep quantity or quality that occurs at least three nights per week for a minimum of 3 months despite adequate opportunity for sleep. This may present as difficulty with falling asleep, staying asleep, or early morning awakenings. The sleep disturbance results in functional impairment or significant distress in at least one area of life (American Psychiatric Association. Arlington, Virginia: APA; 2013). While insomnia is often a symptom of many psychiatric disorders, research has shown that insomnia is an independent risk factor for suicide, even when controlling for mental illness. Studies have shown that there is up to a 2.4 relative risk of suicide death with insomnia after adjusting for depression severity (McCall W, et al. J Clin Sleep Med. 2013;32[9]:135).
 

Nightmares

Nightmares, as defined by the American Psychiatric Association’s DSM-5, are “typically lengthy, elaborate, story-like sequences of dream imagery that seem real and incite anxiety, fear, or other dysphoric emotions” (American Psychiatric Association. Arlington, Virginia: APA; 2013). They are common symptoms in posttraumatic stress disorder (PTSD), with up to 90% of individuals with PTSD experiencing nightmares following a traumatic event (Littlewood DL, et al. J Clin Sleep Med. 2016;12[3]:393). Nightmares have also been shown to be an independent risk factor for suicide when controlling for mental illness. Studies have shown that nightmares are associated with an elevated risk factor of 1.5 to 3 times for suicidal ideation and 3 to 4 times for suicide attempts. The data suggest that nightmares may be a stronger risk factor for suicide than insomnia (McCall W, et al. Curr Psychiatr Rep. 2013;15[9]:389).

Proposed Mechanism

The mechanism linking insomnia and nightmares with suicide has been theorized and studied by researchers. A couple of the most noteworthy proposed psychological mechanisms involve dysfunctional beliefs and attitudes about sleep, as well as deficits in problem solving capability. Dysfunctional beliefs and attitudes about sleep (DBAS) are negative cognitions pertaining to sleep, and they have been shown to be related to the intensity of suicidal ideations. Many of the DBAS are pessimistic thoughts that contain a “hopelessness flavor” to them, which lead to the perpetuation of insomnia. Hopelessness has been found to be a strong risk factor for suicide. In addition to DBAS, insomnia has also shown to lead to impairments in complex problem solving. The lack of problem solving skills in these patients may lead to fewer quantity and quality of solutions during stressful situations and leave suicide as the perceived best or only option.

The biological theories focus on serotonin and hyperarousal mediated by the hypothalamic-pituitary-adrenal (HPA) axis. Serotonin is a neurotransmitter that is involved in the induction and maintenance of sleep. Of interesting note, low levels of serotonin’s main metabolite, 5-hydroxyindoleacetic acid (5-HIAA) have been found in the cerebrospinal fluid of suicide victims. Evidence has also shown that sleep and the HPA axis are closely related. The HPA axis is activated by stress leading to a cascade of hormones that can cause susceptibility of hyperarousal, REM alterations, and suicide. Hyperarousal, shared in context with PTSD and insomnia, can lead to hyperactivation of the noradrenergic systems in the medial prefrontal cortex, which can lead to decrease in executive decision making (McCall W, et al. Curr Psychiatr Rep. 2013;15[9]:389).
 

Treatment Strategies

The benefit of treating insomnia and nightmares, in regards to reducing suicidality, continues to be an area of active research. Many of the previous studies have theorized that treating symptoms of insomnia and nightmares may indirectly reduce suicide. Pharmaceutical and nonpharmaceutical treatments are currently being used to help treat patients with insomnia and nightmares, but the benefit for reducing suicidality is still unknown.

According to the Centers for Disease Control and Prevention, suicide is the 10th leading cause of mortality in the United States, with rates of suicide rising over the past 2 decades. In 2016, completed suicides accounted for approximately 45,000 deaths in the United States (Ivey-Stephenson AZ, et al. MMWR Surveill Summ. 2017;66[18]:1). While progress has been made to lower mortality rates of other leading causes of death, very little progress has been made on reducing the rates of suicide. The term “suicide,” as referred to in this article, encompasses suicidal ideation, suicidal behavior, and suicide death.

Researchers have been investigating potential risk factors and prevention strategies for suicide. The relationship between suicide and sleep disturbances, specifically insomnia and nightmares, has been well documented in the literature. Given that insomnia and nightmares are potentially modifiable risk factors, it continues to be an area of active exploration for suicide rate reduction. While there are many different types of sleep disorders, including excessive daytime sleepiness, parasomnias, obstructive sleep apnea, and restless legs syndrome, this article will focus on the relationship between insomnia and nightmares with suicide.
 

Insomnia

Insomnia disorder, according to the American Psychiatric Association’s DSM-5, is a dissatisfaction of sleep quantity or quality that occurs at least three nights per week for a minimum of 3 months despite adequate opportunity for sleep. This may present as difficulty with falling asleep, staying asleep, or early morning awakenings. The sleep disturbance results in functional impairment or significant distress in at least one area of life (American Psychiatric Association. Arlington, Virginia: APA; 2013). While insomnia is often a symptom of many psychiatric disorders, research has shown that insomnia is an independent risk factor for suicide, even when controlling for mental illness. Studies have shown that there is up to a 2.4 relative risk of suicide death with insomnia after adjusting for depression severity (McCall W, et al. J Clin Sleep Med. 2013;32[9]:135).
 

Nightmares

Nightmares, as defined by the American Psychiatric Association’s DSM-5, are “typically lengthy, elaborate, story-like sequences of dream imagery that seem real and incite anxiety, fear, or other dysphoric emotions” (American Psychiatric Association. Arlington, Virginia: APA; 2013). They are common symptoms in posttraumatic stress disorder (PTSD), with up to 90% of individuals with PTSD experiencing nightmares following a traumatic event (Littlewood DL, et al. J Clin Sleep Med. 2016;12[3]:393). Nightmares have also been shown to be an independent risk factor for suicide when controlling for mental illness. Studies have shown that nightmares are associated with an elevated risk factor of 1.5 to 3 times for suicidal ideation and 3 to 4 times for suicide attempts. The data suggest that nightmares may be a stronger risk factor for suicide than insomnia (McCall W, et al. Curr Psychiatr Rep. 2013;15[9]:389).

Proposed Mechanism

The mechanism linking insomnia and nightmares with suicide has been theorized and studied by researchers. A couple of the most noteworthy proposed psychological mechanisms involve dysfunctional beliefs and attitudes about sleep, as well as deficits in problem solving capability. Dysfunctional beliefs and attitudes about sleep (DBAS) are negative cognitions pertaining to sleep, and they have been shown to be related to the intensity of suicidal ideations. Many of the DBAS are pessimistic thoughts that contain a “hopelessness flavor” to them, which lead to the perpetuation of insomnia. Hopelessness has been found to be a strong risk factor for suicide. In addition to DBAS, insomnia has also shown to lead to impairments in complex problem solving. The lack of problem solving skills in these patients may lead to fewer quantity and quality of solutions during stressful situations and leave suicide as the perceived best or only option.

The biological theories focus on serotonin and hyperarousal mediated by the hypothalamic-pituitary-adrenal (HPA) axis. Serotonin is a neurotransmitter that is involved in the induction and maintenance of sleep. Of interesting note, low levels of serotonin’s main metabolite, 5-hydroxyindoleacetic acid (5-HIAA) have been found in the cerebrospinal fluid of suicide victims. Evidence has also shown that sleep and the HPA axis are closely related. The HPA axis is activated by stress leading to a cascade of hormones that can cause susceptibility of hyperarousal, REM alterations, and suicide. Hyperarousal, shared in context with PTSD and insomnia, can lead to hyperactivation of the noradrenergic systems in the medial prefrontal cortex, which can lead to decrease in executive decision making (McCall W, et al. Curr Psychiatr Rep. 2013;15[9]:389).
 

Treatment Strategies

The benefit of treating insomnia and nightmares, in regards to reducing suicidality, continues to be an area of active research. Many of the previous studies have theorized that treating symptoms of insomnia and nightmares may indirectly reduce suicide. Pharmaceutical and nonpharmaceutical treatments are currently being used to help treat patients with insomnia and nightmares, but the benefit for reducing suicidality is still unknown.

According to the Centers for Disease Control and Prevention, suicide is the 10th leading cause of mortality in the United States, with rates of suicide rising over the past 2 decades. In 2016, completed suicides accounted for approximately 45,000 deaths in the United States (Ivey-Stephenson AZ, et al. MMWR Surveill Summ. 2017;66[18]:1). While progress has been made to lower mortality rates of other leading causes of death, very little progress has been made on reducing the rates of suicide. The term “suicide,” as referred to in this article, encompasses suicidal ideation, suicidal behavior, and suicide death.

Researchers have been investigating potential risk factors and prevention strategies for suicide. The relationship between suicide and sleep disturbances, specifically insomnia and nightmares, has been well documented in the literature. Given that insomnia and nightmares are potentially modifiable risk factors, it continues to be an area of active exploration for suicide rate reduction. While there are many different types of sleep disorders, including excessive daytime sleepiness, parasomnias, obstructive sleep apnea, and restless legs syndrome, this article will focus on the relationship between insomnia and nightmares with suicide.
 

Insomnia

Insomnia disorder, according to the American Psychiatric Association’s DSM-5, is a dissatisfaction of sleep quantity or quality that occurs at least three nights per week for a minimum of 3 months despite adequate opportunity for sleep. This may present as difficulty with falling asleep, staying asleep, or early morning awakenings. The sleep disturbance results in functional impairment or significant distress in at least one area of life (American Psychiatric Association. Arlington, Virginia: APA; 2013). While insomnia is often a symptom of many psychiatric disorders, research has shown that insomnia is an independent risk factor for suicide, even when controlling for mental illness. Studies have shown that there is up to a 2.4 relative risk of suicide death with insomnia after adjusting for depression severity (McCall W, et al. J Clin Sleep Med. 2013;32[9]:135).
 

Nightmares

Nightmares, as defined by the American Psychiatric Association’s DSM-5, are “typically lengthy, elaborate, story-like sequences of dream imagery that seem real and incite anxiety, fear, or other dysphoric emotions” (American Psychiatric Association. Arlington, Virginia: APA; 2013). They are common symptoms in posttraumatic stress disorder (PTSD), with up to 90% of individuals with PTSD experiencing nightmares following a traumatic event (Littlewood DL, et al. J Clin Sleep Med. 2016;12[3]:393). Nightmares have also been shown to be an independent risk factor for suicide when controlling for mental illness. Studies have shown that nightmares are associated with an elevated risk factor of 1.5 to 3 times for suicidal ideation and 3 to 4 times for suicide attempts. The data suggest that nightmares may be a stronger risk factor for suicide than insomnia (McCall W, et al. Curr Psychiatr Rep. 2013;15[9]:389).

Proposed Mechanism

The mechanism linking insomnia and nightmares with suicide has been theorized and studied by researchers. A couple of the most noteworthy proposed psychological mechanisms involve dysfunctional beliefs and attitudes about sleep, as well as deficits in problem solving capability. Dysfunctional beliefs and attitudes about sleep (DBAS) are negative cognitions pertaining to sleep, and they have been shown to be related to the intensity of suicidal ideations. Many of the DBAS are pessimistic thoughts that contain a “hopelessness flavor” to them, which lead to the perpetuation of insomnia. Hopelessness has been found to be a strong risk factor for suicide. In addition to DBAS, insomnia has also shown to lead to impairments in complex problem solving. The lack of problem solving skills in these patients may lead to fewer quantity and quality of solutions during stressful situations and leave suicide as the perceived best or only option.

The biological theories focus on serotonin and hyperarousal mediated by the hypothalamic-pituitary-adrenal (HPA) axis. Serotonin is a neurotransmitter that is involved in the induction and maintenance of sleep. Of interesting note, low levels of serotonin’s main metabolite, 5-hydroxyindoleacetic acid (5-HIAA) have been found in the cerebrospinal fluid of suicide victims. Evidence has also shown that sleep and the HPA axis are closely related. The HPA axis is activated by stress leading to a cascade of hormones that can cause susceptibility of hyperarousal, REM alterations, and suicide. Hyperarousal, shared in context with PTSD and insomnia, can lead to hyperactivation of the noradrenergic systems in the medial prefrontal cortex, which can lead to decrease in executive decision making (McCall W, et al. Curr Psychiatr Rep. 2013;15[9]:389).
 

Treatment Strategies

The benefit of treating insomnia and nightmares, in regards to reducing suicidality, continues to be an area of active research. Many of the previous studies have theorized that treating symptoms of insomnia and nightmares may indirectly reduce suicide. Pharmaceutical and nonpharmaceutical treatments are currently being used to help treat patients with insomnia and nightmares, but the benefit for reducing suicidality is still unknown.